Patrocina

Auspician
 FOTOS PRIMERA JORNADA DE
MEDICINA CARDIORESPIRATORIA
 DR. ALBERTO
MONTOYA
ESPAÑA

CHARLAS

1. Técnica y tips para una correcta auscultación

cardiopulmonar, aprendemos los sonidos principales

2. Enfoque diagnóstico y terapéutico de miocardiopatía

arritmogénica, el holter es imprescindible
3. ¿Es tan frecuente la hipertensión pulmonar como creemos?

4. Colapso traqueal, tratamiento médico y quirúrgico en perros

5. Neumonía una grave enfermedad respiratoria. Abordaje
clínico,diagnóstico y tratamiento

6. No todos los gatos que respiran mal tienen asma.

Como no equivocarnos

7. Sincopes cardiogénicos y su diagnóstico diferencial

8. Manejo de tos crónica en perros. Uso de broncodilatadores
 José Alberto Montoya-Alonso, DMV, MsC, MA,
Bi-PhD

Licenciado y Doctor en Veterinaria por la

Universidad Complutense de Madrid (UCM).
Doctor en Medicina por la Universidad de Las
Palmas de Gran Canaria (ULPGC).
Especialista universitario en Obesidad,
Especialista en bienestar animal y en salud
animal. Acreditado en Medicina interna y
cardiología en pequeños animales y Máster
Universitario en Innovación Educativa y
Evaluación de Programas Formativos por la
Universidad Nacional a Distancia (UNED)

Catedrático de medicina y cirugía animal del

Departamento de Patología Animal, donde ha
sido su director, en la Facultad de Veterinaria de
Las Palmas de Gran Canaria. Responsable del Servicio de Medicina
Veterinaria y del grupo de investigación de Clínica veterinaria e
investigación terapéutica del Instituto Universitario de Investigaciones
Biomédicas y Sanitarias de la ULPGC. Coordinador del Programa de
Doctorado de Investigación en Biomedicina. Académico electo de la Real
Academia de Ciencias Veterinarias de España (RACVE)

Ha sido presidente del grupo de Especialistas en cardiología y aparato

respiratorio (GECAR) de la Asociación Española de Especialistas en
Pequeños Animales (AVEPA), pertenece a la junta directiva de la
European Society of dirofilariosis and Angiostrongylosis. Pertenece a la
European Society of Veterinary Cardiology a la Academy of Veterinary
Cardiology y a la European Society of Veterinary and Comparative
Nutrition

Obtuvo el Eitan Bogin Prize de la International Society of Animal Clinical

Biochemistry (ISACB) en 2004. Es Premio a la Excelencia docente de la
Universidad de Las Palmas de Gran Canaria y fue Veterinario del año en
2007. Ha obtenido el I, II y III Premio laboratorios Boehringer de la
RACVE.

Ha dirigido 22 tesis doctorales y múltiples, suficiencias investigadoras

tesinas, trabajos fin de grado, y trabajos fin de master
Es profesor invitado de varias universidades extrajeras.
Ha participado como profesor y coordinador en más de 270 cursos, talleres,
seminarios, etc. de formación continuada y especialización para clínicos
veterinarios en España, Portugal y América.

Ha presentado más de 400 trabajos en congresos nacionales e

internacionales. Ha dirigido y participado en proyectos y contratos de
investigación suscritos con diferentes organismos públicos y privados en el
campo de la medicina veterinaria y humana.
Ha participado en la organización de más de 60 eventos científicos
Ha publicado más de 130 artículos científicos en revistas nacionales e
internacionales (en un 75% indexados) y editado, publicado y/o participado
en más de 20 libros.
Es miembro del comité científico y del comité editorial de más de 25
publicaciones biomédicas indexadas.
PROCEDURES PRO h CARDIOLOGY h PEER REVIEWED
The Basic
Cardiology
Examination
Wendy W. Mandese, DVM
Amara H. Estrada, DVM, DACVIM (Cardiology)
University of Florida
A thorough physical examination is valuable for diagnos-
ing heart disease and should include extensive examina-
tion of all body systems.
General Appearance
Weight loss is common in patients with advanced car-
diac disease. In one study, >50% of dogs with dilated
cardiomyopathy experienced cardiac cachexia (ie, loss
of lean body mass).1 Low body weight and failure to
grow normally can also be signs of congenital cardiac
disease in pediatric patients.
Ocular Examination
Enlarged retinal vessels, retinal hemorrhage, or retinal
detachment often indicates systemic hypertension,
which can be primary (ie, idiopathic) or secondary to
conditions such as renal or cardiac disease, hyperadre-
nocorticism, diabetes mellitus, pre-eclampsia, and
hyperthyroidism. In patients with inconclusive labora-
tory results, echocardiography can be used to identify
underlying heart conditions that cause hypertension
(eg, hypertrophic cardiomyopathy in cats, myxomatous
mitral valve disease and cardiac overload in dogs). Car-
diac changes secondary to hypertension include myxo-
matous mitral valve disease, left atrial enlargement, or
left ventricular hypertrophy.2
Oral Examination
Pale mucous membranes can indicate shock or anemia,
and hyperemic or injected mucous membranes can indi-
cate infection or polycythemia. Cyanosis occurs pri-
marily in patients with cardiac defects that result in
right-to-left shunting, such as reverse patent ductus
arteriosus, atrial septal defect, and ventricular septal
defect. Other health conditions, such as severe hypo-
thermia or severe respiratory disease, can also cause
cyanosis. In differential cyanosis, the lower extremities
and vulva/prepuce appear cyanotic but the upper
extremities and oral mucous membranes are pink and
well oxygenated.3
Several congenital cardiac defects are associated with dif-
ferential cyanosis, but it is most commonly seen with a
reverse patent ductus arteriosus. Periodontal disease
May 2017 cliniciansbrief.com 91
PROCEDURES PRO h CARDIOLOGY h PEER REVIEWED
should be assessed and noted, as secondary
cardiac complications (eg, endocarditis) are
possible if severe periodontal disease is not
addressed.4
Tracheal Palpation
Tracheal palpation should be performed on
all coughing dogs. Small-breed dogs more
prone to myxomatous mitral valve disease
are also more prone to a collapsing trachea.
In both of these conditions, cough can occur
during exercise or excitement5 and may be
caused by tracheal disease, even if a murmur
is present. Coughing can be heard with
tracheitis or tracheobronchitis and can be
caused by bacterial or viral infection or
environmental allergens.
Respiratory Rate/Effort
Respiration should be evaluated when the
patient is calm. Clients can be trained to take
respiratory rates at home, especially while the
patient is sleeping. Several phone apps are
available to make it easy for clients to obtain
accurate readings. One study suggested that
most dogs and cats without cardiac disease or
with well controlled heart disease will have a
resting respiratory rate of <30 breaths/min at
home.6 Increased respiratory effort can indi-
cate upper airway disease (effort occurs
during inspiration) or lower airway disease
(effort occurs during expiration).
Lung Sounds
Abnormal lung sounds are most common in
patients with primary respiratory disease.
Lung sounds also may be abnormal in patients
with secondary respiratory conditions such as
pulmonary edema and pleural effusion. Aus-
cultation of the lungs is not a sensitive means
of detecting pulmonary edema or pleural effu-
sion in dogs and cats, and many patients have
pulmonary edema with no auscultatory abnor-
malities other than increased bronchovesicu-
lar sounds.7 Patients with severe pulmonary
edema resulting in free fluid in the airways are
92 cliniciansbrief.com May 2017
more likely to have audible crackles; crackles
can also be auscultated in patients with pul-
monary hypertension, bronchitis, and pneu-
monia. Muffled lung sounds can indicate
pleural effusion. Wheezes are associated with
allergic airway disease, bronchitis, and col-
lapsing trachea.
Heart Rate
Stress and anxiety associated with the veteri-
nary environment can markedly increase a
patient’s heart rate. Waiting for a patient’s ini-
tial arrival excitement to subside and asking
the client to be present during examination
can help the clinician obtain a normal heart
rate. The client can also be asked to obtain the
patient’s resting heart rate at home. If an
arrhythmia is present, the type (eg, tachyar-
rhythmia, bradyarrhythmia) should be noted
and the nature characterized.
Pulse
Pulse pressure can be decreased or increased
or have an altered configuration. Decreased
pulse pressure may be seen in patients with
dilated cardiomyopathy, aortic or pulmonic
stenosis, heart failure, hypovolemia, or
shock. Increased pulse pressure can occur
because of excitement and/or pain or hyper-
trophic cardiomyopathy.8 Dogs with aortic
regurgitation commonly have a bounding
pulse. Bounding pulses can also be felt in
patients with patent ductus arteriosus,
severe bradycardia, hyperthyroidism, fever,
or anemia.
Alterations in pulse conformation also may
occur. Dogs with severe subaortic stenosis
can have a weak pulse or a pulse pressure
that increases more slowly and peaks later
during systole (ie, pulsus parvus et tardus).
Conversely, dogs with mitral regurgitation
commonly have a brisk pulse that rises more
rapidly in systole and lasts a shorter time.
Other pulse abnormalities include pulsus par-
adoxus and pulse deficits. Pulsus paradoxus is
an increase in pulse pressure on expiration
and a decrease on inspiration. This occurs
normally but is exaggerated in cardiac tam-
ponade. Pulse deficits can occur with cardiac
tachyarrhythmias in which beats occur so
rapidly that the ventricle does not have time
to fill with an adequate amount of blood
before ejection (eg, fast atrial fibrillation,
ventricular premature beats).7 Pulse should
always be monitored while performing car-
diac auscultation to detect pulse deficits.
Blood Pressure
Obtaining a systolic blood pressure using a
Doppler is a relatively simple procedure. To
obtain the most accurate reading, blood pres-
sure should be measured in a quiet, calm envi-
ronment with the client present, if possible.
Proper technique, including appropriate cuff
width (ie, 40% of the circumference of the
limb or tail) is integral to obtaining an accu-
rate measurement. A minimum of 3 measure-
ments should be obtained, and the variability
between measurements should be <20%.9
Heart Sounds
The first heart sound (S1) is produced by clos-
ing of the mitral and tricuspid valves. S1 is
loudest over the mitral valve area and is
louder, longer, and lower pitched than the
second heart sound (S2). S2 is produced by
closing of the pulmonic and aortic valves.
S2 is shorter and higher pitched than S1.
The third heart sound (S3) is not usually heard
during auscultation of healthy small animals,
and its presence indicates myocardial failure.
The sound is generated during the period of
rapid filling in early diastole when the ventri-
cles suddenly resist expansion.
The fourth heart sound (S4) originates from the
vibration generated by cardiac structures when
the atria contract. It can be a normal finding in
giant-breed dogs and large animals or be asso-
ciated with advanced hypertrophic cardiomy-
opathy. The presence of an S3 or S4 is referred
to as a diastolic gallop. When a diastolic gallop
is present, further evaluation is warranted.
Systolic clicks are found in dogs with chronic
valvular disease and originate from vibra-
tions that occur when chordae tendineae and
the mitral leaflets suddenly resist further
stretching and protrude into the left atrium.10
Muffled heart sounds may indicate the pres-
ence of pericardial or pleural effusion.
Arrhythmias
Sinus arrhythmia is common in dogs, espe-
cially in patients who are relaxed and have a
lower heart rate. The heart rhythm is faster
on inspiration and slower on expiration.
When the patient becomes more excited or
active, the sinus arrhythmia is often no lon-
ger heard. Sinus arrhythmia does not always
correspond to respiration and can occur with
other causes of increased vagal tone (eg, GI
disease).11 Pulses should be palpated in con-
junction with auscultation to determine if
pulse deficits are present. Sinus arrhythmia
was previously thought to be uncommon in
cats, but a 2009 study determined that
relaxed cats in their home environment can
have frequent sinus arrhythmia.12
Common abnormal rhythms include:
h Premature beats with pulse deficits: Asso-
ciated with atrial and ventricular prema-
ture complexes. Can occur in bursts or be
sustained
h Irregularly irregular rhythm: Associated
with atrial fibrillation. Has been described
as “shoes in a dryer”
h Slow arrhythmia with intermittent
pauses: Heard in patients with AV block or
sinus arrhythmia
h Persistent tachycardia or persistent bra-
dycardia: Clients should be informed that
an abnormality in heart rate and/or rhythm
requires additional testing to determine
the cause.
May 2017 cliniciansbrief.com 93
PROCEDURES PRO h CARDIOLOGY h PEER REVIEWED
h Murmurs: Caused by turbulence disturbing
the normal laminar flow of blood, which
most often is caused by dysfunctional valves
or septal defects. Can also have physiologic
causes because of patient size, athletic abil-
ity, or underlying noncardiac disease pro-
cesses (eg, fever, anemia)13
Characterization of murmurs is based on
several criteria:
h Timing in the cycle: A systolic murmur
occurs between S1 and S2 and is common in
small animals. A diastolic murmur occurs
between S2 of one beat and S1 of the follow-
ing beat and is uncommon in small ani-
mals. A continuous murmur can be heard
throughout the cardiac cycle (Table 1).
h Location: Location or point of maximal
intensity (PMI) refers to the valve area at
which the murmur is heard loudest. Recog-
nition of the PMI can help identify the spe-
cific cardiac abnormality (Table 2; Figures
1-5, page 96).
TABLE 1
COMMON PATHOLOGIC CAUSES
OF MURMURS BASED ON TIMING7
Murmur Type Pathologic Cause
Systolic murmur Atrioventricular valve regurgitation
Left-to-right shunt
Increased flow (hyperthyroidism)
Aortic or pulmonic stenosis
Ventricular septal defect/atrial septal defect
(often not audible)
Diastolic murmur Aortic regurgitation
Pulmonary regurgitation
Mitral stenosis
Endocarditis
Continuous murmur Patent ductus arteriosus
94 cliniciansbrief.com May 2017
h Intensity
• Murmurs are graded on a scale of 1 to 6.
This scale can be subjective and may vary
between observers.
– Grade 1/6: Softest murmur audible. May
only be heard in a quiet room after listen-
ing for several minutes. May not be audi-
ble to all observers, and may be transient
– Grade 2/6: Soft but more easily heard.
Often focal over one valve only
– Grade 3/6: Prominent and easily heard.
May radiate to other areas
– Grade 4/6: Loud and radiates widely. Not
accompanied by a palpable thrill
– Grade 5/6: Loud and accompanied by a
palpable thrill
– Grade 6/6: Loud, accompanied by a pal-
pable thrill, and can be heard with the
stethoscope barely touching the thorax
• Innocent murmurs are soft, systolic,
heard best at the mitral or aortic valves,
and often low-grade (grade 1). They do not
radiate. They are often auscultated in
young puppies and kittens and usually
disappear by 3 to 4 months of age.
• Physiologic murmurs are soft and usually
of low intensity (grade 1-2). PMI is at the
heart base in the area of the outflow tracts
(aortic and pulmonic area). These murmurs
typically resolve with resolution of the
underlying disease. They may also be heard
in otherwise healthy animals that are deep
chested and/or athletic. They do not indi-
cate any underlying cardiac disorder that
can be identified by chest radiography or
echocardiography and are common in ani-
mals with anemia and occurs as a result of
changes in blood viscosity.
h Character: Most murmurs have character-
istic sounds on auscultation:7
• Harsh or regurgitant: Mimicked by placing
the back of the tongue close to the roof of
the mouth and blowing out forcefully. Heard
in patients with ventricular septal defects
and atrioventricular valve insufficiency
• Blowing: Mimicked by blowing air with
 TABLE 2

LOCALIZATION OF MURMURS IN COMMON CARDIAC LESIONS7

Condition Left Base Right Base Left Apex Right Apex Right Sternum

Mitral regurgitation Systolic PMI (+/- Systolic referred)

Tricuspid regurgitation Systolic PMI

Aortic regurgitation Diastolic PMI +/- Diastolic (Diastolic referred)

Aortic stenosis Systolic PMI +/- Systolic +/- Systolic

Pulmonic stenosis Systolic PMI

Ventricular septal defect +/- Systolic (often not heard) Systolic PMI

Atrial septal defect +/- Systolic (often not heard)

Tetralogy of Fallot Systolic PMI +/- Systolic

Patent ductus arteriosus Continuous PMI

moderate force through slightly parted
lips. Often heard in patients with aortic or
pulmonic insufficiency
• Machinery: Sounds like the wind blowing
through a tunnel. Most often heard in
patients with patent ductus arteriosus
• Systolic clicks: High frequency sounds
heard over the left apex that may indicate
mitral valve disease
• Crescendo-decrescendo: An ejection mur-
mur most common in patients with atrial
septal defects and aortic or pulmonic
stenosis
Heart murmurs are present in approximately
one-third of apparently healthy adult cats.14-16
The intensity of these murmurs can vary with
Visit cliniciansbrief.com/cardiac-library to
hear a collection of heart sounds associated
with clinical diagnoses.
sympathetic tone and usually increases as
heart rate increases. The murmur can disap-
pear entirely when sympathetic stimulation
abates and heart rate slows. A murmur may
be audible on initial auscultation and may
soften or disappear as the patient relaxes
during the examination.
Hypertrophic cardiomyopathy and systolic
anterior motion of the mitral valve are the
most common diagnoses in cats with mur-
murs caused by heart disease.14-16 Because
benign murmurs and murmurs caused by car-
diac disease are dynamic and audibly indis-
tinguishable, further evaluation is warranted
when a murmur is detected.17
Abdominal Palpation
Ascites and/or liver enlargement may be
present in patients with right-sided heart PMI = point of
maximal intensity
failure.

May 2017 cliniciansbrief.com 95

PROCEDURES PRO h CARDIOLOGY h PEER REVIEWED

STEP-BY-STEP
CARDIAC AUSCULTATION

Cardiac auscultation is best performed in a quiet

room with a standing patient. In anxious dogs, pant-
ing sounds can be mistaken for murmurs. Manually
close the dog’s mouth for a short time during auscul-
tation and give panting breaks as needed. Purring in
cats can also be mistaken for a murmur. Distract the
cat with a toy or change the position or location of
the patient to stop purring.

STEP 1
Place the stethoscope over the left cardiac apex
d FIGURE 3 Postmortem photograph of the right side of
(location of ventricles) and base (location of pul-
the heart in the thoracic cavity. A = aortic valve, RA = right
monary and aortic outflow tracts), right cardiac atrium, RV = right ventricle, T = tricuspid valve. Photo courtesy
apex and base, the length of the sternum, and the of Dr. Lisa Farrina, University of Florida College of Veterinary
thoracic inlet. Medicine Department of Pathology

d FIGURE 1 Position of cardiac apex and base in a left canine d FIGURE 4 Canine left thorax. A = aortic valve, LA = left atrium,
thorax. Illustrations by Ally Mandese and used with permission LV = left ventricle, M = mitral valve, P = pulmonic valve

d FIGURE 2 Canine right thorax. A = aortic valve, RA = right d FIGURE 5 Postmortem photograph of the left side of the
atrium, RV = right ventricle, T = tricuspid valve heart in the thoracic cavity. A = aortic valve, LA = left atrium,
M = mitral valve, P = pulmonic valve

96 cliniciansbrief.com May 2017

STEP 2 Conclusion
Cardiac abnormalities can be identified
Auscultate each heart valve at its PMI (Table 3). during a basic cardiac examination that
includes obtaining a complete history and
TABLE 3 performing a thorough physical examination
and simple diagnostics. Creating a list of dif-
STETHOSCOPE PLACEMENT ferential diagnoses based on the information
FOR CARDIAC EXAMINATION gathered during the cardiac examination can
help the clinician make informed decisions
about the appropriate next diagnostic or
Valve Point of Maximal Intensity therapeutic step. n

Mitral Left 5th intercostal space at costochondral junction

Tricuspid Between right intercostal spaces 3-5 just above

costochondral junction

Pulmonic Between left intercostal spaces 2-4 just above sternum PMI = point of maximal intensity

Aortic Within left intercostal space 4-5 just above costrochondral

junction See page 98 for references.

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PROCEDURES PRO h CARDIOLOGY h CONTINUED FROM PAGE 97
References
1. Freeman LM, Rush JE, Kehayias JJ, et al. Nutrition alterations
and the effect of fish oil supplementation in dogs with heart
failure. J Vet Intern Med. 1998;12(6):440-448.
2. Davies C, Shell L. Systemic hypertension. In: Davies C,
Shell L, eds. Common Small Animal Medical Diagnoses: An
Algorithmic Approach. Saunders; 2002. Accessed on Veterinary
Information Network, April 18, 2017.
3. Kittleson MD. Diagnosis. In: Kittleson MD, Kienle RD, eds. Small
Animal Cardiovascular Medicine. Maryland Heights, MO: Mosby
Elsevier; 2005. Accessed on Veterinary Information Network,
April 18, 2017.
4. Glickman LT, Glickman NW, Moore GE, Goldstein GS, Lewis HB.
Evaluation of the risk of endocarditis and other cardiovascular
events on the basis of the severity of periodontal disease in
dogs. J Am Vet Med Assoc. 2009;234(4):486-494.
5. Tappin SW. Canine tracheal collapse. J Small Anim Pract.
2016;57(1):9-17.
6. Porciello F, Rishniw M, Ljungvall I, Ferasin L, Haggstrom J,
Ohad DG. Sleeping and resting respiratory rates in dogs and
cats with medically-controlled left-sided congestive heart
failure. Vet J. 2016;207:164-168.
7. Kittleson MD, Kienle RD. Physical exam. In: Kittleson MD,
Kienle RD, eds. Small Animal Cardiovascular Medicine.
Maryland Heights, MO: Mosby Elsevier; 2005. Accessed on
Veterinary Information Network, April 18, 2017.
8. Ware WA. Clinical manifestations of cardiac disease. In: Nelson
RW, Couto CG, eds. Small Animal Internal Medicine. 5th ed. St.
Louis, MO: Elsevier; 2014:6.
9. Ferasin L. How to measure blood pressure. Presented at:
British Small Animal Veterinary Congress; 2011. Accessed on
Veterinary Information Network, April 18, 2017.
TALKING POINTS h CONTINUED FROM PAGE 85
References
1. Freeman LM, Chandler ML, Hamper BA, Weeth LP. Current
knowledge about the risks and benefits of raw meat-based
diets for dogs and cats. J Vet Intern Med. 2013;243(11):1549-
1558.
2. Weese JS. Worms & Germs Blog. http://www.
wormsandgermsblog.com
3. Chengappa MM, Staats J, Oberst RD, Gabbert NH, McVey S.
Prevalence of Salmonella in raw meat used in diets of racing
greyhounds. J Vet Diagn Invest. 1993;5(3):372-377.
4. Joff DJ, Schlesinger DP. Preliminary assessment of the risk of
Salmonella infection in dogs fed raw chicken diets. Can Vet J.
2002;43(6):441-442.
5. Finley R, Reid-Smith R, Ribble C, Popa M, Vandermeer M,
Aramini J. The occurrence and antimicrobial susceptibility of
salmonellae isolated from commercially available canine raw
food diets in three Canadian cities. Zoonoses Public Health.
2008;55(8-10):462-469.
6. Nemser SM, Doran T, Grabenstein M, et al. Investigation of
Listeria, Salmonella, and Toxigenic Escherichia coli in various
pet foods. Foodborne Pathog Dis. 2014;11(9):706-709.
7. Strohmeyer RA, Morley PS, Hyatt DR, Dargatz DA, Scorza
AV, Lappin MR. Evaluation of bacterial and protozoal
contamination of commercially available raw meat diets for
dogs. J Am Vet Med Assoc. 2006;228(4):537-542.
8. Weese JS, Rousseau J, Arroyo L. Bacteriological evaluation
of commercial canine and feline raw diets. Can Vet J.
2005;46(6):513-516.
9. Bojanić K, Midwinter AC, Marshall JC, Rogers LE, Biggs PJ,
Acke E. Isolation of Campylobacter spp. from client-owned
98 cliniciansbrief.com May 2017
10. Kvart C, Häggström. Heart sounds and murmurs in dogs
and cats. In: Kvart C, Häggström J. Cardiac Auscultation &
Phonocardiography in Dogs, Horses and Cats; 2002. Accessed
on Veterinary Information Network, April 18, 2017.
11. Kittleson MD. Specific arrhythmias. In: Kittleson MD, Kienle RD,
eds. Small Animal Cardiovascular Medicine. Maryland Heights,
MO: Mosby Elsevier; 2005. Accessed on Veterinary Information
Network, April 18, 2017.
12. Hanås S, Tidholm A, Egenvall A, Holst BS. Twenty-four hour
Holter monitoring of unsedated healthy cats in the home
environment. J Vet Cardiol. 2009;11(1):17-22.
13. Kvart C, Häggström J. Heart sounds and murmurs in dogs and
cats: physiological flow murmurs. In: Kvart C, Häggström J.
Cardiac Auscultation & Phonocardiography in Dogs, Horses and
Cats; 2002. Accessed on Veterinary Information Network, April
18, 2017.
14. Paige CF, Abbott JA, Elvinger F, Pyle RL. Prevalence of
cardiomyopathy in apparently healthy cats. J Am Vet Med
Assoc. 2009;234(11):1398-1403.
15. Wagner T, Fuentes VL, Payne JR, McDermott N, Brodbelt D.
Comparison of auscultatory and echocardiographic findings
in healthy adult cats. J Vet Cardiol. 2010;12(3):171-182.
16. Nakumura RK, Rishniw M, King MK, Sammarco CD. Prevalence
of echocardiographic evidence of cardiac disease in
apparently healthy cats with murmurs. J Feline Med Surg.
2011;13(4):266-271.
17. Côté E, Manning AM, Emerson D, Laste NJ, Malakoff RL,
Harpster NK. Assessment of the prevalence of heart murmurs
in overtly healthy cats. J Am Vet Med Assoc. 2004;225(3):384-
388.
dogs and cats, and retail raw meat pet food in the Manawatu,
New Zealand. Zoonoses Public Health. 2016. doi: 10.1111/
zph.12323
10. Stiver L, Frazier KS, Mauel MJ, Styer EL. Septicemic
salmonellosis in two cats fed a raw meat diet. J Am Anim
Hosp Assoc. 2003;39(6):538-542.
11. Morley PS, Strohmeyer RA, Tankson JD, et al. Evaluation of
the association between feeding raw meat and Salmonella
enterica infections at a Greyhound breeding facility. J Am Vet
Med Assoc. 2006;228(10):1524-1532.
12. Centers for Disease Control and Prevention. Human
salmonellosis associated with animal-derived pet treats—
United States and Canada, 2005. MMWR Morb Mortal Wkly
Rep. 2006;55(25):702-705.
13. Finley R, Reid-Smith R, Weese JS. Human health implications
of Salmonella-contaminated natural pet treats and raw pet
food. Clin Infect Dis. 2006;42(5):686-691.
14. Pitout JD, Reisbig MD, Mulvey M, et al. Association between
handling of pet treats and infection with Salmonella enterica
serotype newport expressing the AmpC beta-lactamase,
CMY-2. J Clin Microbiol. 2003;41(10):4578-4582.
15. Cavallo SJ, Daly ER, Seiferth J, et al. Human outbreak
of Salmonella typhimurium associated with exposure to
locally made chicken jerky pet treats, New Hampshire, 2013.
Foodborne Pathog Dis. 2015;12(5):441-446.
16. Fauth E, Freeman LM, Cornjeo L, Markovich JE, Janecko N,
Weese JS. Salmonella bacteriuria in a cat fed a Salmonella-
contaminated diet. J Am Vet Med Assoc. 2015;247(5):525-530.
 CARDIOMIOPATÍA ARRITMOGÉNICA DEL BÓXER

Laín García y J. Alberto Montoya-Alonso

Facultad de Veterinaria

Universidad de Las Palmas de Gran Canaria

ESPAÑA

 Premio al mejor artículo científico divulgativo veterinario del año

2016, que concede la Real Academia de Ciencias Veterinarias de
España (RACVE) perteneciente al Instituto de España.

Resumen:

El objetivo de este artículo es dar a conocer una cardiomiopatía

relativamente habitual en los perros de raza Bóxer llamada cardiomiopatía
arritmogénica del ventrículo derecho. Se trata de una enfermedad hereditaria
asociada a una serie de mutaciones genéticas que provocan un proceso
degenerativo del miocardio con infiltración fibro-adiposa principalmente en el
ventrículo derecho. Es una enfermedad de tipo eléctrico por lo que, en fases
iniciales no se detectan alteraciones en la radiografía o la ecocardiografía. El
signo clínico más habitual es la presencia de síncopes e intolerancia al
ejercicio, aunque a veces el primer síntoma puede ser una muerte súbita. Se
diagnostica a partir de antecedentes familiares, signos clínicos, alteraciones
en el electrocardiograma y/o registro Holter (complejos ventriculares
prematuros (CVP) derechos), tests genéticos y/o biopsia del miocardio. Esta
última normalmente se realiza post mortem. El fármaco de elección para
reducir el número de CVP es el sotalol. La reducción en el número de
arritmias no implica una reducción del riesgo de muerte súbita. El pronóstico
es más favorable en pacientes jóvenes que no presenten síncopes.

Introducción
1
La cardiomiopatía arritmogénica del Bóxer (en inglés arrhythmogenic right
ventricular cardiomyopathy, ARVC) es una miopatía primaria hereditaria que
afecta principalmente al ventrículo derecho. Consiste en un proceso
degenerativo del miocardio donde se produce una infiltración fibroadiposa y
una atrofia de los miocitos. Esta miopatía predispone a la aparición de
arritmias, muerte súbita, fallo congestivo derecho, etc…Varios estudios han
demostrado que esta patología es muy similar a la cardiomiopatía
arritmogénica ventricular derecha de humanos.

Tanto las arritmias como otras alteraciones electrolíticas pueden detectarse

incluso antes de que aparezcan alteraciones histológicas o disfunción
ventricular. La progresión de la enfermedad no sigue un proceso continuo
sino que se alternan periodos de estabilidad con periodos donde aparecen
arritmias de forma más recurrente. En medicina humana se ha constatado
que ciertos factores ambientales como el ejercicio intenso o procesos que
cursan con inflamación pueden predisponer a la progresión de la
enfermedad. En fases avanzadas, la cardiomiopatía del ventrículo derecho o
la progresión de la afectación hacia el ventrículo izquierdo pueden provocar
la presencia de fallo cardíaco derecho o biventricular. Suele detectarse más
habitualmente en pacientes jóvenes y atletas, los cuales pueden sufrir
muerte súbita asociada a fibrilación ventricular. Se sospecha que estagrave
arritmia puede estar relacionada con apoptosis aguda e inflamación reactiva
de los miocitos.

La cardiomiopatía arritmogénica del Bóxer es una enfermedad hereditaria

genética de transmisión autosómica dominante que se manifiesta en edad
adulta. En humana se ha constatado que existen más de 1400 variantes en
12 genes relacionados con esta cardiomiopatía. De éstas, solamente 411
variantes se han confirmado como patológicas siendo la significancia del
resto todavía desconocida.

Presentación clínica y diagnóstico

2
La presentación clínica de esta patología se puede clasificar en tres posibles
categorías en cuanto al cuadro clínico:

1, perros asintomáticos con arritmias ventriculares ocasionales;

2, perros con taquiarritmias, síncopes e intolerancia al ejercicio;

3, perros con disfunción sistólica miocárdica, insuficiencia cardíaca

congestiva y evidencia de dilatación ventricular izquierda; esta tercera
categoría presenta una incidencia mucho menor respecto a las anteriores.

El motivo principal de visita son los episodios sincopales. El examen físico

suele ser normal, aunque en ocasiones el primer signo clínico es la muerte
súbita del animal. Se pueden auscultar arritmias, y en los pacientes con fallo
sistólico detectarse soplos de regurgitación mitral y tricúspide, edema
pulmonar, taquipnea, crepitaciones pulmonares, ascitis y pulso yugular
positivo.

Recientemente se han desarrollado tests genéticos de diagnóstico que son

capaces de identificar algunas variantes de alteraciones genéticas asociadas
a la patología (http://www.ncstatevets.org/genetics/boxerarvc/). De todos
modos, normalmente el diagnóstico se realiza a partir de la combinación de
varios factores como los antecedentes familiares, la presencia de síncopes o
intolerancia al ejercicio, la detección de extrasístoles ventriculares o
taquicardia ventricular principalmente de morfología derecha, y sobre todo a
partir del estudio anatomopatológico del miocardio.

En la mayoría depacientes afectados el examen físico es completamente

normal. En ocasiones se puede auscultar la presencia de latidos prematuros.
En caso de auscultar un soplo hay que tener en cuenta que los perros de
raza Bóxer pueden presentar soplos fisiológicos debido a su anatomía
cardíaca, o bien estar asociados a una estenosis aórtica. Los pacientes con
ARVC no suelen presentar soplos excepto en la forma donde existe
disfunción sistólica.

Las radiografías suelen ser normales excepto si existe fallo sistólico con
insuficiencia cardíaca congestiva. Normalmente no se aprecian alteraciones

3
estructurales o hemodinámicamente significativas en la ecocardiografía, no
obstante, en algunos casos, se puede detectar dilatación y cierto grado de
disfunción ventricular derecha. En los pacientes de categoría 3 puede haber
también fallo sistólico ventricular izquierdo (dilatación ventricular, fracción de
acortamiento disminuida, etc…) y fallo cardíaco congestivo.

En el electrocardiograma (ECG) suelen aparecer complejos ventriculares

prematuros (CVP) derechos (morfología similar a los bloqueos de rama
izquierda) en las derivaciones I, II y III. Las arritmias se pueden clasificar en
4 grados según su gravedad:

1, CVP simples aislados (ver Figura 1);

2, Bigeminismo, trigeminismo o ambos;

3, parejas ventriculares, tripletes o ambos;

4, fenómeno de R en T, taquicardia ventricular o ambos (ver Figura 2).

Figura 1. Electrocardiograma con un complejo ventricular prematuro derecho

aislado.

4
Figura 2. Taquicardia ventricular paroxística derecha.

De todos modos, el ECG tiene ciertas limitaciones a la hora de detectar

arritmias ya que a menudo se presentan de forma intermitente a lo largo del
día y por lo tanto esta prueba complementaria de diagnóstico solamente
permite analizar un breve período de tiempo de pocos minutos. Por lo tanto
el ECG presenta una buena especificidad pero una baja sensibilidad.

La presencia de CVP en el ECG es motivo suficiente para recomendar el

estudio mediante registro Holter de 24 horas. El registro Holter es el método
de elección para detectar arritmias de naturaleza intermitente ya que permite
periodos de evaluación mucho más largos y en un entorno habitual para el
paciente, sin el estrés que puede padecer cuando acuden a la consulta (ver
Figura 3).

5
Figura 3. Bóxer tras la colocación del dispositivo Holter.

Algunos criadores utilizan esta prueba para realizar un screening de sus

animales y detectar pacientes enfermos asintomáticos. Se han descrito
diferentes sistemas de gradación en cuanto a la gravedad de la enfermedad
en función del recuento de CVP (ver Tabla 1) (ver Figura 4).

6
Figura 4. Registro Holter. Presencia de complejos ventriculares.

Análisis del registro Holter según el recuento de complejos ventriculares

prematuros y episodios de taquicardia ventricular

Holter clase 1 <1000 CVPs simples/24h

Holter clase 2 >1000 CVPs simples /24h
Holter clase 3 <1000 CVPs simples /24h, parejas, tripletes, TV
Holter clase 4 >1000 CVPs simples /24h, parejas, tripletes, TV
TV clase I <200 TV en 24 horas
TV clase II >200 TV en 24 horas
CVP clase A <10000 CVPs en 24 horas
CVP clase B >10000 CVPs en 24 horas

CVPs, complejos ventriculares prematuros; TV, taquicardia ventricular

Tabla 1. Clasificaciones a partir del registro Holter para Bóxers con cardiomiopatía
arritmogénica.

Es importante destacar que, en ocasiones, el registro Holter en un paciente

con ARVC puede no ser concluyente ya que en un estudio realizado con
Bóxer se vio que diariamente existe una variabilidad de hasta el 83% en el
número de CVP que se generan. En tal situación se puede realizar un
segundo estudio Holter o bien antes descartar otras posibles causas de
síncope.

A nivel macroscópico la mayoría de los pacientes presentan un corazón de

aspecto normal, aunque a veces se puede detectar dilatación del ventrículo
derecho o incluso del izquierdo.

7
Estudios realizados a nivel microscópico han determinado que en los Bóxer
afectados existe una importante pérdida de la estructura miocítica del
ventrículo derecho debido a la presencia de infiltrados adiposos o fibro-
adiposos (ver Figura 5). Estos infiltrados también se han detectado en ambos
atrios y en el ventrículo izquierdo. La cantidad de infiltrados en el ventrículo
derecho resultó significativamente mucho mayor en pacientes afectados en
comparación con el grupo control.

Figura 5. Histopatología. Detalle de infiltrados adiposos en ventrículo derecho.

En algunos pacientes afectados se han identificado zonas de miocarditis con

infiltrados linfocíticos multifocales, así como evidencias histológicas de
apoptosis en los miocitos del ventrículo derecho. Algunos investigadores
consideran que los patrones adiposo y fibroadiposo constituyen una
situación clínica evolutiva de la enfermedad mediada por la presencia de
miocarditis, la cual en una fase inicial (forma adiposa) provoca un daño a
nivel miocítico que evoluciona al segundo estadio de la enfermedad (forma
fibroadiposa) debido al efecto reparador sobre el daño ocasionado.

En cuanto a la utilización de marcadores de daño miocárdico se ha visto que

existen niveles elevados de troponina cardiaca I (cTnI) sérica en Bóxer con
ARVC. Se cree que la elevación de los niveles séricos de cTnI se debe a la

8
miocitolisis, atrofia miocárdica y degeneración de las fibras musculares que
presentan los perros afectados. Otros estudios demuestran que la
concentración del marcador péptido natriurético cerebral (BNP) no puede
utilizarse como indicador de ARVC en Bóxer ya que no existe una diferencia
significativa entre animales enfermos y sanos.

Tratamiento

La mayoría de perros afectados no desarrollan disfunción sistólica ni fallo

cardiaco por lo que el tratamiento consiste básicamente en utilizar
antiarrítmicos ventriculares. En pacientes asintomáticos se debe iniciar el
tratamiento deforma inmediata si aparecen más de 1000 CVP en 24 horas, si
hay episodios de taquicardia ventricular, o si se detecta el fenómeno de R en
T. Los pacientes con síncopes o intolerancia al ejercicio idealmente deberían
empezar a medicarse tras haber realizado el registro Holter de 24 horas. En
algunos casos, si los síncopes son frecuentes o se detecta taquicardia
ventricular en el ECG es preferible iniciar el tratamiento lo antes posible.

El objetivo del tratamiento consiste en controlar la frecuencia de aparición de

arritmias malignas y prevenir el riesgo de muerte súbita. Se han descrito
diferentes protocolos antiarrítmicos en perros con ARVC, así como la
implantación de desfibriladores cardio-versores.

Tanto en medicina humana como en veterinaria el antiarrítmico de elección

en pacientes con cardiomiopatía aritmogénica del ventrículo derecho es el
sotalol. Se trata de un beta-bloqueante no selectivo de clase III que es muy
eficaz en la reducción del recuento de arritmias y no suele generar un efecto
pro-arrítmico. La administración de sotalol (1.5-3.5 mg/kg/12h) o bien la
combinación de mexiletina (5-8 mg/kg/8h) junto a atenolol (0.3-0.6
mg/kg/12h) son las pautas terapéuticas más eficaces. Tras 2-3 semanas de
tratamiento se debe realizar un segundo Holter para valorar la eficacia del
fármaco y descartar un efecto proarrítmico del mismo. Se considera que la
medicación está ejerciendo un efecto terapéutico si se observa una
reducción del 85% como mínimo en el número de CVP.También se ha

9
demostrado la eficacia de los ácidos grasos omega-3 presentes en aceites
de pescado como tratamiento para reducir el recuento de arritmias
ventriculares en Bóxer con cardiomiopatía arritmogénica.

Pronóstico

Ningún tratamiento probado es capaz de reducir la incidencia de síncopes ni

el riesgo de muerte súbita. Así mismo, en un estudio retrospectivo realizado
con una población de 62 Bóxer se vio que no había diferencias
estadísticamente significativas según el tratamiento farmacológico
administrado.

En cuanto al pronóstico algunos perros fallecen a consecuencia de una

arritmia grave sin mostrar signos clínicos previamente. Por lo tanto, la
ausencia de signos clínicos no significa que no exista riesgo de muerte
súbita. Mientras algunos pacientes con un número anormal de ectopias
nunca desarrollarán signos clínicos, otros con el mismo grado de afectación
pueden progresar y desarrollar arritmias más graves. En cuanto al tiempo
medio de supervivencia, es superior en perros jóvenes (p<0,001), y en
pacientes sin síncopes (p=0,012) [365 días en Bóxer con síncopes versus
693 días en Bóxer sin síncopes]. Además, la probabilidad de fallecer antes
de un año a partir del momento de diagnóstico es 4,8 veces superior en
perros con síncopes. Por lo tanto, el mejor pronóstico es para pacientes
jóvenes sin presencia de síncopes.

Referencias bibliográficas

1. Avramides D, Protonotarios N, Asimaki A, et al. Arrhythmogenic Right

Ventricular Cardiomyopathy/Dysplasia. Hellenic J Cardiology (2011) 52,
452-461.

10
2. Basso C, Fox PR, Meurs KM, et al. Arrhythmogenic Right Ventricular
Cardiomyopathy Causing Sudden Cardiac Death in Boxer Dogs. A New
Animal Model of Human Disease. Circulation (2004) 109, 1180-11.

3. Baumwart RD, Meurs KM, Atkins CE, et al. Clinical, echocardiographic

and electrocardiographic abnormalities in Boxers with cardiomyopathy
and left ventricular systolic dysfunction: 48 cases (1985-2003). J Am Vet
Med Assoc (2005) 226, 538-541.

4. Caro-Vadillo A, García-Guasch L, Carretón E, et al. Arrhythmogenic right

ventricular cardiomyopathy in Boxer dogs: a retrospective study of
survival. Vet Record (2013). doi: 10.1136/vr.100937.

5. Hariu CD, Carpenter D. Arrhythmogenic right ventricular cardiomyopathy

in Boxers. Compendium: continuing Education for Veterinarians (2010) pp:
E2-E7.

6. Meurs KM, Spier AW, Wright NA, et al. Comparison of the effects of four
antiarrhythmic treatments for familial ventricular arrhythmias in Boxers. J
Am Vet Med Assoc (2002) 221, 522-527.

7. Meurs KM. Boxer dog cardiomyopathy: an update. Vet Clin N Am Small

Anim Pract (2004) 34, 1235-1244.

8. Meurs KM, Lahmers S, Keene BW. Characteristics of ARVC Boxer with

sudden death. Proceedings of the ACVIM Forum. Denver, USA. June 15-
18 2011, p 649.

9. Nelson OL, Lahmers S, Schneider T, et al. The Use of an Implantable

Cardioverter Defibrillator in a Boxer Dog to Control Clinical Signs of
Arrhythmogenic Right Ventricular Cardiomyopathy. J Vet Intern Med
(2006) 20, 1232–1237.

11
10. Palermo V, Stafford Johnson MJ, Sala E, et al. Cardiomyopathy in Boxer
dogs: A retrospective study of the clinical presentation, diagnostic findings
and survival. Journal of Veterinary Cardiology (2011) 13, 45-55.

11. Smith CE, Freeman LM, Rush JE, et al. Omega-3 Fatty Acids in Boxer
Dogs with Arrhythmogenic Right Ventricular Cardiomyopathy. J Vet Intern
Med (2007) 21, 265–273.

12
 Paper

Paper
Arrhythmogenic right ventricular
cardiomyopathy in boxer dogs: a retrospective
study of survival
A. Caro-Vadillo, L. García-Guasch, E. Carretón, J. A. Montoya-Alonso, J. Manubens

The aim of the present study was to retrospectively evaluate survival in a population of
62 boxer dogs with arrhythmogenic right ventricular cardiomyopathy (ARVC), without left
ventricular systolic failure, based on the following factors: age at diagnosis, presence of
syncopal episodes, Holter arrhythmia classification and administered treatment. Medical
records of boxer dogs with a diagnosis of ARVC between 2000 and 2010 were reviewed.
Results showed that median survival time (MST) was longer in younger ARVC dogs than in the
older ones P<0.001). MST was statistically different (P=0.012) between dogs with syncope
(365 days) and dogs without syncope episodes (693 days), the probability of death within
a year being 4.8 times greater in dogs with syncope (95% CI 1.48 to 15.99) than in dogs
without syncope. Regarding Holter classification results, MST was 547.5 days in Holter
class-2 dogs and 365 days in Holter class-4 dogs (P=0.030). There were no differences
regarding treatment options; MST was 365 days (95% CI 193.615 to 536.4) in the sotalol
group, 365 days (95% CI 92.86 to 637.14) in the mexiletine plus atenolol group, and 547.50
days (95% CI 170.45 to 924.55) in the procainamide group (P=0.383). According to this study,
the best prognosis is for the younger boxer dog without syncope. There were no differences in
survival times in relation to the different treatment options used.

Introduction the early phase, individuals are often asymptomatic but can be at risk
Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a famil- of sudden cardiac death. Later, individuals present with symptomatic
ial primary myocardial disease in the boxer dog characterised by the arrhythmias, and right ventricular morphological abnormalities in
progressive replacement of ventricular myocardium (primarily right conventional imaging (Azaouagh and others 2011).
ventricular myocardium) with fatty or fibrofatty tissue which leads to These changes are frequently associated with inflammatory infil-
right ventricular failure, arrhythmias and sudden cardiac death (Meurs trates, which probably play a major part in triggering life-threatening
and others 1999, 2011, Basso and others 2004, 2009, Meurs 2004, arrhythmias. Whether the inflammatory cells are a reaction to cell
2005, Baumwart and others 2005, Hariu and Carpenter 2010, Nakao death (either necrosis or apoptosis) or the consequence of infective
and others 2011, Palermo and others 2011). or immune mechanisms is not known. The role of inflammation
Several researchers have demonstrated that this disease has strik- in ARVC in human beings is unresolved, although inflammation
ing similarities to a human myocardial disease called ARVC (Basso may contribute to disease progression (Azaouagh and others 2011,
and others 2004). Pinamonti and others 2011).
In human beings, arrhythmias and other electrocardiographic Disease progression may result in biventricular heart failure (HF).
abnormalities can be present before histological evidence of myocytes The progressive loss of the right ventricular myocardium can impair
degeneration or clinical presence of right ventricular dysfunction. In the function of the right ventricle and lead to severe pump failure.
When ARVC involves the ventricular septum and the left ventricle,
congestive HF occurs (Azaouagh and others 2011, Pinamonti and
Veterinary Record (2013) doi: 10.1136/vr.100937 others 2011).
Electrical impulse could be interfered with by the fibrofatty
A. Caro-Vadillo, DVM, PhD, de Gran Canaria, Las Palmas de Gran replacement, and this is the cause of ventricular arrhythmias in
Faculty of Veterinary Medicine, Canaria, Arucas, Gran Canaria, Spain human beings. It has been described that the disease progression is
Medicina y Cirugía Animal, University not a continuous process; there are periodic bursts and stable phases.
E-mail for correspondence:
Complutense of Madrid, Madrid, Spain This disease deterioration can be clinically silent in most patients, but
aliciac@vet.ucm.es
L. García-Guasch, DVM, PhD, sometimes the patients suffer life-threatening arrhythmias. It has been
J. Manubens, DVM, Provenance: Not commissioned; described that different environmental factors, exercise or inflamma-
Department of Cardiology and externally peer reviewed tion, might facilitate disease progression. Young people and athletes
Respiratory, Hospital Veterinari Molins, with asymptomatic ARVC can suffer instantaneous sudden death due
Accepted December 18, 2012
Barcelona, Spain to ventricular fibrillation (VF). VF in these patients, is most likely to
E. Carretón, DVM, be related to acute myocyte death and reactive inflammation. In older
J. A. Montoya-Alonso, DVM, PhD, patients with ARVC, VF seems to be infrequent, who more often
Internal Medicine, Faculty of Veterinary have haemodynamically stable ventricular tachycardia (VT) (Basso
Medicine, University of Las Palmas and others 2009, Pinamonti and others 2011).
Paper
ARVC in boxer dogs is a familial disease apparently inherited as an
autosomal dominant trait (Meurs and others 1999). It is an adult-onset
myocardial disease. Harpster described three forms of the disease:
concealed, overt and myocardial dysfunction. Affected dogs can have
many different presentations ranging from being totally asymptomatic
to sudden cardiac death. It is not clear if these forms represent a con-
tinuum of the disease, especially the two first forms (Harpster 1983).
Clinically, the disease is characterised by the development of ven-
tricular tachyarrhythmias. The concealed form is characterised by an
asymptomatic dog with occasional ventricular premature complexes
(VPCs). The VPCs usually show a left bundle branch configuration.
The overt form is characterised by VT and syncope or exercise intol-
erance. The last group developed myocardial systolic dysfunction
(Harpster 1983, Kraus and others 2002, Meurs 2004).
Diagnosis of cardiomyopathy is based on a combination of factors
including the presence of syncopal events, ECG and/or Holter abnor-
malities, echocardiographic findings and a family history of disease
(Meurs and others 1999, Smith 2011).
Treatment considerations usually focus on the use of ventricu-
lar antiarrhythmics. Antiarrhythmic drugs may be prescribed in
an attempt to decrease the number of VPCs and the complexity
of the arrhythmia. Boxer dogs with ARVC are always at risk of sud-
den death, so treatment may be useful in preventing this (Meurs and
others 2002, Meurs 2005, Prosek and others 2006, Thomason and
others 2008, Basso and others 2009, Hariu and Carpenter 2010,
Avramides and others 2011, Azaouagh and others 2011, Smith 2011).
A reduction in VPCs has been demonstrated with several treat-
ment protocols including: sotalol, procainamide and a combination
of mexiletine plus atenolol, both in human (Basso and others 2009,
Friedman and others 2010, Markel and others 2010, Smith 2011,
Avramides and others 2011, Azaouagh and others 2011) and in vet-
erinary medicine (Meurs and others 2002, Meurs 2005, Prosek and
others 2006, Gelzer and others 2010).
Although several studies have been reported in boxer dogs with
ARVC, they failed to provide consistent data regarding the risk stratifi-
cation of the disease. However, Palermo and others did look at survival
in a group of boxer dogs with mainly the myocardial dysfunction and
left ventricular enlargement form of the disease, which were excluded
from this study (Palermo and others 2011). Therefore, the aims of this
study were to retrospectively evaluate survival time in a population of
boxer dogs with ARVC, without left ventricular systolic failure, based
on the following factors: age of diagnosis, presence of syncopal epi-
sodes, Holter arrhythmia classification and administered treatment, as
well as to identify long-term prognostic predictors in a large cohort of
patients with ARVC, specifically focusing on the prognostic impact
of Holter class and other clinical parameters.
Materials and methods
Medical records of client-owned boxer dogs referred to the Hospital
Veterinario Clínico Complutense (Madrid, Spain), Hospital Clínico
Veterinario Universidad Las Palmas de Gran Canaria (Gran Canaria
island, Spain) and Hospital Veterinari Molins (Barcelona, Spain),
between January 2002 and October 2010 in which a diagnosis of
ARVC had been made, were reviewed by just one author. The owners
were informed, and all of them signed an informed consent.
The study was approved by the ethical committee of the
Veterinary Medicine Service of Las Palmas de Gran Canaria
University, and was carried out in accordance with the current
European legislation on animal protection.
The diagnosis inclusion criteria included presence of more than
1000 VPCs in 24 hours Holter recording and normal left ventricular
chamber on echocardiographic examination. Some dogs also present-
ed syncope or exercise intolerance and/or VPCs with increased com-
plexity (couplets, triplets) and/or VT. The left ventricular chamber
was considered to be normal when left ventricular systolic and diastol-
ic diameters, indexed to body surface area were less than 2.91 cm/m2
and 4.35 cm/m2, respectively. These echocardiographic criteria to
include or exclude dogs in the present study are the same described by
Bonagura and Luis Fuentes (2000). These particular indexes are very
similar to the indexes included in Cunningham and others (2008).
Fractional shortening in this group was superior to 25 per cent in all
cases (Bonagura and Luis Fuentes 2000, Cunningham and others
2008, Boon 2011).
Thus, the dogs included in the present study represent the cat-
egory 1 and category 2 forms of Harpster’s boxer cardiomyopathy
classification (Harpster 1983).
In this study, a modification of the Holter ventricular arrhythmia
classification defined by Palermo and others (2011), has been used as
detailed in Table 1.
Dogs with echocardiographic signs of mitral valve disease, con-
genital heart disease (Ebstein anomaly, atrial septal defect), myocar-
dial failure due to supraventricular tachycardia (with normal myo-
cardial function after control of the tachyarrhythmia), pulmonary
hypertension or systemic disease with secondary cardiac effects (eg,
hypothyroidism, renal failure) were excluded. A basic blood analysis
was performed to rule out metabolic causes of arrhythmia (eg, anae-
mia, hypokalaemia, hypoxia). Abdominal ultrasonography was per-
formed in some cases as abdominal masses may cause ventricular
arrhythmias.
Dogs were classified in different groups according to the number
of VT episodes per day, number of VPCs per day, presence of syn-
cope, age at diagnosis and Holter classification as shown in Table 1.
Administered treatments were sotalol (Sotapor, Brystol-Myers Squibb)
at 1.5–3.5 mg/kg/12 hours orally, mexiletine (Mexitil, Boehringer
Ingelheim) plus atenolol (Tenormin, AstraZeneca) at 5–8 mg/kg/8 hours
+0.3–0.6 mg/kg/12hours orally, or procainamide (Biocoryl, Grupo
Uriach) at 20–26 mg/kg/8 hours orally.
The clinical progress of each dog was ascertained by telephone
interview with the owner. The interviews were conducted by spe-
cifically trained senior students, and the results were recorded in an
electronic questionnaire. The questionnaire consisted of questions
with a definite number of possible answers, most commonly yes/no.
The interviewer was not blinded to the clinical status of the dog at
the initial examination. The owner was asked if the dog was dead or
alive. If the dog was dead, the owner was asked if the dog had been
euthanased or died spontaneously, reasons for euthanasia, and, in case
of spontaneous death, the possible causes, including cardiac-related
sudden death, presence of syncope, or progression of HF were probed.
Cardiac-related death was defined as death occurring because of pro-
gression of clinical signs of HF. Dogs that were euthanased because of
refractory HF, were scored as cardiac-related deaths. In this study, sud-
den death was defined as death occurring during sleep or activity such
as running, or within two hours after the dog showed sudden signs of
HF (dyspnea). Sudden death was regarded as cardiac-related if no other
cause of death was obvious.
Data regarding the death was recorded, and survival time was
measured from the date of first presentation. Whether the dog’s death
was due to cardiac-related causes (spontaneous death, euthanasia) was
taken into consideration.
In this study of survival, we considered only cardiac-related
deaths, and patients who suffered a non-cardiac death were not includ-
ed in the study.
Statistical analysis
The Kaplan-Meier method and plot time to event curves were used to
estimate survival. Survival time differences were assessed by log Rank
TABLE 1: Holter classification, ventricular tachycardia
classification and ventricular premature complex grading
for the boxer dog with ARVC included
Holter classification, ventricular tachycardia classification and ventricular prema-
ture complex graduation
Holter class 1 <1000 single VPCs/24 hours
Holter class 2 >1000 single VPCs/24 hours
Holter class 3 <1000 single VPCs/24 hours, couplets, triplets, VT
Holter class 4 >1000 single VPCs/24 hours, couplets, triplets, VT
VT class I <200 runs/24 hours
VT class II >200 runs/24 hours
VPCs class A <10000/24 hours
VPCs class B >10000/24 hours
VT, ventricular tachycardia; VPCs, ventricular premature complexes
 Paper

A B
1,0 1,0

0,8 0,8

Accum survival
Accum survival
a.(MST=693 days)
0,6 0,6
c.(MST=620 days)

0,4 0,4

b.(MST=15 days)
0,2 0,2
d.(MST=187 days)

0,0 0,0
0 500,0 1000,0 1500,0 2000,0 0 500,0 1000,0 1500,0 2000,0
Days Days

C D
1,0 1,0

0,8 0,8
Accum survival

Accum survival
0,6 e.(MST=547 days) 0,6
g.(MST=693 days)

0,4 0,4

0,2 0,2
f.(MST=365 days)
h.(MST=365 days)

0,0 0,0
0 500,0 1000,0 1500,0 2000,0 0 500,0 1000,0 1500,0 2000,0
Days Days

FIG 1: Kaplan-Meier survival curves in boxer dogs with arrhythmogenic right ventricular cardiomyopathy (ARVC) according to:(A)
ventricular tachycardia (VT) classification. a, Kaplan-Meier survival curve in ARVC dogs, VT class I. b, Kaplan-Meier survival curve in ARVC
dogs, VT class II. (B) ventricular premature complex (VPC) classification. a, Kaplan-Meier survival curve in ARVC dogs, VPC class A. b,
Kaplan-Meier survival curve in ARVC dogs, VPC class B. (C) Holter classification. a, Kaplan-Meier survival curve in ARVC dogs, Holter class
2. b, Kaplan-Meier survival curve in ARVC dogs, Holter class 4. (D) Presence or absence of syncope. a, Kaplan-Meier survival curve in ARVC
dogs without syncope. b, Kaplan-Meier survival curve in ARVC dogs with syncopal episodes

test. The cross-tabs, Fisher’s exact test and odds ratio were used to esti-
mate risk of death within a year. A Cox regression multivariable analy-
sis (stepwise method for variable selection) was done. A P value <0.05
was considered significant. The statistical analyses were performed
using a commercially available software program: SPSS V.19.0.
Results
A total of 62 boxer dogs of both sexes met the inclusion criteria for the
study. Males were over-represented (63 per cent (39/62) male, 37 per cent
(23/62) female; ratio 1.7:1). The mean age of presentation was 7.7 years
old (min: three years, max: 12.2 years). The most common presenting
clinical sign was syncope in 68 per cent (42/62) of the boxer dogs, where-
as exercise intolerance was present in 24 per cent (15/62) of the dogs.
Twenty-four hours Holter monitoring was performed in all the dogs
included. The morphology of VPCs was consistent with a right ven-
tricular origin (left bundle branch block pattern). The majority of dogs
76 per cent (47/62) were Holter class 4 (>1000 VPCs in 24 hours, with
increased complexity (couplets, triplets) and/or VT. The mean±sd of the
VPCs in the 62 dogs was 8748.66±7178.975 (min: 1129; max: 21869).
The mean±sd of the VT episodies in the 62 dogs was 186.18±341730
(min: 0; max: 2347).
According to inclusion criteria, echocardiography findings were
normal in 100 per cent of the dogs prior to treatment.
Median survival time (MST) was 365 days (mean±sd: 561±62.6),
min: 7 days, max:1971 days for the complete group of patients.
There was a significant association between survival and VT class
(P<0.001), with a MST of 693 days (mean 748) in dogs with VT class
I (<200 runs/24 hours) vs 15 days (mean 169) in dogs with VT class II
(>200 runs/24 hours) Table 2, Figure 1A.
There was a significant association between survival and the
number of VPCs in 24 hours Holter monitoring (P=0.01) with a MST
of 620 days (mean 706) in dogs with VPCs class A (<10.000/24 hours)
vs 182 days (mean 360) in dogs with VPCs class B (>10.000/24 hours)
Table 2, Figure 1B.
There was a significant association between survival and Holter
class (P=0.03) with a MST of 547 days (mean 799) in dogs with
Holter class 2 vs 365 days (mean 485) in dogs with Holter class 4 Table
2, Figure 1C.
There was a significant association between survival and syncope
(P=0.012), with a MST of 693 days (mean 445) in dogs without syn-
cope vs 365 days (mean 805) in dogs with syncope Table 2, Figure 1D.
There was a significant association between survival and age at
initiation of treatment (P<0.001) with a MST of 1460 days in dogs
younger than four years at treatment initiation vs 620 days in dogs
between four and eight years and 292 days for dogs older than eight
years Table 2 Figure 2.
There were no differences in survival between males (MST of 457
days) and females (MST of 650 days) (P=0.345).
There were no differences with regards to survival, among the three
treatment options used (P=0.383), with a MST of 365 days (95% CI
193.615 to 536.4) (mean 475) for sotalol treatment, a MST of 365 days
(95% CI 92.86 to 637.14) (mean 595) for mexiletine plus atenolol
treatment and a MST of 547 days (95% CI 170.45 to 924.55) (mean
632) for procainamide treatment Table 2.
The probability of death within a year (odds ratio), of dogs with
VT class II is 20 times greater (95% CI 4 to 99.5; P<0.001) than in the
group of dogs with VT class I. The probability of death within a year,
of dogs with VPCs class B is 5.43 times greater (95% CI 1.79 to 16.46;
Paper

TABLE 2: Mean and sd of the days of survival in the different groups of boxer dogs with ARVC
MEAN±sd (days)

Age at treatment <4 years 4–8 years >8 years

n=5 n=30 n=27 P<0.001
1262.9±317.7 657.26±81.6 324.31±62.9
Treatment options Sotalol mexiletine+atenolol Procainamide
n=23 n=21 n=18 P=0.564
474.82±394.7 594.8±561 631.9±533.2
Syncope Yes No
n=42 n=20 P=0.012
805.22±129.7 444.86±62.3
Holter class Class 2 Class 4
n=15 n=47 P=0.03
798.66±169.5 485.29±59.6
VT class I II
n=42 n=20 P<0.001
747.6±73.6 169±50
VPCs class A B
n=36 n=26 P=0.01
706.3±82.7 360±82

ARVC, arrhythmogenic right ventricular cardiomyopathy; VT, ventricular tachycardia

P=0.004) than in the group of dogs with VPCs class A. The prob-
ability of death within a year, of dogs with Holter class 4 is 2.47 times
greater than in dogs with Holter class 2, however, this result was not
statistically significant (95% CI 0.73 to 8.3; P=0.235). The probability
of death within a year, of dogs with syncope is 4.875 times greater
(95% CI 1.48 to 15.99; P=0.013) than in dogs without syncope.
The hazard ratio, for the complete duration of the study, calculat-
ed by Cox proportional hazard multivariable analysis, for VT was 4.8
(95% CI 2.63 to 8.99; P<0.001). There were no other variables (VPC,
presence/absence of syncope, Holter class) statistically significant for
this Cox proportional stepwise method.
The hazard ratio, for one year, calculated by Cox proportional
hazard multivariable analysis, for VT was 6.05 (95% CI 2.92 to 12.51;
P<0.001). There were no other variables (VPC, presence/absence of
syncope, Holter class) statistically significant for this Cox proportional
stepwise method.
Discussion
Boxer dog cardiomyopathy in Spain seems to progress in the same
way as the disease in other countries, although some differences have
been described between different families of boxer dogs (Palermo and
others 2011).
The signalment for the dogs in this study was similar to the
descriptions in previous publications. Males were over-represented
(Harpster 1983, 1991, Baumwart and others 2005, Meurs and others
2011, Palermo and others 2011).
Mean age at presentation was similar to that reported by Palermo
and others (2011), by Harpster (1983), by Basso and others (2004) and
by Baumwart and others (2005).
The most common clinical sign detected in the present study was
syncope (68 per cent of boxer dog). It would be reasonable to suggest
that syncope, in this study, is associated with ventricular arrhyth-
mias. The presence of VT episodies and bradycardias as causes of
syncope, coexisting in boxer dogs has been described (Thomason and
others 2008). No evidence of bradycardia was found in the 24 hours
Holter recordings in this study, therefore, in these patients syncope
should be the result of rapid VT. In the present study, a significant
risk of death within the first year after the diagnosis in dogs with
syncope versus dogs without syncope has been found. In human
patients presenting with syncope for which a diagnosis is not made,
the likelihood of sudden death is low, other studies would suggest
this is also the case in dogs (Barnett and others 2011). It is useful to
consider the deaths recorded in this study in the light of other studies
that have been completed which report typical life expectancies of
different dog breeds. Eichelberg and Seine (1996), reported an over-
all life expectancy of 10 years based on a sample of 9248 dogs. On
that basis, it might be considered that boxer dogs presenting with
collapse, syncope or exercise intolerance are more likely to suffer a
premature death.
The fact that boxer dogs with ARVC and syncope live for a short-
er time, has been proved in the present study; the probability of death
within a year is 4.875 times greater for dogs with syncope.

1,0
0-4 years
4,1-8 years
8,1-12 years

0,8
Accum survival

a.(MST=1460 days)
0,6

b.(MST=620 days)
0,4

0,2
c.(MST=292 days)

0,0

0 500,0 1000,0 1500,0 2000,0

Days

FIG 2: Kaplan-Meier survival curves in the different groups of boxer dogs with arrhythmogenic right ventricular cardiomyopathy (ARVC)
according to age of initial diagnosis. (a) Kaplan-Meier survival curve in ARVC dogs younger than four years old. (b) Kaplan-Meier survival
curve in ARVC dogs between four and eight years old. (c) Kaplan-Meier survival curve in ARVC dogs older than eight years

The presence of frequent VT episodes was associated negatively
with survival in our study, unlike the findings reported by Palermo
and others (2011). In human beings, VT is an independent and nega-
tive predictor of mortality (Basso and others 2009). In this report, it
has been found that VT means a high risk of death within one year.
It is probable that VT degenerates into VF leading to sudden death in
the dogs used in this study. The number of VT episodes was the only
variable associated with a statistically significant hazard ratio risk of
death. This was probably due to the fact that the total number of
VPCs and syncope episodes are closely related to the number of VT
episodes.
Similarly, the presence of a greater number of VPCs involved a
high risk of death. Although the cut-off value to define the normal
number of VPCs in boxer dog is not determined, it is unusual to have
ventricular ectopy. It has been suggested that a small number of VPCs
could be normal, especially in older dogs (Palermo and others 2011).
In the present study, a negative correlation between number of VPCs
and survival time has been found.
MST was significantly longer in the younger group of dogs at
the time of diagnosis. ARVC, although genetically determined, is
an acquired and progressive disease which shows an age-related pen-
etrance both in human beings and dogs (Meurs 2005, Basso and oth-
ers 2009, Avramides and others 2011, Smith 2011). In human beings,
VF is the mechanism of instantaneous sudden death in young people
and athletes with ARVC, and VF is most likely related to a phase
of disease progression, due to acute myocytes death and reactive
inflammation.
The reason why a better prognosis has been observed in younger
dogs may be that VF is rare in older patients with long-lasting ARVC
(Basso and others 2009). In accordance with the results of the present
study, dogs that lived longer are less prone to sudden death. Despite
the hypothesis that in dogs the disease progresses over time, the natu-
ral history of boxer dog cardiomyopathy requires further study. So,
even though this disease seems to be progressive in nature, according
to Harpster, in this report a better survival in younger dogs is found.
Another reason besides lack of evidences of inflammatory response
could be that early treatment (drug and restriction of vigorous exer-
cise) was able to slow down the progression of the disease (Basso and
others 2009). More studies are needed to clarify this point.
It has been described that striatin genotype was significantly asso-
ciated with sudden death at an earlier age than dogs without sudden
death which live longer (Meurs and others 2011). In the present study,
genetic studies, to corroborate this possibility as the reason for longer
MST in the younger dogs, were not carried out.
Treatment is aimed mainly at the prevention and management
of malignant arrhythmias and sudden death. Different antiarrhyth-
mic regimes to treat ARVC in dogs have been described (Meurs and
others 2002) as well as a successful use of an implantable cardiovert-
er-defibrillator in boxer dogs (Nelson and others 2006). Differences
between survival times in relation to the treatment options used were
not found in the current study. The drug chosen for an individual ani-
mal is usually selected on the basis of a combination of factors, includ-
ing clinical experience, adverse effects, ease of administration and cost
of the drug. In human beings, sotalol proved to be highly effective
in patients with ARVC, and inducible as well as non-inducible VT.
D,l-sotalol is a non-selective β-blocker with class III antiarrhythmic
properties. Its antiarrhythmic efficacy has been demonstrated both
in boxer dogs with spontaneous VT as well as human patients with
VT that were refractory to class I antiarrhythmics (Meurs and others
2002, Avramides and others 2011).
The reason for the selection of a β-blocker as a ventricular
antiarrhythmic is its effect in modulation of the autonomic nerv-
ous system that could be involved in the development of VT. An
excitement or exercise trigger for VT in boxer dogs has been reported
(Meurs and others 2011). Patients being treated with sotalol or other
antiarrhythmic drugs that block potassium channels may have an
acceptable degree of QT prolongation or develop marked lengthening
of the QT interval and even torsades de pointes. Such incidents can
usually be attributed to development of excessive bradycardia, electro-
lyte abnormalities, a decline in renal function, initiation of a new drug
that affects cardiac repolarisation, or metabolism of the antiarrhyth-
Paper
mic drug (Friedman and others 2010). In human beings, another class
III antiarrhythmic drug, amiodarone, was associated with a poor
long-term outcome (Pinamonti and others 2011). However, in another
study, amiodarone had superior efficacy in preventing ventricular
arrhythmias (Marcus and others 2009).
Mexiletine is an orally available class Ib antiarrhythmic drug
similar to lidocaine; mexiletine which inhibits fast sodium channels
and reduces arrhythmias in canine in vitro models of repolarisation
abnormalities with triggered activity as well as in human beings with
long QT wave syndrome. Previous antiarrhythmic drug studies in
boxer dogs found mexiletine to be effective for reduction of VT when
combined with atenolol, with minimal proarrhytmic effects. Atenolol
alone did not significantly reduce the number of VPCs and arrhyth-
mia grade (Meurs and others 2002). The administration of β-blockers
can aggravate or precipitate bradycardia-related syncope (Thomason
and others 2008). However, in this study, a worse prognosis in the
group of dogs treated with either sotalol or atenolol plus mexiletine in
comparison with the procainamide group has not been found.
Potential benefits of combination therapy of sotalol with mexile-
tine have been shown in human clinical trials as well as in German
shepherd dogs with inherent ventricular arrhythmias (Prosek and oth-
ers 2006, Gelzer and others 2010, Smith 2011). This combination has
not been used in this study.
Procainamide is a class Ia antiarrhytmic drug that affects normal
and abnormal tissues, with conduction-slowing and vasodilatory
properties. In human beings, it has been recommended for haemo-
dynamically stable ventricular and atrial arrhythmias with preserved
ventricular function (Markel and others 2010). Although in some
situations, procainamide could not eliminate VT, the heart rate is
decreased improving haemodynamic stability. The incidence of proar-
rhythmia in dogs treated is not known. Although procainamide did
not induce significant reduction in VPCs, it is less expensive than
sotalol and sometimes this justifies its use.
As mentioned above, none of the treatment protocols were related
to survival time. Although proven efficacy in ventricular arrhythmia
for the treatment protocol used (Meurs and others 2002, Gelzer and
others 2010, Azaouagh and others 2011, Smith 2011) may be another
factor which could have influenced the survival as neurocardiogenic
bradycardia as inducer of VT or VF (Thomason and others 2008),
progression of the disease to another form or proarrhythmia effects
of the antiarrhytmic drug used. However, this study detects a direct
relationship in the number and complexity of VPCs and the risk of
sudden death, therefore, the ability of a treatment to alter the arrhyth-
mia could have an impact on survival.
According to other studies, the administration of fish oil could
decrease ventricular arrhythmia and the risk of sudden death in boxer
dogs with ARVC (Smith and others 2007). This has not been used in
this study.
In conclusion, MST was significantly longer in young boxer dogs,
in dogs without syncopal episodes and in the VT class I group. As
regards therapeutic options, there were no statistically significant dif-
ferences in MST between the three groups.
As far as the probability of death within the first year after diagno-
sis is concerned, this risk is doubled for a cohort of dogs with syncope
and VPCs more than 10000 per day, and six times more for dogs with
VT episodes over 200 per day.
Limitations
This was a retrospective cohort study with a fixed sample size and
was susceptible to bias, confounding and incomplete power to detect
more modest, yet still clinically important, survival associations.
Because of the retrospective nature of the study, most of the dogs
had not subsequently undergone cardiac evaluations, so we cannot
establish a progression from arrhythmia to other forms of left ven-
tricular dysfunction.
Another limitation was the absence of postmortem examinations
to assert the final diagnosis of the dogs. Genetic characterisation was
not available; therefore, potential differences in clinical features and
prognosis impact of different genetic substrates cannot be ascertained.
In addition, in this study, only clinical and Holter parameters at enrol-
ment have been analysed since the onset of the disease in the single
 Paper
patient is unknown; that kind of evaluation was performed at differ-
ent stages of the disease in different patients. An extensive follow-up
study to assess the progression of clinical, echo dysfunctions of right
and left ventricular chambers and Holter test and their possible prog-
nostic role is advisable.
As regards treatment, this study only considered the effect of the
different protocols on survival time. It did not consider other clinical
factors (eg, frequency of syncope) that could improve the overall con-
dition of the animal prior to death.
To this end, the present study included 62 ARVC dogs, a cohort
size that exceeds any prior publication evaluating survival time and
probability of death within a year in boxer dog population.
Preliminary results of this study were reported in 17th FECAVA Eurocongress,
7–10 September, 2011. Istanbul, Turkey.
References
AVRAMIDES, D., PROTONOTARIOS, N., ASIMAKI, A. & MATSAKAS, E.
(2011) Arrhythmogenic right ventricular cardiomyopathy/dysplasia. Hellenic Journal of
Cardiology 52, 452–461
AZAOUAGH, A., CHURZIDSE, S., KONORZA, T. & ERBEL, R. (2011)
Arrhythmogenic right ventricular cardiomyopathy/dysplasia: a review and update.
Clinical Research in Cardiology 100, 383–394
BARNETT, L., MARTIN, M. W. S., TODD, J., SMITH, S. & COBB, M. (2011) A ret-
rospective study of 153 cases of undiagnosed collapse, syncope or exercise intolerance:
the outcomes. Journal of Small Animal Practice 52, 26–31
BASSO, C., FOX, P. R., MEURS, K. M., TOWBIN, J. A., SPIER, A. W., CALABRESE,
F., MARON, B. J. & THIENE, G. (2004) Arrhythmogenic right ventricular cardiomyo-
pathy causing sudden cardiac death in Boxer dogs. A New Animal Model of Human Disease.
Circulation 109, 1180–1185
BASSO, C., CORRADO, D., MARCUS, F.I., NAVA, A. & THIENE, G. (2009)
Arrhythmogenic right ventricular cardiomyopathy. The Lancet 373, 1289–1300
BAUMWART, R. D., MEURS, K. M., ATKINS, C. E., BONAGURA, J. D.,
DeFRANCESCO, T. C., KEEN, B. W., KOPLITZ, S., LUIS FUENTES, V., MILLER,
M.W., RAUSCH, W. & SPIER, A.W. (2005) Clinical, echocardiographic and electro-
cardiographic abnormalities in Boxers with cardiomyopathy and left ventricular systolic
dysfunction: 48 cases (1985–2003). Journal of the American Veterinary Medical Association
226, 538–541
BONAGURA, J. D. & LUIS FUENTES, V. (2000) Echocardiography. In: Textbook of
Veterinary Internal Medicine. 5th edn. Eds. S. J. Ettinger, E. C. Feldman. WB Saunders,
Philadelphia. pp 834–873
BOON, J. A. (2011) Veterinary Echocardiography. 2th edn. Wiley-Blackwell, Iowa,
USA
CUNNINGHAM, S. M., RUSH, J. E., FREEMAN, L. M., BROWN, D. J. & SMITH,
C. E. (2008) Echocardiographic ratio indices in overtly healthy Boxer dogs screened for
heart disease. Journal of Veterinary Internal Medicine 22, 924–930
EICHELBERG, H. & SEINE, R. (1996) Life expectancy and cause of death in dogs. The
situation in mixed breeds and various dogs breeds. Berliner und Munchener tierarztliche
Wochenschrift 109, 292–303
FRIEDMAN, P. L., MONTGOMERY, S. & MATAS, N. (2010) Sotalol and a Broken
Heart. Journal of Cardiovascular Electrophysiology 21, 207–210
GELZER, A. R. M., KRAUS, M. S., RISHNIW, M., HEMSLEY, S. A. & MOïSE,
N. S. (2010) Combination therapy with mexiletine and sotalol suppresses inherited
ventricular arrhythmias in German shepherd dogs better than mexiletine or sotalol
monotherapy: a randomized cross-over study. Journal of Veterinary Cardiology 12, 93–106
HARIU, C. D. & CARPENTER, D. (2010) Arrhythmogenic right ventricular cardio-
myopathy in Boxers. Compendium: continuing Education for Veterinarians. pp E2–E7
HARPSTER, N. (1983) Boxer cardiomyopathy. In: Current Veterinary Therapy VIII. Ed.
R. Kirk. WB Saunders. pp 329–337
HARPSTER, N. (1991) Boxer cardiomyopathy: a review of the long-term benefits
of antiarrhythmic therapy. Veterinary Clinical North America Small Animal Practice 21,
989–1004
KRAUS, M. S., MOÏSE, N. S., RISHNIW, M., KYKES, N. & ERB, H. N. (2002)
Morphology of ventricular arrhythmias in the Boxer as measured by 12-lead electro-
cardiography with pace-mapping comparison. Journal of Veterinary Internal Medicine 16,
153–158
MARCUS, G. M., GLIDDEN, D. V., PLONSKY, B., ZAREBA, W., SMITH, L. M.,
CANNOM, D. S., ESTES, M., MARCUS, F. & SCHEINMAN, M. M. (2009)
Efficaccy of antiarrhythmic drugs in arrhythmogenic right ventricular cardiomyopa-
thy: a report from the North American ARVC registry. Journal of the American College of
Cardiology 54, 609–615
MARKEL, D. T., GOLD, L. S., ALLEN, J., FAHRENBRUCH, C. E., REA, T. D.
EISENBERG, M. S. & KUDENCHUK, P. J. (2010) Procainamide and survival in
ventricular fibrillation out-of-hospital cardiac arrest. Academic Emergency Medicine 17,
617–623
MEURS, K. M. (2004) Boxer dog cardiomyopathy: an update. Veterinary Clinical North
American Small Animal Practice 34, 1235–1244
MEURS, K. M. (2005) Right ventricular arrhythmic cardiomyopathy: an update on
Boxer cardiomyopathy. Proceedings of The North American Veterinary Conference.
Orlando January 8–12, 2005. pp 122–123
MEURS, K. M. SPIER, A. W., MILLER, M. W., LEHMKUHL, L. & TOWBIN, J. A.
(1999) Familial ventricular arrhythmias in boxers. Journal of Veterinary Internal Medicine
14, 437–439
MEURS, K. M., SPIER, A. W., WRIGHT, N. A., ATKINS, C. E., DeFRANCESCO, T.
C., GORDON, S. G., HAMLIN, R. L., KEENE, B. W., MILLER, M. W. & MOÏSE,
N. S. (2002) Comparison of the effects of four antiarrhythmic treatments for familial
ventricular arrhythmias in Boxers. Journal of the American Veterinary Medical Association
221, 522–527
MEURS, K. M., LAHMERS, S. & KEENE, B. W. (2011) Characteristics of ARVC Boxer
with sudden death. Proceedings of the ACVIM Forum. Denver, USA. June 15–18,
2011. p 649
NAKAO, S., HIRAKAWA, A., YAMAMOTO, S., KOBAYASHI, M. & MACHIDA, N.
(2011) Pathological features of arrhythmogenic right ventricular cardiomyopathy in
middle-aged dogs. Journal of Veterinary Medical Science 73, 1031–1036
NELSON, O. L., LAHMERS, S., SCHNEIDER, T. & THOMPSON, P. (2006) The Use
of an Implantable cardioverter defibrillator in a Boxer dog to control clinical signs of
arrhythmogenic right ventricular cardiomyopathy. Journal of Veterinary Internal Medicine
20, 1232–1237
PALERMO, V., STAFFORD JOHNSON, M. J., SALA, E., BRAMBILLA, P. G. &
MARTIN, M. W. S. (2011) Cardiomyopathy in Boxer dogs: a retrospective study of
the clinical presentation, diagnostic findings and survival. Journal of Veterinary Cardiology
13, 45–55
PINAMONTI, B., DRAGOS, A. M., PYXARAS, S. A., MERLO, M., PIVETTA, A.,
BARBATI, G., DI LENARDA, A., MORGERA, T., MESTRONI, L. & SINAGRA,
G. (2011) Prognostic predictors in arrhythmogenic right ventricular cardiomyopathy:
results from a 10-year registry. European Heart Journal 32, 1105–1113
PROSEK, R., ESTRADA, A. & ADIN, D. (2006) Comparison of sotalol and mexiletine
versus stand alone sotalol in treatment of Boxer dogs with ventricular arrhythmias.
Proceedings of the ACVIM Forum. Louisville, USA. May 31-June 3, 2006. pp 748
SMITH, C. E., FREEMAN, L. M., RUSH, J. E., CUNNINGHAM, S. M. & BIOURGE,
V. (2007) Omega-3 fatty acids in Boxer dogs with arrhythmogenic right ventricular
cardiomyopathy. Journal of Veterinary Internal Medicine 21, 265–273
SMITH, W. (2011) Guidelines for the diagnosis and management of arrhythmogenic
right ventricular cardiomyopathy. Heart, Lung and Circulation 20, 757–760
THOMASON, J. D., KRAUS, M. S., SURDYK, K. K., FALLAW, T. & CALVERT, C.
A. (2008) Bradycardia-associated syncope in 7 Boxers with ventricular tachycardia
(2002–2005). Journal of Veterinary Internal Medicine 22, 931–936
 Downloaded from veterinaryrecord.bmj.com on January 14, 2013 - Published by group.bmj.com

Arrhythmogenic right ventricular

cardiomyopathy in boxer dogs: a
retrospective study of survival
A. Caro-Vadillo, L. García-Guasch, E. Carretón, et al.

Veterinary Record published online January 12, 2013

doi: 10.1136/vr.100937

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 ENFERMEDADES CARDIORRESPIRATORIAS DE PEQUEÑOS ANIMALES

Actualización en hipertensión
pulmonar arterial en perros.
Conceptos básicos
Bernardo Serrano Parreño, DVM.
Elena Carretón Gómez, DVM, MSc, PhD.
J. Alberto Montoya-Alonso, DVM, MSc, MA, PhD.
Servicio de Medicina Veterinaria.
Facultad de Veterinaria de la Universidad de Las Palmas de Gran Canaria
alberto.montoya@ulpgc.es

La hipertensión pulmonar se define como un aumento de la presión arterial diastólica

y/o sistólica de la arteria pulmonar.
La fisiopatología de la hipertensión arterial pulmonar es compleja y multifactorial. Ésta
se produce por una disfunción endotelial que conduce a un desequilibrio de agentes
vasoactivos con predominio de la vasoconstricción.
La clasificación clínica de los pacientes con hipertensión pulmonar se basa
en la causa subyacente de la misma, mientras que la clasificación funcional
agrupa a los pacientes en clases según la gravedad de los signos clínicos
producidos por la hipertensión pulmonar.
Una vez identificada la causa primaria de la hipertensión pulmonar, el trata-
miento es fundamentalmente farmacológico mediante la administración de
fármacos que ayuden a reducir la presión de la arteria pulmonar y la carga
sobre el ventrículo derecho, con el fin de reducir la sintomatología, mejorar
la calidad de vida y el tiempo de supervivencia. Los principales síntomas aso-
ciados a esta patología son disnea, intolerancia al ejercicio, tos y síncopes.

70 Canis et Felis Número 133 - Abril 2015

 Actualización en hipertensión pulmonar arterial en perros. Conceptos básicos

INTRODUCCIÓN
La hipertensión pulmonar (HTP) se define como un aumento de la presión
arterial diastólica y/o sistólica a nivel de la circulación pulmonar. De manera
más específica, la HTP puede definirse como sistólica cuando la presión ar-
terial pulmonar sistólica es superior a 30 mm Hg, o bien diastólica cuando
la presión arterial pulmonar diastólica es superior a 15 mm Hg. Aunque es
posible determinar estas presiones de manera directa a través de cateterismo
cardiaco del lado derecho, este procedimiento requiere sedación o anestesia,
siendo un procedimiento invasivo, no exento de riesgo para la vida del animal
y económicamente no accesible para veterinarios y clientes. De forma alter-
nativa, la presión arterial pulmonar puede valorarse mediante ecocardiografía
transtorácica evaluando de forma subjetiva algunas alteraciones, tales como
la dilatación de la arteria pulmonar y de las cámaras derechas, y el análisis
mediante Doppler de la regurgitación de la válvula tricúspide y de la valvular
pulmonar. La HTP puede presentarse como una enfermedad tanto de origen
primario como secundario. Entre las posibles etiologías, se incluyen: 1- pato-
logías que causen aumento de presión en atrio izquierdo, como endocardiosis
mitral y cardiomiopatía dilatada, 2- patologías que supongan sobrecarga de
volumen a nivel de circulación pulmonar, como defectos del septo interven-
tricular o conducto arterioso persistente, 3- patologías que cursen con un
aumento de la resistencia vascular, causada por enfermedades obstructivas
o por oclusión de la circulación pulmonar, como pudiera ser un tumor de
base cardiaca, 4- patologías pulmonares crónicas. En medicina veterinaria, el
incremento de presión a nivel de atrio izquierdo es causa más común de HTP
(45% de los casos).

FISIOPATOLOGÍA
La fisiopatología de la HTP arterial es compleja y multifactorial. Ésta se pro-
duce por una disfunción endotelial que conduce a un desequilibrio de agentes
vasoactivos (endotelina-1, óxido nítrico, prostaciclina, etc.), con predominio de
la vasoconstricción. Comprender los eventos y mecanismos en la constricción
y dilatación de los vasos pulmonares puede ayudar a un mejor enfoque pro-
nóstico y terapéutico del paciente. La hipoxia alveolar es una respuesta se-
cundaria a la vasoconstricción de los vasos pulmonares, la vasoconstricción
permite que la sangre sin oxígeno sea derivada hacia zonas del pulmón que se
encuentran más ventiladas mejorando la ventilación-perfusión. Inicialmen-
te es una respuesta fisiológica favorable pero en condiciones crónicas puede
conducir a HTP.

CLASIFICACIÓN CLÍNICA
Se ha propuesto una clasificación de la HTP basada en la presentación clínica
y las opciones de tratamiento.

Número 133 - Abril 2015 Canis et Felis 71

 ENFERMEDADES CARDIORRESPIRATORIAS DE PEQUEÑOS ANIMALES

Clase clínica I: Hipertensión arterial pulmonar

Incluye pacientes con enfermedad vascular arteriolar pulmonar. En seres hu-
manos la forma más común es la idiopática. Aunque se ha descrito HTP idiopá-
tica en perros, se trata de una presentación poco habitual; no obstante, existen
referencias de pacientes con HTP en los que no ha podido identificarse una cau-
sa determinada. En perros, las causas más comunes de HTP clase I incluyen
enfermedades congénitas y dirifilatiosis cardiopulmonar.

Clase clínica II: Hipertensión venosa pulmonar

Los pacientes englobados en esta categoría desarrollan una HTP secundaria
a cardiopatías que afectan el lado izquierdo del corazón. Debido a un aumento
de presión en el atrio izquierdo, se produce una elevación en la presión venosa
pulmonar, lo que puede provocar la aparición de edema pulmonar e hipoxia,
así como una HTP reactiva.
Cuando la presión venosa pulmonar excede de 25 mmHg, la presión arterial pul-
monar aumenta en un intento por mantener el flujo sanguíneo pulmonar pero
finalmente se desarrolla hipertrofia arteriolar. La enfermedad cardiaca del lado
izquierdo es la causa más frecuente de HTP, tanto en seres humanos como en
perros. Aunque menos usual, se ha descrito HTP clase II tanto en seres humanos
como en perros con miocarditis y distensión atrial secundaria a fibrilación atrial.

Clasificación clínica III: Enfermedad pulmonar o hipoxia

La HTP también puede ser secundaria a enfermedad pulmonar primaria o
hipoxia crónica. Las enfermedades respiratorias relacionadas más a menudo
con HTP clase III en personas son la enfermedad pulmonar obstructiva cró-
nica, enfermedad intersticial pulmonar y el trastorno respiratorio del sueño.
En perros se asocia a fibrosis pulmonar, neumonía, enfermedad traqueo-
bronquial y neoplasias. Debido a una predisposición racial, hasta 40% de los
WestHighland White Terriers con enfermedad pulmonar intersticial crónica
presentan cierto grado de HTP.

Clase clínica IV: Enfermedad tromboembólica

La HTP clase IV es producida por el desarrollo de trombos o émbolos. En hu-
manos, la obstrucción de la arteria pulmonar se relaciona con tromboembolis-
mos, tumores y cuerpos extraños. En perros, el tromboembolismo pulmonar
se asocia a la presencia de anemia hemolítica inmunomediada, neoplasias,
neuropatías y enteropatías perdedoras de proteínas, hiperadrenocorticismo,
sepsis y traumatismo. Dada la posibilidad de émbolos por gusanos, la diri-
filatiosis cardiopulmonar canina puede incluirse también en esta categoría.

Clase clínica V: Otras causas

La HTP clase V comprende causas diversas de HTP. En personas, la clase V
incluye trastornos que de manera indirecta alteran el flujo sanguíneo cardiaco
(p. ej. policitemia vera primaria), enfermedades granulomatosas y enferme-

72 Canis et Felis Número 133 - Abril 2015

 Actualización en hipertensión pulmonar arterial en perros. Conceptos básicos

dades que conducen a la destrucción del parénquima pulmonar. En medicina

veterinaria se ha documentado en muy pocas ocasiones; sin embargo, proba-
blemente la situación más habitual sea aquella que cursa con compresión de
la vasculatura pulmonar (por ejemplo, tumores de base cardiaca).

CLASIFICACIÓN FUNCIONAL
Mientras que la clasificación clínica se basa en la causa subyacente de la HTP,
la clasificación funcional agrupa a los pacientes según la gravedad de los sig-
nos clínicos producidos por la HTP.

Clase funcional I
Esta clase incluye pacientes con HTP que no sufren intolerancia al ejercicio y
que pueden ejercitarse sin signos de disnea, fatiga, dolor torácico o síncope.

Clase funcional II
Los pacientes de la clase II no presentan síntomas en reposo pero muestran
una leve disnea, intolerancia al ejercicio, dolor torácico o síncope al realizar
algún tipo de actividad física.

Clase funcional III

La HTP de estos pacientes produce limitaciones notables en el desarrollo de
actividad física y manifiestan intolerancia al ejercicio, disnea, fatiga, dolor to-
rácico y síncopes incluso durante actividad física muy leve; sin embargo, du-
rante el reposo no presentan sintomatología.

Clase funcional IV
Esta clase terminal incluye pacientes con HTP que son incapaces de desa-
rrollar ningún tipo de actividad física, de manera que cualquier ejercicio físico
desemboca en una intensa sintomatología. Estos pacientes son sintomáticos
incluso en reposo y además presentan insuficiencia cardiaca derecha.

DIAGNÓSTICO
1. PRESENTACIÓN CLÍNICA Y EXAMEN FÍSICO
Las alteraciones más frecuentemente observadas durante la auscultación
son un soplo cardiaco por insuficiencia mitral y/o tricuspídea, y un desdobla-
miento de S2, el cual se relaciona normalmente con el cierre de las cúspides
de las válvulas aórtica y pulmonar. También se puede auscultar crepitaciones
pulmonares o sonidos pulmonares broncovesiculares aumentados. Los sín-
tomas a los que con mayor frecuencia hace referencia el propietario son tos,
disnea, letargia, episodios sincopales, intolerancia al ejercicio, ascitis y ciano-
sis. La HTP se presenta con mayor frecuencia en razas pequeñas y en perros
de edad mediana y geriatras.

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 ENFERMEDADES CARDIORRESPIRATORIAS DE PEQUEÑOS ANIMALES

2. PRUEBAS DE LABORATORIO

Debe obtenerse un perfil analítico básico para determinar alteraciones hema-

tológicas y serológicas así como un urianálisis. Se recomienda realizar sero-
logía para dirifilatiosis ya que ésta es una de las enfermedades más comunes
relacionadas con HTP en zonas endémicas.

Los hallazgos laboratoriales más comunes suelen ser leucocitosis moderada

(provocado por grandes trombos pulmonares), eritrocitos nucleados (que es
un potencial indicador de hipoxia) y policitemia, además de eosinofilia, baso-
filia, monocitosis y anemia no regenerativa en pacientes con dirifilatiosis. A
su vez puede cursar con trombocitopenia secundaria a coagulación intravas-
cular diseminada, como hallazgo en pacientes con tromboembolismo agudo.
En presencia de grandes trombos pulmonares, pueden aparecer leucogra-
mas inflamatorios y, en caso de tromboembolismo pulmonar, es de utilidad
la determinación plasmática de dímero-D. En el desarrollo de insuficiencia
cardíaca derecha, se puede desarrollar hipoalbuminemia si se produce ascitis
debido a la congestión hepática.

Se han descrito elevaciones de NT-proBNP (péptido natriurético secretado por

el miocardio en respuesta al aumento de la distensión) en pacientes con HTP
precapilar, y con HTP de moderada a severa, respecto a perros no hipertensos
o con HTP leve. También se ha observado una fuerte correlación positiva entre
la presión arterial sistólica estimada por el pico de regurgitación tricuspídea y
las concentraciones plasmáticas de NT-proBNP. Además, el incremento de la
troponina I cardiaca, como biomarcador de lesión miocárdica, se ha asociado
a menores tiempos de supervivencia en pacientes.

3. ELECTROCARDIOGRAFÍA

El electrocardiograma no es una prueba específica para diagnóstico o evalua-

ción de la HTP. Cuando aparecen alteraciones evaluables mediante esta técnica,
se desarrollan de forma secundaria a la enfermedad subyacente; puede obser-
varse una desviación del eje eléctrico hacia la derecha o dextroeje por cardio-
megalia derecha, arritmias supraventriculares o ventriculares asociado a enfer-
medad cardiaca izquierda, o bien bradiarritmias y bloqueos atrioventriculares
por un aumento del tono parasimpático ocasionado por enfermedad pulmonar.

4. RADIOGRAFÍA

En muchas ocasiones las radiografías torácicas son normales, no siendo pa-

tognomónicas de la enfermedad. No suelen ser específicas para el diagnóstico
de HTP pero se pueden evidenciar cambios que lo sugieran, dependiendo de la
causa subyacente de hipertensión pulmonar. Dentro de estos cambios se en-
cuentran cardiomegalia generalizada, cardiomegalia derecha y/o dilatación de
la arteria pulmonar (Figura 1). Cuando la HTP es secundaria a enfermedad
valvular mitral crónica se aprecian signos de insuficiencia cardiaca derecha,

74 Canis et Felis Número 133 - Abril 2015

 Actualización en hipertensión pulmonar arterial en perros. Conceptos básicos

junto a los hallazgos típicos de la cardiopatía izquierda (elevación de la tráquea

y compresión bronquial, aumento de tamaño de la silueta de atrio y ventrículo
izquierdo, dilatación de venas pulmonares, áreas de edema intersticial-alveo-
lar, etc.) a los que pueden asociarse patrones radiológicos compatibles con
bronquitis crónica, bronquiectasia, fibrosis pulmonar o colapso traqueobron-
quial. En los casos de síndrome de Eisenmenger, los pulmones parecen hipo-
perfundidos y la arteria pulmonar principal y las arterias lobares proximales
se encuentran dilatadas. En los casos de dirifilatiosis, con frecuencia la radio-
grafía torácica muestra arterias pulmonares dilatadas y tortuosas, dilatación
de las arterias lobares, dilatación y brusca terminación de las arterias pulmo-
nares periféricas (más evidente en los lóbulos caudales), cambios alveolares e
intersticiales, dilatación de ventrículo derecho con infiltrados pulmonares co-
rrespondientes a hemorragias o edema y, con menos frecuencia, efusión pleu-
ral y áreas de consolidación pulmonar y atelectasia (Figuras 2a y b).

Figura 1: Estudio radiográfico de silueta cardiaca en proyección dorso ventral (DV), con signo de
agrandamiento de cámaras derechas (signo de D invertida) y patrón hipervascular arterial y arteria
pulmonar dilatada.

Número 133 - Abril 2015 Canis et Felis 75

 ENFERMEDADES CARDIORRESPIRATORIAS DE PEQUEÑOS ANIMALES

Figura 2: (a) Estudio radiográfico de silueta cardiaca en proyección dorso ventral (DV) de un perro
con Dirifilatiosis donde se aprecia cardiomegalia, dilatación del tronco pulmonar y arterias pulmo-
nares y arterias lobares aumentadas. (b) Estudio radiográfico latero-lateral derecho en el que se
observa un patrón vascular e intersticial con aumento de la silueta cardiaca principalmente de las
cámaras derechas.

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 Actualización en hipertensión pulmonar arterial en perros. Conceptos básicos

5. ECOCARDIOGRAFÍA
La ecocardiografía es la técnica de elección para diagnosticar HTP, ya que
permite medir de manera no invasiva la presión y velocidades de flujo, visua-
lizar cambios de remodelación en cámaras cardiacas, y determinar la función
cardiaca relacionada a cambios por HTP.
La determinación de la velocidad máxima de regurgitación de la válvula tricús-
pide es el método ecocardiográfico más comúnmente empleado para diagnos-
ticar HTP, aunque no siempre es detectable. En ausencia de elevaciones en la
postcarga derecha asociada a alteraciones congénitas, como por ejemplo una
estenosis pulmonar, un pico de velocidad de regurgitación tricuspídea mayor a
2.8 m/s se considera anormal e indicativo de HTP (Figuras 3a y 3b).

a b

Figura 3a: Vista de cuatro cámaras en corte paraesternal longitudinal izquierdo, donde se aprecia
insuficiencia tricuspídea mediante Doppler color.
Figura 3b: Doppler contínuo con velocidades de regurgitación tricuspídea superiores a 2,7 m/s (imagen
cedida por H. V. Molins).

En ausencia de obstrucción del tracto de salida del ventrículo derecho, la

presión sistólica ventricular derecha es una estimación de la presión arterial
pulmonar sistólica y, por tanto, puede ayudar a identificar y a clasificar la HTP.
La presión arterial pulmonar sistólica tiene rangos que van desde los 15 a 25
mmHg en perros sanos, sin embargo, ésta puede incrementarse en ciertas
condiciones fisiológicas, como puede ser habitar a elevada altitud o en perros
de trabajo con elevada masa muscular. Las HTP se clasifica desde leve (30-50
mmHg), moderada (50-80 mmHg) a grave (>80 mmHg).
La presencia de insuficiencia pulmonar permite evaluar la presión arterial
pulmonar diastólica. La insuficiencia pulmonar ocurre en diástole y permite
diferenciar la presión de arteria pulmonar-ventrículo derecho. Esta medida es
útil en caso de que la regurgitación tricuspídea no sea evidente. La velocidad
de la insuficiencia pulmonar de 2.2 m/s o más o un gradiente de presión de 19

Número 133 - Abril 2015 Canis et Felis 77

 ENFERMEDADES CARDIORRESPIRATORIAS DE PEQUEÑOS ANIMALES

mmHg o mayor es sugerente de HTP (Figura 4). Aun así, el flujo de regurgita-
ción pulmonar puede no estar presente en todos los pacientes con HTP.

Figura 4: Doppler color y espectral de arteria pulmonar con presencia de jet regurgitante dias-
tólico.

Los pacientes con HTP tienen mayor postcarga ventricular derecha, por lo que las
dimensiones de las cámaras derechas pueden ser normales o bien pueden pre-
sentarse dilatadas de forma leve a grave (Figura 5). Se puede apreciar cierto grado
de hipertrofia ventricular derecha y dilatación del ventrículo derecho, movimiento
septal paradójico y aplanamiento del septo interventricular debido a una sobrecar-
ga de presión ventricular derecha (Figura 6).Normalmente también se identifica
dilatación de la arteria pulmonar en pacientes con HTP (Figura 7). El diámetro nor-
mal de la arteria pulmonar principal en relación a la aorta en el corte paraesternal
derecho a nivel de la base en eje corto es de 0.98 (relación PA/Ao). En los casos
de infección por dirifilatiosis pulmonar los parásitos se visualizan en la arteria
pulmonar o en las cavidades derechas como dos líneas paralelas hiperecoicas.

Figura 5: Corte pa-

raesternal longitudinal
derecho de cuatro
cámaras, en el que se
observa dilatación de
las cámaras derechas
en relación al ventrícu-
lo izquierdo y aurícula
izquierda.

78 Canis et Felis Número 133 - Abril 2015

 Actualización en hipertensión pulmonar arterial en perros. Conceptos básicos

Figura 6: El aplana-
miento septal es uno
de los parámetros
subjetivos en modo B
que pueden sugerir un
aumento de presión
en cámaras derechas
secundario a hiperten-
sión pulmonar.

Figura 7: Dilatación
de la arteria pulmonar
principal. En la imagen
se aprecia un marcado
incremento en la ratio
pulmonar: aorta.

Otros parámetros, como los perfiles de velocidad de flujo sistólico en el Doppler

espectral de la arteria pulmonar, pueden ser de utilidad en el diagnóstico. En
pacientes con presión arterial pulmonar normal, se registra un perfil tipo I, con
velocidades de aceleración y desaceleración iguales produciendo una apariencia
simétrica. Conforme aumentan las presiones arteriales pulmonares, se registra
un perfil asimétrico debido a una rápida aceleración inicial y a una velocidad pico
temprana. Este perfil asimétrico sucede como resultado de una mayor tasa de
aumento en las presiones vasculares pulmonares y se le conoce como perfil tipo
II. Los perfiles tipo II se relacionan con HTP leve a moderada. En casos graves hay
una rápida aceleración con una velocidad pico inicial y una muesca sistólica me-
dia también presente, a lo cual se le conoce como perfil tipo III. La muesca sistóli-
ca indica flujo sanguíneo inverso, secundario a presiones vasculares pulmonares
elevadas y presenta un 80% de sensibilidad y especificidad para diagnosticarla.

Número 133 - Abril 2015 Canis et Felis 79

 ENFERMEDADES CARDIORRESPIRATORIAS DE PEQUEÑOS ANIMALES

Otras medidas que se han uti-

lizado para ayudar al diagnós-
tico de HTP en perros son los
tiempos de intervalo ventricu-
lar sistólico, como es el tiempo
de aceleración (TA), tiempo de
eyección (TE), la relación TA/
TE, así como el periodo de pre-
eyección (PPE) (Figura 8). Estos
valores reflejan cambios en la
carga de ventrículo derecho de-
mostrándose que una relación
TA/TE igual o inferior de 0.31, y
un valor de TA igual o inferior a
0.58 ms son predictivos de HTP.
Estos cambios pueden ayudar
en el diagnóstico cuando otros
hallazgos clínicos lo sugieran y
no se detecte la medida Doppler
Figura 8: Perfil Doppler de flujo sistólico de arteria de regurgitación tricuspídea.
pulmonar con mediciones de tiempo de acelera-
La excursión sistólica del anillo
ción, desaceleración, de eyección y período de pre-
eyección. (Imagen cedida por H. V. Molins). plano tricuspídeo (TAPSE) es un
parámetro ecocardiográfico que
ha sido desarrollado en humanos
para evaluar la función sistólica de ventrículo derecho. Éste mide el desplaza-
miento apical de la porción lateral del anillo de la válvula tricúspide durante
la sístole desde el modo M. En pacientes con HTP, los valores de TAPSE por
debajo de los rangos de referencia se asocian a una disminución de la función
sistólica ventricular derecha y se relaciona a una alta mortalidad. El TAPSE se
mide en modo M a nivel del aspecto lateral del anillo de la válvula tricúspide
mediante el corte paraesternal izquierdo de cuatro cámaras (Figura 9).

TRATAMIENTO
Una vez se ha podido identificar y tratar la causa subyacente de la HTP, se puede
completar el tratamiento utilizando medicamentos para ayudar a reducir la pre-
sión arterial pulmonar y la carga sobre el ventrículo derecho con el fin de mejorar
los signos clínicos como la intolerancia al ejercicio, la disnea, la tos, y reducir los
episodios de síncopes para mejorar la calidad de vida y el tiempo de supervivencia.

1. Análogos de la prostaciclina
La prostaciclina es un agente vasodilatador, inhibidor de la actividad plaqueta-
ria y que presenta efectos antiproliferativos. Entre los análogos de la prostaci-
clina se encuentran el epoprostenol, treprostinil, y el iloprost. El epoprostenol y
trepostinil se administran por vía intravenosa, el treprostinil puede administrar-

80 Canis et Felis Número 133 - Abril 2015

 Actualización en hipertensión pulmonar arterial en perros. Conceptos básicos

Figura 9: Medición del TAPSE. Modo M a nivel del aspecto lateral del anillo de la válvula tricúspide
visto en el corte apical de cuatro cámaras por la ventana paraesternal izquierda centrado en el
ventrículo derecho.

se por vía subcutánea y el iloprost puede ser administrado vía inhalatoria. En

humanos, estos medicamentos mejoran la sintomatología y la supervivencia.
Los efectos secundarios a su administración incluyen anemia, trombocitopenia,
hipotensión y síntomas gastrointestinales. Se ha observado que estos fármacos
son eficaces a nivel experimental en el tratamiento de la HTP canina pero aún
no hay evidencias clínicas publicadas. Dado su elevado coste económico, su
administración al paciente veterinario resulta impracticable.

2. Antagonistas de la endotelina
Es posible reducir la presión arterial pulmonar al antagonizar las acciones
de la endotelina 1. Los antagonistas de la endotelina más comunes incluyen
bosentán, sitaxsentan y ambrisentan. En humanos, estos medicamentos ad-
ministrados vía oral han demostrado mejorar la intolerancia al ejercicio, la
presión arterial pulmonar y la resistencia pulmonar. El bosentán se ha eva-
luado en perros de forma experimental; en estos pacientes, el bosentán fue
eficaz y redujo el remodelamiento vascular, mejoró la función miocárdica y
redujo el remodelamiento ventricular. Estos medicamentos, aunque menos
caros que los análogos de la prostaciclina, se consideran prohibitivos por su
coste en pacientes veterinarios y aún no se han llevado a cabo pruebas clíni-
cas en pacientes con HTP no inducida experimentalmente.

Número 133 - Abril 2015 Canis et Felis 81

 ENFERMEDADES CARDIORRESPIRATORIAS DE PEQUEÑOS ANIMALES

3. Óxido nítrico y nitratos

El óxido nítrico es un vasodilatador administrado por vía inhalatoria, mientras
que el dinitrato de isosorbide y el mononitrato de isosorbide son vasodilata-
dores de administración vía oral. En humanos, los nitratos son prescritos por
sus efecto vasodilatador frente a la isquemia miocárdica, teniendo un valor
limitado en el tratamiento de la HTP. Estos medicamentos no son utilizados
de manera común en medicina veterinaria a causa de sus efectos colaterales
potencialmente graves. La L-arginina, precursor del óxido nítrico, ha sido ad-
ministrada en humanos con HTP observándose una mejora en las concentra-
ciones de óxido nítrico y ocasionando vasodilatación.

4. Inhibidores de la fosfodiesterasa 5
Hay varios inhibidores de la fosfodiesterasa 5 (PDE-5, por sus siglas en inglés)
incluyendo al sildenafil, tadalafil y vardenafil. Estos medicamentos inhiben de
manera específico a la PDE-5, la cual se encuentra en concentraciones elevadas
en los vasos pulmonares. La PDE-5 degrada al monofosfato de guanosina cíclico
(cGMP), de forma que cuando la PDE-5 es inhibida, las concentraciones de cGMP
aumentan y se promueve la vasodilatación. En humanos, los inhibidores de PDE-5
causan vasodilatación arterial pulmonar pero hay diferencias sutiles entre las tres
sustancias con respecto al inicio y duración de acción, el grado de reducción de la
resistencia vascular pulmonar y la habilidad para revertir la hipertrofia cardiaca.
El sildenafil es un inhibidor de la PDE-5 de corta duración. Se ha evaluado en
el tratamiento de la HTP canina y ha demostrado reducir la presión arterial
pulmonar, mejorar la calidad de vida y aumentar el tiempo de supervivencia.
En algunos pacientes presenta algunos efectos secundarios gastrointestina-
les y, aunque es un producto relativamente caro, puede ser accesible para
la mayoría de los propietarios. Se considera el fármaco de elección para el
tratamiento de la HTP en perros. La dosis recomendada de sildenafil es de 1
a 3 mg/kg por vía oral cada 8 a 12 horas.
El pimobendan y el levosimendan son fármacos de mecanismo dual; ejercen
efectos inotrópicos positivos relacionados con la sensibilización al calcio, así
como efectos vasodilatadores mediados por la inhibición de la PDE-3. Desde
el punto de vista clínico, el pimobendan ha demostrado mejorar la HTP se-
cundaria a enfermedad degenerativa de la válvula mitral (clase clínica II).

PRONÓSTICO
Los cambios estructurales que se producen a nivel pulmonar y que dan lugar
a la HTP son irreversibles. Por lo tanto, según la respuesta al tratamiento ad-
ministrado en función a la patología causante de la HTP, el pronóstico variará y
será más favorable o desfavorable a corto y medio plazo. A largo plazo, el pro-
nóstico siempre debe ser reservado. Éste suele ser peor en aquellos pacientes
con HTP secundaria a una patología pulmonar crónica, en comparación a los
casos secundarios a incrementos de presión en el lado izquierdo del corazón.

82 Canis et Felis Número 133 - Abril 2015

 Actualización en hipertensión pulmonar arterial en perros. Conceptos básicos

BIBLIOGRAFÍA
1. ATKINSON, K. J., FINE, D. M., THOMBS, L. A., GORELICK, J. J. & DURHAM, H. E. 2009. Evaluation of
Pimobendan and N-Terminal Probrain Natriuretic Peptide in the Treatment of Pulmonary Hypertension
Secondary to Degenerative Mitral Valve Disease in Dogs. Journal of Veterinary Internal Medicine, 23, 1190-1196.
2. BACH, J. F., ROZANSKI, E. A., MACGREGOR, J., BETKOWSKI, J. M. & RUSH, J. E. 2006a. Retrospective
evaluation of sildenafil citrate as a therapy for pulmonary hypertension in dogs. Journal of veterinary
internal medicine, 20, 1132-1135.
3. CHIAVEGATO, D., BORGARELLI, M., D’AGNOLO, G. & SANTILLI, R. A. 2009. Pulmonary Hypertension
in Dogs with Mitral Regurgitation Attributable to Myxomatous Valve Disease. Veterinary Radiology &
Ultrasound, 50, 253-258.
4. FLEMING E. Pulmonary hypertension. Compend Contin Educ Vet 2006;28:720–30.
5. GLAUS, T. M., SOLDATI, G., MAURER, R. & EHRENSPERGER, F. 2004. Clinical and pathological charac-
terisation of primary pulmonary hypertension in a dog. Vet Rec, 154, 786-89.
6. JOHNSON, L., BOON, J. & ORTON, E. 1999. Clinical characteristics of 53 dogs with Doppler-derived
evidence of pulmonary hypertension: 1992-1996. J Vet Intern Med, 13, 440-7.
7. KELLIHAN, H. B. & STEPIEN, R. L. 2010. Pulmonary hypertension in dogs: diagnosis and therapy. Vet
Clin North Am Small Anim Pract, 40, 623-41.
8. KELLIHAN, H. B. & STEPIEN, R. L. 2012. Pulmonary hypertension in canine degenerative mitral valve
disease. J Vet Cardiol, 14, 149-64.
9. KELLUM HB, STEPIEN RL. Sildenafil citrate therapy in 22 dogs with pulmonary hypertension. J Vet Intern
Med 2007;21(6):1258–64.
10. KIM, H., YUNG, G. L., MARSH, J. J., KONOPKA, R. G., PEDERSEN, C. A., CHILES, P. G., MORRIS, T. A.
& CHANNICK, R. N. 2000. Endothelin mediates pulmonary vascular remodelling in a canine model of
chronic embolic pulmonary hypertension. European Respiratory Journal, 15, 640-648.
11. MCLAUGHLIN, V. V., ARCHER, S. L., BADESCH, D. B., BARST, R. J., FARBER, H. W., LINDNER, J. R.,
MATHIER, M. A., MCGOON, M. D., PARK, M. H. & ROSENSON, R. S. 2009. ACCF/AHA 2009 Expert Consensus
Document on Pulmonary HypertensionA Report of the American College of Cardiology Foundation Task
Force on Expert Consensus Documents and the American Heart Association Developed in Collaboration
With the American College of Chest Physicians; American Thoracic Society, Inc.; and the Pulmonary
Hypertension Association. Journal of the American College of Cardiology, 53, 1573-1619.
12. MONTOYA, A. J.-A. & CARRETÓN, E. 2012. Dirifilatiosis pautas de manejo clínico, Barcelona, España,
Multimedica Ediciones Veterinarias.
13. OYAMA, M. A. & SISSON, D. D. 2004. Cardiac Troponin-I Concentration in Dogs with Cardiac Disease.
Journal of veterinary internal medicine, 18, 831-839.
14. PARADIES, P., SPAGNOLO, P. P., AMATO, M. E., PULPITO, D. & SASANELLI, M. 2014. Doppler echocar-
diographic evidence of pulmonary hypertension in dogs: a retrospective clinical investigation. Veterinary
Research Communications, 38, 63-71.
15. QUINN, R. L. & WILLIAMS, J. G. 2011a. Canine pulmonary hypertension Part 1: An in-depth review of its
pathophysiology and classifications. Veterinary Medicine, 6, 454-9.
16. QUINN, R. L. & WILLIAMS, J. G. 2011b. Canine pulmonary hypertension, Part 2: Diagnosis and treatment.
Veterinary Medicine, 6, 26-36.
17. SCHOBER, K. & BAADE, H. 2006. Doppler echocardiographic prediction of pulmonary hypertension in
West Highland white terriers with chronic pulmonary disease. J Vet Intern Med, 20, 912-20.
18. SERRES, F., CHETBOUL, V., GOUNI, V. & AL, E. 2007. Diagnostic Value of Echo-Doppler and Tissue Doppler
Imaging in Dogs with Pulmonary Arterial Hypertension. J Vet Intern Med, 21, 1280-89.
19. SILVA, A. C., OBERLENDER, G., MANTOVANI, M. M., MUZZI, R. A. L., PEREIRA, L. J. & ZANGERONIMO, M.
G. 2014. Efficacy of sildenafil therapy for pulmonary hypertension in dogs: a systematic review. Archivos
De Medicina Veterinaria, 46, 277-287.
20. SIMONNEAU, G., GATZOULIS, M. A., ADATIA, I., CELERMAJER, D., DENTON, C., GHOFRANI, A., SANCHEZ,
M. A. G., KUMAR, R. K., LANDZBERG, M., MACHADO, R. F., OLSCHEWSKI, H., ROBBINS, I. M. & SOUZA,
R. 2013. Updated Clinical Classification of Pulmonary Hypertension. JACC, 62, 34-41.
21. STEPIEN, R. 2009. Pulmonary arterial hypertension secondary to chronic left-sided cardiac dysfunction
in dogs. J Small Anim Pract, 50, 34-43.

Número 133 - Abril 2015 Canis et Felis 83

CONSULTANT ON CALL h CARDIOLOGY h PEER REVIEWED

Pulmonary
Hypertension From
a Non-cardiologist
Perspective
Elizabeth Rozanski, DVM, DACVIM (Small Animal),
DACVECC
Tufts University

PROFILE Genetic Implications

Definition
h Pulmonary hypertension (PHTN) is an
increase in pulmonary arterial pressures
(PAP).
• Normal systolic PAP is <25 mm Hg. Clini-
cal signs of PHTN are typically seen at
>50 mm Hg.
• In dogs with severe signs (eg, syncope),
pressures close to 100 mm Hg are
common.1
• Clinical signs may be common with higher
pressures.
Systems
h The cardiopulmonary system is primarily
affected, but with severe PHTN, limited
cardiac output affects the entire patient
by causing exercise intolerance, respiratory
h There are no known genetic influences.
h Certain dog breeds may be likely to develop
mitral valve disease (MVD), which may
result in PHTN, and West Highland white
terriers (Westies) are considered at PHTN appears
increased risk for pulmonary fibrosis that to be recognized
may lead to the development of secondary more frequently
PHTN.2 with more
widespread
Incidence & Prevalence availability of
h Unknown, but PHTN appears to be recog- echocardiography.
nized more frequently with more wide-
spread availability of echocardiography.
h Geographic distribution is worldwide; the
presence of heartworm disease will increase
the likelihood of PHTN, and high altitude
(>2000 m, about 6560 ft) may worsen PTHN.3 MVD = mitral valve disease
PAP = pulmonary arterial
Signalment pressure

distress, and syncope. h Dogs are much more commonly affected PHTN = pulmonary
hypertension
than cats.

February 2016 cliniciansbrief.com 85

CONSULTANT ON CALL h CARDIOLOGY h PEER REVIEWED

intolerance are the most common signs.

• Some dogs have cough associated with
CATEGORIES OF CANINE PULMONARY HYPERTENSION4
either MVD or chronic pulmonary disease.
PHTN is classified into 5 categories in humans. Some veterinarians use the h There are no specific history and clinical

human classification model (below); others prefer to categorize cases as signs that clearly signify PHTN.
primary (rare) and secondary. Regardless, suspicion or documentation h Westies with pulmonary fibrosis or dogs
of PHTN should prompt a complete patient evaluation for underlying with heartworm disease should prompt
medical disease resulting in PHTN. specific concern for PHTN.
1. Pulmonary arterial hypertension, including idiopathic, congenital
heart disease, some connective tissue disorders, and, in developing Physical Examination
countries, schistosomiasis h A split or, less commonly, loud S2 is classi-
2. Left-sided heart failure, the most common cause of PHTN in humans cally appreciated on cardiac auscultation,
and in dogs as is mild-to-moderate tachycardia.
h Other possible abnormalities include signs
3. Chronic pulmonary disease (eg, pulmonary fibrosis, chronic bronchitis);
of right-sided heart failure (eg, jugular
also considered common in dogs
venous distension, hepatomegaly, ascites).
4. Chronic pulmonary thromboembolism

5. Miscellaneous, which includes various other causes (eg, polycythemia, DIAGNOSIS

vasculitis). Heartworm disease, which is common in dogs, may lead to
the development of PHTN.
h Westies are more commonly affected by
pulmonary fibrosis, which may lead to
secondary PHTN, than other breeds.2
h Can affect any age but tends to occur in
Definitive Diagnosis
h The gold standard in humans for diagnosis
of pulmonary arterial hypertension is a
right-heart catheterization for direct
assessment of pressure; although this
is possible in dogs and cats, it is rarely
performed.
h In veterinary medicine, PHTN is most com-

older patients.1 monly inferred by echocardiography.

h Both sexes are equally affected.1 • Echocardiography may provide an esti-
mate of PAP based on the speed (m/sec) of
Risk Factors the tricuspid or pulmonary regurgitant jet.
h Advancing age and/or presence of • Echocardiography is also useful to iden-
long-standing MVD or chronic pulmonary tify structural changes in the heart,
disease including paradoxical septal motion,
enlarged right heart, and a volume-
Pathophysiology underloaded (small) left heart.
h Depends on the underlying cause but • From the clinician’s standpoint, echocardi-
includes increasing pressures associated ography should be considered the most
with chronic pulmonary venous hyperten- useful method to document PHTN (Figure 1).
CT = computed sion or chronic pulmonary disease.
tomography
• In congenital heart disease, there may be Differential Diagnosis
MVD = mitral valve
disease primary arterial disease; with thrombotic h Before an echocardiogram, other differen-
PAP = pulmonary disease, there is occlusion to blood flow. tials include mitral valve disease with con-
arterial pressure gestive heart failure and other cardiac
PHTN = pulmonary History & Clinical Signs disease (eg, pericardial effusion with tam-
hypertension
h Respiratory distress, syncope, and exercise ponade, dilated cardiomyopathy), upper

86 cliniciansbrief.com February 2016

 airway disease, or pneumonia.
h With syncope, differential diagnoses may

include seizure or arrhythmia.

h After echocardiographic confirmation of

PHTN, the focus should shift to identifying

the cause of PHTN.

Laboratory Findings
h Laboratory testing is typically unremark-
able unless there is underlying systemic
disease, including heartworm disease.
h Hypercoagulable conditions may lead to

pulmonary thromboembolism.
• Hypercoagulability may be difficult to
1A
detect on routine laboratory testing.
h NT pro-BNP, while emerging as a useful

marker in cardiac disease, is typically ele-

vated in PHTN and may inadvertently result
in treatment for congestive heart failure,5
which may or may not be present.
h Higher doses of furosemide may result in

worsening syncope in dogs with PHTN

without left-sided cardiac disease.

Imaging
h Echocardiography is the most definitive
diagnostic imaging.
h Thoracic radiographs are useful for evalua- 1B
tion but may underestimate the severity of
the PHTN.
d Echocardiographic Doppler study documenting high tricuspid
• However, it may be possible to appreciate regurgitant velocity consistent with pulmonary hypertension.
right-sided enlargement (reverse “D”) The modified Bernoulli equation [change in pressure = 4 ×
or pulmonary arterial enlargement (regurgitant velocity)2] may be used to estimate the systolic
(Figure 2, next page). PAP. In the example shown, the tricuspid regurgitant velocity
h Computed tomography (CT) and, particu- is 4.1 m/sec; thus, estimated PAP is 67 mm Hg.
larly, CT-angiography is useful to evaluate
lung parenchyma and to determine if pul-
monary thromboembolism is present.
h Abdominal ultrasonography is helpful to

evaluate the patient for other underlying

conditions and to evaluate the hepatic
vessels (Figure 3, page 89).
Laboratory testing is typically
unremarkable unless there is
Postmortem Findings
h Postmortem findings may reflect the
underlying systemic disease,
underlying cause. including heartworm disease.

February 2016 cliniciansbrief.com 87

CONSULTANT ON CALL
Fluid therapy is
contraindicated
in most cases of
PHTN because
of volume
overload of the
right side of
the heart.
ACE = angiotensin-
converting enzyme
PHTN = pulmonary
hypertension
PAP = pulmonary
arterial pressure
88 cliniciansbrief.com
h CARDIOLOGY h PEER REVIEWED
2A
2B
d Lateral and VD thoracic radiographs of a
dog with PHTN, showing mild right-sided
enlargement of the heart and enlarged
pulmonary arteries (arrows).
TREATMENT
Inpatient vs Outpatient
h Decisions should be based on the stability
of the patient.
h Severely affected animals benefit from
inpatient oxygen therapy, as oxygen is a
potent pulmonary vasodilator.
h Mildly affected patients may be treated at
home.
February 2016
Medical
h Oxygen is administered if patient is
severely affected and sildenafil (1-3 mg/kg
orally 2 to 3 times a day) is the most com-
monly used medication.
h Even in patients without pulmonary throm-
boembolism as an underlying cause, vascu-
lar stasis may lead to an increased risk for
thrombotic disease, but the role of antico-
agulant therapy in patients with PHTN
remains unclear.
h Dogs with inflammatory lung disease may
benefit from glucocorticoids; those with
heart failure benefit from standard therapy
with furosemide, pimobendan, and
angiotensin-converting enzyme (ACE)
inhibitors.
h Fluid therapy is contraindicated in most
cases of PHTN because of volume overload
of the right side of the heart.
h Sildenafil may be the most useful specific
drug for PHTN.
h Other drug therapy may be warranted by
the underlying condition.
Contraindications
h Nitrates (eg, nitroglycerin) are contraindi-
cated in dogs receiving sildenafil.
h Furosemide may result in worsening of
cardiac output and is not indicated in dogs
that do not have concurrent left-sided
congestive heart failure.
Precautions/Interactions
h Anesthesia is considered high-risk in dogs
with severe PHTN.
• Procedures should only be performed
when the benefit outweighs the risk and
ideally with a veterinary anesthesiologist.
Nutritional
h Maintenance of a normal body condition is
a goal.
h Some dogs experience loss of appetite and
may require coaxing to eat adequate
amounts.
Activity
h Activity should be limited based on degree
of patient’s comfort.
h Excessive exertion should be avoided.

• In moderately-to-severely affected dogs,

exercise should be limited.
–Smaller patients may be carried up and
down stairs.

Client Education
h Client education is important, as PHTN is a
severe condition that tends to progress
over time. 3
Alternative Therapy d Abdominal ultrasound image documenting enlarged hepatic
h None proven; fish oil supplementation may vessels consistent with right-sided heart failure.
be considered to decrease inflammation
and help decrease platelet adhesion

FOLLOW-UP

Patient Monitoring
h Monitoring should include evaluation for
worsening respiratory distress or exercise
intolerance.
h Recheck echocardiography may be useful
to monitor changes in PAP, although pul-
monary pressures may not correlate with
At-Home Treatment
h Exercise should be restricted.
h Treat for primary condition, if identified.
• Sildenafil, possibly pimobendan
h Anticoagulants are likely warranted in

clinical signs. humans, and possibly in dogs.

• Changes in right ventricular motion and h Home oxygen therapy, if possible.

left ventricular filling are good at assess-

ing response, but tricuspid regurgitation
and perfusion index gradients rarely
change substantially.
Complications
Future Follow-Up
h Recheck regularly; monitor for develop-
ment of right-sided heart failure or azote-
mia secondary to low cardiac output.
h Ascites may be drained as needed for

h PHTN is a progressive disease, and cardio- patient comfort.

pulmonary failure is the most likely ulti-
COST KEY
mate outcome.
IN GENERAL
h Most dogs are euthanized for humane rea- $ = up to $100
sons associated with respiratory distress, Relative Cost
$$ = $101–$250
syncope, or heart failure. h $$$-$$$$$: Diagnosis of PHTN with echo-
cardiography alone is $$$; if CT or other
$$$ = $251–$500
h Sudden death is possible.

h Concurrent administration of nitrates may imaging is pursued, costs will increase to $$$$ = $501–$1000
be associated with severe hypotension and $$$$$. $$$$$ = more than
should be avoided. h Sildenafil is expensive for daily use. $1000

February 2016 cliniciansbrief.com 89

CONSULTANT ON CALL h CARDIOLOGY
Prognosis
h Prognosis is fair; some dogs with less
profound signs will do well for
months to perhaps a year; badly
affected dogs may not survive to hos-
pital discharge.
h Dogs with mild-to-moderate PHTN
associated with MVD often do quite
well, and the development of PHTN is
not a particularly ominous sign in
these dogs.
h As in all diseases, owner expectations
and decisions influence survival
times.
Prevention and Management
h Heartworm preventive therapy is
warranted for all dogs in endemic
regions.
References
1. Kellihan HB, Stepien RL. Pulmonary hyper-
tension in dogs: diagnosis and therapy. Vet Clin
North Am Small Anim Pract. 2010:40(4):623-641.
2. Glaus TM, Hässig M, Baumgartner C, Reusch CE.
Pulmonary hypertension induced in dogs by
hypoxia at different high-altitude levels. Vet Res
Commun. 2003;27(8):661-670.
3. Schober KE, Baade H. Doppler
echocardiographic prediction of pulmonary
hypertension in West Highland white terriers
with chronic pulmonary disease. J Vet Intern
Med. 2006;20(4):912-920.
4. Ryan JJ, Thenappan T, Luo N, et al. The WHO
classification of pulmonary hypertension: A
case-based imaging compendium. Pulm Circ.
2012;2(1):107-121.
5. Kellihan HB, Mackie BA, Stepien RL. NT-proBNP,
NT-proANP and cTnI concentrations in dogs
with pre-capillary pulmonary hypertension.
J Vet Cardiol. 2011;13(3):171-182.
Suggested Reading
Arita S, Arita N, Hikasa Y. Therapeutic effect of
low-dose imatinib on pulmonary arterial
hypertension in dogs. Can Vet J. 2013;54(3):
255-561.
MVD = mitral valve disease
PHTN = pulmonary hypertension
90 cliniciansbrief.com February 2016
h PEER REVIEWED
h Other methods of prevention have not
been established.
h If possible, affected dogs should not
live at high altitudes and should not
vacation in the mountains.
• Air travel should be avoided in
affected dogs.
Future Considerations
h Improved awareness may open up
therapeutic options such as treatment
with endothelin receptor antagonists
(eg, bosentan) or with tyrosine kinase
inhibitors, which have been used with
some success in humans (although, to
date, no evidence exists in dogs).
• These drugs are expensive and may
have significant side effects. n
Brown AJ, Davison E, Sleeper MM. Clinical efficacy
of sildenafil in treatment of pulmonary arterial
hypertension in dogs. JVIM. 2010;24(4):850-854.
Chiavegato D, Borgarelli M, D’Agnolo G, Santilli RA.
Pulmonary hypertension in dogs with mitral
regurgitation attributable to myxomatous
valve disease. Vet Radiol Ultrasound. 2009:50(3):
253-258.
Johnson L, Boon J, Orton EC. Clinical
characteristics of 53 dogs with Doppler-derived
evidence of pulmonary hypertension: 1992-
1996. J Vet Intern Med. 1999;13(5):440-447.
Rush JE, Keene BW, Fox PR. Pericardial disease in
the cat: A retrospective evaluation of 66 cases.
JAAHA. 1990;26:39-46.
Serres FJ, Chetboul V, Tissier R, et al. Doppler
echocardiography-derived evidence of
pulmonary arterial hypertension in dogs with
degenerative mitral valve disease: 86 cases
(2001-2005). JAVMA. 2006:229(11):1772-1778.
Stepian RL, Whitely NT, Dubielzig RR. Idiopathic or
mesothelioma-related pericardial effusion:
clinical findings and survival in 17 dogs studied
retrospectively. Small Anim Pract. 2000:
41(8):342-347.
VETORYL® CAPSULES
(trilostane)
5 mg, 10 mg, 30 mg, 60 mg and 120 mg strengths
Adrenocortical suppressant for oral use in dogs only.
BRIEF SUMMARY (For Full Prescribing Information,
see package insert.)
CAUTION: Federal (USA) law restricts this drug to
use by or on the order of a licensed veterinarian.
DESCRIPTION: VETORYL Capsules are an orally
active synthetic steroid analogue that blocks
production of hormones produced in the adrenal
cortex of dogs.
INDICATION: VETORYL Capsules are indicated for
the treatment of pituitary- and adrenal-dependent
hyperadrenocorticism in dogs.
CONTRAINDICATIONS: The use of VETORYL
Capsules is contraindicated in dogs that have
demonstrated hypersensitivity to trilostane. Do not
use VETORYL Capsules in animals with primary
hepatic disease or renal insufficiency. Do not use in
pregnant dogs. Studies conducted with trilostane in
laboratory animals have shown teratogenic effects
and early pregnancy loss.
WARNINGS: In case of overdosage, symptomatic
treatment of hypoadrenocorticism with
corticosteroids, mineralocorticoids and intravenous
fluids may be required. Angiotensin converting
enzyme (ACE) inhibitors should be used with caution
with VETORYL Capsules, as both drugs have
aldosterone-lowering effects which may be additive,
impairing the patient’s ability to maintain normal
electrolytes, blood volume and renal perfusion.
Potassium sparing diuretics (e.g. spironolactone)
should not be used with VETORYL Capsules as
both drugs have the potential to inhibit aldosterone,
increasing the likelihood of hyperkalemia.
HUMAN WARNINGS: Keep out of reach of children.
Not for human use. Wash hands after use. Do not
empty capsule contents and do not attempt to divide
the capsules. Do not handle the capsules if pregnant
or if trying to conceive. Trilostane is associated with
teratogenic effects and early pregnancy loss in
laboratory animals. In the event of accidental
ingestion/overdose, seek medical advice immediately
and take the labeled container with you.
PRECAUTIONS: Hypoadrenocorticism can develop
at any dose of VETORYL Capsules. A small
percentage of dogs may develop corticosteroid
withdrawal syndrome within 10 days of starting
treatment. Mitotane (o,p’-DDD) treatment will reduce
adrenal function. Experience in foreign markets
suggests that when mitotane therapy is stopped, an
interval of at least one month should elapse before
the introduction of VETORYL Capsules. The use of
VETORYL Capsules will not affect the adrenal tumor
itself. Adrenalectomy should be considered as an
option for cases that are good surgical candidates.
The safe use of this drug has not been evaluated in
lactating dogs and males intended for breeding.
ADVERSE REACTIONS: The most common adverse
reactions reported are poor/reduced appetite,
vomiting, lethargy/dullness, diarrhea, elevated liver
enzymes, elevated potassium with or without
elevated sodium, elevated BUN, decreased Na/K
ratio, weakness, elevated creatinine, shaking, and
renal insufficiency. Occasionally, more serious
reactions, including severe depression, hemorrhagic
diarrhea, collapse, hypoadrenocortical crisis or
adrenal necrosis/rupture may occur, and may result
in death.
Distributed by:
Dechra Veterinary Products
7015 College Boulevard, Suite 525
Overland Park, KS 66211
VETORYL is a trademark of
Dechra Ltd. © 2015, Dechra Ltd.
NADA 141-291, Approved by FDA
ASK THE EXPERT h RESPIRATORY MEDICINE
Common
Pulmonary
Diseases in Dogs
Douglas Palma, DVM, DACVIM (SAIM)
The Animal Medical Center
New York, New York
YOU HAVE ASKED ...
What should I know about
common canine pulmonary
diseases?
THE EXPERT SAYS ...
Pulmonary disease is a common cause of
respiratory signs in dogs. A thorough
history and examination help localize
the pulmonary parenchyma rather than
other parts of the respiratory system.
Signalment, clinical onset and progres-
sion, geographic location, and additional
organ involvement can help prioritize
differential diagnoses.
Patients with pulmonary disease may
exhibit coughing, increased respiratory
rate, dyspnea, and/or exercise intoler-
h PEER REVIEWED
ance. Depending on cause and nonrespi-
ratory involvement, nonspecific clinical
signs (eg, lethargy, inappetence, weight
loss) may be present. Many patients may
have a mixed pattern of breathing char-
acterized by increased inspiratory and
expiratory effort, as the disease pro-
cesses may involve concurrent airway
obstruction and altered lung compliance.
Therefore, a pure restrictive (decreased
tidal volume, increased respiratory rate)
or obstructive (increased expiratory
effort) pattern of breathing is often not
observed.
The following are pulmonary diseases
frequently encountered in dogs.
Pneumonia
Bacterial Pneumonia
Pneumonia may be community-acquired
(ie, characterized by bronchopneumonia
October 2016 cliniciansbrief.com 77
ASK THE EXPERT h RESPIRATORY MEDICINE h PEER REVIEWED

CDV = canine distemper

virus
CIV = canine influenza
virus
EB = eosinophilic
bronchopneumopathy
PCR = polymerase chain
reaction
RT-PCR = reverse
transcription
polymerase chain
reaction
A ent, many older patients are clinically
in a dog with a history of being housed in
the community) or secondary to altered
pulmonary defenses, aspiration, or
hematogenous infection.
Community-acquired pneumonia is
most common in young dogs and in dogs
with recent exposure to kennels or shel-
ters.1 Exposure to other dogs makes Bor-
detella bronchiseptica most common, but
other opportunistic pathogens may be
involved.1 Streptococcus zooepidemicus,
another emerging bacterial pathogen, is
associated with development of hemor-
rhagic pneumonia.2
Aspiration pneumonia is more common
in older patients. Clinical history is
important to help identify potential
underlying causes. The most commonly
reported causes of aspiration pneumonia
in dogs include esophageal disease, vom-
iting, neurologic disorders, laryngeal
disease, and postanesthetic aspiration.3
Opportunistic infections complicate the
initial aspiration event. A mixed popula-
tion of bacteria with an anaerobic popu-
lation is common. Aspiration pneumonia
is typically characterized by a distribu-
tion to the most dependent lung lobe (ie,
right middle). However, distribution to
any lung or multiple lungs is possible.4
Although respiratory signs may be pres-
silent; pneumonia must be considered in
dogs with nonspecific signs of lethargy,
inappetence, and/or fatigue.

Dogs with bacterial pneumonia are typi-

cally presented with acute-onset cough-
ing, lethargy, inappetence, and/or
respiratory distress. An inflammatory
leukogram and pyrexia, although com-
mon, are not always present. Radiographs
may reveal an interstitial-to-alveolar
pattern with a cranioventral distribution
(Figure 1). Atypical distributions can also
B occur.5

Culture-directed therapy is ideal; how-

ever, empiric treatment with knowledge
of common organisms is reasonable.6
Multidrug-resistant organisms are more
common following recent antibiotic
exposure.7,8

Viral Pneumonia
Viral pneumonia is generally associated
with canine distemper virus (CDV) or
canine influenza virus (CIV). Emerging
d FIGURE 1 (A) Bronchopneumonia. Cranioventral distribution of alveolar disease
with air bronchograms. (B) A patchy distribution can be observed on the lateral viral pathogens (eg, canine pantropic
projection. The changes overlying the heart may be missed in subtle cases. coronavirus, canine pneumovirus) have

78 cliniciansbrief.com October 2016

recently been described.9 Canine herpes-
virus can, albeit rarely, induce intersti-
tial pneumonia.10,11

CDV should be suspected in poorly vacci-

nated dogs with multiorgan involvement.
Dogs with CDV may have exhibited only
respiratory signs before developing char-
acteristic nonrespiratory signs.12 Radio-
graphs may reveal a diffuse interstitial
pattern (Figure 2). Diagnosis is sup-
ported by compatible clinical signs and
complementary diagnostic testing (ie,
real-time reverse transcription poly- d FIGURE 2 CDV pneumonia with a diffuse interstitial pattern confirmed by
merase chain reaction [RT-PCR], serol- multisystemic signs, urine RT-PCR, and necropsy
ogy, CSF pleocytosis). Conjunctival
scraping and tissue-based immunohisto-
chemistry may confirm diagnosis.

CIV may involve the pulmonary paren-

chyma and is often complicated by
opportunistic bacteria. Patients typi-
cally are presented with lethargy,
anorexia, nasal discharge, and cough-
ing. PCR of the nasal cavity or orophar-
ynx within 3 to 5 days of infection may
confirm organism presence. Patients
with clinical signs lasting longer than
5 days may require serologic testing.13
d FIGURE 3 Eosinophilic bronchopneumopathy. Note the heavy, patchy
Fungal Pneumonia bronchointerstitial pattern.
The incidence of fungal disease varies
widely by geographic region. Dogs with buminemia, hyperglobulinemia, nonre-
fungal pneumonia are generally young generative anemia, and monocytosis;
and exhibit signs of generalized illness hypercalcemia and eosinophilia are less
(eg, lethargy, weight loss, pyrexia, common. An inflammatory leukogram
decreased appetite). Many patients with may be observed. Radiographs often
pulmonary involvement do not show show a miliary pattern and may show
respiratory signs; coughing and respira- hilar lymphadenopathy. A combination
tory distress are most common among of serologic and antigen testing may sup-
those that do.14-16 Additional organ sys- port diagnosis. Cytology or tissue histo-
tems (eg, dermatologic, GI, ocular, mus- pathology may identify the organism.18-21
culoskeletal) may be affected.17
Eosinophilic Bronchopneumopathy
Blood testing is somewhat nonspecific. Eosinophilic bronchopneumopathy
Common abnormalities include hypoal- (EB) is an idiopathic inflammatory

October 2016 cliniciansbrief.com 79

ASK THE EXPERT h RESPIRATORY MEDICINE h PEER REVIEWED

hypersensitivity disorder associated ment for pneumonia, have peripheral

with acute onset coughing, gagging,
retching, and/or respiratory distress.
Radiographs may reveal a diffuse bron-
chointerstitial pattern or alveolar dis-
ease (Figure 3, previous page). Patients
with EB have airway cytology support-
ive of eosinophilic inflammation and
are negative for parasitic testing.
eosinophilia, or have uncharacteristi-
cally severe diffuse bronchointersitial
patterns; further diagnostic investiga-
tion is indicated to confirm eosino-
philic inflammation and rule out other
causes. Treatment with corticosteroids
is often successful; however, relapse
can occur after dose tapering.22

EB’s acute nature, occurrence in young Pulmonary Edema

animals, and radiographic findings Noncardiogenic and cardiogenic edema
EB = eosinophilic may mimic pneumonia. EB should be are common causes of pulmonary paren-
bronchopneumopathy
suspected in patients that fail treat- chymal changes in dogs.

A C

B D

d FIGURE 4 (A & B) Congestive heart failure. Note the left-sided cardiomegaly, pulmonary venous
congestion, and interstitial pulmonary pattern. Edema is not exclusively perihilar. (C & D) Noncardiogenic
edema with bilateral, symmetrical caudodorsal distribution without venous congestion or cardiomegaly

80 cliniciansbrief.com October 2016

Cardiogenic edema is caused by
increased hydrostatic pressure and is
readily diagnosed by thoracic radio-
graphic documentation of left-sided
cardiomegaly, pulmonary venous conges-
tion, and a patchy interstitial or alveolar
pattern (frequently perihilar). Echocar-
diographic evaluation may support diag-
nosis.23 Natriuretic peptides may provide
additional insight in differentiation
between congestive heart failure and
other causes of respiratory distress (Fig-
ure 4). Plasma B-type natriuretic peptide
has been shown to have discriminatory
value in dogs; however, some degree of
overlap exists between groups.24
Noncardiogenic edema is a low-pressure
edema characterized by increased blood
vessel permeability. Seizures, electrocu-
tion, strangulation or upper airway
obstruction, local pulmonary disease,
and systemic inflammatory response
syndrome (ie, acute respiratory distress
syndrome) are the most commonly
reported causes.25,26
Thorough clinical history and physical
examination are necessary to identify
potential underlying causes. Careful
auscultation of the upper airways is
important. Radiographs often reveal
bilateral, caudodorsal interstitial, and/
or alveolar disease. Radiographic pro-
gression can occur for as long as 48
hours.27
Lungworms
Lungworms may cause bronchitis and
pneumonia. Chronic coughing is the
most common clinical sign. Acute-onset
exercise intolerance and/or respiratory
distress may also be seen.
Radiographic evaluation can vary from
a diffuse bronchointerstitial pattern to
d FIGURE 5 Crenosoma vulpis (ie, lungworm). Note the patchy, unstructured
interstitial densities. Larvae were recovered on bronchoscopy.
patchy interstitial or alveolar infiltrates
(Figure 5).28 Bullae may occasionally be
appreciated in association with some
infections (eg, Paragonimus kellicotti).29-31
Peripheral eosinophilia is not always
present with infection. Eosinophilic
inflammation on airway cytology sup-
ports diagnosis. Identification of larvae
or oocysts via fecal testing (eg, Baer-
mann technique, fecal centrifugation)
or airway sampling confirms diagno-
sis.32 False-negative results can occur;
any patient with eosinophilic bronchitis
should be treated empirically. An
extended course of fenbendazole (ie,
2 weeks) is generally recommended to
treat most pulmonary worms.
Lung Lobe Torsion
Spontaneous lung lobe torsion occurs in
dogs (most commonly pugs and Afghan
hounds33), can occur in any lung lobe,
and may be secondary to pleural effusion
or thoracic surgery. The right middle
lung lobe is overrepresented in deep-
chested dogs; the left cranial lung lobe
is overrepresented in pugs.33,34
October 2016 cliniciansbrief.com 81
ASK THE EXPERT h RESPIRATORY MEDICINE h PEER REVIEWED
Nonspecific illness and respiratory signs
may be appreciated. Leukocytosis, left
shift, and pyrexia may be present.34
Radiographs often reveal an alveolar pat-
tern, trapped gas (vesiculated), and/or
pleural effusion. Bronchial malposition-
ing is uncommon (Figure 6).35 Confirma-
tion via ultrasonography, bronchoscopy,
and/or CT is recommended.36,37 Pleural
fluid varies widely in gross and cytologic
appearance. Although nonspecific, the
presence of pleural fluid, alveolar disease,
and acute respiratory signs is suggestive.
Immediate lung lobectomy is warranted.
Pulmonary Neoplasia
Radiographs usually reveal structured
interstitial densities within pulmonary
parenchyma.38 These lesions may repre-
sent primary or metastatic lesions. Clin-
ical signs are typically absent, although
coughing is most common. Acute respi-
ratory signs may occur secondary to
generation of pleural effusion or bleed-
ing from a lesion (ie, hemangiosarcoma
metastasis). Depending on the extent of
PAH = pulmonary
arterial hypertension disease, anorexia, lethargy, and weight
PE = pulmonary loss may be appreciated.39
embolism
A B
d FIGURE 6 (A & B) Lung lobe torsion. Note classic vesicular pattern associated with gas trapping and pleural effusion. Bronchial attenuation
or displacement is subtle and often absent.
82 cliniciansbrief.com October 2016
Pulmonary neoplasia may, on occasion,
have a more diffuse nature. This is com-
mon with pulmonary lymphoma40 and
is sometimes seen with carcinoma
(author experience). Pulmonary lym-
phoma can have a rapid clinical course
and mimic acute disorders. A diffuse,
unstructured interstitial pattern is typi-
cally appreciated. Additionally, bron-
chointerstitial, alveolar, and nodular
patterns may be observed (Figure 7).40
Diagnosis of pulmonary lymphoma
requires airway cytology, pulmonary
fine-needle aspiration, and/or confirma-
tion on nonpulmonary samples.41
Carcinoma frequently causes anorexia
and weight loss and should be consid-
ered in older patients with refractory
pneumonia.42
Pulmonary Embolism
Pulmonary embolism (PE) should be
suspected in dogs with acute respiratory
signs, hypoxemia, and minimal radio-
graphic changes. More common disor-
ders should be ruled out. Radiographic
findings vary from normal to patchy/
wedge-shaped alveolar/interstitial infil- A
trates. Pulmonary oligemia may be
appreciated in some patients (Figure 8,
next page).

Diagnostics should focus on document-

ing a predisposing hypercoagulable
state and attempting to confirm throm-
bosis. d-dimers, contrast angiography,
echocardiography, nuclear medicine,
and thoracic CT may indicate PE.43-45
Microvascular thrombosis may only be
documented on necropsy. However, no
test can reliably rule out PE; therefore,
treatment must be considered for B
patients in which the condition is sus-
pected. Optimal management has not
been described; however, anticoagulant
therapy is standard in human patients.
Thrombolytic therapy is standard in
humans with massive pulmonary throm-
boembolism (hemodynamically unsta-
ble). Recently, subpopulations of
submassive pulmonary thromboembo-
lism (hemodynamically stable) have
benefitted from thrombolytic therapy.46
Optimal thrombolytic protocols have not
been designed for dogs or cats. d FIGURE 7 (A) Pulmonary lymphoma with a diffuse, patchy bronchointerstitial
pattern confirmed on bronchoalveolar lavage and peripheral lymph node
aspiration. (B) Pulmonary carcinoma with a diffuse, severe bronchointerstitial
Pulmonary Arterial Hypertension pattern confirmed on bronchoalveolar lavage and postmortem examination.
Pulmonary arterial hypertension (PAH) Note: Pulmonary and hilar lymphadenopathy are not always present.
may be a primary vascular disorder or
secondary to cardiac disease, pulmonary
disease, or pulmonary embolism. The breath, exercise intolerance, collapse,
most commonly cited causes of PAH in syncope, right-sided congestive heart
dogs include chronic acquired valvular failure [rare]). Coughing is common and
disease, pulmonary disease, pulmonary is often associated with secondary causes
overcirculation, and heartworm dis- of PAH.52 Radiographic features and
ease.47-52 Primary pulmonary hyperten- physical examination results generally
sion has been described in dogs in reflect the underlying disease process;
association with a pulmonary arteriopa- rarely, pulmonary edema may be
thy53 and a primary pulmonary veno- observed.55 Investigation may be war-
occlusive condition.54 Patients may be ranted in at-risk patients (ie, patients
subclinical or may show signs of hypoxia with diffuse crackles, West Highland
(eg, weakness, fatigue, shortness of terriers with pulmonary fibrosis).

October 2016 cliniciansbrief.com 83

ASK THE EXPERT h RESPIRATORY MEDICINE h PEER REVIEWED
Documentation of PAH can be performed
indirectly with echocardiography.56,57
Direct pulmonary arterial measurement
is rarely performed. PAH often contrib-
utes to signs with any chronic cardiopul-
monary disease; thus, screening is
recommended. Phosphodiesterase type
V inhibitors (eg, sildenafil,49,50,58 tadala-
fil59), pimobendan,60 and imatinib61 may
be considered, depending on cause.
d FIGURE 8 Pulmonary embolism confirmed on
necropsy. Note the right caudal lung field
oligemia, which signifies vascular occlusion.
d FIGURE 9 Idiopathic pulmonary fibrosis with a
diffuse bronchointerstitial pattern. Idiopathic
PAH = pulmonary arterial
pulmonary fibrosis was confirmed on lung
hypertension
biopsy.
84 cliniciansbrief.com October 2016
Interstitial Lung Diseases
Interstitial lung diseases are an uncom-
mon cause of respiratory disease in gen-
eral. The most common interstitial lung
disease is idiopathic pulmonary fibrosis,
which occurs most commonly in West
Highland terriers.62 Because of the
interstitial location of interstitial lung
diseases, histopathology is required for
definitive diagnosis.63 Common signs
include exercise intolerance, labored
breathing, syncope, and weakness.64
Coughing is typically not present.
Examination may reveal crackles,
fatigue, cyanosis, and a restrictive
breathing pattern.
Radiographs may reveal a diffuse,
unstructured interstitial pattern (Fig-
ure 9). Subtle changes in interstitial
opacity may go unnoticed despite severe
histologic disease.62
Thoracic CT may provide strong support
with a characteristic diffuse “ground
glass” appearance.65 This remains non-
specific, however, and may be caused by
other conditions. Additional supportive
diagnostics may include bronchoalveolar
lavage biomarkers (eg, endothelin-1)66 as
well as echocardiography to document
secondary pulmonary hypertension.
Additional Disorders
Other pulmonary conditions in dogs
include atypical infections (eg, Mycobac-
terium spp, protozoal),67,68 traumatic
injuries (eg, pulmonary contusions,
near-drowning), and inhaled irritants
(eg, pneumonitis, smoke). It is important
to note that the lungs may represent a
manifestation of systemic disease (eg,
leptospirosis, acute respiratory distress
syndrome, anaphylaxis, transfusion-
related acute lung injury). n
See page 105 for references.
ASK THE EXPERT h RESPIRATORY MEDICINE h CONTINUED FROM PAGE 84
References
1. Radhakrishnan A, Drobatz KJ, Culp WT, King LG.
Community-acquired infectious pneumonia in
puppies: 65 cases (1993-2002). J Am Vet Med Assoc.
2007;230(10):1493-1497.
2. Priestnall S, Erles K. Streptococcus zooepidemicus: an
emerging canine pathogen. Vet J. 2011;188(2):142-148.
3. Kogen DA, Johnson LR, Sturges BK, Jandrey KE,
Pollard RE. Etiology and clinical outcome in dogs
with aspiration pneumonia: 88 cases (2004-2006).
J Am Vet Med Assoc. 2008;233(11):1748-1755
4. Kogan DA, Johnson LR, Jandrey KE, Pollard RE. Clin-
ical, clinicopathologic, and radiographic findings in
dogs with aspiration pneumonia: 88 cases (2004–
2006). J Am Vet Med Assoc. 2008;233(11):1742-1747.
5. Jameson PH, King LA, Lappin MR, Jones RL. Compar-
ison of clinical signs, diagnostic findings, organisms
isolated, and clinical outcome in dogs with bacterial
pneumonia: 93 cases (1986-1991). J Am Vet Med Assoc.
1995;206(2):206-209.
6. Proulx A, Hume DZ, Drobatz KJ, Reineke EL. In vitro
bacterial isolate susceptibility to empirically selected
antimicrobials in 111 dogs with bacterial pneumonia.
J Vet Emerg Crit Care. 2014;24(2):194-200.
7. Angus JC, Jang SS, Hirsh DC. Microbiological study
of transtracheal aspirates from dogs with suspected
lower respiratory tract disease: 264 cases (1989-1995).
J Am Vet Med Assoc.. 1997;210(1):55-58.
8. Proulx A, Hume, Drobatz KJ, Reineke EL. In vitro
bacterial isolate susceptibility to empirically selected
antimicrobials in 111 dogs with bacterial pneumonia.
J Vet Emerg Crit Care (San Antonio). 2014;(24)2:194-200.
9. Priestnall SL, Mitchell JA, Walker CA, Erles K, Brownlie
J. New and emerging pathogens in canine infectious
respiratory disease. Vet Pathol. 2014;51(2):492-504.
10. Larsen RW, Kiupel M, Agerholm JS. Prevalence of canid
herpesvirus-1 infection in stillborn and dead neonatal
puppies in Denmark. Acta Vet Scand. 2015;52:1.
11. Kumar S, Driskell EA, Cooley AJ, et al. Fatal canid her-
pesvirus 1 respiratory infections in 4 clinically healthy
adult dogs. Vet Pathol. 2015;52(4):681-687.
12. Pandher K, Podell B, Gould DH, Johnson BJ, Thomp-
son S. Interstitial pneumonia in neonatal canine pups
with evidence of canine distemper virus infection.
J Vet Diagn Invest. 2006;18(2):201-214.
13. Dubovi EJ, Njaa BL. Canine Influenza. Vet Clin North Am
Small Anim Pract. 2008;38(4):827-835.
14. Johnson LR, Herrgesell EJ, Davidson AP, Pappagianis
D. Clinical, clinicopathologic, and radiographic find-
ings in dogs with coccidioidomycosis: 24 cases (1995-
2000). J Am Vet Med Assoc. 2003;222(4):461-466.
15. Clinkenbeard KD, Cowell RL, Tyler RD. Disseminated
histoplasmosis in dogs: 12 cases (1981-1986). J Am Vet
Med Assoc. 1988;193(11):1443-1447.
16. Arceneaux KA, Taboada J, Hosgood G. Blastomycosis
in dogs: 115 cases (1980-1995). J Am Vet Med Assoc.
1998;213(5):658-664.
17. Roudebush P. Mycotic pneumonias. Vet Clin North Am
Small Anim Pract. 1985;15(5):949-969.
18. Bromel C, Sykes JE. Epidemiology, diagnosis, and
treatment of blastomycosis in dogs and cats. Clin Tech
Small Anim Pract. 2005;20(4):233-239.
19. Arceneaux KA, Taboada J, Hosgood G. Blastomycosis
in dogs: 115 cases (1980-1995). J Am Vet Med Assoc.
1998;213(5):658-664.
20. Spector D, Wheat LJ, Beamis D, et al. Antigen testing
for the diagnosis of blastomycosis. J Vet Intern Med.
2006;20(3):711-712.
21. Hage CA, Knox KS, Davis TE, Wheat LJ. Antigen detec-
tion in bronchoalveolar lavage fluid for diagnosis of
fungal pneumonia. Curr Opin Pulm Med. 2011;17(3):
167-171.
22. Clercx C, Peeters D, Snaps F, et al. Eosinophilic
bronchopneumopathy in dogs. J Vet Intern Med.
2000;14(3):282-291.
23. Diana A, Guglielmini C, Pivetta M, et al. Radiographic
features of cardiogenic pulmonary edema in dogs with
mitral regurgitation: 61 cases (1998-2007). J Am Vet Med
Assoc. 2009;235(9):1058-1063.
24. Smith KF, Quinn RL, Rahilly LJ. Biomarkers for differ-
entiation of causes of respiratory distress in dogs and
cats: part 1—Cardiac diseases and pulmonary hyper-
tension. J Vet Emerg Crit Care (San Antonio). 2015;25(3):
311-329.
25. Drobatz KJ, Saunders HM, Pugh CR, Hendricks JC.
Noncardiogenic pulmonary edema in dogs and cats: 26
cases (1987-1993). J Am Vet Med Assoc. 1995;206(11):1732-
1736.
26. Hughes D. Pulmonary Edema. In: King LG, ed. Textbook
of Respiratory Diseases in Dogs and Cats. St. Louis, MO:
Elsevier; 2004;487-497.
27. Bachmann M, Waldrop JE. Noncardiogenic edema.
Compend Contin Educ Vet. 2012;34(11):E1.
28. Sherding RG. Parasites of the lung. In: King LG, ed. Text-
book of Respiratory Diseases in Dogs and Cats. St. Louis,
MO: Elsevier; 2004;548-559.
29. Pechman RD. The radiographic features of pulmonary
paragonimiasis in the dog and cat. J Am Vet Radiol Soc.
1976;17(5):182-191.
30. Pechman RD Jr. Pulmonary paragonimiasis in dogs
and cats: a review. J Small Anim Pract. 1980;21(2):87-95.
31. Herman LH, Helland DR. Paragonimiasis in a cat. J Am
Vet Med Assoc. 1966;149(6):753-757.
32. Bihr T, Conboy GA. Lungworm (Crenosoma vulpis)
infection in dogs on Prince Edward Island. Can Vet J.
1999;40(8):555-559.
33. Murphy KA, Brisson BA. Evaluation of a lung lobe tor-
sion in Pugs: 7 cases (1991-2004). J Am Vet Med Assoc.
2006;228(1): 86-90.
34. Neath PJ, Brockman DJ, King LG. Lung lob torsion
in dogs: 22 cases (1981-1999). J Am Vet Med Assoc.
2000;217(7):1041-1044.
35. d’Anjou MA, Tidwell AS, Hecht S. Radiographic diag-
nosis of lung lobe torsion. Vet Radiol Ultrasound.
2005;46(6):478-484.
36. Caivano D, Birettoni F, Bufalari A, et al. Contrast-
enhanced ultrasound findings in three dogs with
lung lobe torsion. J Vet Med Sci. 2015;78(3)427-430.
37. Seiler G, Schwarz T, Vignoli M, Rodriguez D. Computed
tomography features of lung lobe torsion. Vet Radiol
Ultrasound. 2008;49(6):504-508.
38. Barrett LE, Pollard RE, Zwingenberger A, Zierenberg-
Ripoll A, Skorupski KA. Radiographic characterization
of primary lung tumors in 74 dogs. Vet Radiol Ultra-
sound. 2014;55(5):480-487.
39. Baez JL, Sorenmo U. Pulmonary and bronchial neopla-
sia. Textbook of Respiratory Diseases in Dogs and Cats.
St. Louis, MO: Elsevier; 2004;508-516.
40. Geyer NE, Reichle JK, Valdés-Martínez A, et al.
Radiographic appearance of confirmed pulmonary
Continues on page 108
October 2016 cliniciansbrief.com 105
ASK THE EXPERT h RESPIRATORY MEDICINE h CONTINUED FROM PAGE 105
lymphoma in cats and dogs. Vet Radiol Ultrasound.
2010;51(4):386-390.
41. Hawkins EC, Morrison WB, DeNicola DB, Blevins WE.
Cytologic analysis of bronchoalveolar lavage fluid from
47 dogs with multicentric malignant lymphoma. J Am
Vet Med Assoc. 1993;203(10):1418-1425.
42. Bertazzolo W, Zuliani D, Pogliani E, Caniatti M, Bussa-
dori C. Diffuse bronchiolo-alveolar carcinoma in a dog.
J Small Anim Pract. 2002;43(6):265-268.
43. LaRue MJ, Murtaugh RJ. Pulmonary thromboembo-
lism in dogs: 47 cases (1986-1987). J Am Vet Med Assoc.
1990;197(10):1368-1372.
44. Goggs R, Benigni L, Fuentes VL, Chan DL. Pulmo-
nary embolism. J Vet Emerg Crit Care (San Anto-
nio). 2009;19(1):30-52.
45. Johnson LR, Lappin MR, Baker DC. Pulmonary throm-
boembolism in 29 dogs: 1985-1995. J Vet Intern Med.
1999;13(4):338-345.
46. Nakamura S, Takano H, Kubota Y, Asai K, Shimizu W.
Impact of the efficacy of thrombolytic therapy on the
mortality of patients with acute submassive pulmo-
nary embolism: a meta-analysis. J Thromb Haemost.
2014;12(7):1086-1095.
47. Johnson L, Boon J, Orton EC. Clinical characteristics
PRACTICE MARKETPLACE h CONTINUED FROM PAGE 107
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108 cliniciansbrief.com October 2016
of 53 dogs with Doppler derived evidence of pul-
monary hypertension: 1992-1996. J Vet Intern Med.
1999;13(5):440-447
48. Pyle RL, Abbott J, MacLean H. Pulmonary hyperten-
sion and cardiovascular sequelae in 54 dogs. Int J Appl
Res Vet Med. 2004;2(2):99.
49. Bach JF, Rozanski EA, MacGregor J, et al. Retrospective
evaluation of sildenafil citrate as a therapy for pul-
monary hypertension in dogs. J Vet Intern Med. 2006;
20(5):1132-1135.
50. Kellum HB, Stepien RL. Sildenafil citrate therapy in 22
dogs with pulmonary hypertension. J Vet Intern Med.
2007;21(6):1258-1264.
51. Serres F, Chetboul V, Gouni V, et al. Diagnostic value
of echo-Doppler and tissue Doppler imaging in dogs
with pulmonary arterial hypertension. J Vet Intern Med.
2007;21(6):1280-1289.
52. Kellihan HB, Stepien, RL. Pulmonary hyperten-
sion in dogs: diagnosis and therapy. Vet Clin North Am
Small Anim Pract. 2010;40(4):623-640.
53. Zabka TS, Campbell FE, Wilson DW. Pulmonary arte-
riopathy and idiopathic pulmonary arterial hyperten-
sion in six dogs. Vet Pathol. 2006;43(4):510 -522.
54. Williams K, Andrie K, Cartoceti A, et al. Pulmonary

veno-occlusive disease: a newly recognized cause of
severe pulmonary hypertension in dogs. Vet Pathol.
2016;53(4):813-822.
55. Kellihan HB, Waller KR, Pinkos A, Steinberg H, Bates
ML. Acute resolution of pulmonary alveolar infiltrates
in 10 dogs with pulmonary hypertension treated with
sidenafil citrate: 2005-2014. J Vet Cardiol. 2015;17(3):182-
191.
56. Johnson LR. Diagnosis of pulmonary hypertension.
Clin Tech Small Anim Pract. 1999;14(4):231-236.
57. Johnson L, Boon J, Orton EC. Clinical characteris-
tics of 53 dogs with Doppler-derived evidence of
pulmonary hypertension: 1992-1996. J Vet Intern
Med. 1999;13(5):440-447.
58. Brown AJ, Davison E, Sleeper MM. Clinical efficacy of
sildenafil in treatment of pulmonary arterial hyperten-
sion in dogs. J Vet Intern Med. 2010;24(4):850-854.
59. Hori Y, Kondo C, Matsui M, et al. Effect of the phos-
phodiesterase type 5 inhibitor tadalafil on pulmonary
hemodynamics in a canine model of pulmonary
hypertension. Vet J. 2014;202(2):334-339
60. Atkinson KJ, Fine DM, Thombs LA, et al. Evaluation
of pimobendan and N-terminal probrain natriuretic
peptide in the treatment of pulmonary hypertension
secondary to degenerative mitral valve disease in
dogs. J Vet Intern Med. 2009;23(6):1190-1196.
61. Arita S, Arita N, Hikasa Y. Therapeutic effect of low-
dose imatinib on pulmonary arterial hypertension in
dogs. Can Vet J. 2013;54(3):255-261.
62. Heikkila-Laurila HP, Rajamaki MM. Idiopathic
pulmonary fibrosis in West Highland white terriers.
Vet Clin North Am Small Anim Pract. 2014;44(1):129-142.
63. Norris CR, Griffey SM, Walsh, P. Use of keyhole lung  Anorexia
biopsy for diagnosis of interstitial lung diseases in
dogs and cats: 13 cases (1998-2001). J Am Vet Med Assoc.
2002; 221(10):1453-1459.
64. Reinero CR, Cohn LA. Interstitial Lung Diseases. Vet
Clin North Am Small Anim Pract. 2007;33(5):937-947.
65. Johnson S, Corcoran BM, Wotton PR, Schwarz T,
Sullivan M. Thoracic high-resolution computed
tomographic findings in dogs with canine
idiopathic pulmonary fibrosis. J Small Anim Pract.
2005;46(8):381-388.
66. Krafft E, Heikkila HP, Jespers P, et al. Serum
and bronchoalveolar lavage fluid endothelin-1
concentrations as diagnostic biomarkers of canine
idiopathic pulmonary fibrosis. J Vet Intern Med.
2011;25(5):990-996.
67. Martinho AP, Franco MM, Ribeiro MG, et al.
Disseminated Mycobacterium tuberculosis infection
in a dog. Am J Trop Med Hyg. 2013;88(3):596-600.
68. Dubey JP, Lindsay DS, Lappin MR. Toxoplasmosis and
other intestinal coccidial infections in cats and dogs.
Vet Clin North Am Small Anim Pract. 2009;39(6):
1009-1034.
October 2016 cliniciansbrief.com
CAUTION: Federal (USA) law restricts this drug to use by or on the order of a licensed veterinarian.
Description:
NexGard® (afoxolaner) is available in four sizes of beef-flavored, soft chewables for oral administration to dogs and puppies
according to their weight. Each chewable is formulated to provide a minimum afoxolaner dosage of 1.14 mg/lb (2.5 mg/
kg). Afoxolaner has the chemical composition 1-Naphthalenecarboxamide, 4-[5- [3-chloro-5-(trifluoromethyl)-phenyl]-4,
5-dihydro-5-(trifluoromethyl)-3-isoxazolyl]-N-[2-oxo-2-[(2,2,2-trifluoroethyl)amino]ethyl.
Indications:
NexGard kills adult fleas and is indicated for the treatment and prevention of flea infestations (Ctenocephalides felis), and
the treatment and control of Black-legged tick (Ixodes scapularis), American Dog tick (Dermacentor variabilis), Lone Star tick
(Amblyomma americanum), and Brown dog tick (Rhipicephalus sanguineus) infestations in dogs and puppies 8 weeks of age
and older, weighing 4 pounds of body weight or greater, for one month.
Dosage and Administration:
NexGard is given orally once a month, at the minimum dosage of 1.14 mg/lb (2.5 mg/kg).
Dosing Schedule:
Body Afoxolaner Per Chewables
Weight Chewable (mg) Administered
4.0 to 10.0 lbs. 11.3 One
10.1 to 24.0 lbs. 28.3 One
24.1 to 60.0 lbs. 68 One
60.1 to 121.0 lbs. 136 One
Over 121.0 lbs. Administer the appropriate combination of chewables
NexGard can be administered with or without food. Care should be taken that the dog consumes the complete dose, and
treated animals should be observed for a few minutes to ensure that part of the dose is not lost or refused. If it is suspected
that any of the dose has been lost or if vomiting occurs within two hours of administration, redose with another full dose. If
a dose is missed, administer NexGard and resume a monthly dosing schedule.
Flea Treatment and Prevention:
Treatment with NexGard may begin at any time of the year. In areas where fleas are common year-round, monthly
treatment with NexGard should continue the entire year without interruption.
To minimize the likelihood of flea reinfestation, it is important to treat all animals within a household with an approved flea
control product.
Tick Treatment and Control:
Treatment with NexGard may begin at any time of the year (see Effectiveness).
Contraindications:
There are no known contraindications for the use of NexGard.
Warnings:
Not for use in humans. Keep this and all drugs out of the reach of children. In case of accidental ingestion, contact a
physician immediately.
Precautions:
The safe use of NexGard in breeding, pregnant or lactating dogs has not been evaluated. Use with caution in dogs with a
history of seizures (see Adverse Reactions).
Adverse Reactions:
In a well-controlled US field study, which included a total of 333 households and 615 treated dogs (415 administered
afoxolaner; 200 administered active control), no serious adverse reactions were observed with NexGard.
Over the 90-day study period, all observations of potential adverse reactions were recorded. The most frequent reactions
reported at an incidence of > 1% within any of the three months of observations are presented in the following table. The
most frequently reported adverse reaction was vomiting. The occurrence of vomiting was generally self-limiting and of short
duration and tended to decrease with subsequent doses in both groups. Five treated dogs experienced anorexia during the
study, and two of those dogs experienced anorexia with the first dose but not subsequent doses.
Table 1: Dogs With Adverse Reactions.
Treatment Group
Afoxolaner Oral active control
N1 % (n=415) N2 % (n=200)
Vomiting (with and without blood) 17 4.1 25 12.5
Dry/Flaky Skin 13 3.1 2 1.0
Diarrhea (with and without blood) 13 3.1 7 3.5
Lethargy 7 1.7 4 2.0
5 1.2 9 4.5
1
Number of dogs in the afoxolaner treatment group with the identified abnormality.
2
Number of dogs in the control group with the identified abnormality.
In the US field study, one dog with a history of seizures experienced a seizure on the same day after receiving the first
dose and on the same day after receiving the second dose of NexGard. This dog experienced a third seizure one week after
receiving the third dose. The dog remained enrolled and completed the study. Another dog with a history of seizures had
a seizure 19 days after the third dose of NexGard. The dog remained enrolled and completed the study. A third dog with a
history of seizures received NexGard and experienced no seizures throughout the study.
To report suspected adverse events, for technical assistance or to obtain a copy of the MSDS, contact Merial at 1-888-637-
4251 or www.merial.com/NexGard. For additional information about adverse drug experience reporting for animal drugs,
contact FDA at 1-888-FDA-VETS or online at http://www.fda.gov/AnimalVeterinary/SafetyHealth.
Mode of Action:
Afoxolaner is a member of the isoxazoline family, shown to bind at a binding site to inhibit insect and acarine ligand-gated
chloride channels, in particular those gated by the neurotransmitter gamma-aminobutyric acid (GABA), thereby blocking pre-
and post-synaptic transfer of chloride ions across cell membranes. Prolonged afoxolaner-induced hyperexcitation results in
uncontrolled activity of the central nervous system and death of insects and acarines. The selective toxicity of afoxolaner
between insects and acarines and mammals may be inferred by the differential sensitivity of the insects and acarines’
GABA receptors versus mammalian GABA receptors.
Effectiveness:
In a well-controlled laboratory study, NexGard began to kill fleas four hours after initial administration and demonstrated >99%
effectiveness at eight hours. In a separate well-controlled laboratory study, NexGard demonstrated 100%
effectiveness against adult fleas 24 hours post-infestation for 35 days, and was ≥ 93% effective at 12 hours post-infestation
through Day 21, and on Day 35. On Day 28, NexGard was 81.1% effective 12 hours post-infestation. Dogs in both the treated
and control groups that were infested with fleas on Day -1 generated flea eggs at 12- and 24-hours post-treatment (0-11
eggs and 1-17 eggs in the NexGard treated dogs, and 4-90 eggs and 0-118 eggs in the control dogs, at 12- and 24-hours,
respectively). At subsequent evaluations post-infestation, fleas from dogs in the treated group were essentially unable to
produce any eggs (0-1 eggs) while fleas from dogs in the control group continued to produce eggs (1-141 eggs).
In a 90-day US field study conducted in households with existing flea infestations of varying severity, the effectiveness of
NexGard against fleas on the Day 30, 60 and 90 visits compared with baseline was 98.0%, 99.7%, and 99.9%, respectively.
Collectively, the data from the three studies (two laboratory and one field) demonstrate that NexGard kills fleas before they
can lay eggs, thus preventing subsequent flea infestations after the start of treatment of existing flea infestations.
In well-controlled laboratory studies, NexGard demonstrated >97% effectiveness against Dermacentor variabilis, >94%
effectiveness against Ixodes scapularis, and >93% effectiveness against Rhipicephalus sanguineus, 48 hours post-infestation for
30 days. At 72 hours post-infestation, NexGard demonstrated >97% effectiveness against Amblyomma americanum for 30 days.
Animal Safety:
In a margin of safety study, NexGard was administered orally to 8 to 9-week-old Beagle puppies at 1, 3, and 5 times the
maximum exposure dose (6.3 mg/kg) for three treatments every 28 days, followed by three treatments every 14 days, for
a total of six treatments. Dogs in the control group were sham-dosed. There were no clinically-relevant effects related to
treatment on physical examination, body weight, food consumption, clinical pathology (hematology, clinical chemistries, or
coagulation tests), gross pathology, histopathology or organ weights. Vomiting occurred throughout the study, with a similar
incidence in the treated and control groups, including one dog in the 5x group that vomited four hours after treatment.
In a well-controlled field study, NexGard was used concomitantly with other medications, such as vaccines, anthelmintics,
antibiotics (including topicals), steroids, NSAIDS, anesthetics, and antihistamines. No adverse reactions were observed
from the concomitant use of NexGard with other medications.
Storage Information:
Store at or below 30°C (86°F) with excursions permitted up to 40°C (104°F).
How Supplied:
NexGard is available in four sizes of beef-flavored soft chewables: 11.3, 28.3, 68 or 136 mg afoxolaner. Each chewable size
is available in color-coded packages of 1, 3 or 6 beef-flavored chewables.
NADA 141-406, Approved by FDA
Marketed by: Frontline Vet Labs™, a Division of Merial, Inc.
Duluth, GA 30096-4640 USA
Made in Brazil.
®NexGard is a registered trademark, and TMFRONTLINE VET LABS
is a trademark, of Merial. ©2015 Merial. All rights reserved.
1050-4493-03
Rev. 1/2015
109
 COLAPSO TRAQUEAL
J. Alberto Montoya Alonso
Medicina veterinaria
Facultad de Veterinaria
Universidad de Las Palmas de Gran Canaria
35413-Arucas (Las Palmas)

Resumen

En el colapso traqueal existe una reducción de la luz traqueal en cualquier

parte de su longitud. Habitualmente hay una disminución del diámetro dorso-

ventral que se traducirá en un alargamiento de la membrana traqueal dorsal.

Esta membrana dorsal ocupará un espacio en la luz traqueal con importancia

dentro del mecanismo del colapso. No se conocen las causas pero podría estar

ligado a un problema en el cartílago 1. Es muy frecuente observarlo en razas

miniatura. La sintomatología suele ser una dificultad en la inspiración y ataques

paroxísticos de tos definidos como“graznido de ganso”. El diagnóstico que

confirme el proceso será endoscópico y radiográfico. El tratamiento efectivo es

dificultoso ya que requiere la colocación de una prótesis endotraqueal o stent

“a medida”, tratamiento médico y una gran colaboración por parte del

propietario .

Definición

La tráquea es un conducto flexible que une las vías áereas altas (área nasal,

oral, faríngea y laringe) y bajas (bronquios y bronquiolos). Está formada por

anillos cartilaginosos en forma de “C” conectados por ligamentos anulares. La

parte abierta de estos anillos está completada por el músculo o membrana

traqueal dorsal.2

La situación de colapso es una reducción dinámica del diámetro de la luz

traqueal cervical y/o torácica.

La reducción del diámetro traqueal suele ser dorso-ventral y conlleva un

alargamiento de la membrana traqueal dorsal que será el causante del

colapso traqueal dinámico.

Etiología

Se desconoce aunque se han descrito problemas en la función de los

cóndrocitos que conducirá a defectos en el cartílago traqueal.

Hay una mayor incidencia de esta enfermedad en razas como el Yorkshire

Terrier, Caniche, Pomerania, Bichón Maltés,Pug, Chihuahua y, en general,

perros miniatura. Estos animales, una nutrición deficiente o factores

metabólicos pueden acabar con una alteración de la condrogénesis y del

metabolismo del cartílago.

Se pensó en una inervación deficiente de la membrana traqueal pero no se ha

demostrado.

En estudios realizados en la Universidad de Queensland durante dos años se

encontró que de 2780 perros el 0,5% presentaban esta patología. De 521

perros de raza miniatura el 2,7% (14 perros) tenían colapso traqueal. En

diversos estudios se ratificó que suelen ser perros de edad media (6-7 años).

Patología

La tráquea es una estructura de cierta flexibilidad pero que apenas cambia con

las variaciones de presión durante la respiración.

Inspiración. Cae la presión progresivamente de la glotis a los bronquiolos.

Habrá un aumento del flujo de aire hacia los pulmones.
Espiración. Las estructuras cartilaginosas de las paredes de las vías
respiratorias deberían evitar el colapso cuando aumente la
presión intrapleural.

Algunos animales afectados tienen una carencia de condroitín sulfato y

glucosaminoglicanos. Esto se traduce en una carencia de agua en la matriz del

cartílago y, por lo tanto, debilitamiento.El debilitamiento del cartílago facilita el

aplanamiento de la tráquea cervical en inspiración y al aplanamiento de las

vías respiratorias intratorácicas durante la espiración o durante la tos.

La obstrucción crónica da lugar a disnea y tos que induce a su vez laringo-

traqueo-bronquitis crónica. Estos trastornos unidos a otros concurrentes

(obstrucción de vías respiratorias altas, bronquitis crónica o insuficiencia

cardíaca crónica) pueden producir grave sintomatología. La obesidad agrava

más el proceso al alterarse la distensibilidad torácica y del diafragma, con lo

que asistiremos a una disminución en la expansión del pulmón en la inspiración

y a una tendencia evidente al colapso de las vías respiratorias.

Está descrita la intubación endotraqueal y las infecciones respiratorias como

Desencadenantes del cuadro.

Síntomas

El colapso cervical suele producir tos u obstrucción inspiratoria. El colapso

Intratorácico suele producirse durante la espiración y los signos suelen ser

más fuertes. Pueden coincidir ambos colapsos o no e incluso podemos

observar colapsos bronquiales sin que ocurran los traqueales.

Son frecuentes los ataques paroxísticos descritos como “graznido de ganso”.

Los signos pueden ser provocados por agitación, presión sobre la tráquea,

condiciones ambientales (elevada temperatura o humedad) o al comer o beber.

La tos puede acabar en vómito debido al intento de eliminar secreciones

acumuladas en las vías respiratorias.

Diagnóstico
. La exploración del animal:

- Perros de raza miniatura

- Ataques paroxísticos de tos en “graznido de ganso”, sobre todo en
agitación.
- Perros obesos
- Sensibilidad traqueal
- Traquea aplanada
- Ruidos inspiratorios y/o dificultad espiratoria a la auscultación

.Radiografías Torácicas en inspiración y espiración que nos ayudarán a ver los

posibles cambios dinámicos del colapso.

.Traqueobroncoscopia. Mediante este procedimiento podemos visualizar el

grado, la extensión y la gravedad del colapso. Es recomendable realizar en el

mismo procedimiento y lavado traqueobronquial que nos ayuden a realizar un

análisis citológico y un cultivo de las muestras recogidas.

La endoscopia de las vías respiratorias bajas es la técnica exploratoria indicada

y más útil para el estudio y diagnóstico de trastornos patológicos de dichas

vías, al proporcionar una visión directa y permitir al mismo tiempo obtener

muestras de tejidos, estructuras específicas o muestras de lavado. Esta prueba

es fundamental cuando queremos valorar anormalidades estructurales (colapso

traqueal), presencia de masas, comprobar el estado de las paredes de la

traquea y bronquios, observar la posible inflamación de las vías respiratorias,

presencia de exudados, torsiones lobares o la hemorragia pulmonar. También

es útil para recoger muestras para su análisis posterior.

Indicaciones de la traqueobroncoscopia:

 tos persistente
 expectoración
 hemoptisis
 lesión obstructiva
 aspiración de cuerpo extraño
 extracción de cuerpo extraño
 colapso traqueal
 lavados traqueales
  toma de exudados
 pólipos intraluminales
 diagnóstico de parasitosis
 tumores endotraqueales y endobronquiales
 toma de biopsias
 procesos infecciosos
 procesos crónicos

Esta contraindicada la realización de esta prueba en casos de disnea severa

por un proceso pulmonar o en casos de infección aguda del tracto respiratorio.

Para realizar la traqueobroncoscopia se pueden utilizar endoscopios

rígidos o flexibles. La broncoscopia se puede realizar con endoscopios rígidos

o flexibles dependiendo del tamaño de la tráquea. Los inconvenientes que nos

encontramos con estos aparatos son muchos, aparatos grandes no pueden ser

utilizados en animales pequeños y aparatos muy pequeños nos reducirán

mucho la ventana de imagen.

Lo ideal es utilizar anestesia inhalatoria, usando el tubo endotraqueal del

máximo grosor que nos permita un movimiento cómodo del endoscopio o un

sistema que comunique el oxígeno y anestésico a la tráquea a través del canal

de trabajo. Durante todo el procedimiento, el paciente debe ser monitorizado

(pulso, color de mucosas, tiempo de relleno capilar, frecuencia y calidad de

pulso y frecuencia respiratoria).

El endoscopio debe ser introducido a través de la laringe, evitando la

contaminación del mismo si queremos realizar toma de muestras. Una vez

dentro de la traquea, el ligamento traqueal (en posición dorsal), nos permite

situarnos. A nivel de la bifurcación de la traquea, se divisa la carina como un

delgado pilar. El bronquio derecho está más cerca de la traquea mientras que

el izquierdo forma un arco.

Cada bronquio se explora individualmente teniendo en cuenta que el

derecho es de más fácil exploración al encontrarse más cercano a la carina 3.

ANORMALIDADES TRAQUEO-BRONCOSCOPICAS DE LA TRAQUEA

Anormalidad Correlación clínica

Tráquea
Hiperemia, exceso de moco Inflamación
Mb. Traqueal redundante Colapso traqueal
Anillos aplanados Colapso traqueal
Estrechamiento uniforme hipoplasia traqueal
Estrechamiento trauma previo
Lesión en masa Anillo fracturado,
granuloma por c.e.,
neoplasias.

Tangner y Hobson propusieron un sistema de clasificación del colapso traqueal

según el grado de colapso2.observado en la traqueobroncoscopia.

Fig.1

Tratamiento

.Corticoesteroides

Para reducir la inflamación pero tienen el inconveniente que aumentan el jadeo

y el peso del animal.

.Broncodilatadores.

Pueden ir bien al disminuir la probabilidad del colapso respiratorio.

Teofilina 20 mg/kg/2 veces al día.

. Antibióticos.

Si es posible por cultivo del lavado traqueobronquial.

. Antitusivos.

Deben ser agentes potentes como el Butorfanol 0,5-1 mg/kg/2-4 veces al día.

.Tratar la insuficiencia cardíaca.

.Tratar la obesidad.

. Cambio de correa a arnés

. Evitar el calor, la humedad, la agitación y el estrés.

.Quirúrgico.

Se trata de la implantación de prótesis de anillo:

- Son pacientes muy pequeños por lo que es complicado.

- Puede producirse parálisis laríngea en un 20% de los casos.
- Hay un índice alto de complicaciones inmediatas a la cirugía.
- Hay un índice alto de complicaciones a medio y largo plazo.

. Stent endotraqueal.

Este puede ser un sistema rápido, eficaz y relativamente sencillo frente a otras

técnicas quirúrgicas (más agresivas) descritas para este fin.

Un stent es una red expansora del diámetro traqueal que se libera dentro de la

tráquea a través de un procedimiento endoscópico.

Una vez hemos medido la longitud del colapso, la longitud total de la tráquea y

el diámetro traqueal normal, seleccionaremos el modelo más apropiado para

nuestro paciente de aquellos que nos puedan suministrar los fabricantes de

Stent para humana. Es decir, realizaremos un estudio radiográfico y

endoscópico de la lesión, y consultando los distintos modelos existentes,

seleccionaremos aquel que expanda la zona estenosada, comprobando el

movimiento del stent y los posibles daños secundarios, haciendo controles a

los 30, 60 y 90 días.

Ventajas e inconvenientes de la técnica:

Ventajas:

 Rapidez
  Eficacia desde el primer momento
 Técnica no invasiva
 Fácil recolocación si se descoloca
 Fácil de comprobar radiológicamente
 Gran porcentaje de recuperación frente a otras técnicas
 Se puede extraer sin problemas secundarios

Inconvenientes:

 Descolocación
 Granuloma cicatricial post-stent
 Precio
 Dificultad de acceder al material por ser de humana (muchas
trabas legales)
 Rotura traqueal
 Hemorragias
J. Alberto Montoya-Alonso, Laín García-Guasch

ASMA BRONQUIAL FELINO

J. Alberto Montoya-Alonso, DVM, PhD, MSc, MA
Lain García-Guasch, DVM, PhD, MSc,
Facultad de Veterinaria de Las Palmas de Gran Canaria
35416- Arucas (Las Palmas)- ESPAÑA

El asma felino es una de las patologías respiratorias más frecuentes en gatos.

Consiste en una enfermedad inflamatoria crónica de las vías aéreas inferiores
(bronquios y bronquiolos) a menudo de causa no identificada. Suele afectar a
pacientes jóvenes o de mediana edad. Se ha observado cierta predisposición en
gatos siameses. Los signos clínicos típicos incluyen un cuadro de tos, estornudos,
intolerancia al ejercicio y distrés respiratorio agudo.

El tracto respiratorio dispone de ciertos mecanismos simples de defensa que

protegen a los pulmones de un agente nocivo externo. A partir de un estímulo
irritante o inflamatorio del epitelio respiratorio se produce:

- Inflamación y edema del epitelio bronquial.

- Hipertrofia e hiperactividad de la mucosa glandular con una mayor secreción
de moco.
- Contracción de la musculatura lisa bronquial.

Estos cambios comportan una reducción en el diámetro del tracto respiratorio, el

consiguiente incremento en la resistencia al paso de aire por las vías aéreas, y una
mayor inflamación que dará lugar a los signos clínicos.

La ley descrita por Poiseuille postula que el flujo de aire que circula a través del
bronquio es proporcional al radio elevado a la 4ª potencia (r4). Por lo tanto, siguiendo
esta ley, pequeños incrementos en el diámetro bronquial implicará una importante
mejoría en cuanto a los signos clínicos del paciente.

La obstrucción grave de las vías aéreas genera un estado de hiperinsuflación

pulmonar debido a la dificultad para exhalar completamente el aire. En ocasiones
tiene como consecuencia la dilatación permanente de las vías aéreas
(bronquiectasia) y una reducción en la elasticidad pulmonar (enfisema).

Por desgracia no existen signos clínicos ni ninguna prueba de laboratorio disponible

en la clínica rutinaria que sirva para diagnosticar que nuestro paciente presenta
asma bronquial felino.

El diagnóstico se realiza por eliminación tras descartar todas las posibles causas de
disnea aguda, estornudos y tos en gatos. El diagnóstico diferencial de un gato con

Asma bronquial felino-1

J. Alberto Montoya-Alonso, Laín García-Guasch

sospecha de asma bronquial debe incluir la bronquitis crónica, edema pulmonar o

secundario a insuficiencia cardiaca (es importante recordar que los fallos cardiacos
en gato no suelen dar tos), infecciones víricas, bacterianas o por Mycoplasma spp,
cuerpos extraños en vías aéreas (poco frecuente), parásitos del tracto respiratorio
como Paragonimus, Aelurostrongylus y Capillaria (poco frecuentes), infección por
Bordetella, enfermedades del parénquima pulmonar, derrame pleural, neumotórax,…
También hay que valorar si en el entorno del gato puede identificarse la presencia de
alergenos, polución ambiental, humo, aerosoles irritantes,…

Signos clínicos:

Los signos clínicos más frecuentemente asociados a un gato con asma incluyen
disnea, taquipnea, ortopnea, intolerancia al ejercicio, tos paroxística de grado medio
a moderado, y distrés espiratorio agudo. En los casos graves, debido a la
broncoconstricción suelen presentarse respirando con la boca abierta, con cianosis,
y en posición esternal con abducción de los codos (Imagen 1). Por desgracia estos
signos clínicos también se observan en pacientes cardiópatas descompensados.
Para determinar si los signos clínicos son de origen cardiaco, o bien secundarios a
un problema respiratorio es útil fijarse en la temperatura corporal. Los pacientes que
presentan un shock cardiogénico suelen estar hipodérmicos debido al bajo gasto
cardiaco, mientras que los gatos asmáticos sueles tener una temperatura corporal
normal. A diferencia de lo que ocurre en un gato asmático, un gato cardiópata no
suele presentar tos.

El examen físico debe realizarse sin generar ningún tipo de estrés. Puede ser
totalmente normal en reposo pero en ocasiones se observa una espiración forzada,
reflejo traqueal positivo, y se pueden auscultar sibilancias y crepitaciones. La
auscultación puede ser totalmente normal. Debido al atrapamiento de aire puede
identificarse una menor compresión de la caja torácica y un aspecto de tórax en
tonel.

En la bronquitis crónica el gato presenta una tos de aparición diaria de al menos dos
meses de duración y que no responde al tratamiento con broncodilatadores; en
cambio el asma, al ser una broncoconstricción aguda provoca una tos intermitente
que responde muy bien al tratamiento.

Radiografía:

Las radiografías pueden ser normales pero es habitual identificar evidencias de

engrosamiento de las paredes bronquiales (“donuts” y “vías de tren”) por la
inflamación (Imagen 2). Se puede observar un incremento en la radiolucencia
pulmonar sobre todo en los campos periféricos que indica la presencia de
atrapamiento de aire (“air trapping”), y un aplanamiento del diafragma debido a la

Asma bronquial felino-2

J. Alberto Montoya-Alonso, Laín García-Guasch

hiperinsuflación pulmonar. En un bajo porcentaje de los casos puede identificarse

atelectasia del lóbulo pulmonar medio derecho (Imagen 3). También en muy raras
ocasiones puede haber neumotórax o fracturas de costillas. A menudo se observa
aerofagia.

Analítica laboratorial:

El 20% de los gatos asmáticos presenta eosinofilia periférica, pero este hallazgo no
es específico ya que también se observa en pacientes sanos. También puede
asociarse a la presencia de parásitos intestinales, pulmonares, ectoparásitos o
filarias. Aunque es infrecuente, si el paciente presenta hipoxemia crónica puede
haber elevaciones en el hematocrito.

En el examen coprológico por flotación se debe buscar huevos de Paragonimus y

Capillaria; y mediante la cámara de Bareman larvas de Aelurostrongylus.

El examen citológico de la muestra obtenida por lavado broncoalveolar (BAL) suele

mostrar evidencias de inflamación de las vías aéreas ya que hay un incremento en el
número de eosinófilos y neutrófilos. Es complicado interpretar cultivos
bacteriológicos positivos ya que también se obtienen crecimientos a partir de
muestras de gatos sanos. En cambio se ha observado que el Micoplasma spp. crece
en el 25% de los cultivos de gatos asmáticos y no a partir de muestras de gatos
sanos.

Tratamiento

Tratamiento de emergencia:

Cuando un gato se presenta con un cuadro de distrés respiratorio agudo y grave

(con cianosis o respirando con la boca abierta), antes de realizar ninguna prueba de
diagnóstico se debe estabilizar al paciente reduciendo al mínimo el estrés. Se debe
administrar oxígeno al 40%-60% (mediante una cámara de oxigenación, incubadora,
flow-by,…) y un broncodilatador (terbutalina 0.01 mg/kg IM, IV, SC; Terbasmin®). Si
es posible, administrar también un broncodilatador inhalado. El de elección es el
albuterol (Ventolin®). Se trata de un β2-agonista de acción rápida muy efectivo en las
crisis agudas ya que relaja la musculatura bronquial e incrementa el diámetro de las
vías aéreas a los 5 minutos de haber sido administrado. Su efecto alcanza las 3-6
horas. La aminofilina tiene una actividad broncodilatadora menor que la terbutalina
por lo que no es un fármaco de primera elección.

A menudo es aconsejable sedarlo para poder manejarlo con mayor tranquilidad. El

tener que tomar esta decisión puede ser complicado ya que de entrada
desconocemos la causa del distrés respiratorio y pueden aparecer complicaciones

Asma bronquial felino-3

J. Alberto Montoya-Alonso, Laín García-Guasch

asociadas a los efectos secundarios de los fármacos administrados (sobre todo si se

trata de un paciente cardiópata). Se debe evitar el uso de fármacos y dosis que
puedan causar depresión respiratoria o que favorezcan a la aparición de arritmias. Si
no se dispone de un acceso acceso intravenoso y pensamos que puede ser un
paciente cardiópata, una buena combinación de fármacos es butorfanol (0.05-0.2
mg/kg) junto a midazolam (0.2-0.5 mg/kg) IM. Otra alternativa sería administrar
acepromacina (0.01-0.05 mg/kg) más ketamina (0.2 mg/kg) IM ya que la ketamina
tiene también potencialmente propiedades broncodilatadoras. Si se dispone de
acceso intravenoso se puede administrar igualmente la combinación de butorfanol
más midazolam, o también diazepam (5 mg/mL) más ketamina (100 mg/mL)
mezclados en proporción 1:1 y administrando 0.05-0.15 mL/Kg.

Lo esperable sería obtener una respuesta positiva en los primeros 30-45 minutos
con la consiguiente reducción de la frecuencia respiratoria y el esfuerzo espiratorio.
Si no responde favorablemente se debe volver a administrar el broncodilatador y
añadir una cortisona de acción rápida (dexametasona 0.25-2 mg/kg IV, IM). Si no
responde buscar otras causas de disnea y plantearse si es mejor intubar al gato y
realizar ventilación por presión positiva junto a la administración de oxígeno. En
cuanto sea posible realizar pruebas complementarias de diagnóstico (radiografías,
ecocardiografía, BAL,…) para descartar el resto de patologías.

Mediante pulsioximetría puede medirse el nivel de saturación de hemoglobina, que

debe mantenerse como mínimo al 92% ya que niveles menores de saturación se
correlacionan con una presión parcial de oxígeno arterial demasiado baja. Un nivel
de saturación inferior al 92% o bien una presión arterial de oxígeno por debajo de
75-80 mmHg indica un grado de hipoxemia de moderado a grave.

Pautas de terapia crónica:

En primer lugar, en caso de identificarlo, se debe eliminar la exposición al alergeno o

sustancia irritante responsable.

- Pacientes con crisis esporádicas:

En los pacientes en los que las crisis de disnea no ocurren de forma diaria se puede
administrar albuterol inhalado (Ventolin®) cada vez que el gato presente los signos
clínicos. En estos casos se presume que al no aparecer los síntomas de forma diaria
no existe suficiente inflamación de las vías aéreas como para administrar anti-
inflamatorios. Si la incidencia de aparición incrementa considerablemente se debe
plantear la necesidad de administrar una terapia más agresiva.

- Pacientes con crisis diarias:

Asma bronquial felino-4

J. Alberto Montoya-Alonso, Laín García-Guasch

En los pacientes que presentan síntomas de forma diaria pero que no tienen
dificultad respiratoria entre crisis las asmáticas, se puede administrar corticoides
inhalados como la fluticasona (Flixotide® de 220 μg) cada 12 horas, y tener
preparado albuterol (Ventolin®) para cuando tenga una cuadro asmático más fuerte.
Se puede observar cierta mejoría a las 24 horas de haber iniciado el tratamiento con
glucocorticoides inhalados, pero el máximo efecto no se alcanza hasta los 7-14 días.

Los gatos con cuadros asmáticos de grado moderado no presentan síntomas de

forma sostenida a lo largo de todo el día pero ya empiezan a tener una calidad de
vida algo peor. En estos casos se puede administrar fluticasona cada 12 horas,
albuterol cuando presente los episodios asmáticos, y prednisona a dosis de 1 mg/kg
PO cada 12 horas durante 5 días y posteriormente cada 24 horas durante 5 días
más. Tras 10 días de tratamiento con cortisona el paciente suele mejorar bastante y
se puede eliminar dicha medicación.

Cuando el paciente presenta síntomas clínicos en reposo la administración de

corticoides es el tratamiento más efectivo. Inicialmente se administra a dosis altas
(1-2 mg/kg bid PO durante 7-10 días) y a continuación se va reduciendo la
dosificación durante 2-3 meses. Se debe intentar pasar a corticoides inhalados,
aunque puede resultar caro y mal tolerado ya que el riesgo de efectos secundarios
es mucho menor en relación a la medicación administrada por vía oral. La
fluticasona (Flixotide®) se considera la formulación más potente y efectiva con el
mayor tiempo de acción y una mínima absorción a nivel sistémico. También es
necesario administrar albuterol (Ventolin®) cada 6-8 horas. Otro broncodilatador de la
misma familia es el salmeterol (Serevent®). Tarda unos 15-30 minutos en actuar pero
la duración de su efecto es mayor (> 12 horas). A diferencia del albuterol, éste no se
recomienda como tratamiento de elección en una crisis aguda sino como adyuvante
al tratamiento crónico con glucocorticoides. Algunos pacientes pueden necesitar
además una dosis mínima de cortisona vía oral, de mantenimiento, para controlar los
síntomas. En gatos que no toleran medicación vía oral se puede administrar acetato
de metilprednisolona a 10-20 mg/gato IM, SC cada 2-4 semanas.

En los gatos que no toleran la mediación mediante inhaladores se puede administrar

broncodilatadores agonistas β-adrenérgicos como la terbutalina (Terbasmin®) a
dosis de 0.625 mg PO bid. Los posibles efectos secundarios incluyen taquicardia,
nerviosismo e hipotensión. Otra opción son los derivados de las metilxantinas
(teofilina y aminofilina). Hasta hace unos años se podía administrar preparaciones
orales de larga duración (Theo-Dur®) a dosis de 20-25 mg/kg PO sid pero
actualmente se han retirado del mercado.

Los antibióticos no suelen administrarse ya que raramente los problemas

bronquiales en gatos se asocian a infecciones bacterianas del tracto respiratorio. Se
ha comprobado que a partir de muestras de BAL de gatos sanos se obtienen

Asma bronquial felino-5

J. Alberto Montoya-Alonso, Laín García-Guasch

resultados de cultivos falsamente positivos. La única excepción es en caso de

obtener crecimiento positivo de Mycoplasma spp en el cultivo ya que este
microorganismo no suele detectarse en cultivos de muestras tomadas de animales
sanos. Por ese motivo, se considera una buena opción administrar doxiciclina a
dosis de 10 mg/kg PO cada 24 horas hasta tener resultados del cultivo.

La serotonina es un mediador liberado por los mastocitos que interviene en el

proceso de contracción de la musculatura lisa bronquial. Estudios in vitro han
demostrado que la ciproheptadina posee un efecto antagonista de la serotonina. No
existen suficientes estudios in vivo publicados pero la dosis propuesta es de 1-4
mg/gato PO bid en gatos que no responden a la medicación con cortisona y
broncodilatadores. Los efectos secundarios incluyen letargia e incremento del
apetito.

Otros fármacos como la ciclosporina A, antagonistas de los receptores de

leucotrienos, anticuerpos anti-interleukinas, magnesio,… se han probado en humana
pero no hay suficientes estudios que demuestren su aplicación en veterinaria.

Pronóstico

La mayor parte de los gatos con problemas bronquiales responden bien a la terapia
pero el propietario debe ser consciente de que puede tratarse de una medicación
que tenga que administrarse de por vida para evitar recidivas.

Asma bronquial felino-6

Guideline and Recommendation
J Vet Intern Med 2017;31:279–294

Antimicrobial use Guidelines for Treatment of Respiratory Tract

Disease in Dogs and Cats: Antimicrobial Guidelines Working Group
of the International Society for Companion Animal Infectious
Diseases
M.R. Lappin, J. Blondeau, D. Boothe, E.B. Breitschwerdt, L. Guardabassi, D.H. Lloyd, M.G. Papich,
S.C. Rankin, J.E. Sykes, J. Turnidge, and J.S. Weese
Respiratory tract disease can be associated with primary or secondary bacterial infections in dogs and cats and is a com-
mon reason for use and potential misuse, improper use, and overuse of antimicrobials. There is a lack of comprehensive
treatment guidelines such as those that are available for human medicine. Accordingly, the International Society for Compan-
ion Animal Infectious Diseases convened a Working Group of clinical microbiologists, pharmacologists, and internists to
share experiences, examine scientific data, review clinical trials, and develop these guidelines to assist veterinarians in making
antimicrobial treatment choices for use in the management of bacterial respiratory diseases in dogs and cats.
Key words: Bronchitis; Pneumonia; Pyothorax; Rhinitis.

T his document contains guidelines for the treatment

of bacterial causes of feline upper respiratory tract
disease (URTD), canine infectious respiratory disease
complex (CIRDC; previously known as canine infec-
tious tracheobronchitis or kennel cough complex),
bronchitis, pneumonia, and pyothorax that were final-
ized in 2016 by the Antimicrobial Guidelines Working
Group of the International Society for Companion
Animal Infectious Diseases (www.iscaid.org). During
the development of the guidelines, other veterinary rec-
ommendations on antimicrobial treatment1–4 and corre-
sponding guidelines for human medicine were
evaluated, with consideration of the differences among
species.5,6
The committee unanimously believes that there are
limitations in objective, published information relevant
to the treatment of bacterial respiratory diseases in dogs
and cats. Thus, the Working Group used a modification
of the Delhi method for consensus building in the devel-
opment of these guidelines.7 The Working Group
From the Colorado State University, Fort Collins, CO (Lappin);
University of Saskatoon, Saskatoon, SK (Blondeau); Auburn
University, Auburn, AL (Boothe); North Carolina State University,
Raleigh, NC (Breitschwerdt, Papich); University of Copenhagen,
Copenhagen, Denmark (Guardabassi); Royal Veterinary College,
London, UK (Lloyd); University of Pennsylvania, Philadelphia, PA
(Rankin); University of California, Davis, CA (Sykes); Ontario
Veterinary College, Guelph, ON (Weese); and the The Women’s
and Children Hospital, Adelaide, SA, Australia (Turnidge).
An overview of the guidelines was presented at the 2016 American
College of Veterinary Internal Medicine Forum, Denver, Colorado.
Corresponding author: M.R. Lappin, Colorado State University,
300 West Drake Road, Fort Collins, CO 80523; e-mail: mlappin@
colostate.edu.
Submitted May 22, 2016; Revised September 5, 2016;
Accepted November 7, 2016.
Copyright © 2017 The Authors. Journal of Veterinary Internal
Medicine published by Wiley Periodicals, Inc. on behalf of the Ameri-
can College of Veterinary Internal Medicine.
This is an open access article under the terms of the Creative
Commons Attribution-NonCommercial License, which permits use,
distribution and reproduction in any medium, provided the original
work is properly cited and is not used for commercial purposes.
DOI: 10.1111/jvim.14627
Abbreviations:
CIRDC canine infectious respiratory disease complex
FCV feline calicivirus
FHV-1 feline herpesvirus 1
PCR polymerase chain reaction
URI upper respiratory infection
URTD feline upper respiratory tract disease
reviewed the literature and met in person to develop the
initial draft of the guidelines. This was followed by a
number of revisions completed electronically in an
attempt to build consensus with the wording of each
recommendation within the Working Group. The
Working Group recommendations were then provided
to all guidelines committee members who were asked to
independently select whether they agreed, were neutral,
or disagreed with a recommendation. A updated draft
of the document was then completed and provided to 6
experts in the field that were not members of the Work-
ing Group who were asked to rate each recommenda-
tion by means of the same system. For those
recommendations that received any “disagree” votes
from the 17 total reviewers (Working Group and out-
side reviewers), the percentage distribution of all review-
ers and appropriate comments are presented.
As with all guidelines, the antimicrobial use guideli-
nes for the treatment of bacterial respiratory tract infec-
tions in dogs and cats should be interpreted as general
recommendations that are reasonable and appropriate
for the majority of cases. The Working Group acknowl-
edges the variability among cases and these guidelines
should not be considered standards of care that must be
followed in all circumstances. Rather, they should be
considered the basis of decision-making, with the poten-
tial that different or additional approaches might be
required in some cases. Further, although these guideli-
nes are designed as international guidelines that are
appropriate for all regions of the world, the Working
Group realizes that regional differences in antimicrobial
resistance rates, antimicrobial availability, prescribing
280
patterns, and restrictions on use of some agents exist.
The user of this document is obligated to be familiar
with local and regional regulations that might restrict
use of certain antimicrobials listed in this document.
Diagnostic and treatment recommendations contained
in these guidelines are largely limited to those relating
to bacterial infection.
Feline Upper Respiratory Tract Disease
Definitions and Causes
Feline upper respiratory tract disease is a syndrome
consisting of clinical signs that can include serous to
mucopurulent ocular and nasal discharges, epistaxis,
sneezing, and conjunctivitis.8–11 Clinical signs can be
acute (≤10 days) or chronic (>10 days). The term “up-
per respiratory infection (URI)” is reserved for cats
with clinical signs of URTD that are directly associated
with one or more of the known pathogenic viral, bacte-
rial, or fungal organisms.
It is believed that the majority of cats with acute clin-
ical signs of URTD have feline herpesvirus 1 (FHV-1)-
or calicivirus (FCV)-associated URI. Some of the cats
with viral infections can develop secondary bacterial
infections.12–15 Staphylococcus spp., Streptococcus spp.,
Pasteurella multocida, Escherichia coli, and anaerobes
are organisms that are commonly cultured from the sur-
face of the upper respiratory mucous membranes from
healthy cats.16,17 However, several bacterial species,
including Chlamydia felis, Bordetella bronchiseptica,
Streptococcus canis, Streptococcus equi subspp. zooepi-
demicus, and Mycoplasma spp., have been isolated or
detected by molecular techniques such as the poly-
merase chain reaction (PCR) from cats with URTD
without the presence of pathogenic viruses, suggesting a
primary role in some cats.16,18–22 The presence of puru-
lent or mucopurulent nasal or ocular discharges might
increase the suspicion that primary or secondary bacte-
rial infection is present, but there is no definite proof of
this association because viral or fungal agents can also
induce mucopurulent discharges.
Diagnosis of Acute Bacterial Upper Respiratory
Infection (≤10 Days Duration)
For cats with signs of URTD of ≤10 days’ duration,
a thorough history should evaluate in particular the
vaccination status, the presence or exposure to other
cats, whether cats are allowed outdoors, contact with a
shelter, kennel or veterinary hospital, health status of
in-contact cats, health status of in-contact humans,
exposure to dogs that might be boarded or have
recently come from a shelter (possible increased risk of
infection by B. bronchiseptica), likelihood of foreign
body contact (including house plants), and a history of
recent stress which is thought to reactivate FHV-1
infection in some cats.17 Careful ocular, oral, and otic
examination to evaluate for other primary problems is
indicated. Thoracic auscultation should be performed to
evaluate for evidence of concurrent lower respiratory
Lappin et al
disease. The Working Group recommends that all cats
with suspected bacterial URI be evaluated for the pres-
ence of feline leukemia virus antigen and feline immun-
odeficiency virus antibodies in serum in accordance
with the American Association of Feline Practitioners
Retrovirus Panel Report.23 Although these retroviruses
do not cause respiratory disease directly, both have
been associated with lymphoma (which could cause
URTD) and both can cause immunosuppression that
could predispose to severe viral and bacterial URIs.
Many diagnostic tests could be performed to assess for
evidence of primary or secondary bacterial URI (See the
Diagnosis of Chronic Bacterial Upper Respiratory Infec-
tion (>10 Days of Duration) section). It is the opinion
of the Working Group that there is limited benefit to per-
forming cytology of nasal discharges to diagnose bacte-
rial infection and guide the antimicrobial choice.
If nasal discharges are serous and lack a mucopuru-
lent or purulent component, the Working Group
believes that antimicrobial treatment is not recom-
mended because of the likelihood of uncomplicated
viral infection.
If acute bacterial URI is suspected based on purulent
or mucopurulent discharge, in the absence of evidence of
the cause of URTD based on history and physical exami-
nation findings, the Working Group recommends a per-
iod of observation without immediate use of an
antimicrobial drug. This might vary in duration based on
other clinical findings (See the Treatment of Suspected
Acute Bacterial Upper Respiratory Infection section). In
humans, antimicrobial treatment is recommended only if
clinical signs have not improved after 10 days or have
worsened after 5–7 days.24 A more extensive workup for
an underlying cause can be postponed until after the per-
iod of observation, up to 10 days after the onset of clini-
cal signs if the cat develops chronic URTD.
Aerobic bacterial culture and antimicrobial suscepti-
bility test results from nasal discharges are difficult to
interpret because (1) some pathogenic organisms (eg,
Chlamydia and Mycoplasma) cannot be cultured on
standard laboratory media and (2) positive culture
might not be associated with bacterial infection due to
growth of commensal organisms. Thus, the Working
Group recommends that aerobic bacterial culture and
antimicrobial susceptibility testing not be performed on
nasal secretions collected from cats with acute bacterial
URI.
Results from Mycoplasma spp. culture (or PCR
assay), and molecular diagnostic procedures for FHV-1,
FCV, and C. felis are difficult to interpret in individual
cats. Mycoplasma spp., FHV-1, FCV, and C. felis can
be grown or amplified by molecular assays from both
healthy or diseased cats, and vaccine strains of B. bron-
chiseptica, FHV-1, FCV, and C. felis can be detected by
molecular diagnostic assays for varying periods of time
depending on the vaccine type.25,26 When positive,
molecular diagnostic tests for FCV, FHV-1, or C. felis
might be useful to support a diagnosis of infection in
the presence of suggestive clinical signs and the absence
of a history of recent vaccination. However, if an out-
break of URI is suspected in populations of cats like
 Respiratory Treatment Guidelines 281

Table 1. First-line antimicrobial options for bacterial respiratory infections in the dog and cat.
Infection Type First-Line Drug Options
Acute bacterial upper respiratory Doxycyclinea or amoxicillin per os (PO)
infection (URI) in cats
Chronic bacterial URI in cats Doxycycline or amoxicillin PO
Base the choice on C&Sb if available
Canine infectious respiratory disease complex Doxycyclinea or amoxicillin–clavulanate PO
(bacterial component)
Bacterial bronchitis (dogs or cats) Doxycyclinea PO
Base changes if needed on clinical responses and
C&S if available
Pneumonia in animals with extensive contact with Doxycyclinea PO
other animals that have no systemic manifestations Base changes if needed on clinical responses
of disease (ie, fever, lethargy, dehydration) and C&S if available
Pneumonia with or without clinical evidence of sepsisc Parenteral administration of a fluoroquinoloned and a
penicillin or clindamycine initially
Base oral drug choices to follow on clinical responses
and C&S results if available
Pyothorax (dogs or cats)b Parenteral administration of a fluoroquinoloned and a
penicillin or clindamycine initially combined with
therapeutic lavage initially
Base oral drug choices to follow on clinical responses
and C&S results if available
a
Minocycline has been substituted in some situations when doxycycline is unavailable or of greater expense. See Table 2 for dose recom-
mendations.
b
Culture and antimicrobial susceptibility testing = C&S.
c
For animals with clinical findings of life-threatening disease, the consensus of the Working Group was to administer dual agent treat-
ment parenterally with the potential for de-escalation of treatment and switch to oral drugs based on clinical responses and culture and
antimicrobial susceptibility testing. See Table 2 for dose differences by route and the text for further recommendations for oral or par-
enteral administration.
d
Enrofloxacin is often chosen as there is a veterinary product for parenteral administration and the drug has a wide spectrum against
Gram-negative organisms and Mycoplasma spp. There are other drugs with a wide spectrum against Gram-negative bacteria that can be
substituted based on antimicrobial susceptibility testing or clinician preference. See Table 2 for a discussion of how to administer enrofloxa-
cin and for other drug choices. Enrofloxacin should be administered at ≤5 mg/kg/24 h in cats to lessen risk of retinal degeneration. One
reviewer noted that IV ciprofloxacin could also be used; however, the other reviewers (94%) believed that enrofloxacin should be used as
labeled for veterinary use.
e
When enrofloxacin or other drugs with Gram-negative activity are administered parenterally to animals with life-threatening disease,
concurrent administration of other parenteral drugs with activity against anaerobes and Gram-positive bacteria is recommended. Common
choices include ampicillin or clindamycin. Which of these drugs to choose will depend on the most likely infectious agent suspected and
historical antimicrobial resistance in the geographical region. For example, Enterococcus spp. and Streptococcus spp. are more likely to be
susceptible to a penicillin, and Toxoplasma gondii and Neospora caninum are more likely to be susceptible to clindamycin. Cephalosporins
are generally not recommended for the treatment of anaerobic infections because of unpredictable activity and lack of evidence for their
efficacy. Please see the text for further discussion of other potential drug choices or combinations.

those in shelters, catteries, boarding facilities, or multi-
ple cat households, these assays also might be indicated,
particularly if severe clinical disease is occurring. If pos-
sible, several affected cats should be evaluated to
increase sensitivity and positive predictive value of the
assay results.
Treatment of Suspected Acute Bacterial Upper
Respiratory Infection
Some cats with mucopurulent nasal discharge main-
tain normal appetite and attitude and experience spon-
taneous resolution of illness within 10 days without
antimicrobial treatment. The Working Group recom-
mends that antimicrobial treatment be considered
within the 10-day observation period only if fever,
lethargy, or anorexia is present concurrently with
mucopurulent nasal discharge.
If antimicrobial treatment is chosen for a cat with
acute bacterial URI, the optimal duration of treatment
is unknown and so this recommendation is based on
experiences of the Working Group members that are
clinicians. The Working Group recommends empirical
administration of doxycycline (Tables 1 and 2) for 7–
10 days to cats with suspected acute bacterial URI as
the first-line antimicrobial option.27,28 The Working
Group believes that doxycycline is a good first choice
because it is well tolerated by cats; most B. bronchisep-
tica isolates from cats are susceptible to doxycycline
in vitro (by unapproved standards for testing), despite
resistance to other agents such as beta-lactams and
sulfonamides,29–31 and doxycycline is effective in vivo
for the treatment of cats with C. felis infections,27,32–34
and Mycoplasma spp. infections.35 Doxycycline is also
effective for the treatment of a variety of chlamydial
and mycoplasma infections in cats and other
282
Table 2. Antimicrobial treatment options for respiratory tract infections in the dog and cat.
Drug Dose
Amikacin Dogs: 15 mg/kg, IV/IM/SC, q24h
Cats: 10 mg/kg, IV/IM/SC, q24h
Amoxicillin 22 mg/kg, PO, q12h
Amoxicillin–clavulanate Dogs: 11 mg/kg, PO, q12h
Cats: 12.5 mg/kg, PO, q12h
(dose based on
combination of
amoxicillin–clavulanate
Ampicillin-sulbactam 20 mg/kg, IV, IM, q6–8h
Ampicillin sodium 22–30 mg/kg, IV, SQ, q8h
Azithromycin 5–10 mg/kg, PO, q12h day 1
and then q3 days (Longer
intervals are not indicated)
Cefazolin 25 mg/kg, SQ, IM, IV, q6h
Cefadroxil Dogs: 11–22 mg/kg, PO, q12h
Cats: 22 mg/kg, PO, q24h
Cefoxitin 10–20 mg/kg, IV, IM, q6–8h
Cefovecin 8 mg/kg, SC, once. Can be repeated
once after 7–14 days
Cephalexin 22–25 mg/kg, PO, q12h
Chloramphenicol Dogs: 50 mg/kg, PO, q8h
Cats: 50 mg/cat, PO q12h
Lappin et al
Comments
Not recommended for routine use but might be useful for the
treatment of multidrug-resistant organisms or if parenteral
enrofloxacin or ciprofloxacin are contraindicated. Potentially
nephrotoxic. Avoid in dehydrated animals and those with renal
insufficiency
Might be useful for the treatment of secondary bacterial URI
caused by Pasteurella spp. and Streptococcus spp., some
Staphylococcus spp. and many anaerobic bacteria. Ineffective
against beta-lactamase-producing bacteria, most Bordetella
bronchiseptica isolates, all Mycoplasma spp., and Chlamydia felis in
cats. One Working Group member supports the use of amoxicillin
q8h because of the short plasma half-life
Used as a first-line option for secondary bacterial URI from
Pasteurella spp., Streptococcus spp., methicillin-susceptible
Staphylococcus spp. (including penicillinase-producing strains),
many anaerobic bacteria, and most B. bronchiseptica isolates.
Ineffective against all Mycoplasma spp., and inferior to other drugs
for C. felis in cats. One Working Group member supports the use
of amoxicillin q8h because of the short plasma half-life
Used alone parenterally for cases with uncomplicated secondary
bacterial pneumonia (Gram-positive and anaerobic bacteria). Used
concurrently with another drug with wider Gram-negative activity
if life-threatening disease exists
Used parenterally for cases with uncomplicated secondary bacterial
pneumonia (Gram-positive and anaerobic bacteria). Used
concurrently with another drug with Gram-negative activity if life-
threatening disease exists
Used for primary bacterial diseases (in particular Mycoplasma spp.)
and for pneumonia of undetermined etiology because the spectrum
includes Toxoplasma gondii and Neospora caninum
Used parenterally for cases with uncomplicated secondary bacterial
pneumonia (Gram-positive and anaerobic bacteria). Used
concurrently with another drug with wider Gram-negative activity
if life-threatening disease exists. Ineffective against
B. bronchiseptica, Mycoplasma spp., and C. felis in cats, and
enterococci
Used PO for secondary bacterial URI from Pasteurella spp., and
some Staphylococcus spp. and Streptococcus spp., and many
anaerobic bacteria. Ineffective against B. bronchiseptica,
Mycoplasma spp., and C. felis in cats, and Enterococcus spp.
Resistance might be common in Enterobacteriaceae in some regions
Used parenterally for cases with secondary bacterial pneumonia
(Gram-positive and anaerobic bacteria). Has a greater Gram-
negative spectrum than first-generation cephalosporins. Ineffective
against B. bronchiseptica, Mycoplasma spp., and C. felis in cats,
and Enterococcus spp
Might be effective for the treatment of secondary bacterial URI
caused by Pasteurella spp., some Staphylococcus pseudintermedius
and Streptococcus spp. Ineffective for B. bronchiseptica,
Mycoplasma spp., and C. felis in cats and Enterococcus spp.
Pharmacokinetic data are available to support the use in dogs and
cats, with a duration of 14 days (dogs) and 21 days (cats)
See cefadroxil comments
Reserved for multidrug-resistant infections with few other options.
Effective for the primary bacterial pathogens, penetrates tissues
well, and has an excellent spectrum against anaerobes and so
might be considered for the treatment of pneumonia when the
owner cannot afford dual antimicrobial agent treatment.
Myelosuppression can occur, particularly with long-term treatment.
Owners should be instructed to wear gloves when handling the
drug because of rare idiosyncratic aplastic anemia in humans
(continued)
 Respiratory Treatment Guidelines
Table 2 (Continued)
Drug Dose
Clindamycin Dogs: 10 mg/kg, PO, SC, q12h
Cats: 10–15 mg/kg, PO, SC, q12h
Doxycycline 5 mg/kg, PO, q12h
Or
10 mg/kg, PO, q24h
Enrofloxacin Dogs: 5–20 mg/kg PO, IM, IV q24h
Cats: 5 mg/kg, PO, q24h
Gentamicin Dogs: 9–14 mg/kg, IV, q24h
Cats: 5–8 mg/kg, IV, q24h
Imipenem–cilastatin 3–10 mg/kg, IV, IM q8h
Marbofloxacin 2.7–5.5 mg/kg PO q24h
Meropenem Dogs: 8.5 mg/kg SC q12h
Or 24 mg/kg IV q12h
Cats: 10 mg/kg q12h, SC, IM, IV
Minocycline Dogs: 5 mg/kg, PO, q12h
Cats: 8.8 mg/kg PO q24h or
50 mg/cat PO q24h
Orbifloxacin 2.5–7.5 mg/kg PO q12h for tablets
7.5 mg/kg, PO, q12h for the oral
suspension in cats
Ormetoprim- 27.5 mg/kg, PO q24h in dogs
sulfadimethoxine Note: dosing is based on total
sulfadimethoxine-ormetoprim
concentration (5 to 1 ratio)
Pradofloxacin 5.0 mg/kg PO q24h if tablets are
used in dogs or cats
7.5 mg/kg PO q24h if oral
suspension for cats is used
283
Comments
Activity against most anaerobic bacteria, many Gram-positive
bacteria and some mycoplasmas. Not effective for most Gram-
negative bacteria and some Bacterioides spp.
Used for dogs or cats with URI, CIRDC, or bronchitis that is likely
to be associated with B. bronchiseptica, Mycoplasma spp., and
C. felis (cats). An injectable formulation is available if parenteral
administration is needed. Either the hyclate or monohydrate salts
can be used. Can be used in kittens and puppies >4 weeks of age
without enamel discoloration
Active against most isolates of B. bronchiseptica, Mycoplasma spp.,
and C. felis (cats) as well as many secondary Gram-negative and
Gram-positive bacteria. Practically no activity against Enterococcus
spp and anaerobic bacteria. Associated with risk of retinopathy in
cats and so do not exceed 5 mg/kg/d of enrofloxacin in this
species. All quinolones are associated with cartilage problems in
growing puppies and kittens. Enrofloxacin is not approved for
parenteral use in cats and is not soluble enough to be injected
directly. It can precipitate and can chelate with cations in some
fluid solutions. One Working Group member recommends never
with the 5 mg/kg dose in dogs because of likely induction of
resistant strains and 1 Working Group member does not
recommend the drug for cats because the 5 mg/kg dose might
induce resistance and higher doses can induce retinal degeneration
Not recommended for routine use but might be useful for the
treatment of multidrug-resistant organisms or if parenteral
enrofloxacin is contraindicated. Potentially nephrotoxic. Avoid in
dehydrated animals and those with renal insufficiency
Reserve for the treatment of multidrug-resistant infections,
particularly those caused by Enterobacteriaceae or Pseudomonas
aeruginosa. Recommend consultation with a respiratory or infectious
disease veterinary specialist or veterinary pharmacologist before use
Effective for the primary bacterial pathogens B. bronchiseptica,
Mycoplasma spp., and C. felis (cats) as well as many secondary
infections with Gram-negative and Gram-positive organisms.
Limited efficacy against Enterococcus spp. and anaerobic bacteria.
Available as an injectable solution in some countries
Reserve for the treatment of multidrug-resistant infections,
particularly those caused by Enterobacteriaceae or P. aeruginosa.
Recommend consultation with an infectious disease veterinary
specialist or veterinary pharmacologist before use
Similar to doxycycline and can be used for dogs or cats with URI,
CIRDC, or bronchitis that is likely to be associated with
B. bronchiseptica, Mycoplasma spp., and C. felis (cats)
See Marbofloxacin comments. The oral suspension is well tolerated
by cats
See comments on trimethoprim–sulfonamide-containing products
Effective for the primary bacterial pathogens B. bronchiseptica,
Mycoplasma spp., and C. felis (cats) as well as many secondary
infections with Gram-negative and Gram-positive organisms. In
contrast to other veterinary fluoroquinolones, pradofloxacin has
activity against some anaerobic bacteria. The drug is labeled in
some countries for the treatment of acute infections of the upper
respiratory tract of cats caused by susceptible strains of Pasteurella
multocida, Escherichia coli and the S. intermedius group (including
S. pseudintermedius). The use of pradofloxacin in dogs has been
associated with myelosuppression and is extra-label in North
America
(continued)
284 Lappin et al

Table 2 (Continued)

Drug Dose Comments

Piperacillin-tazobactam
Trimethoprim-
sulfamethoxazole,
trimethoprim-sulfadiazine
50 mg/kg IV q6h for
immunocompetent animals,
or 3.2 mg/kg/h CRI, after loading
dose of 3 mg/kg IV, for other
animals
15 mg/kg PO q12h
Note: dosing is based on total
trimethoprim + sulfadiazine
concentration
Antipseudomonal penicillin. Used for life-threatening pneumonia or
pyothorax for the treatment of Gram-negative (including some
ESBL), Gram-positive and anaerobic bacteria. Ineffective for
Mycoplasma, T. gondii, and N. caninum
Generally avoided in respiratory tract infections that might involve
anaerobic bacteria (particularly pyothorax). Might be less effective
that other first-line choices for some primary bacterial pathogens
other than Streptococcus spp. Concerns regarding adverse effects
exist (KCS, folate deficiency anemia, blood dyscrasias) in some
dogs, especially with prolonged treatment. If prolonged (>7 day)
treatment is anticipated, baseline Schirmer’s tear testing is
recommended, with periodic re-evaluation and owner monitoring
for ocular discharge. Avoid in dogs that might be sensitive to
potential adverse effects such as KCS, hepatopathy,
hypersensitivity, and skin eruptions, and owners of treated dogs
should be informed of the clinical findings to be monitored.

CIRDC, canine infectious respiratory disease complex; URI, upper respiratory infection.

mammalian host species. It also has activity against
many opportunistic bacterial pathogens that are compo-
nents of the normal microbiota of the respiratory tract.
Of the 17 reviewers, 16 (94%) agreed with this Working
Group recommendation and 1 disagreed because there
is no breakpoint data for this antimicrobial for B. bron-
chiseptica or other bacteria in cats and there are no
pharmacokinetics, controlled clinical trials, susceptibility
data, or pharmacodynamic data on which to base the
recommendation.
Due to delayed esophageal transit time for capsules
and tablets, cats are prone to drug-induced esophagitis
and resultant esophageal strictures.36,37 Although any
table or capsule could cause this problem, doxycycline
hyclate tablets and clindamycin hydrochloride cap-
sules have been reported most frequently to cause
problems.38–40 Thus, tablets and capsules should be given
coated with a lubricating substance, followed by water,
administered in a pill treat, concurrently with at least
2 mL of a liquid, or followed by a small amount of
food.37 Doxycycline formulated and approved for use in
cats is available in some countries and should be used if
available. The use of compounded suspensions of doxy-
cycline should be avoided because marketing of such for-
mulations is in violation with regulations in some
countries, including the USA. In addition, compounded
aqueous-based formulations of doxycycline are associ-
ated with a variable loss of activity beyond 7 days.41
Minocycline pharmacokinetics are now available for cats
and this tetracycline should be evaluated further for effi-
cacy against infectious disease agents in cats.42
The Working Group considers amoxicillin to be an
acceptable alternate first-line option for the treatment
of acute bacterial URI when C. felis and Mycoplasma
are not highly suspected. This is based on evidence that
cats administered amoxicillin for the treatment of sus-
pected secondary bacterial infections in shelter cats with
acute bacterial URI often have apparent clinical
responses.20,43 Cats administered amoxicillin and
clavulanate potassium (amoxicillin–clavulanate) had
apparent clinical responses in 1 study of shelter cats
with acute bacterial URI and so this drug also could be
considered as an alternative to doxycycline in regions
where a high prevalence of beta-lactamase-producing
organisms has been identified (eg, based on regional
antibiograms).44
In 1 study of shelter cats with suspected bacterial URI,
the injectable cephalosporin, cefovecin was inferior to
doxycycline or amoxicillin–clavulanate.44 One limitation
of this study was the lack of a negative control group.44
Thus, it is the opinion of the Working Group that more
evidence is needed before cefovecin can be recommended
for the treatment of bacterial URI in cats (Table 2).
Monitoring Treatment of Suspected Acute Bacterial
Upper Respiratory Infection
Most cats with this syndrome will rapidly improve
within 10 days with or without antimicrobial adminis-
tration. If an antimicrobial drug was prescribed and
was ineffective and bacterial infection is still suspected
after the first 7–10 days of administration, the Working
Group recommends that a more extensive diagnostic
workup should be offered to the owner. An alternate
antimicrobial agent with a different spectrum should be
considered only if the owner refuses a diagnostic
workup and careful re-evaluation of the cat still sup-
ports the presence of a bacterial infection without an
obvious underlying cause (see the Diagnosis of acute
bacterial Upper Respiratory Infection section). Longer
duration of treatment might be required to clear the
carrier state of C. felis.33,34
Diagnosis of Chronic Bacterial Upper Respiratory
Infection (>10 Days of Duration)
A more extensive diagnostic workup should be con-
sidered for cats with URTD of >10 days of duration,
 Respiratory Treatment Guidelines
particularly in the face of therapeutic failure after treat-
ment of suspected acute bacterial URI as described.
The diagnostic workup should be performed to eval-
uate for other causes including Cuterebra spp. and fun-
gal diseases as well as noninfectious causes of URTD
including allergic diseases, neoplasia, foreign bodies,
nasopharyngeal stenosis, oronasal fistulas, nasopharyn-
geal polyps, and trauma.8–11 Referral to a specialist is
recommended if advanced imaging or rhinoscopy capa-
bilities are not available. If other treatable causes of
URTD are not identified, The Working Group recom-
mends that nasal lavage or brushings (for cytology, aer-
obic bacterial culture and antimicrobial susceptibility
testing, Mycoplasma spp. culture or PCR, and fungal
culture) and nasal tissue biopsy for histopathological
examination with or without cultures (if not evaluated
by lavage) should be performed. Of the 17 reviewers,
16 (94%) agreed with the recommendation and 1 dis-
agreed and stated that the results of nasal tissue cul-
tures in cats with chronic URTD are always impossible
to interpret.
In 1 study, nasal lavage specimens gave a higher
sensitivity for bacterial growth than tissue biopsy
specimens.45 However, as discussed previously, bacterial
culture results can be difficult to impossible to interpret
as bacteria can be cultured from the nasal cavity of
healthy cats. For example, multidrug-resistant bacteria
can colonize and be grown from the nasal passages in
the absence of infection. The purpose of culture and
susceptibility testing in cats with chronic bacterial URI
is usually to identify the antimicrobial susceptibility of
severe secondary bacterial infections that occur sec-
ondary to an untreatable underlying cause (eg, idio-
pathic inflammatory rhinitis). Antimicrobial treatment
of these cats might provide relief from severe clinical
signs, but it should be recognized that these cats will
continue to be predisposed to opportunistic infections,
often with antimicrobial-resistant bacteria. Therefore,
use of antimicrobials should be limited to those cats
with severe clinical signs.
The Working Group recommends consultation with
an internal medicine specialist with expertise in infec-
tious disease, clinical pharmacologist, or clinical micro-
biologist before treating multidrug-resistant organisms
(resistant to ≥3 drug classes) isolated from nasal lavage
cultures.
Treatment of Chronic Feline Bacterial Upper
Respiratory Infection
In cats with chronic bacterial URI, the antimicrobial
agent should be selected on the basis of culture and
antimicrobial susceptibility test results if available. If an
organism with resistance against a previously prescribed
antimicrobial agent is identified and the clinical
response is poor, an alternate drug should be substi-
tuted (Table 2).
Pradofloxacin is a veterinary fluoroquinolone that is
approved in some countries for the treatment of acute
infections of the upper respiratory tract caused by
susceptible strains of P. multocida, E. coli and the
285
Staphylococcus intermedius group.46 In 1 study of shel-
ter cats, a pradofloxacin protocol was equivalent to
amoxicillin for the treatment of suspected bacterial
URI.20 The other veterinary fluoroquinolones (en-
rofloxacin, orbifloxacin, and marbofloxacin [Table 2])
have also been used by veterinarians to treat suspected
feline bacterial URI.47 In the first study, all cats were
administered an antibiotic;20 a placebo control study
evaluating pradofloxacin for the treatment of bacterial
URI in cats has not been published to our knowledge.
Because of concerns about the emergence of, and ani-
mal and public health consequences of, resistance to flu-
oroquinolones and third-generation cephalosporins, the
Working Group recommends that these drugs should
be reserved for situations where culture and susceptibil-
ity results indicate potential efficacy and when other
antimicrobial agents (eg, doxycycline, amoxicillin) are
not viable options. Moreover, there is no clinical evi-
dence indicating that fluoroquinolones and third-genera-
tion cephalosporins are superior to doxycycline and
amoxicillin in the treatment of chronic bacterial URI in
cats.
Although azithromycin pharmacokinetics have been
determined in cats,48,49 azithromycin and amoxicillin
protocols for the treatment of suspected bacterial upper
respiratory tract infections in shelter cats were equiva-
lent in 1 study where all cats were administered an
antibiotic.43 Azithromycin is also not as efficacious as
doxycycline for the treatment of feline ocular chlamy-
diosis in a study in which all cats were administered an
antibiotic.33 Thus, the Working Group recommends
that azithromycin should be reserved for situations
when chlamydiosis is not likely and when other antimi-
crobial agents (eg, doxycycline, amoxicillin) are not
viable options. Of the 17 reviewers, 16 (94%) agreed
with this recommendation. One reviewer commented
that there is evidence that azithromycin treatment in
people produces therapeutic benefits for infections of
the respiratory tract via mechanisms that are not attrib-
uted to the antibacterial properties.49 However, at this
time, the Working Group does not advocate for the
administration of azithromycin to animals only for its
disease-modifying properties or immunomodulatory
effects.
If Pseudomonas aeruginosa is isolated in pure or
nearly pure culture and believed to be the cause of a
secondary infection, extensive flushing of the nasal cav-
ity under anesthesia should be performed to remove
loculated secretions. Although use of drug combinations
(such as a fluoroquinolone combined with a beta-lactam
[Table 2]) has been recommended to treat P. aeruginosa
infections because of the tendency of this organism to
rapidly develop resistance, monotherapy with a fluoro-
quinolone is accepted for the treatment of P. aeruginosa
otitis/osteomyelitis in human patients, unless resistance
is encountered.50,51 Regardless of whether monotherapy
or combination treatment is chosen, the Working
Group recommends that antimicrobials be selected on
the basis of culture and susceptibility testing and that a
clinical microbiologist, clinical pharmacologist, or inter-
nal medicine specialist with expertise in infectious
286
disease be consulted before initiating treatment. Of the
17 reviewers, 15 (88%) agreed with this recommenda-
tion and 2 were neutral (12%).
Optimal duration of the treatment of chronic bacte-
rial URI in cats with no other underlying disease is
unknown. The consensus of the Working Group was to
administer the chosen antimicrobial for at least 7 days
and if the drug is tolerated and showing a positive clini-
cal effect, the drug should be continued as long as there
is progressive clinical improvement and for at least
1 week past clinical resolution of nasal disease or pla-
teau in response to treatment. However, the Working
Group acknowledges that stopping treatment sooner
might also be effective in some cats.
If mucopurulent discharge with or without sneezing
recurs after treatment in a cat that has had a thorough
diagnostic evaluation, the previously effective antimicro-
bial agent is usually prescribed empirically again, for at
least 7–10 days, to assess for the treatment response.
The Working Group recommends avoidance of
repeated empirical treatment on a regular basis when-
ever possible. However, some cats with suspected
chronic bacterial URI require such an approach to les-
sen clinical signs of disease even though clinical cure is
never achieved. The Working Group believes there is
currently no known optimal protocol for repeated
empirical treatment for chronic URI in cats. Evidence
from the human infectious disease literature shows
organisms cultured from patients within 3 months of
primary treatment had a higher likelihood of resistance
to the treatment drug or class used. As such, some res-
piratory treatment guidelines in human medicine recom-
mend a different drug (or drug class) if used within
3 months of the initial treatment.52 Until further data
are available, the Working Group recommends use of
the previously effective antimicrobial drug with switch
to a different drug class or a more active drug within
the class if treatment is ineffective after a minimum of
48 hours. Collection of specimens for culture and sus-
ceptibility is recommended if neither of these
approaches is successful.
There is no evidence to support the use of topical
(intranasal) antiseptic or antimicrobial administration
for the treatment of acute or chronic bacterial URI.
However, topical administration of 0.9% saline solu-
tion is believed to have has a mild mucolytic effect and
might be effective in clearing nasal secretions in some
cats.
Many cats with chronic URTD have complete diag-
nostic evaluations performed and the only finding is lym-
phocytic–plasmacytic or mixed inflammation identified
on histopathological evaluation without a known under-
lying cause (idiopathic feline rhinosinusitis). Although
chronic infection with respiratory viruses has been specu-
lated to play a role in this disease, the true underlying eti-
ology remains enigmatic.16,22 Although there was no
association among Bartonella spp. test results among cats
with and without URTD in shelters in 1 study or with
chronic rhinosinusitis in another study, additional
research is required to ascertain the role of Bartonella
spp. in feline chronic rhinosinusitis.53,54
Lappin et al
Monitoring Treatment of Chronic Bacterial Upper
Respiratory Infection
Because results of bacterial culture and antimicrobial
susceptibility testing from specimens collected from the
nasal cavity are difficult to interpret, monitoring the
efficacy of treatment of cats with suspected chronic bac-
terial URI is usually based on clinical signs of disease.
Canine Infectious Respiratory Disease Complex
Definition and Causes
The clinical syndrome associated with CIRDC is gen-
erally characterized by an acute onset of cough with or
without sneezing. Nasal and ocular discharges can also
occur depending on the infectious agent that is
involved. Fever is uncommon but might be present. The
viruses that have been implicated include canine aden-
ovirus 2, canine distemper virus, canine respiratory
coronavirus, canine influenza viruses, canine her-
pesvirus, canine pneumovirus, and canine parainfluenza
virus.55–59 Bacteria implicated as primary pathogens in
this complex include B. bronchiseptica, S. equi sub-
species zooepidemicus, and Mycoplasma spp.55,59–63
Dogs with canine distemper virus infection often have
diarrhea and can have mucopurulent ocular and nasal
discharge that might be confused with mucopurulent
discharges caused by primary bacterial pathogens.
Because of its significance to the health of other dogs
and for prognosis, the possibility of underlying distem-
per virus infection should always be considered in
young dogs with mucopurulent ocular and nasal dis-
charges, even when other signs of distemper are absent.
Infection with S. equi subspecies zooepidemicus should
be suspected if cases of acute hemorrhagic pneumonia
or sudden death are reported.64
Co-infections with multiple respiratory pathogens are
common in dogs with CIRDC and each of the agents
can be harbored by dogs with no clinical signs. Vaccines
are available for some of the causes of CIRDC in some
countries and include canine parainfluenza virus, canine
adenovirus 2, canine distemper virus, H3N8 canine
influenza virus, H3N2 influenza virus, and B. bron-
chiseptica. With the exception of canine distemper virus,
the immunity induced by vaccination does not prevent
colonization and shedding of the organisms and clinical
signs of disease can develop in vaccinated dogs (2011
AAHA Canine Vaccination Guidelines; www.aahanet.
org). However, morbidity is generally decreased in vac-
cinates compared with dogs that are not vaccinated
when exposed to the pathogens.
Diagnosis of Bacterial Causes of CIRDC
A thorough history and physical examination should
be performed on all dogs with suspected CIRDC. Many
diagnostic tests could be performed to assess for evi-
dence of primary or secondary bacterial CIRDC. It is
the opinion of the Working Group that there is limited
benefit to performing cytology of nasal discharges to
diagnose bacterial infection and guide the antimicrobial
 Respiratory Treatment Guidelines
choice. Aerobic bacterial culture and antimicrobial sus-
ceptibility testing, Mycoplasma spp. culture (or PCR
assay), and molecular diagnostic procedures for canine
parainfluenza virus, canine adenovirus 2, canine distem-
per virus, canine respiratory coronavirus, canine influ-
enza viruses, canine herpesvirus, pneumovirus,
B. bronchiseptica, and Mycoplasma spp. (or M. cynos
alone) can be performed. However, each of these organ-
isms can be grown or detected by molecular methods
from healthy and diseased dogs and vaccine strains of
the organisms can be amplified by molecular diagnostic
assays.65 Molecular assays might also be of limited sen-
sitivity by the time dogs are presented for examination
because viral shedding rates tend to peak very early in
disease. Thus, these tests are generally not recom-
mended by the Working Group for single cases with
typical clinical presentations, no evidence of pneumonia,
and when high-risk populations (eg, breeding kennels)
are not involved.
If an outbreak of CIRDC is suspected in populations
of dogs like those in shelters, breeding kennels, board-
ing facilities, or multiple dog households, molecular
assays might be indicated, along with bacterial culture
and serological testing for viral pathogens, particularly
if poor response to treatment or severe clinical disease
is occurring. If possible, specimens from respiratory
discharges should be collected from several affected
dogs and assayed individually to increase sensitivity
and positive predictive value and necropsy should
be performed if there are fatalities. If clinical signs
consistent with pneumonia develop, a more extensive
diagnostic evaluation is indicated (See the Pneumonia
in Dogs and Cats section).
Treatment of Suspected Bacterial Canine Infectious
Respiratory Disease Complex
The majority of cases of CIRDC are currently
believed to be viral in etiology and so antimicrobial
administration is often not indicated. Most dogs with
clinical signs of CIRDC including mucopurulent nasal
discharge maintain normal appetite and attitude and
might resolve spontaneously within 10 days without
antimicrobial treatment. The Working Group recom-
mends that antimicrobial treatment be considered
within the 10-day observation period only if fever,
lethargy, or inappetence is present together with mucop-
urulent discharges.
If bacterial CIRDC is suspected in dogs with mucop-
urulent nasal discharge, fever, lethargy, or inappetence
but no clinical evidence of pneumonia (eg, crackles or
wheezes on thoracic auscultation), the Working Group
recommends administration of doxycycline empirically
for 7–10 days as the first-line antimicrobial option
(Table 1). Doxycycline is believed to have clinical activ-
ity against Mycoplasma. As in cats, doxycycline is well
tolerated by dogs and isolates of B. bronchiseptica from
dogs are typically susceptible in vitro to doxycy-
cline.60,66 However, the susceptibility testing studies
used an unapproved standard. Optimal duration of
treatment for dogs with bacterial causes of CIRDC is
287
unknown and the 7–10-day recommendation was based
on the clinical experiences of the Working Group. Of
the 17 reviewers, 15 (88%) agreed with this recommen-
dation and 2 disagreed. One reviewer stated that if there
is no evidence of pneumonia and the case is not at high
risk of pneumonia (brachycephalic, collapsing airways;
immunosuppressed), antimicrobial treatment is not indi-
cated at all. The other dissenting reviewer disagreed
with the recommendation because there is no break-
point data for doxycycline for B. bronchiseptica or
Mycoplasma spp. in dogs and so whether the agents are
truly susceptible to the drug is unknown.
Additional antimicrobial susceptibility data for sec-
ondary bacterial agents like Pasteurella spp., Streptococ-
cus spp., Staphylococcus spp., and anaerobes are
needed. For Pasteurella spp. and Streptococcus spp.,
amoxicillin is usually adequate, whereas strains of Sta-
phylococcus spp. are usually susceptible in vitro to
amoxicillin–clavulanic acid. Thus, these antimicrobials
are considered by the Working Group to be alternate
first-line antimicrobials for the treatment of secondary
bacterial infections in this syndrome if treatment with
doxycycline fails or is not possible (eg, it is not well tol-
erated). However, it should also be recognized that
some B. bronchiseptica isolates and all mycoplasmas are
resistant to amoxicillin–clavulanate. Of the 17 reviewers,
13 (77%) agreed, 3 reviewers (18%) disagreed, and 1
reviewer was neutral (6%). Reviewers that provided
negative comments were concerned that because the
concentrations of beta-lactams in bronchial secretions
are unknown for dogs and cats, the use of these drugs
could be ineffective if tracheobronchitis without pneu-
monia was present. Another concern was that use of
amoxicillin–clavulanate more likely selects for resistance
phenotypes of clinical concern (eg, methicillin resistance
in staphylococci).
Inhalational aminoglycoside treatment has been anec-
dotally mentioned as beneficial for the management of
dogs with B. bronchiseptica-associated CIRDC. How-
ever, in the absence of controlled studies for safety or
efficacy, the Working Group does not recommend this
treatment protocol for dogs with suspected bacterial
CIRDC.
Monitoring Treatment of Bacterial Canine Infectious
Respiratory Disease Complex
This disease syndrome is usually self-limited or
responds quickly to antimicrobial treatment. Thus, pri-
mary or repeated diagnostic tests are rarely needed
unless pneumonia is suspected. Bacterial culture is not
recommended after successful treatment. Canine infec-
tious respiratory disease complex has not been associ-
ated with chronic upper respiratory disease in the dogs.
Most dogs with bacterial CIRDC have clinical signs
that resolve quickly and so if the first drug chosen is
ineffective and bacterial disease is still suspected after
the first 7 days, the Working Group recommends that a
more extensive diagnostic workup should be considered
before considering use of other drug classes like fluoro-
quinolones or azithromycin.
288 Lappin et al
Bacterial Bronchitis in Dogs and Cats
Definition and Causes
Inflammation of the bronchi in dogs and cats is asso-
ciated with many different conditions including inhaled
irritants; infections by bacteria, viruses, Dirofilaria
immitis, respiratory parasites (tissue migration of Toxo-
cara canis); pharyngeal or esophageal dysfunction; and
allergies.67 Acute inflammation of the bronchi can occur
secondary to the primary infectious disease agents dis-
cussed in the acute and chronic URI in cats section and
in CIRDC section. In general, the clinical manifesta-
tions, diagnostic plan, and treatment plan are as
described in those sections. However, some dogs and
cats infected with the primary bacterial pathogens
B. bronchiseptica and Mycoplasma spp. can develop
chronic bronchitis or bronchopneumonia.68 In addition,
dogs and cats with other inflammatory diseases of the
bronchi or anatomic defects of the larynx and trachea
(eg, laryngeal paralysis, collapsing airways) might
develop secondary bacterial bronchitis. The source of
those bacteria is thought to be the natural oral micro-
biota. Thus, the same bacteria described for secondary
bacterial URI in cats and secondary bacterial CIRDC
in dogs might be associated with bronchitis. However,
many dogs with chronic bronchitis do not have large
numbers of bacteria cultured after bronchoalveolar
lavage and so the syndrome is not always associated
with bacterial infection.69,70
Diagnosis of Suspected Bacterial Bronchitis
The primary clinical manifestation of bacterial
bronchitis in dogs and cats is cough, with or without
signs of respiratory distress. Dogs or cats with
chronic cough, with or without prior evidence of URI
or CIRDC should have a full physical examination
performed, which should include thorough tracheal
and thoracic auscultation. Thoracic radiographs
should be made on full inspiration to evaluate for
pulmonary and cardiac changes that could be associ-
ated with cough. In dogs, radiographs should include
the cervical and intrathoracic trachea and both inspi-
ratory and expiratory radiographs can be performed
to identify collapsing airways. Alternately, fluoroscopy
is available in some veterinary clinics for diagnosis of
collapsing airways. Some dogs and cats with bacterial
bronchitis have radiographic evidence of thickened
bronchi, but others have normal radiographs even
though inflammation exists on cytology of airway
washings. Computed tomography can also be used
to determine the extent of disease. Other causes of
bronchial inflammation should be explored (D. immitis
serology, fecal flotation, fecal sedimentation, Baer-
mann test, laryngeal function evaluation) as indicated
by the history.
If radiographic evidence of bronchial disease is pre-
sent or suspected based on clinical findings, airway
washings for cytological examination are indicated to
determine the type of inflammation that is present and
to obtain materials for Mycoplasma spp. culture and
aerobic bacterial culture and antimicrobial susceptibil-
ity testing. Mycoplasma PCR assay results do not
always correlate with those of culture and might reflect
oral contamination.71 Specimens obtained by bron-
choscopy are most accurate for diagnosis, but collec-
tion of specimens by other methods like tracheal
washing is acceptable if diffuse disease is present and
bronchoscopy is not available, not affordable or of too
great a risk to the animal. The results of analysis of
bronchoalveolar lavage and brush specimens are not
always in agreement.72
The presence of neutrophilic inflammation, intracellu-
lar bacteria, and positive bacterial culture with charac-
teristic radiographic findings suggests primary or
secondary bacterial bronchitis. However, the trachea is
not sterile in normal dogs and low numbers of bacteria
cultured in the absence of cytological evidence of intra-
cellular bacteria might not imply bacterial infection.
Treatment of Suspected Bacterial Bronchitis
While waiting for results of culture and antimicro-
bial susceptibility testing, the Working Group recom-
mends either no antimicrobial treatment or, if the
clinical disease is severe, empirical administration of
doxycycline for 7–10 days (Tables 1 and 2). The use of
doxycycline is recommended based on its in vitro activ-
ity against B. bronchiseptica isolates from dogs and
cats,31,66,73 reports of positive clinical responses to
doxycycline in cats with respiratory Mycoplasma infec-
tions, and a low rate of adverse effects.74,75 Of the 17
reviewers, 16 (94%) agreed with this Working Group
recommendation and 1 disagreed because there is no
breakpoint data for this antimicrobial drug for these
bacteria in dogs. Depending on the clinical and labora-
tory testing results, antimicrobial treatment is contin-
ued, initiated, or modified based on antimicrobial
susceptibility testing with the drug that is selected
being one believed to penetrate the blood bronchus
barrier based on data from other species. If a positive
response is obtained in the first 7–10 days, treatment
should be continued to 1 week past resolution of clini-
cal signs of disease. Optimal duration of treatment for
this syndrome is unknown and so this recommendation
was based on the experiences of the clinicians on the
Working Group. Dogs that fail to respond to antimi-
crobial treatment are likely to have primary chronic
(noninfectious) bronchitis.
Most veterinary microbiology laboratories do not
report antimicrobial susceptibility results for Myco-
plasma spp. and this genus can be difficult to culture.
Thus, the antimicrobial choices for dogs with suspected
or proven Mycoplasma-associated bronchitis are often
made empirically. Doxycycline or minocycline is com-
monly used by veterinarians for this syndrome and is
likely to have a therapeutic effect for pets with sus-
pected Mycoplasma spp. bronchitis.68,76 Veterinary fluo-
roquinolones and azithromycin are other drugs that
might be effective for the treatment of Mycoplasma spp.
infections.
 Respiratory Treatment Guidelines
Monitoring Treatment of Bacterial Bronchitis
If bronchitis is associated with Mycoplasma spp. or
B. bronchiseptica, clinical resolution might be obtained
with 1 course of antimicrobial treatment. In some cases,
prolonged antimicrobial treatment might be needed. In
the event that another primary cause of inflammation
such as allergic bronchitis exists and secondary bacterial
infections are occurring, recurrent treatment might be
required. Controlling inflammation associated with the
primary disease syndrome might also lessen recurrence
of secondary bacterial bronchitis.77 Repeated thoracic
radiographs can be taken to follow bronchial changes,
but this is of limited sensitivity. In some cases, repeated
cytology and culture might be indicated.
Pneumonia in Dogs and Cats
Definition and Causes
Inflammation of the lungs (pneumonia) can occur
after a variety of insults. In dogs and cats, although
uncommon, primary bacterial pneumonia can occur
after infection with B. bronchiseptica, Mycoplasma
spp., S. equi zooepidemicus, S. canis, and Yersinia
pestis.61–64,68,78–80 Of 65 puppies <1 year of age with
“community acquired” pneumonia in the United States,
49% were infected with B. bronchiseptica.80 Dogs with
B. bronchiseptica infection were younger and had more
severe disease than dogs from which other bacteria were
cultured. Most cases of bacterial pneumonia in dogs
and cats are secondary to other primary inflammatory
events like viral infections or aspiration of oral, esopha-
geal, or gastric contents during vomiting or regurgita-
tion (commonly associated with megaesophagus), after
aspiration because of pharyngeal or laryngeal function
abnormalities, during anesthesia recovery, and after
inhalation of foreign bodies.81–83 In addition, bacterial
pneumonia can develop in the presence of immunodefi-
ciency syndromes. Secondary bacterial pneumonia
potentially could develop as a result of other pulmonary
or airway diseases like neoplasia, ciliary dyskinesia,
bronchiectasis, and collapsing airways.
Common organisms isolated from dogs and cats with
lower respiratory disease include E. coli, Pasteurella
spp., Streptococcus spp, B. bronchiseptica, Enterococcus
spp., Mycoplasma spp., S. pseudintermedius and other
coagulase-positive Staphylococcus spp., and Pseu-
domonas spp.78–80,84–87
Diagnosis of Bacterial Pneumonia
Dogs and cats that develop cough that is associated
with fever, lethargy, inappetence, or tachypnea should
be evaluated for the presence of pneumonia by a full
physical examination, complete blood cell count, and
thoracic radiographs. If clinicopathologic findings and
thoracic radiological findings (alveolar lung disease)
support a diagnosis of bacterial pneumonia, collection
of a transtracheal, endotracheal, or a bronchoalveolar
lavage specimen for cytologic examination, aerobic
289
bacterial culture, and antimicrobial susceptibility and
Mycoplasma spp. culture is recommended.
Culture and susceptibility testing should be recom-
mended to the client and performed before starting
antimicrobial drug treatment, provided that the animal is
sufficiently stable; however, antimicrobial treatment
should not be unduly delayed. Although no controlled
data are available for dogs and cats, the clinical opinion
of the Working Group is that antimicrobial treatment
should be initiated as soon as possible and within
1–2 hours if clinical signs of sepsis exist.
In addition, not all cases of aspiration pneumonia
require antimicrobial treatment, because clinical disease
might be primarily or solely chemical pneumonitis from
aspirated materials. Anaerobic bacteria are sometimes
associated with pneumonia, particularly if there is a his-
tory of aspiration, or grass awn foreign bodies are pre-
sent. However, some commercial laboratories have
difficulty culturing these agents and most do not pro-
vide antimicrobial susceptibility data; thus, antimicro-
bial agents with an anaerobic spectrum are often
included for the treatment of bacterial pneumonia in
dogs and cats when anaerobic culture is not available
or likely to be reliable.
In cases with probable aspiration pneumonia, multi-
ple bacteria are often cultured making it difficult to
determine which is involved with continued inflamma-
tion. Care should also be exercised when interpreting
the significance of few or rare organisms, mixed culture,
or presence of possible airway contaminants such as
coagulase-negative staphylococci or Bacillus spp. If an
endoscope is used to collect a lavage specimen, the pos-
sibility of endoscope-related contamination should also
be considered, particularly when unusual species such
as Serratia or Stenotrophomonas are isolated.88
The Working Group recommends consulting with a
clinical microbiologist or specialist with expertise with
infectious diseases or pulmonology for interpretation of
culture and antimicrobial susceptibility results from
endotracheal or bronchoalveolar lavage specimens. Fif-
teen reviewers (88%) agreed, 1 disagreed (6%), and 1
(6%) was neutral to this Working Group recommenda-
tion. The person that disagreed believes that a consulta-
tion is only needed for difficult cases.
Because bacterial pneumonia is often associated with
an underlying disease process, attempts to identify and
manage current problems should be made. In cats and
dogs that have life-threatening bacterial pneumonia or
are oxygen dependent, airway sampling might not be
feasible. Although more data are required to clarify the
usefulness of blood cultures (aerobic and anaerobic) in
animals with severe pneumonia, it is the consensus
opinion of the Working Group to consider blood cul-
tures in these animals before starting empirical antimi-
crobial drug treatment as an alternative way to obtain
isolates for targeted antimicrobial susceptibility to guide
long-term management. Empirical antimicrobial treat-
ment should not be delayed in an effort to stabilize
affected animals and obtain a pre-antimicrobial airway
sample. Thirteen reviewers (82%) agreed, 3 were neutral
(18%), and 1 (6%) disagreed with this Working Group
290 Lappin et al
recommendation. The primary comment was that blood
culture for this purpose in children is known to be
insensitive and false-positive results can be obtained.89
Treatment of Suspected Bacterial Pneumonia
The Working Group discussed whether antimicrobial
treatment should be delayed while waiting until the
results of culture and antimicrobial susceptibility testing
are available. However, as not all clients can afford the
diagnostic procedures and pneumonia can be a life-
threatening disease, the consensus opinion was to pro-
vide empirical antimicrobial treatment while waiting for
test results with potential for de-escalation of treatment
based on antimicrobial susceptibility testing. While hos-
pitalized, parenteral antimicrobial treatment is generally
recommended by the Working Group for the treatment
of animals with pneumonia, regardless of the severity of
disease. Once the animal is discharged, treatment can
be continued by means of the oral route. It is the opin-
ion of the Working Group that doxycycline is a reason-
able empiric choice for dogs or cats with mild
pneumonia that is suspected to be from infection with
B. bronchiseptica or Mycoplasma spp. (eg, the animal is
from a shelter or boarding environment) and no other
systemic signs of disease like fever, dehydration,
lethargy, or respiratory distress are present. This is
based on the known susceptibility of these organisms to
doxycycline (see Section on Canine Infectious Respira-
tory Disease Complex) and published case reports of
successful treatment with doxycycline (Table 2).74,75,78
Fifteen reviewers (88%) agreed and 2 (12%) disagreed
with this Working Group recommendation. One
reviewer stated that they doubted that pneumonia
would be present without fever and if pneumonia exists,
it should be treated with bactericidal drugs. The other
dissenting reviewer commented on the lack of break-
point data for doxycycline and the bacteria from dogs
and cats as well as the concern that doxycycline might
not penetrate into the extracellular fluids of the lungs.
Azithromycin is used by some veterinarians empiri-
cally in dogs with uncomplicated pneumonia, but the
Working Group believes that data supporting this rec-
ommendation are lacking.
Streptococcus equi subspecies zooepidemicus strains
isolated from dogs are susceptible to penicillin, amoxi-
cillin, and ampicillin. Administration of amoxicillin–
clavulanate is unnecessary if this organism is suspected
because streptococci are not known to produce
beta-lactamases.90
Not all dogs or cats with acute aspiration pneumonia
have a bacterial infection. However, aspirated bacteria
can cause infection secondary to the chemical inflamma-
tion associated with aspiration. If the dog or cat is
acutely affected and has no evidence of systemic sepsis,
the Working Group believes that either no treatment or
parenteral administration of a beta-lactam antimicrobial
like ampicillin, ampicillin-sulbactam, or the first-genera-
tion cephalosporin cefazolin might be sufficient
(Table 2). Thirteen reviewers (82%) agreed, 3 were neu-
tral (18%), and 1 (6%) disagreed with this Working
Group recommendation. The primary comments were
that the risk of not treating a case was greater than the
perceived benefit of withholding treatment or that oral
medications could be adequate for this syndrome. How-
ever, if megaesophagus or other esophageal motility dis-
orders exist, parenteral administration of the
antimicrobial drug is indicated.
If clinical findings in dogs or cats with pneumonia
suggest the existence of sepsis (eg, injected mucous
membranes, hypoglycemia), the Working Group recom-
mends concurrent parenteral administration of either
enrofloxacin or marbofloxacin (available in injectable
form in some countries) combined with a drug with
Gram-positive and anaerobic spectra until bacterial cul-
ture and antimicrobial susceptibility testing results
return. In 1 study, most bacteria from the lower airways
of dogs with respiratory disease were susceptible to
enrofloxacin.91 Other drugs for parenteral use with a
Gram-negative spectrum might be indicated in lieu of
enrofloxacin based on culture and antimicrobial suscep-
tibility testing (Table 2). The Working Group states
that common options for Gram-positive and anaerobic
bacteria include ampicillin or clindamycin administered
parenterally (Table 2). Which of these drugs to choose
while waiting on antimicrobial susceptibility test results
will depend on the most likely infectious agent sus-
pected, previously prescribed antimicrobials (if any),
and historical antimicrobial resistance in the geographi-
cal region. Fourteen reviewers (82%) agreed and 3
(18%) disagreed with this Working Group recommen-
dation. The primary comment was that if Bacteroides
spp. were present, clindamycin could be ineffective and
that metronidazole could be considered another option.
Drugs that could be administered PO for outpatient
treatment of bacterial pneumonia should be selected on
the basis of culture and antimicrobial susceptibility
results for organisms isolated from the lower airways,
de-escalating whenever possible. If culture and antimi-
crobial susceptibility testing was not performed, the
antimicrobial drug class or classes that were initially
prescribed and associated with clinical response is/are
chosen for continued oral treatment.
Inflammatory responses to bacterial pneumonia
increase pulmonary pathology. Thus, glucocorticoids are
used concurrently in some human patients with bacterial
pneumonia.92,93 However, it was the consensus opinion
of the Working Group that further data are needed from
dogs and cats before a definitive recommendation can be
made in regard to the use of systemic or inhaled gluco-
corticoids, which have the potential to contribute to
adverse outcomes due to immunosuppression.
Monitoring Treatment of Bacterial Pneumonia
The current recommendation in most veterinary text-
books is to treat bacterial pneumonia for 4–6 weeks,
but evidence to support this duration of treatment in
either cats or dogs is lacking. Although such lengthy
courses of antimicrobial treatment might be necessary
for some animals with severe pulmonary involvement or
those with immunodeficiency syndromes, it is the
 Respiratory Treatment Guidelines
consensus opinion of the Working Group that shorter
courses of appropriate treatment, such as those used to
treat pneumonia in humans, might be effective in some
situations. In the face of insufficient data supporting a
shorter course of treatment, the Working Group recom-
mends re-evaluation of animals with pneumonia no
later than 10–14 days after starting treatment. At that
point, decisions to extend treatment should be based on
clinical, hematological, and radiographic findings. Addi-
tional studies evaluating durations of treatment that are
shorter than 4–6 weeks are required.
Pyothorax in Dogs and Cats
Definition and Causes
In cats with pyothorax, the bacteria isolated from
thoracic fluid are most commonly a mixture of oropha-
ryngeal anaerobes including Fusobacterium, Prevotella,
Porphyromonas, Bacteroides, Peptostreptococcus,
Clostridium, Actinomyces, and Filifactor villosus. Pas-
teurella spp, Streptococcus spp., and Mycoplasma spp.
have also been isolated.94–97 Less commonly, Staphylo-
coccus spp., Gram-negative bacteria other than Pas-
teurella, and organisms such as Nocardia spp. and
Rhodococcus equi have been isolated. Wounds resulting
from cat fights and URI are risk factors for pyothorax
in cats.97
Bacteria isolated from dogs with pyothorax are most
commonly mixed anaerobes (Prevotella spp., Peptostrep-
tococcus spp., Propionibacterium acnes, Clostridium spp.,
Bacteroides spp., Fusobacterium spp.) and Enterobacte-
riaceae, especially E. coli and Klebsiella pneumo-
niae.94,98–100 Streptococcus canis, Staphylococcus spp,
Enterococcus spp., Corynebacterium spp., Bacillus spp.,
Trueperella (formerly Arcanobacterium) pyogenes, Pas-
teurella, Acinetobacter, Capnocytophaga spp., Enterobac-
ter spp., Stenotrophomonas maltophila, Aeromonas
hydrophila, Achromobacter xylosoxidans, Serratia mar-
cescens and Pseudomonas spp. Actinomyces spp. and to
a lesser extent Nocardia spp. and Streptomyces spp.
have been implicated in canine pyothorax.99 Pyothorax
in dogs commonly results from migrating plant foreign
bodies or trauma but can also result from bite wound
inoculation.94,98–103
Diagnosis of Pyothorax in Dogs and Cats
Thoracic radiographs should be made to evaluate for
the presence of lung consolidation in the dog or cat
after therapeutic thoracocentesis. A pleural fluid speci-
men should be submitted for cytologic analysis, aerobic
bacterial culture, and antimicrobial susceptibility test-
ing, as well as culture for anaerobic bacteria and Myco-
plasma spp. (cats) if available. Performance of Gram
stain and acid-fast stains might provide addition infor-
mation. Detection of actinomycetes and Mycoplasma
spp. requires specialized growth conditions and pro-
longed incubation, and so the laboratory should be
informed that Actinomyces spp., Nocardia spp., or
Mycoplasma spp. are differential diagnoses.
291
Treatment of Pyothorax in Dogs and Cats
The Working Group recommends that treatment of
pyothorax include IV fluid administration and critically,
drainage of pus after placement of chest tubes with
intermittent or preferably continuous suction with or
without lavage.96–103 Surgical debridement might be
required in some cases. Sixteen reviewers (94%) agreed,
and 1 (6%) disagreed with this Working Group recom-
mendation. The primary comment was that evidence
supporting the definitive need for thoracic lavage was
lacking. However, based on lack of data supporting its
use, the Working Group does not recommend adminis-
tration of antimicrobial drugs into the pleural space.
The Working Group recommends the combination of
parenteral administration of enrofloxacin or mar-
bofloxacin (when available in parenteral form) with a
penicillin or clindamycin combined with therapeutic
drainage of the pleural space with or without lavage for
the initial treatment or canine and feline pyothorax
pending the results of culture and antimicrobial suscepti-
bility testing. Sixteen reviewers (94%) agreed and 1 (6%)
disagreed with this Working Group recommendation.
The primary comment was that pradofloxacin adminis-
tered PO as a single drug could be effective if available.
Treatment with an antimicrobial drug with activity
against anaerobes should be continued regardless of cul-
ture results because fastidious anaerobic bacteria could
be present. If combination treatment was initiated and
the bacterial isolates are susceptible to both drugs in
the initial treatment regime, then either of the treatment
drugs could be discontinued. If organisms are grown
that are resistant to one of the drugs and clinical
improvement is not noted, that antimicrobial agent
should be discontinued. A second drug to which the iso-
late is susceptible should be substituted if the animal
has not responded sufficiently. If organisms are grown
that are resistant to both antimicrobials or clinical evi-
dence of improvement is not evident, antimicrobial
treatment should be changed to a drug to which the
organisms are susceptible in vitro. Fifteen reviewers
(88%) agreed, 1 was neutral (6%), and 1 (6%) dis-
agreed with this Working Group recommendation. The
dissenting reviewer stated that mixed culture results can
be difficult to interpret and so if the animal’s clinical
condition improves on the first therapeutic regimen,
changes should not be made.
Consultation with a specialist is recommended when
multidrug-resistant organisms are isolated. In all situa-
tions, the clinical condition must be considered when
interpreting culture results, and continuing apparently
effective treatment despite in vitro resistance is recom-
mended because of the potential that the offending
organism was not isolated.
Monitoring Treatment of Pyothorax
It has been recommended that cats with pyothorax
be treated for a minimum of 3 weeks and ideally 4–
6 weeks.97,101 Additional research is required to deter-
mine whether shorter periods of antimicrobial drug
292 Lappin et al
treatment might be adequate. Serial thoracic radiogra-
phy might be useful to determine whether antimicro-
bial treatment needs to be continued, although further
study is also required to determine whether persistent
radiographic abnormalities correlate with the need for
additional antimicrobial drug treatment. At a mini-
mum, follow-up radiography should be performed for
10–14 days after starting treatment and at completion
of treatment. If the pyothorax persists or reoccurs
after cessation of antimicrobials, repeated thoracocen-
tesis should be performed for cytological assessment
and for culture and antimicrobial susceptibility testing.
Conclusions
The Working Group emphasizes the need for addi-
tional prospective studies to evaluate different treat-
ments and treatment durations in dogs and cats with
bacterial respiratory diseases so that more accurate rec-
ommendations can be made. For the same purpose,
research is needed to develop standard practices for col-
lection of clinical specimens and interpretation of cul-
ture results.
Acknowledgments
The Working Group thanks the following individuals
for a prepublication review of the document and for
providing votes to be used with the panel recommenda-
tions; Leah Cohn (University of Missouri), Joshua
Daniels (The Ohio State University), Eleanor Hawkins
(North Carolina State University), Steve Holloway
(Advanced PetCare Australia), Lynelle Johnson
(University of California, Davis), and Carol Reneiro
(University of Missouri).
Grant support: The work was supported by the Inter-
national Society for Companion Animal Infectious Dis-
eases (ISCAID; www.iscaid.org).
Conflict of Interest Declaration: Jane Sykes serves as
Associate Editor for the Journal of Veterinary Internal
Medicine. She was not involved in review of this manu-
script. M.G. Papich has received consulting fees,
research support, and gifts from Bayer and Zoetis,
who are sponsors of some of the antibiotics recom-
mended in this manuscript. He receives royalties from
a book (published by Elsevier) that was the source of
dosages listed in this paper.
Off-label Antimicrobial Declaration: This document
describes off-label antimicrobial use in multiple sections.
References
1. Morley PS, Michael DA, Thomas EB, et al. Antimicrobial
drug use in veterinary medicine. ACVIM consensus statement. J
Vet Intern Med 2005;19:617–629.
2. Guardabassi L, Houser GA, Frank LA, et al. Guidelines to
antimicrobial use in dogs and cats. In: Guardabassi L, Jensen LB,
Kruse H, eds. Guide to Antimicrobial Use in Animals. Blackwell
Publishing; 2008:183–206.
3. Danish Small Animal Veterinary Association (SvHKS).
Antimicrobial Use Guidelines for Companion Animal Practice.
Danish Small Animal Veterinary Association; 2013. Available at:
http://www.fecava.org/sites/default/files/files/DSAVA_Antibiotic
Guidelines%20-%20v1-1_3(1).pdf. Accessed December 8, 2016.
4. Swedish Veterinary Association. Guidelines for the clinical
use of antimicrobials in the treatment of dogs and cats, 2009.
Available at: www.svf.se. Accessed December 8, 2016.
5. Lionel A, Mandell LA, Richard G, et al. Infectious Diseases
Society of America/American Thoracic Society consensus guideli-
nes on the management of community-acquired pneumonia in
adults. Clin Infect Dis 2007;44:27–72.
6. Bradley JS, Byington CL, Shah SS, et al. The management
of community-acquired pneumonia in infants and children older
than 3 months of age: Clinical Practice Guidelines by the Pediatric
Infectious Diseases Society and the Infectious Diseases Society of
America. Clin Infect Dis 2011;53:325–376.
7. Murphy MK, Black NA, Lamping DL. Consensus develop-
ment methods, and their use in clinical guideline development.
Health Technol Assess 1998;2:1–88.
8. Allen HS, Broussard J, Noone KM. Nasopharyngeal dis-
eases in cats: A retrospective study of 53 cases (1991–1998). J Am
Anim Hosp Assoc 1999;35:457–461.
9. Henderson SM, Bradley K, Day MJ. Investigation of nasal
disease in the cat-a retrospective study of 77 cases. J Feline Med
Surg 2004;6:245–257.
10. Demko JL, Cohn LA. Chronic nasal discharge in cats: 75
cases (1993–2004). J Am Vet Med Assoc 2007;230:1032–1037.
11. Quimby J, Lappin MR. Feline focus: Update on feline
upper respiratory diseases: Introduction and diagnostics. Compend
Contin Educ Vet 2009;31:554–564.
12. Helps CR, Lait P, Damhuis A. Factors associated with
upper respiratory tract disease caused by feline herpesvirus, feline
calicivirus, Chlamydophila felis and Bordetella bronchiseptica in
cats: Experience from 218 European catteries. Vet Rec
2005;156:669–773.
13. Bannasch MJ, Foley JE. Epidemiologic evaluation of multi-
ple respiratory pathogens in cats in animal shelters. J Feline Med
Surg 2005;7:109–119.
14. Di Martino B, Di Francesco CE, Meridiani I. Etiological
investigation of multiple respiratory infections in cats. New Micro-
biol 2007;30:455–461.
15. Veir JK, Ruch-Gallie R, Spindel ME, et al. Prevalence of
selected infectious organisms and comparison of two anatomic
sampling sites in shelter cats with upper respiratory tract disease.
J Feline Med Surg 2008;10:551–557.
16. Johnson LR, Foley JE, De Cock HE. Assessment of infec-
tious organisms associated with chronic rhinosinusitis in cats.
J Am Vet Med Assoc 2005;227:579–585.
17. Quimby J, Lappin MR. Update on feline upper respiratory
diseases: Condition-specific recommendations. Compend Contin
Educ Vet 2010;32:1–10.
18. Welsh RD. Bordetella bronchiseptica infections in cats.
J Am Anim Hosp Assoc 1996;32:153–158.
19. Binns SH, Dawson S, Speakman AJ, et al. Prevalence and
risk factors for feline Bordetella bro nchiseptica infection. Vet Rec
1999;144:575–580.
20. Spindel ME, Veir JK, Radecki SV. Evaluation of prad-
ofloxacin for the treatment of feline rhinitis. J Feline Med Surg
2008;10:472–479.
21. Hartmann AD, Hartmann K, Helps CR, et al. Efficacy of
pradofloxacin in cats with feline upper respiratory tract disease
due to Chlamydophila felis or Mycoplasma infections. J Vet Intern
Med 2008;22:44–52.
22. Burns RE, Wagner DC, Leutenegger CM. Histologic and
molecular correlation in shelter cats with acute upper respiratory
infection. J Clin Microbiol 2011;49:2454–2460.
23. Levy J, Crawford C, Hartmann K, et al. Feline retrovirus
management guidelines. Compend Contin Educ Vet 2008;
2009:10.
 Respiratory Treatment Guidelines
24. Wong DM, Blumberg DA, Lowe LG. Guidelines for the
use of antimicrobials in acute upper respiratory tract infections.
Am Fam Physician 2006;74:956–966.
25. Maggs DJ, Clark HE. Relative sensitivity of polymerase
chain reaction assays used for detection of feline herpesvirus and
commercial vaccines. Am J Vet Res 2005;66:1550–1555.
26. Ruch-Gallie RA, Veir JK, Hawley JR. Results of molecular
diagnostic assays targeting feline herpesvirus-1 and feline cali-
civirus in adult cats administered modified live vaccines. J Feline
Med Surg 2011;13:541–545.
27. Sykes JE, Studdert VP, Browning GF. Comparison of the
polymerase chain reaction and culture for the detection of feline
Chlamydia psittaci in untreated and doxycycline-treated experimen-
tally infected cats. J Vet Intern Med 1999;13:146–152.
28. Schulz BS, Wolf G, Hartmann K. Bacteriological and
antimicrobial sensitivity results in 271 cats with respiratory infec-
tions. Vet Rec 2006;158:269–270.
29. Egberink H, Addie D, Belak S, et al. Bordetella bronchisep-
tica infection in cats. ABCD guidelines on prevention and manage-
ment. J Feline Med Surg 2009;11:610–614.
30. Schwarz S, Alesık E, Grobbel M, et al. Antimicrobial sus-
ceptibility of Pasteurella multocida and Bordetella bronchiseptica
from dogs and cats as determined in the BfT-GermVet monitoring
program 2004–2006. Berl Munch Tierarztl Wochenschr
2007;120:423–430.
31. Speakman AJ, Dawson S, Corkill JE, et al. Antimicrobial
susceptibility of canine Bordetella bronchiseptica isolates. Vet
Microbiol 2000;71:193–200.
32. Sturgess CP, Gruffydd-Jones TJ, Harbour DA. Controlled
study of the efficacy of clavulanic acid-potentiated amoxycillin in
the treatment of Chlamydia psittaci in cats. Vet Rec 2001;149:73–
76.
33. Owen WM, Sturgess CP, Harbour DA, et al. Efficacy of
azithromycin for the treatment of feline chlamydophilosis. J Feline
Med Surg 2003;5:305–311.
34. Sparkes AH, Caney SM, Sturgess CP, et al. The clinical
efficacy of topical and systemic therapy for the treatment of feline
ocular chlamydiosis. J Feline Med Surg 1999;1:31–35.
35. Kompare B, Litster AL, Leutenegger CM, et al. Random-
ized masked controlled clinical trial to compare 7-day and 14-day
course length of doxycycline in the treatment of Mycoplasma felis
infection in shelter cats. Comp Immunol Microbiol Infect Dis
2013;36:129–135.
36. Westfall DS, Twedt DC, Steyn PF, et al. Evaluation of eso-
phageal transit of tablets and capsules in 30 cats. J Vet Intern
Med 2001;15:467–470.
37. Bennett AD, MacPhail CM, Gibbons DS, et al. A compar-
ative study evaluating the esophageal transit time of eight healthy
cats when pilled with the FlavoRx pill glide versus pill delivery
treats. J Feline Med Surg 2010;12:286–290.
38. Melendez LD, Twedt DC, Wright M. Suspected doxycy-
cline-induced esophagitis and esophageal stricture formation in
three cats. Feline Pract 2000;28:10–12.
39. German AJ, Cannon MJ, Dye C. Oesophageal strictures in
cats associated with doxycycline therapy. J Feline Med Surg
2005;7:33–41.
40. Beatty JA, Swift N, Foster DJ, et al. Suspected clin-
damycin-associated oesophageal injury in cats: 5 cases. J Feline
Med Surg 2006;8:412–419.
41. Papich MG, Davidson GS, Fortier LA. Doxycycline con-
centration over time after storage in a compounded veterinary
preparation. J Am Vet Med Assoc 2013;242:1674–1678.
42. Tynan BE, Papich MG, Kerl ME, et al. Pharmacokinetics
of minocycline in domestic cats. J Feline Med Surg 2016;18:257–
263.
43. Ruch-Gallie R, Veir JK, Spindel MM, et al. Efficacy of
amoxicillin and azithromycin for the empirical treatment of cats
293
with upper respiratory infections. J Feline Med Surg 2008;10:542–
550.
44. Litster AL, Wu CC, Constable PD. Comparison of the
efficacy of amoxicillin-clavulanic acid, cefovecin, and doxycycline
in the treatment of upper respiratory tract disease in cats
housed in an animal shelter. J Am Vet Med Assoc 2012;241:
218–226.
45. Johnson LR, Kass PH. Effect of sample collection method-
ology on nasal culture results in cats. J Feline Med Surg
2009;11:645–649.
46. Lees P. Pharmacokinetics, pharmacodynamics and thera-
peutics of pradofloxacin in the dog and cat. J Vet Pharmacol Ther
2013;36:209–221.
47. Dossin O, Gruet P, Thomas E. Comparative field evalua-
tion of marbofloxacin tablets in the treatment of feline upper res-
piratory infections. J Small Anim Pract 1998;39:286–289.
48. Hunter RP, Lynch MJ, Ericson JF, et al. Pharmacokinetics,
oral bioavailability and tissue distribution of azithromycin in cats.
J Vet Pharmacol Ther 1995;18:38–46.
49. Parnham MJ, Erakovic HV, Giamarellos-Bourboulis EJ,
et al. Azithromycin: Mechanisms of action and their relevance for
clinical applications. Pharmacol Ther 2014;143:225–245.
50. Meyers BR, Mendelson MH, Parisier SC. Malignant exter-
nal otitis. Comparison of monotherapy vs. combination therapy.
Arch Otolaryngol Head Neck Surg 1987;113:974–978.
51. Hollis S, Evans K. Management of malignant (necrotising)
otitis externa. J Laryngol Otol 2011;125:1212–1217.
52. Vanderkooi OG, Low DE, Green K, et al. Predicting
antimicrobial resistance in invasive pneumococcal infections. Clin
Infect Dis 2005;40:1288–1297.
53. McInnis CL, Clark L, Brewer M, et al. Prevalence of Bar-
tonella spp. DNA in conjunctival cells collected from shelter cats
with and without conjunctivitis. J Vet Intern Med 2015;29:285.
54. Berryessa NA, Johnson LR, Kasten RW, et al. Microbial
culture of blood samples and serologic testing for bartonellosis in
cats with chronic rhinosinusitis. J Am Vet Med Assoc
2008;233:1084–1089.
55. Mochizuki M, Yachi A, Ohshima T, et al. Etiologic study
of upper respiratory infections of household dogs. J Vet Med Sci
2008;70:563–569.
56. Ellis JA, McLean N, Hupaelo R, et al. Detection of coron-
avirus in cases of tracheobronchitis in dogs: A retrospective study
from 1971 to 2003. Can Vet J 2005;46:447–448.
57. Erles K, Brownlie J. Canine respiratory coronavirus: An
emerging pathogen in the canine infectious respiratory disease
complex. Vet Clin North Am Small Anim Pract 2008;38:815–825.
58. Renshaw RW, Zylich NC, Laverack MA, et al. Pneu-
movirus in dogs with acute respiratory disease. Emerg Infect Dis J
2010;16:993–995.
59. Priestnall SL, Mitchell JA, Walker CA, et al. New and
emerging pathogens in canine infectious respiratory disease. Vet
Pathol 2014;51:492–504.
60. Keil DJ, Fenwick B. Role of Bordetella bronchiseptica in
infectious tracheobronchitis in dogs. J Am Vet Med Assoc
1998;212:200–207.
61. Chalker VJ, Brooks HW, Brownlie J. The association of
Streptococcus equi subsp. zooepidemicus with canine infectious res-
piratory disease. Vet Microbiol 2003;95:149–156.
62. Chalker VJ, Owen WM, Paterson C, et al. Mycoplasmas
associated with canine infectious respiratory disease. Microbiology
2004;150:3491–3497.
63. Priestnall S, Erles K. Streptococcus zooepidemicus: An
emerging canine pathogen. Vet J 2011;88:142–148.
64. Pesavento PA, Hurley KF, Bannasch MJ, et al. A clonal
outbreak of acute fatal hemorrhagic pneumonia in intensively
housed (shelter) dogs caused by Streptococcus equi subsp. zooepi-
demicus. Vet Pathol 2008;45:51–53.
294 Lappin et al
65. Ruch-Galle R, Moroff S, Lappin MR. Adenovirus 2,
Bordetella bronchiseptica, and parainfluenza molecular diagnostic
assay results in puppies after vaccination with modified live vacci-
nes. J Vet Intern Med 2016;30:164–166.
66. Johnson LR, Queen EV, Vernau W, et al. Microbiologic
and cytologic assessment of bronchoalveolar lavage fluid from
dogs with lower respiratory tract infection: 105 cases (2001–2011).
J Vet Intern Med 2013;27:259–267.
67. Rozanski E. Canine chronic bronchitis. Compend Contin
Educ Vet 2014;44:107–116.
68. Chandler JC, Lappin MR. Mycoplasmal respiratory infec-
tions in small animals: 17 cases (1988–1999). J Am Anim Hosp
Assoc 2002;38:111–119.
69. Peeters DE, McKiernan BC, Weisiger RM. Quantitative
bacterial cultures and cytological examination of bronchoalveolar
lavage specimens in dogs. J Vet Intern Med 2000;14:534–541.
70. McKiernan BC. Diagnosis and treatment of canine chronic
bronchitis. Twenty years of experience. Compend Contin Educ
Vet 2000;30:1267–1278.
71. Johnson LR, Drazenovich NL, Foley JE. A comparison of
routine culture with polymerase chain reaction technology for the
detection of Mycoplasma species in feline nasal samples. J Vet
Diagn Invest 2004;16:347–351.
72. Zhu BY, Johnson LR, Vernau W. Tracheobronchial brush
cytology and bronchoalveolar lavage in dogs and cats with chronic
cough: 45 cases (2012–2014). J Vet Intern Med 2015;29:526–532.
73. Speakman AJ, Binns SH, Dawson S, et al. Antimicrobial
susceptibility of Bordetella bronchiseptica isolates from cats and a
comparison of the agar dilution and E-test methods. Vet Micro-
biol 1997;54:63–72.
74. Bongrand Y, Blais MC, Alexander KA. Atypical pneumo-
nia associated with a Mycoplasma isolate in a kitten. Can Vet J
2012;53:1109–1013.
75. Trow AV, Rozanski EA, Tidwell AS. Primary mycoplasma
pneumonia associated with reversible respiratory failure in a cat.
J Feline Med Surg 2008;10:398–402.
76. Mulholland S, Gavranich JB, Gillies MB, et al. Antimicro-
bials for community-acquired lower respiratory tract infections
secondary to Mycoplasma pneumoniae in children. Cochrane Data-
base Syst Rev 2012;12:9.
77. Bexfield NH, Foale RD, Davison LJ, et al. Management of
13 cases of canine respiratory disease using inhaled corticosteroids.
J Small Anim Pract 2006;47:377–382.
78. Jameson PH, Jones RL, King LA, et al. Comparison of
clinical signs, diagnostic findings, organisms isolated, and clinical
outcome in dogs with bacterial pneumonia: 93 cases (1986–1991).
J Am Vet Med Assoc 1995;206:206–209.
79. Velineni S, Timoney JF, Russell K, et al. Clones of Strepto-
coccus zooepidemicus from outbreaks of hemorrhagic canine pneu-
monia and associated immune responses. Clin Vaccine Immunol
2014;21:1246–1252.
80. Radhakrishnan A, Drobatz KJ, Culp WT, et al. Commu-
nity-acquired infectious pneumonia in puppies: 65 cases (1993–
2002). J Am Vet Med Assoc 2007;230:1493–1497.
81. Kogan DA, Johnson LR, Sturges BK, et al. Etiology and
clinical outcome in dogs with aspiration pneumonia: 88 cases
(2004–2006). J Am Vet Med Assoc 2008;233:1748–1755.
82. Tart KM, Babski DM, Lee JA. Potential risks, prognostic
indicators, and diagnostic and treatment modalities affecting sur-
vival in dogs with presumptive aspiration pneumonia: 125 cases
(2005–2008). J Vet Emerg Crit Care 2010;20:319–329.
83. Viitanen SJ, Lappalainen A, Rajam€aki MM. Co-infections
with respiratory viruses in dogs with bacterial pneumonia. J Vet
Intern Med 2015;29:544–551.
84. Angus JC, Jang SS, Hirsh DC. Microbiological study of
transtracheal aspirates from dogs with suspected lower respiratory
tract disease: 264 cases (1989–1995). J Am Vet Med Assoc
1997;210:55–58.
85. Proulx A, Hume DZ, Drobatz KJ, et al. In vitro bacterial
isolate susceptibility to empirically selected antimicrobials in 111
dogs with bacterial pneumonia. J Vet Emerg Crit Care
2014;24:194–200.
86. Dear JD. Bacterial pneumonia in dogs and cats. Compend
Contin Educ Vet 2014;44:143–159.
87. Rheinwald M, Hartmann K, Hahner M, et al. Antimicro-
bial susceptibility of bacterial isolates from 502 dogs with respira-
tory signs. Vet Rec 2014;10:1136.
88. Chan CM, Ridgway MD, Mitchell MA, et al. Association
between Mycoplasma-specific polymerase chain reaction assay
results and oral bacterial contamination of bronchoalveolar
lavage fluid samples from dogs with respiratory tract disease:
121 cases (2005–2012). J Am Vet Med Assoc 2013;243:1573–
1579.
89. Pui-Ying IT, Bernstein E, Ma X, et al. Blood culture in
evaluation of pediatric community-acquired pneumonia: A
systematic review and meta-analysis. Hosp Pediatr 2015;5:
324–336.
90. Drawz SM, Bonoma RA. Three decades of beta-lactamase
inhibitors. Clin Microbiol Rev 2010;23:160–201.
91. Rheinwald M, Hartmann K, H€ahner M. Antimicrobial sus-
ceptibility of bacterial isolates from 502 dogs with respiratory
signs. Vet Rec 2015;176:357.
92. Meijvis SC, Hardeman H, Remmelts HH, et al.
Dexamethasone and length of hospital stay in patients with
community-acquired pneumonia: A randomized, double-blind, pla-
cebo-controlled trial. Lancet 2011;11:2023–2030.
93. Confalonieri M, Annane D, Antonaglia C, et al. Is
prolonged low-dose glucocorticoid treatment beneficial in
community-acquired pneumonia? Curr Infect Dis Rep
2013;15:158–166.
94. Walker AL, Jang SS, Hirsh DC. Bacteria associated with
pyothorax of dogs and cats: 98 cases (1989–1998). J Am Vet Med
Assoc 2000;216:359–363.
95. Demetriou JL, Foale RD, Ladlow J, et al. Canine and
feline pyothorax: A retrospective study of 50 cases in the UK and
Ireland. J Small Anim Pract 2002;43:388–394.
96. Waddell LS, Brady CA, Drobatz KJ. Risk factors, prognos-
tic indicators, and outcome of pyothorax in cats: 80 cases (1986–
1999). J Am Vet Med Assoc 2002;221:819–824.
97. Barrs VR, Allan GS, Martin P, et al. Feline pyothorax: A
retrospective study of 27 cases in Australia. J Feline Med Surg
2005;7:211–222.
98. Rooney MB, Monnet E. Medical and surgical treatment of
pyothorax in dogs: 26 cases (1991–2001). J Am Vet Med Assoc
2002;221:86–92.
99. Johnson MS, Martin MW. Successful medical treatment of
15 dogs with pyothorax. J Small Anim Pract 2007;48:12–16.
100. Boothe HW, Howe LM, Boothe DM, et al. Evaluation of
outcomes in dogs treated for pyothorax: 46 cases (1983–2001).
J Am Vet Med Assoc 2010;236:657–663.
101. MacPhail CM. Medical and surgical management of
pyothorax. Vet Clin North Am Small Anim Pract 2007;37:975–
988.
102. Lee KC. Surgical or medical management of pyothorax in
dogs? Vet Rec 2014;174:605–606.
103. Stillion JR, Letendre JA. A clinical review of the patho-
physiology, diagnosis, and treatment of pyothorax in dogs and
cats. J Vet Emerg Crit Care 2015;25:113–129.
 SÍNCOPE CARDIOGÉNICO EN EL PERRO
Montoya, J.A.
Medicina interna veterinaria
Facultad de Veterinaria de Las Palmas de Gran Canaria
35416- Las Palmas
alberto.montoya@ulpgc.es

Definición y clasificación
El síncope cardiogénico consiste en una pérdida súbita, aguda,
transitoria y reversible de la consciencia debida a la restricción del
flujo sanguíneo cerebral, como consecuencia de un rápido descenso
del gasto cardiaco y es un síndrome que acompaña a muchos procesos
cardiovasculares.

El gasto cardiaco depende de forma directa de dos factores: el

volumen sistólico y la frecuencia cardiaca. Cuando los síncopes se
producen por una disminución del volumen sistólico se denominan
mecánicos u obstructivos; cuando lo que se modifica es la frecuencia
cardiaca se denominan eléctricos o arrítmicos.

Etiología
Los síncopes mecánicos están producidos por: miocardiopatías
(dilatada e hipertrófica) y miocarditis, taponamientos cardiacos y
pericarditis constrictivas; valvulopatías y endocardiopatías restrictivas
así como endocarditis bacterianas. Hay que mencionar los asociados
a Dirofilaria immitis, a neoplasias cardiacas como el quemodectoma y
el hemangiosarcoma, a cuadros de hipertensión sistémica o pulmonar
grave o a defectos cardiacos congénitos (estenosis pulmonar o aórtica
y ductus arterioso persistente). Sin embargo, la causa más frecuente
de la presentación de síncopes mecánicos es la descompensación de
cuadros de insuficiencia cardiaca congestiva.

Los síncopes eléctricos se producen por arritmias y pueden

ser taquiarrítmicos y bradiarrítmicos (estos últimos también
denominados síncopes de Stokes-Adams). Tanto las taquiarritmias
supraventriculares (extrasístoles y taquicardias supraventriculares,
flúter y fibrilación atrial), como las ventriculares pueden generarlos.
También las bradiarritmias (bradicardia sinusal, paro sinusal y

1
bloqueos A-V de 2º y 3º grado) y el síndrome del seno enfermo se
asocian a la aparición de este cuadro.

En la mayoría de las ocasiones y en función de la alteración

cardiovascular primaria los cuadros sincopales son de origen
electromecánico.

Patogenia
El gasto cardiaco debe cubrir las necesidades orgánicas en cada
momento y esto se consigue mediante mecanismos compensadores
cardiovasculares que dirigidos por el sistema nervioso autónomo
modifican y adaptan en cada momento el volumen sistólico y la
frecuencia cardiaca.

Cuando una disminución brusca y severa del gasto cardiaco

implican un fallo en el riego sanguíneo cerebral suficiente se
provoca el síncope, que se explica debido a que el metabolismo
cerebral depende en su totalidad de la perfusión de oxígeno aportado
por la sangre.

En los casos de síncopes obstructivos, hay una causa

mecánica que dificulta u obstaculiza la eyección del flujo sanguíneo
durante la sístole, o bien provoca una disminución de la capacidad
de llenado diastólico de los ventrículos. Generalmente, los síncopes
de este grupo, suelen ir asociados a aumentos súbitos del gasto
cardiaco a los que el corazón no puede responder.

En los síncopes arrítmicos lo que se produce es una alteración

eléctrica cardiaca y cuando la frecuencia cardiaca se altera, por un
aumento o por una disminución, surge una brusca reducción del
gasto cardiaco que puede provocar la insuficiencia cardiaca aguda.
Estas arritmias pueden desencadenar también alteraciones a nivel de
la perfusión coronaria y de la funcionalidad miocárdica,
favoreciendo aún más la aparición del síncope.
Los síncopes taquiarrítmicos, son de esfuerzo o de estrés y en
ellos lo que se produce es un aumento de la frecuencia cardiaca, que
paradójicamente, no se acompaña de un incremento del gasto
cardiaco, porque se produce un acortamiento de los periodos
diastólicos (periodos de llenado ventricular) que genera una
disminución del volumen sistólico y por tanto del gasto cardiaco.

2
 Las bradiarritmias severas, también originan un brusco
descenso el gasto cardiaco como consecuencia de que se sobrepasan
los límites del incremento compensatorio del volumen diastólico
ventricular y del volumen total. Este tipo de síncopes pueden
desencadenarse por dos situaciones: *disminuciones severas de la
frecuencia; y/o *bloqueos del impulso, sobre todo en los casos de
bloqueos atrio-ventriculares completos o incompletos, donde el
impulso no es transmitido a los ventrículos, y éstos dejan de
contraerse durante un periodo de tiempo variable.

Sintomatología
La sintomatología que aparece en los pacientes incluye, por lo
general: mucosas pálidas, bradicardia, hipotensión, debilidad, pulso
yugular y/o filiforme. En los de origen mecánico pueden auscultarse
soplos y cambios de los ruidos cardiacos (alteraciones de la
intensidad, desdoblamientos y/o galopes).

Dependiendo de la duración del déficit de riego cerebral,

aparecen nuevos síntomas más o menos intensos. Si tiene una
duración menor de 10 segundos solamente se produce una
disminución parcial de los reflejos y aturdimiento con debilidad
muscular y/o temblores, pudiendo pasar, incluso, desapercibido para
el dueño. Cuando dura más de 20 segundos el animal presenta pérdida
de consciencia, respiración sincopada y convulsiones. Con una
duración superior al medio minuto aparecen convulsiones más
intensas y relajación de esfínteres. Si el síncope dura más de 3-4 min.
, el animal puede morir o recuperarse parcialmente quedando secuelas
graves en el sistema nervioso central.

En la mayoría de los casos la recuperación suele ser rápida,

aunque después del ataque puede aparecer taquicardia, agitación,
congestión de mucosas, nauseas y vómitos, alteraciones de la visión y
emisión de sonidos extraños. El propietario suele referir que el animal
pasa un tiempo nervioso, asustado y confuso. Si el ataque ha sido muy
prolongado el paciente puede presentar un estado somnoliento,
relajado, adinámico y semicomatoso durante unas horas.

3
 Diagnóstico
Es muy importante realizar una historia clínica completa para
orientar el problema, ya que en muy pocos casos tendremos ocasión
de presenciar un ataque y, además, la información de los propietarios
suele ser escasa y poco exacta.

La anamnesis incluirá los datos referentes a edad, raza, sexo,

peso, tipo de alimentación, vacunaciones, desparasitaciones y
padecimientos anteriores.

En cuanto a las características de los ataques se debe conocer el

momento de presentación; sus relaciones con el ejercicio, el estrés, la
comida y la administración de fármacos; la forma de presentación,
frecuencia, duración e intensidad de los mismos. Es importante que el
propietario realice la descripción completa del ataque incluyendo la
fase prodrómica, el ataque propiamente dicho y el comportamiento
del paciente después del mismo.

Se debe realizar un completo examen general y una exploración

cardiológica completa que incluya radiología, electrocardiografía y
ecocardiografía y medida de las presiones arteriales. Unas pruebas
laboratoriales, que incluyan al menos: hematología completa y
determinaciones de proteínas séricas, glucosa, urea, creatinina, ALT,
gamma-GT, calcio, potasio, y análisis coproparasitológico son
necesarias para descartar otras causas potenciales de convulsiones en
el perro, y a menudo es difícil diagnosticar un síncope cardiogénico.

Diagnóstico diferencial
Los datos recogidos de la anamnesis, exploración y técnicas
complementarias permiten evaluar el estado del paciente y orientar al
clínico hacia un diagnóstico certero. Sin embargo, hay que realizar un
diagnóstico diferencial entre este proceso y otras alteraciones que
pueden presentar una sintomatología similar (Tabla nº 1), como son:
enfermedades nerviosas, alteraciones pulmonares, anemias e
hipovolemias, enfermedades metabólicas (hipoglucemia, síndrome de
Addison, diabetes mellitus), alteraciones electrolíticas, enfermedades
musculares, afecciones renales o hepáticas y, en perros jóvenes,
parasitosis masivas; y que deben tenerse en cuenta a la hora de
investigar la etiología del episodio y aplicar el tratamiento adecuado.

4
 Tratamiento
La primera norma a tener en cuenta es que el síncope en sí no
debe tratarse, sino que hay que tratar la causa primaria.

Los síncopes mecánicos puros son siempre consecuentes a una

alteración cardiovascular grave, por lo que nosotros recomendamos
instaurar una pauta de tratamiento integral de la insuficiencia cardiaca
establecida (diuréticos, vasodilatadores, inótropos positivos, dieta
hiposódica). En caso de instaurar tratamiento sintomático, este podría
encaminarse básicamente a mejorar el gasto cardiaco, empleando
medidas hipertensoras como la administración de soluciones: salina
fisiológica, ringer o ringer-lactato por vía IV rápida, junto con dosis
bajas de diazepam en caso que existan convulsiones.

En lo que respecta a los síncopes eléctricos taquiarrítmicos

hay que conocer el tipo de arritmia que está produciendo el síncope,
así como su causa, para administrar el tratamiento específico. Así en
las supraventriculares los fármacos de elección son los digitálicos, los
beta-bloqueantes o los bloqueantes del canal del calcio. En las
ventriculares se emplean lidocaina, procainamida, mexiletina,
bloqueantes del canal del calcio y beta-bloqueantes.

En los síncopes bradiarrítmicos debe realizarse inicialmente

una prueba de estimulación con atropina. Para ello, se administra
atropina a dosis de 0.04 mg/kg. por vía intramuscular, después
durante 30 minutos, se debe mantener monitorizado al animal o
realizar un E.C.G. cada 5 minutos. Si existe respuesta se puede
intentar el tratamiento con agentes vagolíticos como atropina,
propantelina o glicopirrolato. Dado que la atropina tiene numerosos
efectos secundarios, que estos tratamientos son muy prolongados y
que su administración es compleja (la vía oral es difícil debido al
sabor amargo del preparado y la administración parenteral es molesta
para el animal), no constituye el fármaco de elección a largo plazo y
es preferible el empleo de beta-simpaticomiméticos.

Si no encontramos respuesta a la atropina el pronóstico se

agrava y debemos realizar la prueba de estimulación con isoproterenol
(igual que la de atropina pero empleando 0.01 mg/kg. IM); si es
positiva podemos emplear en el tratamiento los agentes beta-

5
adrenérgicos como isoproterenol, orciprenalina, hexoprenalina,
terbutalina o teofilina.

Si el animal no responde ni a la prueba de la atropina ni a la del

isoproterenol, el único tratamiento posible es la implantación de un
marcapasos. No obstante hemos encontrado casos de baja respuesta al
isoproterenol con buena calidad de vida y supervivencia prolongada
empleando simpaticomiméticos.

Como hemos citado, es frecuente encontrar cuadros de etiología

electromecánica en los que el tratamiento debe ser mixto, intentando
mantener al animal con un gasto cardiaco suficiente para evitar la
presentación de los síncopes.

6
1. ORIGEN METABOLICO
 Hepatoencefalia.
Insuficiencia hepática-cirrosis
Shunt porto-cava
 Azotemia
Insuficiencia renal
 Hipoglucemia
Parasitosis intestinales masivas
Insulinoma
Hipoglucemia funcional (perros de caza)
Estrés
Idiopática (razas “toy” 6-12 semanas de vida)
Glucosuria renal
Síndrome de malaabsorción intestinal
Septicemia
Hipoglucemia pre- y posparto
 Diabetes mellitus
 Hipocalcemia
Lactación
Enfermedad renal crónica
Hiperparatiroidismo
Ejercicio muy intenso
 Hipomagnesemia
 Hipercaliemia
Hipoadrenocorticismo
Retención urinaria
Cetoacidosis
 Hiperlipemia

2. ORIGEN TOXICO Y YATROGENICO

 Plomo
 Etilenglicol
 Estricnina
 Organoclorados
 Organofosforados
 Hidralacina, acepromazina

3. ORIGEN NERVIOSO
 Neoplasias cerebrales
 Encefalitis
 Malformaciones congénitas
Hidrocefalia
Lisencefalia
 Traumatismo craneal
 Edema cerebral
 Congestión y hemorragia cerebrales
 Epilepsia esencial

4. OTRO ORIGEN
 Alteraciones respiratorias
Hipoxemia
Síncope tusígeno
Derrame pleural
 Hipertermia
 Reacciones de hipersensibilidad y alergia
 Enfermedades hematológicas

TABLA 1. DIAGNOSTICO DIFERENCIAL DE SÍNCOPES

CARDIOGÉNICOS EN EL PERRO

7
FARMACO DOSIS VIA
Atropina (Sulfato) 0.02-0.04 mg/kg. IV, SC, PO
Dexametasona 2-4 mg/kg/día IV
Diazepam 1-2 mg/kg. IV
Glicopirrolato 0.002-0.01 mg/kg. IV, IM
Hexoprenalina 0.05 mg/kg/8-12 h. IV, IM, SC, PO
Isoproterenol 0.01 mg/kg/6-8-12 h. IV, IM, SC
Midazolam 0.11 mg/kg. IV,IM
Orciprenalina 1 mg/kg/8-12 h. PO
Propantelina 11-2 mg/kg/8-12 h. PO
Teofilina 10 mg/kg/8-12 h. PO
Terbutalina 1,25-5 mg/animal/8-12 h. PO

TABLA 2: FARMACOS UTILIZADOS EN EL TRATAMIENTO DEL SINCOPE

CARDIOGENICO

8
9
 BRONQUITIS CRÓNICA CANINA: Enfoque práctico
J. Alberto Montoya-Alonso, DVM, PhD, MSc, MA
Elena Carretón, DVM, MSc
Facultad de Veterinaria de Las Palmas de Gran Canaria
35416- Arucas (Las Palmas)- ESPAÑA
amontoya@dpat.ulpgc.es

Definición:

Presencia de tos crónica y pertinaz durante un período igual o superior a dos meses
consecutivos. Se asocia a modificaciones irreversibles de las vías aéreas. El proceso original o
causa subyacente no se ha identificado.

Numerosos autores coinciden en destacar el período mínimo de la persistencia de la tos en 2

meses, ya que este dato tiene importantes derivaciones para el clínico debido a que la bronquitis
crónica no puede ser diagnosticada sin descartar cuidadosamente otra enfermedad activa.

Afecta a perros y gatos a partir de 8 años sin predisposición de raza o sexo. Sin embargo, se ha
observado una mayor predisposición en gatos siameses y en perros de razas pequeñas como
Caniche, Pequinés, Pomeranian. Probablemente afecte el modo de vida urbano que hace que los
animales estén inhalando humo de coches. Dichas razas también están predispuestas a padecer
colapso traqueal y valvulopatía mitral con compresión del tronco bronquial principal.

Etiología:

Normalmente la causa no se descubre porque la enfermedad es detectable cuando aparecen los

signos clínicos en etapas avanzadas,

Procesos inmunomediados:
Hipersensibilidad a irritantes inhalados, contaminantes atmosféricos; ozono, dióxido de azufre,
humo de tabaco, polvo.
Factores genéticos

Procesos infecciosos:
o Micoplasma en gatos
o Bordetella bronchiséptica en perros, secundario a estados de inmunodeficiencia
o A su vez, las infecciones pueden ser secundarias a la propia bronquitis crónica, siendo
difícil establecer relación causa-efecto

Infestaciones parasitarias
o Oslerus osleri en perros.
o Capillaria aerophila ,Crenosoma vulpis, en gatos.
o Mammonogamus spp.
Otros procesos como la discinesia ciliar
Factores predisponentes a bronquitis crónica canina y felina.

Sintomatología

El cuadro clínico de esta enfermedad suele manifestarse con toses secas, más frecuentes por la
noche o a primeras horas de la mañana. Es frecuente que los propietarios confundan la tos con
vómitos si estas toses son en cuadros paroxísticos, más o menos intensos y con arcadas finales.
También pueden asociarlo con intentos del animal para expulsar algo “clavado” en la orofaringe.

Debemos por tanto realizar una cuidadosa anamnesis de manera que lleguemos a diferenciar un
cuadro de vómitos primario de un problema respiratorio con emesis secundaria refleja.

1
La tos puede ser más evidente tras algunos ejercicios físicos y después de periodos de excitación,
alegría o estrés. Un dato importante a tener en cuenta es que la sintomatología es variable en
función de la estación del año y de las condiciones meteorológicas de modo que suele empeorar
esta sintomatología durante la primavera y el otoño.

Otro síntoma que aparece con frecuencia es la disnea e incapacidad de adaptación a los cambios
bruscos de la temperatura ambiental.

En general la actitud del paciente suele ser normal y solo en raras ocasiones encontramos
pacientes deprimidos, anoréxicos o con pérdida de peso. Esta sintomatología es más frecuente en
los casos de bronquitis infecciosa.

Tos duradera de más de dos meses. Acompañada de

Anamnesis hipersecreción de moco por la noche e improductiva, seca y
áspera durante el día.
El animal empieza a demostrar intolerancia al ejercicio y la tos
aumenta después de realizarlo.

Lo normal es que estado general no esté afectado.

Examen físico Los pacientes suelen presentar sobrepeso
Disnea.
Auscultación Puede ser normal.
Espiración prolongada, sibilancias, aumento de los sonidos
broncovesiculares y crujidos.
Estertores espiratorios finales con respiración abdominal en
cuadros avanzados por el colapso traqueal.
Se puede observar un segundo tono cardíaco aumentado en
animales con hipertensión pulmonar secundaria

Sintomatología de la bronquitis crónica canina y felina.

Diagnóstico:

Podemos empezar a sospechar de bronquitis crónica cuando en la anamnesis nos revelen que el
animal presenta tos continuada diaria desde hace varias semanas, evidencia de moco excesivo y
además que el animal haya dado negativo a pruebas de detección de filarias y no presente signos
de insuficiencia cardiaca, neumonía u otras enfermedades respiratorias crónicas. Además
utilizaremos diversas técnicas diagnósticas:

1. Diagnóstico Radiológico:
Debemos tener en cuenta que puede darse un patrón bronquial normal, a pesar de observar unos
signos clínicos evidentes.
Nos resultará útil para descartar otras causas de tos crónica o descubrir complicaciones como
neumonía, bronquiectasia o enfermedad cardiaca.
Veremos, como signo específico, densidades o infiltrados periféricos debidos a la falta de drenaje
del moco.
Engrosamiento bronquial (con forma de buñuelos o raíles de tren) según la proyección verticales o
longitudinal con manguito peribronquiolar.
Las densidades intersticiales y peribronquiales en perros viejos son normales, muestran cambios
histológicos asociados a la edad.
La existencia de infiltraciones alveolares puede indicar coexistencia de bronconeumonía o edema
pulmonar.
Si observamos dilataciones saculares de los bronquios estaremos frente un hallazgo de
bronquiectasia secundaria a bronquitis crónica.
También es común un cuadro intersticial leve en bronquitis crónica.
Puede producirse secuestro de aire y como consecuencia observaremos los pulmones inflados,
por lo tanto aparecerá radiotransparencia y aplanamiento del diafragma por el empuje de los
pulmones contra éste.
En casos graves se observa bronquiectasia, neumonía y atelectasia.
En el gato pueden encontrarse atelectasias en el lóbulo medio derecho.

2
Si realizamos radiografías durante la espiración evidenciaremos el colapso en las grandes vías
aéreas
Además puede observarse cardiomegalia debido al cor pulmonale

2. Diagnóstico Broncoscópico:
Algunos autores recomiendan realizar broncoscopia para descartar otras enfermedades o cuando
el animal no responde al tratamiento.
Es útil para obtener muestras representativas de las vías aéreas profundas para citología y cultivo.
Observaremos de forma característica: mucosa eritematosa, engrosada, edematosa, contorno de
vías respiratorias irregular, colapso total o parcial de vías desde los bronquios principales hasta los
de tercer orden, sobre todo durante la espiración pasiva, se ven hileras o placas de moco denso.
La bronquiectasia también puede reconocerse con la broncoscopia
Pueden observarse proliferaciones polipoides o nodulares proyectadas hacia la luz bronquial.

3. Electrocardiograma:
-Arritmia sinusal respiratoria
-Marcapasos migratorios
-Ondas p pulmonares

4. Pruebas Laboratoriales:
Hemograma: Normalmente no se observa nada específico. No obstante, podemos observar
neutrofilia madura generada por el estrés, así como policitemia por la hipoxemia crónica. Anemia,
leucocitosis neutrofílica y desvío a la izquierda si hay una bronconeumonía secundaria.
Observaremos eosinofilia en procesos alérgicos o parasitarios, más común en los gatos

Bioquímica sérica: Suele ser inespecífica. Se recomienda realizar análisis antigénico para
dirofilariosis, sobre todo en perros que vivan en zonas endémicas.

Análisis fecal: Recomendable realizarlo para detectar gusanos pulmonares

Análisis de filarias

Análisis de orina

Análisis de gases en sangre arterial: Se registra hipoxemia, PaO2< 80mmHg en le 30% de

los casos. Hipercapnia poco frecuente, PaCO2> 40mmHg hallazgo serio de hipoventilación
asociado a trabajo respiratorio

Curva de volumen pulmonar:

o Relación tiempo espiración /tiempo inspiración alta, mayor o igual a 1,31.
o Flujo de aire al 25% del volumen corriente reducido por el estrechamiento o
colapso de vías.
o Desequilibrio en la ventilación/perfusión.

Estas pruebas se recomienda realizarlas para comprobar si el tratamiento es eficaz y el animal

va recuperando su función pulmonar.

5. Examen de líquido traqueobronquial:

El examen citológico nos revela: neutrófilos degenerados lo cuál nos indica infección
bacteriana o bronconeumonía, eosinófilos, signo de parasitismo, alergia o hipersensibilidad (tener
en cuenta parásitos cardíacos, muy comunes en gatos), pueden aparecer también macrófagos y
linfocitos así como hiperplasia de células epiteliales bronquiales.
Se debe hacer un cultivo del fluido traqueobronquial y un análisis de sensibilidad en perros con
diagnóstico de bronquitis crónica y que en sus radiografías y análisis broncoscópico se evidencie
bronquiectasia.
La presencia de un número pequeño de bacterias en un cultivo no necesariamente implica la
existencia de infección.
Para que los resultados de los cultivos traqueobronquiales y de las pruebas de sensibilidad sean
interpretados correctamente es necesario que las muestras sean recogidas de de las vías aéreas
bajas y no de la faringe.

6. Diagnóstico diferencial:
La bronquitis crónica se diagnostica basándonos en la exclusión clínica de otras enfermedades
respiratorias crónicas.

3
En perros, más de 60 procesos cursan con tos, ya que es el signo más evidente y el motivo de
consulta.

Tratamiento:

1. EDUCACIÓN DEL DUEÑO:

Advertirle de que su animal presenta lesiones irreversibles y por tanto el animal
se halla ante una enfermedad incurable. Explicarle el objetivo de la terapia que vamos a
aplicar.

2. TERAPIA DEL PACIENTE:

MEDIDAS CORRECTORAS Y DE MANTENIMIENTO:

1. Evitar el contacto del animal con: humo, polvo, limpia hogares, etc., porque pueden
provocar colapso traqueal, dando lugar a excitación y estrés en el paciente lo que le
provoca ataques de tos paroxística.

2. Dar al paciente pienso dietético para reducir peso, así se mejorará la ventilación y la
oxigenación arterial, y se reducirá el estrés del sistema cardiovascular.

3. Recomendar ejercicio ligero.

4. Oxigenoterapia si el animal sufre episodios de hipoxemia y bronconeumonía severas.

MEDIDAS PRINCIPALES: van encaminadas a:

1. Aliviar la inflamación y la obstrucción provocada por la hipersecreción de moco con

Antiinflamatorios y Broncodilatadores.

2. Controlar la tos siempre que esta sea improductiva, lo que es indicativo de que la
inflamación ya se está resolviendo con Antitusígenos.

3. Controlar la infección con Antibióticos, que deberán se de amplio espectro y

lipolíticos.

4. Hidratar las vías aéreas con nebulización.

5.

Glucocorticoides Prednisona o Dosis de inicio: 0.5-1mg/kg 10-14 Efectos

de acción corta. días/12h. Oral y parenteral. secundarios:
o Si remite la tos: reducir la dosis a la hepatomegalia,
mitad cada 10-14 días hasta el debilidad
mínimo que produce mejoría. muscular,
o Si no remite: combinación con disminución de
broncodilatadores como el las defensas,
Salbutamol inducción a la
obesidad.
Antiinflamatorios.

Broncodilatadores.
Los broncodilatadores de utilidad en la clínica de pequeños animales puede dividirse en tres
grandes grupos: Broncodilatadores directos, bases xánticas y anticolinérgicos, de los cuales,
desde el punto de vista terapéutico, solo interesan los dos primeros, ya que los anticolinérgicos,
como la atropina, tienen efectos secundarios no deseables en la mayoría de los casos.

4
Metilxantinas Teofilina Perros: 20 mg/kg/24h Puede producir efectos
secundarios como:
hiperexcitabilidad, taquicardia y
distrés gastrointestinal.
Reducir la dosis si se observa
mejoría.
Si no responde al tratamiento o
se sospecha de toxicidad, medir
la concentración plasmática de
Aminofilina teofilina 4,5h después de la
administración de teofilina de
liberación lenta y 1,5 h después,
Perros: 11 mg/kg/8h si es de liberación rápida.
Oxifilina

Se suele usar en perros Toys

en forma de elixir 14
mg/kg/8h.

Agonistas β2 Salbutamol Perros: 0.1 mg/kg /8h Si se aprecia mejoría

simpaticomiméticos reducir la dosis.
Clembuterol 0,6 ug/kg/12h
Procaterol 1 ug/kg/12h
Terbutalina 100 ug/kg/8h

Antitusívos
Los fármacos antitusívos como el dextrometorfano tienen un valor muy limitado y no son efectivos
en líneas generales. Los supresores narcóticos como la codeína, sí son más efectivos pero en
casos de complicaciones infecciosas pueden agravar el cuadro puesto que afectan de modo
negativo a los mecanismos de defensa normal facilitando el acumulo de secreciones respiratorias.

Hidrocodona 0.22mg/kg /6-12h, PO

Butorfanol 0.05-0,1mg/kg/6-8h, PO ó SC
Codeína 1-2mg/kg/6-12h PO.
Dihidrocodeína 0,5-1mg/kg /
Butamirato 0,1mg/kg/12h, PO.
Clorbutinol 0,5mg/kg/12h, PO.
Dextrometrofano 1-2mg/ kg /6-8h, PO.
Antitusívos

Fenobarbital 2-6mg/Kg /día/8-12h, PO

Perros: 0.05-0.01mg/kg, IV, IM o SC
0.55-2,2 mg/kg/6-8 h, PO
Acepromazina Gatos: 0,11-0,22 mg/kg, IV, IM o SC; 1,1-2,2
mg/kg/8-12h, PO
Tranquilizantes

5
Doxicilina 2.5-5 mg/kg /12 h. PO
Cloramfenicol 50mg/kg /8h. PO
Enrofloxacina 5-10mg/kg /12 h PO ó 20-40 La Enrofloxacina inhibe el
mg/kg7día PO metabolismo de la teofilina,
dando lugar a niveles tóxicos
en sangre. Reducir la dosis de
teofilina al 30%.
En infecciones severas: 15mg/kg /12h. PO
Cloramfenicol y Trimetropín-
sulfa

Clindamicina con 11mg/kg /12h. PO

Enrofloxacina o
Ciprofloxacina
Gentamicina nebulizada Aplicar con un nebulizador
desechable durante 10
minutos.
Antibióticos

Profilaxis y Prevención:

Se recomiendan controles rutinarios de parásitos como Filarias.

Mantener una higiene bucal regular para evitar la aspiración microbiana a las vías.
Evitar el contacto prolongado con los factores predisponentes citados, sobre todo los que sean de
carácter doméstico (humo de cigarro, limpiadores, polvo, etc.).

Lecturas Recomendadas:

Caro A: Enfermedades pulmonares obstructivas crónicas del perro y el gato. E. Montoya-Alonso

JA: Enfermedades respiratorias en pequeños animales. Buenos Aires, Inter-Médica, 2005, pp:121-
125.

Kuehn NF: Chronic Bronchitis in Dogs. En: King LG: Textbook of Respiratory Disease in Dogs and
Cats. Saunders, 2004, pp: 379-387.

Nielssen A & Taylor SM: Enfermedades de la vía respiratoria baja. En: Morgan RV, Bright RM &
Swartout MS: Clínica de pequeños animales. Sauders-Elsevier, 2.004, pp: 167-168.

6
 FOTOS PRIMERA JORNADA DE
MEDICINA CARDIORESPIRATORIA
 DR. LINA
SANZ
CHILE

CHARLAS

1. Abordaje clínico, diagnóstico y terapéutico del gato con tos

2. Patologías pleurales
3. Diagnóstico radiográfico de las principales urgencias
respiratorias felinas y caninas
Dra. Lina Sanz Aguirre
2018

Dra. Lina Sanz Aguirre

Instituto de Medicina Felina y
Centro Opción Felina
LA TOS
 REFLEJO PROTECTIVO
 ESTIMULACIÓN DE MECANORECEPTORES O
QUIMIORECEPTORES EN LA VÍA AÉREA
 BRONQUIOLOS Y ALVEOLOS NO TIENE
RECEPTORES ….. SI ENFERMEDAD PULMONAR
GENERA TOS ES POR EXTENSIÓN A VÍAS DE
MÁS DIÁMETRO

PROTOCOLO FRENTE A ANTECEDENTE DE TOS

 ASEGURARSE QUE ES TOS Y NO ARCADA,
VÓMITO, REGURGITACIÓN
 SUELEN SER ATAQUES PAROXÍSTICOS
 EN JÓVENES PREDOMINAN CAUSAS
INFECCIOSAS
 EN ADULTOS PREDOMINA ASMA (ORIENTALES
Y SIAMESES CON MÁS FRECUENCIA)
PROTOCOLO FRENTE A ANTECEDENTE DE TOS
 FRECUENCIA Y NATURALEZA DE LA TOS

 SUAVE Y PRODUCTIVA… ENFERMEDAD DE

PARÉNQUIMA

 SECA Y DURA … ENFERMEDAD DE VÍA AÉREA

PROTOCOLO FRENTE A ANTECEDENTE DE TOS

 INICIO Y DURACIÓN

 AGUDA … CUERPO EXTRAÑO INHALADO, ASMA,

TRAUMA, ENFERMEDAD INFECCIOSA

 CRÓNICA …. BRONQUITIS CRÓNICA, ASMA ,

NEOPLASIA
APROXIMACIÓN DIAGNÓSTICA
 AUSCULTAR LARINGE, TRÁQUEA Y CAMPOS
PULMONARES
 PALPACIÓN LARINGE Y TRÁQUEA
 PALPACIÓN Y RESISTENCIA DE TÓRAX
ANTERIOR

EXÁMENES COMPLEMENTARIOS
 SANGUÍNEOS NO DAN LA CAUSA PERO
APORTAN; INCLUYENDO TEST RETROVIRAL
 HIPERGLOBULINEMIA, NEUTROFILIA SUGIEREN
INFLAMATORIO E INFECCIOSO
 EOSINOFILIA SUGIERE PROCESO ALÉRGICO O
PARASITARIO
 ANEMIA REGENERATIVA SUGIERE ANEMIA –
HEMORRAGIA
 ERITROCITOSIS SUGIERE HIPOXIA CRÓNICA
TOS AGUDA
 PUEDE CONSIDERARSE TERAPIA EMPÍRICA
 EXAMEN NASOFARÍNGEO BAJO ANESTESIA
PARA CUERPOS EXTRAÑOS INHALADOS
 TRAQUEOSCOPÍA PARA CUERPOS EXTRAÑOS
EN TRÁQUEA
 ANTIMICROBIANOS SUELEN INDICARSE,
MÍNIMO 3 SEMANAS
 DOXICICLINA 10 MG/KG CADA 12 HORAS A 24 HORAS
***
 AZITROMICINA 5 – 10 MG /KG CADA 12 HORAS Y LUEGO
DOSIS MÁS BAJAS
 AMOXICILINA CON ÁCIDO CLAVULÁMICO

TOS CRÓNICA (mayor a 2 semanas)

 BRONQUITIS Y ASMA ES LO MÁS FRECUENTE
 SI SE PRESCRIBIRÁN CORTICOIDES DEBEN SER
SOLO INHALADOS MIENTRAS SE DEFINE EL
DIAGNÓSTICO
 DOXICICLINA POR MÍNIMO DE TRES SEMANAS
Y ANTIELMÍNTICOS SUELEN USARSE
 LIMPIEZA Y MANEJO DEL AMBIENTE
 ASMA FELINA

 Limitación al flujo aéreo en la vía aérea baja que

resuelve espontáneamente o con medicación.
 Combinación de inflamación, mucus acumulado y
contracción del músculo liso bronquial
 Signos desde toses esporádicas a ahogo dramático
 Se reconoce en ocasiones como complejo asma /
bronquitis

ASMA FELINA

 Proceso crónico del árbol bronquial con

signología similar a la bronquitis crónica
 BRONQUITIS CRÓNICA : Genera toses a diario en
todos los casos; debe excluirse para el diagnóstico
de asma. Generada por dirofilaria, pneumonia,
parásitos pulmonares y neoplasia.
 ASMA FELINA

 En humanos el asma se diagnostica por estudios

dinámicos que requieren cooperación.
 En ocasiones , entonces, no podemos distinguir
entre asma y bronquitis en felinos que tengan tos
como único signo

ASMA FELINA
 Felinos predispuestos a severo asma por
hiperreactividad bronquial:
 Mayor cantidad de músculo liso en pared
bronquial y ductos alveolares
 Mayor cantidad de cartílago elástico respecto al
hialino en bronquiolos
 Mayor cantidad de células globoides y glándulas
submucosas
 Mayor viscosidad mucus
 Mayor cantidad de mastocitos pulmonares
(serotonina!!!)
 ASMA FELINA

 Ante cualquier noxa el epitelio respiratorio bajo se

hipertrofia, entra en metaplasia, se erosiona y
finalmente se ulcera.
 Las células caliciformes y glándulas submucosas se
hipertrofian y generan gran cantidad de mucus
viscoso
 Se infiltra la mucosa y submucosa bronquial con
células inflamatorias.
 ASMA FELINA

 Signos serán tos, ruido respiratorio (resuello o

wheeze) y letargia por la limitación de la vía aérea
dada por mucus, edema y estrechamiento por
infiltrados.. En gatos se suma la broncoconstricción

ASMA FELINA

 Por las fórmulas de Bernouilli y Poiseuile- Hagen la

disminución en el diámetro genera incremento de la
velocidad y cae la presión.
 Un 50% de reducción luminal hace caer en 16 veces el
volumen de aire
 Degranulación de proteínas catiónicas desde
eosinófilos
 ASMA FELINA

 La patogenia incluye la interacción entre linfocitos

T activados y eosinófilos (LBA)
 Son CD4 activados por aeroalergenos, liberan IL-5
la cual promueve eosinófilopoyesis, activación y
supervivencia de eosinófilos ( Perfil de citoquinas T
helper 2)

ASMA FELINA

 Los gatos generan:

 IgE alergeno – específicos, IgG e IgA en suero y
LBA alergeno – específicos
 Hiperreactividad en vía aérea
 Eosinofilia en vía aérea
 Perfil de citoquinas agudo T H - 2
 ASMA FELINA

 Prevalencias:
 1% de población general
 5 a 15% en siameses

 Edad promedio 2 a 8 años para el inicio

ASMA FELINA
 Signología:
 Tos por la mayor sensibilidad de la vía aérea
 Resuellos por el paso de aire forzado por espacios
estenosados
 Cépitos por excesivo mucus, espiratorios
 Letargia
 Asintomáticos entre crisis los casos leves, no así los
severos.
 ASMA FELINA

 Signología:
 Puede estimularse la tos por compresión de pared
toráxica.
 Disnea espiratoria obstructiva de leve a severa
(cianosis y boca abierta)
 Signos parten episódicos y luego se cronifican
 Signos frente al alergeno

ASMA FELINA

 Diagnóstico:
 Broncoconstricción reversible es pauta
 Aplicar terbutalina por inhalación o parenteral
(agonista β2) 0,01 mg/Kg i.m. y reevaluar en 5 a 10
minutos… es el único criterio aprobado de distinción
clínica entre BC y AF
 En su defecto …dexametasona 2 mg/Kg
 ASMA FELINA

 Diagnóstico:
 Examen físico es irrelevante
 Baja condición corporal, cianosis, diestress, crépitos
en crónicos
 Por flotación y prueba Baermann excluir
Aelurostrongylus abstrusus o Eucoleus aerophila
(formalmente Capillaria aerophila)

ASMA FELINA

 Diagnóstico radiográfico:

 Radiografías normales o anormales

 Patrón bronquial con anillos y líneas de ferrocarril
 Hiperluscencia lobar por enfisema , con
aplanamiento diafragmático, redondeamiento de
ángulos lumbofrénicos y costofrénicos, ángulos
lumbofrénicos caudales al último par costa,
paralelismo costal
 ASMA FELINA
 Diagnóstico radiográfico:

 Esternón convexo ventralmente, tórax biconvexo

lateralmente
 Colapso del lobo medio derecho en 15% de casos,
evidencia de atelectasia (orientación dorsoventral
en el árbol bronquial)
 Infiltrados y patrón miliar diseminado por
tapones mucosos y/o áreas atelectásicas.

ASMA FELINA
 Diagnóstico radiográfico:

 Radiografías NO distinguen de bronquitis crónica

 Radiografías similares a pneumonitis intersticial
, neoplasia y otros
 Radiografía se mantiene similar entre controles
!!!!
 Tomar tres a cuatro proyecciones
 ASMA FELINA

 Broncoscopía:

 Raramente requerida!!!
 Procedimiento puede comprometer la vida en estos
casos
 Luego de 6 a 7 días de terapia agresiva que incluya
corticoides, si no existen cambios en la signología,
se prescribe con especialistas

ASMA FELINA
 Citología traqueobronquial:
 20 a 25% de eosinófilos en LBA son comunes en
gatos sanos
 Su presencia no indica alergia o parasitismo
 Macrófagos, neutrófilos se recolectan de sanos y
enfermos en igual cantidad…
 Obtenida por LBA o lavado transtraqueal

 No recomendado
 ASMA FELINA

 Cultivo traqueobronquial:

 Parénquima sano NO es estéril

 Incluso Klebsiella y Pseudomonas desde gatos sanos
 Solo relevante Mycoplasma , que al igual que
algunos virus (VHF-1) degrada la endopeptidasa
neutra (que degrada sustancia P, proteína que
genera broncoconstricción y edema)

ASMA FELINA
 Diferenciales:

 Para el status asthmaticus es la falla cardíaca

congestiva izquierda por cardiomiopatía… muy
inusual
 Para lo crónico: toda otra pneumopatía que genera
tos : bronquitis crónica, dirofilarias, H1N1,
parásitos, neoplasia.
 ASMA FELINA
 Terapia:

 Broncodilatador y antiinflamatorio es lo básico

 Disminuir de peso en CC alta
 Disminuir stress ambiental
 Fenbendazole (antígeno tratable) 50 mg/Kg/14 ds
 En Aelurostrongylus abstrusus también se puede
aplicar tópico imidacloprid / moxidectin

ASMA FELINA
 Terapia Corticoides:

 Es lo más efectivo a largo plazo

 Disminuye citoquinas
 Corticoides inhalatorios
 Con toses mayores a una crisis por semana 1 – 2
mg/Kg de prednisolona cada 12 horas por 5 a 7 días…
baja sostenida lenta en 2 meses y siempre seguir con
inhalatorio (propionato de futicasona Provent®)
 ASMA FELINA
 Terapia Corticoides:

 Inyectable solo acetato de metilprednisolona

10 a 20 mg i.m. en gatos que no toleran otra
administración
 Cada 4 a 8 semanas
 Efectos adversos
 ASMA FELINA

 Terapia Broncodilatadores:

 Usar agonistas de receptores β2 selectivos para evitar

efectos cardiovasculares.
 Sulfato de terbutalina
 Sulfato de albuterol

ASMA FELINA

 Terapia Broncodilatadores:

 Sulfato de terbutalina
 Relaja músculo liso bronquial, vascular y uterino
 Tabletas, jarabes, puff y parenteral (sc o im)
 0,01 mg /Kg i.m. en crisis (clínica u hogar)
 0,1 - 0,2 mg/Kg oral cada 8 horas
 ASMA FELINA
 Terapia Broncodilatadores:

 Sulfato de terbutalina
 Frecuencia cardíaca alcanza los 240 lpm y respiratoria
baja un 50% cuando es efectiva
 Monitorear kalemia
 Cuidado con cardiomiopatía pre existente

ASMA FELINA

 Terapia Broncodilatadores:

 Sulfato de albuterol (salbutamol)

 Tabletas, jarabes y puff
 Solo usar el inhalador, con 90 µg por puff
 ASMA FELINA

 Terapia Broncodilatadores:

 Metilxantinas
 Aminofilina no recomendada
 Teofilina 4 mg/Kg oral cada 8 a 12 horas. En
preparación de larga acción 25 mg/Kg cada 24 horas

ASMA FELINA

 Terapia Antitusivos:

 No indicados
 Tos es productiva
 ASMA FELINA
 Terapia Mucolíticos:

 No se necesitan habitualmente
 Principales autores no lo usan
 Bromhexina 2 mg/Kg oral cada 12 horas por 7 a 10
días y bajar dosis a la mitad por 7 a 10 días más
 Acetilcisteína nebulizada, 5 a 10 mg/Kg por 30
minutos cada 12 horas (viene al 10 y 20%).. PERO
IRRITA

ASMA FELINA
 Terapia Espectorantes:
 No se utilizan
 Inducen vómito (guafenesin)

 Terapia Antibióticos:
 Más de 105 organismos por ml
 Basado en sensibilidad
 Doxiciclina con Mycoplasma en cualquier
concentración
 ASMA FELINA
 Terapia Ciproheptadina:

 Antiserotónínico
 Solo en gatos que no responden a dosis máximas
de broncodilatadores y corticoides
 2 – 4 mg total PO cada 12 horas… depresión a las 24
horas y si hay efectos benéficos se ven luego de 4 a
7 días

ASMA FELINA
 Terapia Antileucotrienos:

 LTC4, LTD4, LTE4

 Generan hipersecresión de mucus, edema por
incremento de permeabilidad,
broncoconstricción y quemotaxis a eosinófilos y
PMN
 No hay evidencia fuerte de su beneficio en estos
casos
 Zafirlukast 1 a 2 mg/Kg/bid – Montelukast 0,5 – 1
mg/Kg/sod.
 ASMA FELINA
 Tubos de inhalación:

 70% lo usan de inmediato, 20% requieren

acostumbrarse, 10% no lo tolerarán.
 Efectos óptimos en 1 a 2 semanas
 Preferir broncodilatador y corticoide por separado
 Flovent ® de 110 a 220 µg cada 12 horas

ASMA FELINA
 Recomendación Dr Phil Padrid:

 Solo tos : fluticasona 110 mcg bid (2 puff) y

albuterol bid (2 puff)
 Tos y despertar nocturno: fluticasona 220 mcg bid
, albuterol bid, prednisolona 1 mg/Kg/sod 5 ds
 Signos marcados: Igual al anterior con
prednisolona 1 -2 mg/Kg cada 12 horas, luego cada
24 y dosis descendientes
 ASMA FELINA
 Recomendación Dr Phil Padrid:

 En emergencia
 Reposo, escasa manipulación
 Oxígeno 10 – 20 minutos
 Terbulatlina (o dexa) inyectable
 Esperar 5 – 10 minutos
 Terbutalina cada 30 minutos por 4 veces si es
necesario
 Luego mantención de caso grave.

PNEUMONIAS

 INFLAMACIÓN DEL PARÉNQUIMA

PULMONAR
 INFRECUENTE
 VARIADAS ETIOLOGÍAS
 BACTERIAS SUELEN SER SECUNDARIAS
PNEUMONIAS
 Bacterias patógenas incluyen:
 Escherichia coli
 Klebsiella
 Pasteurella (también primario)
 Pseudomonas
 Bordertella (también primario)
 Streptococcus sp
 Nocardia
 Actinomices

PNEUMONIAS

 Condiciones asociadas:
 Aspiración por esofagopatía o recuperación
anestésica
 Enfermedad metabólica como la pneumonitis
urémica, hiperadrenocorticismo y diabetes
mellitus
 Trauma contuso, penetrante o Cx
 Inmunosupresión por drogas, neoplasias o
retrovirus
 Infección preexistente
ANTECECENTES

 Pneumonia por Mycoplasma es infrecuente y

secuela de severa enfermedad del tracto
respiratorio alto
 Chlamidophila felis puede generarla en gatitos
 Casos parasitarios y protozoarios son frecuentes
 Casos fúngicos suelen ser por Criptococcus
neoformans

ANTECECENTES

 Pneumonitis virales por calicivirus en

gatitos o secundarias a FIV
 Se denomina pneumonitis intersticial
 Producto de algunas cepas muy patógenas
 Infrecuente
ANTECECENTES
 Micosis menos frecuentes (USA) incluyen:
 Blastomicosis
 Histoplasmosis
 Aspergilosis
 Candidiasis
 Aspergilosis
 Coccidiomicosis
▪ Tipo intersticial
▪ Testear FIV – FeLV
▪ Fluconazol, itrakonazol

PNEUMONIAS

 Signos:
 Tos infrecuente, puede ser productiva
 Disnea de predominio espiratorio
 Disnea restrictiva
 Fiebre
 Letargia y anorexia
 Halitosis
 Respirar con boca abierta
 Auscultación con crépitos, sibilancias, silencio
en consolidación
 Ocasionalmente descarga nasal y disneas mixta
BORDETELLA BRONCHIPSEPTICA

 Cocobacilo aerobio gram (-)

 Seroprevalencias de 24 a 79%
 Aislamientos de 3 a 11%
 Mayores prevalencias en gaterías, albergues o
múltiples gatos en casa
 Sin relación con agentes clásicos del complejo
respiratorio alto
 Stress de parto induce eliminación desde
orofaringe

BORDETELLA BRONCHIPSEPTICA

 Principal causa de pneumonia infecciosa

primaria
 Mayor prevalencia en menores de 10
semanas
 Afecta cilios, libera toxinas
 Depresión, disnea, cianosis, muerte
 Nódulos grises en necropsia y exudado
purulento al corte
BORDETELLA BRONCHIPSEPTICA

 Toxinas:
- Dermonecrótica: inflamación
- Citotoxina: cilioestasis
- Enzimática: altera fagocitosis
(PMN)

BORDETELLA BRONCHIPSEPTICA

 Inmunidad materna corta de 2-6 sem

 Importancia del perro y cerdo en la
epidemiología
 Terapia no suele eliminar el agente
 Puede ser zoonosis en
inmunocomprometidos o esplenectomizados
BORDETELLA BRONCHIPSEPTICA

 Cuadros altos orofaríngeos suelen limitarse

en 10-14 días
 Signos 5-6 días por la inflamación mediada
por citoquinas
 Algunos cronifican asintomáticos (41%)

BORDETELLA BRONCHIPSEPTICA

 Altamente contagiosa
 Lavado broncoalveolar o transtraqueal
 Cultivo dirigido en la orden
 Medio carbón – cefalexina
 Terapia según antibiograma
 Empírico : doxiciclina (10 mg/Kg/24 hr),
oxitetraciclina, enrofloxacino y otras
quinolonas. Algunas cepas amoxi –
clavulámico
BORDETELLA BRONCHIPSEPTICA

 Terapia clásica:
- Doxiciclina 10 mg/kg/24 hrs
con Prednisolona 1 mg/kg/24 hr por
10 días y 0,5 mg/kg por 10 días
- Nebulizaciones 14 días (3ml agua)
- NaCl
- Inhalaciones
Diseminan hasta 5 meses pos infección

BORDETELLA BRONCHIPSEPTICA

 Prevención:
 Disminuir hacinamiento
 Eliminar excretores orofaríngeos de
reproducción (hembras)
 Reducción stress
 Desinfectantes
 Vacunación Novibac Bb ®
 Diagnóstico
pneumonia

 Examen clínico
 Radiografías (alveolar, bronquial, intersticial ,
nodular, consolidaciones; linfoadenomegalia
en micobacterias, hongos y linfoma)
 Neutrofilia con o sin D a I
 Neutropenia por secuestro
 Neutrófilos tóxicos

Diagnóstico
pneumonia

 Anemia NN en cronicidad
 Hipoxemia PaO2 menor a 80 mmHg o SPO2
menor al 90% - 92%
 Citología por aspiración percutánea, LTT, LBA
 Cultivo Bb, aerobios, anaerobios y hongos
 Test especiales
Diagnóstico diferencial
pneumonia

 Asma / bronquitis
 Pneumonia eosinofílica
 H5N1
 Linfoma pulmonar intersticial
 Neoplasia primaria (carcinoma broncogénico,
CCE) o metastásica

Aelurostrongylus abstrusus

 Nemátodo metastrongylidae
 Frecuente infestación
 Huésped: - babosa, caracol (intermedios)
- Roedores , aves, reptiles, anfibios
(paraténicos)
 Bronquiolitis y neumonia
 Adultos en alvéolos , bronquiolos y pequeñas
ramas de arteria pulmonar
Aelurostrongylus abstrusus

 Huevos pasan a L1 en alvéolos

 L1 deglutidas y salen con defecaciones
 Pueden sobrevivir meses
 Ingeridas por moluscos terrestres
 Gato ingiere caracoles, babosas o paraténicos
 Larva llega al pulmón por sangre o linfa en 24
h (L3 penetra digestivo)

Aelurostrongylus abstrusus

 Adulto macho 5 mm
 Adulto hembra 9 mm
 Larva en fecas de 3,6 mm con cola en S
 Prepatencia de 34 a 42 días
Aelurostrongylus abstrusus

 Se genera gran respuesta inflamatoria

 Casos asintomáticos autolimitantes en 3-4
meses (menos de 50 larvas)
 Tos es signo predominante
 Escaso compromiso sistémico … asma
 En ocasiones disnea
 Pneumonia intersticial y/o bronquitis –
bronquiolitis

Aelurostrongylus abstrusus

 Puede generar pleuritis con nódulos de 10 mm

 Infiltrados de linfocitos, macrófagos y
eosinófilos
 Genera hiperplasia e hipertrofia epitelial que
puede quedar como secuela , generalmente sin
impacto clínico
Aelurostrongylus abstrusus

 Radiografía muestra cambios 2 – 6 semanas

pos infección
 Cambios pueden ser severos incluyendo
patrones miliares
 Técnica de Baerman en fecas
 Citología pulmonar por punción , LTT, LBA

Aelurostrongylus abstrusus

 Terapia
 Febendazole 50 mg/kg/día por 10-20 días
- Ivermectina 0,4 mg/kg SC única
- Mebendazol 30 mg/kg/24 hr por 5 días
- Imidacloprid / moxidectina tópico
Dra. Lina Sanz Aguirre
2018
Dra. Lina Sanz Aguirre
2018

Dra. Lina Sanz Aguirre

Instituto de Medicina Felina y
Centro Opción Felina
  Aplicaciones de radiología simple y
contrastada, no intervencionista

 Muchas de las técnicas se van reemplazando

por TAC simple y contrastado, especialmente en
emergencias luego de estabilización

 “Radiografía de Urgencia”

 Ecografía y radiografía SON

COMPLEMENTARIAS … en tórax y
abdomen tener ambas
 Excepciones suelen involucrar tejido
óseo o mineralizaciones
 Las radiografías, excepto casos aislados,
pueden esperar
 Si se obtendrá ecografía… partirmos con
Radiografía
  Las radiografías DEBEN esperar

 CUANDO SE HABLA DE RADIOGRAFÍAS

NOS REFERIMOS A

ESTUDIOS RADIOGRÁFICOS
 Dos proyecciones en abdomen
 Pueden ser tres a cuatro en
gastrointestinal y estudio de masas
 Dos proyecciones en mediastino
 Cuatro proyecciones en broncoalveolar
y espacio pleural
Indicaciones
 Estudio de cavidad nasal y senos paranasales

 Estudio de cuello y tórax

 Estudio de tórax : 4 proyecciones para

broncoalveolar y espacio pleural

 Estudio de tórax : 2 proyecciones para mediastino en

general

Consideraciones
 Paciente estable que tolere manipulación
 Aprovechar su estado anestesiado / sedado
 Solo xilaxina altera en forma consistente
diagnósticos intra toráxicos
 Extremar simetría y adecuada técnica
 No olvidar pick de inspiración y centrado
 Controles en proceso broncoalveolar cada 12 a
28 horas (Morgan, 2009)
 Posterior a toracocéntesis.
HVS 2018

HVS 2018
Pneumomediastino
 Considerar en pacientes con distress respiratorio,
mala oxigenación y radiografía “sin grandes
cambios”
 Este diagnóstico DEBE BUSCARSE (Similar a TEP)
 Signos patognomónicos en LL
 Puede generar Pneumotórax pero no a la inversa
 Grave o crónico genera pneumoretroperitoneo

HVS 2018
Tromboembolismo pulmonar
 Buscar cada arteria para considerar su vena
vecina
 Ocasionalmente afecta a vasos lobares
principales
 Se evalúa todo el tórax y no solo los puntos de
observación oficiales
 No olvidar glomérulonefritis,
hiperadrenocorticismo, pancreatitis, PPIF, CID,
neoplasias
 Si existe arteritis deformante la única causa es
Dirofilaria

Vet praxis 2015

 Vet praxis 2015

Vet praxis 2015

Efusión pleural
 Estudio de tres a CUATRO proyecciones
POSTERIOR a toracocéntesis bilateral
 Análisis de fluido citoquímico y de patología
imprescindible
 Test Rivalta obligatorio en felinos
 Signos patognomónicos (VD)
 Evaluar redondeamiento de márgenes de pleura
visceral
 Diferencias entre especies !!
 SIGNOS RADIOGRÁFICOS
 FLUIDO ENCAPSULADO NO SE MODIFICA SEGÚN
DECÚBITO

 FLUIDO típico SE MODIFICA SEGÚN DECÚBITOS

 100 ML MÍNIMO EN RAZA MEDIANA
 50 ML PEQUEÑOS Y GATOS

HVS 2018
 HVS 2018

Pneumotórax
 Signo patognomónico es mejor visualizado en V-
D
 Requiere buena técnica
 Se obtiene posterior a toracocéntesis bilateral
 HVS 2018

Trauma esternal
 Luxacíón
 Luxofractura
 Diferenciar malformaciones congénitas
 HVS 2018

HVS 2018
Masa mediastinal craneal
 Más frecuente en felinos que caninos
 Mayor generación de Sindrome de Claude
Bernard Horner en caninos que felinos (**)
 Raramente se mineraliza
 Tiene signo patognomónico
 Puede o no tener efusión pleural – mediastinal

HVS 2018
 HVS 2018

Efusión mediastinal
 Buscar fisuras reversas o mediastinales
 Signo patognomónico en V-D o D-V
 Simetría necesaria
 Puede existir efusión pleural concomitante
Efusión en politrauma
 Importante la toracocéntesis previa
 Evaluación de pared costal, esternón, columna
toráxica, articulación escápulohumeral,
integridad de diafragma
 No siempre se logra simetría en trauma de pared
toráxica y/o pacientes inestables

HVS 2018
 HVS 2018

Rotura diafragmática traumática

 Signo patognomónico en VD
 Requiere EXTREMA SIMETRÍA
 Se privilegia Llder, Llizq y DV
 Muchos signos comunes a otras patologías
 HVS 2018

HVS 2018
Hemiparálisis de diafragma
 Confirmación RADIOGRÁFICA o fluroscópica
 Se confunde con Rotura Diafragmática
 Proyección DV o VD con signo patognomónico

HVS 2018
 HVS 2018

Hipoplasia de tráquea
 Confirmación RADIOGRÁFICA
 Signo patognomónico
 Proyección L-L
 Suele coexistir con otros procesos
TASA TRAQUEOTORÁXICA
MEDICIÓN ENTRADA TORÁXICA:
Entre T1 y su ángulo cráneoventral y
Esternebra I a la altura de la porción más
craneal de la I costilla y llegando al punto de
menor espesor del manubrio

TASA TRAQUEOTORÁXICA
MEDICIÓN TRÁQUEA:
Perpendicular al eje mayor y a la altura
de intersección de la línea de la entrada
toráxica con el centro del lumen traqueal
TASA TRAQUEOTORÁXICA
0,21 +/- 0,03 RAZAS GENERALES,
MESO O LONGICEFÁLICOS
0,16 +/- 0,03 RAZAS BRAQUICEFÁLICAS
0, 13 +/- 0,038 BULL DOG INGLÉS
0,11 +/- 0,03 BULLDOG INGLÉS
(rango de 0,07 a 0,21)

TASA TRAQUEOTORÁXICA
Diámetro tráquea / esternebra a VII
cervical….
0,18 en DSH
0,20 en Persas
Diámetro tráquea / ancho tercio proximal
de III costilla
1,59 DSH
1,71 Persas
 HVS 2018

HVS 2018
Masas que comprimen vía aérea
 Proyección L-L da más información
 Masas en cuello o mediastino
 Requieren de citología / biopsia

HVS 2018
 HVS 2018

Cardiomegalia
 Conocer diferencias entre especies
 Se REQUIERE foco, simetría y pick de inspiración
 Evaluación cualitativa
 Evaluación cuantitativa
 En urgencia suele obtenerse luego del manejo
 Evaluación de fallo cardíaco congestivo derecho e
izquierdo
 HVS 2018

HVS 2018
HVS 2018

HVS 2018
HVS 2018

HVS 2018
Colapso lobo medio derecho
 Pneumonia
 Torsión lobar
 Aspiración
 Asma felino
 Carcinoma broncogénico

Colapso lobo medio derecho

 Lineal o abultado en L-L
 Se aprecia en V.-D / D-V o existe shift
 HVS 2018

Patrón alveolar
 Signo patognomónico
 El más fácil patrón de diagnóstico
 El más relevante patrón
HVS 2018

HVS 2018
Patología de esófago
 Siempre dos vistas
 Cuello y tórax
 VD da pronóstico
 LL con signos patognomónicos

HVS 2018
 HVS 2018

HVS 2018
Bulla Pulmonar
 Diagnóstico en estudios simétricos
 Diferenciar de masa / asbceso

HVS 2018
 HVS 2018

Contusión Pulmonar
 Falsos negativos primeras horas
 Patrones mixtos
 Evaluar pared toráxica y patrones concomitantes
 Dificultad con enfisema subcutáneo
HVS 2018

HVS 2018
Broncopatía
 Puede generar crisis respiratoria
 Bronquiectasia y enfisema son irreversibles
 Suele existir cambios en corazón derecho (cor
pulmonare)
 Suele existir hipertensíón

Dra. Lina Sanz Aguirre

2018
 FOTOS PRIMERA JORNADA DE
MEDICINA CARDIORESPIRATORIA
 DR. PAULO
MALLEA
CHILE

CHARLAS

1. Anestesia en el paciente cardiópata felino complicaciones

y su manejo

2. Tips en anestesia de paciente cardiópata canino geriatra

F e l i n e H y p e r t ro p h i c
C a rd i o m y o p a t h y :
An Update
Jonathan A. Abbott, DVM

KEYWORDS
 Feline  Hypertrophic cardiomyopathy
 Feline myocardial disease

INTRODUCTION/HISTORICAL PERSPECTIVE

Recently proposed classifications of human cardiomyopathies have emphasized the

etiology or molecular basis of myocardial disease.1,2 Although the cause of a few
specific breed-associated feline cardiomyopathies has been determined, feline
myocardial disease remains largely idiopathic.3,4 Accordingly, morphopathologic/
functional designations remain valid. Given that premise, cardiomyopathy can be
defined as a heart muscle disease that is associated with dysfunction.5 Hypertrophic
cardiomyopathy (HCM) is a disorder in which myocardial hypertrophy develops in the
absence of hemodynamic load or metabolic cause; it is morphologically characterized
by hypertrophy of a non-dilated ventricle.6–8 Feline HCM is a diagnosis of exclusion
that is valid when hypertrophy is echocardiographically evident in the absence of
disorders such as systemic hypertension or hyperthyroidism.
The recognition of cardiomyopathies, and specifically HCM, is recent. The clinical
characteristics of the entity that has become known as HCM were first described in
human patients during the late 1950s.9 The recognition of feline HCM occurred some-
what later. The association between feline cardiac disease and the occurrence of
systemic arterial thromboembolism was reported by Holzworth, but early reports of
thromboembolic phenomena do not specifically relate these events to heart muscle
disease.10,11 In 1970, Liu12 retrospectively evaluated the postmortem features of
acquired feline diseases that had resulted in congestive heart failure. Characteristic
pathologic findings of advanced feline HCM, including left ventricular hypertrophy
(LVH); left ventricular fibrosis; and left atrial dilation, were described but the term cardio-
myopathy was not used. The use of the term cardiomyopathy in reference to feline heart
disease seems to have first appeared in 1973.13 Later publications, including an issue of
this periodical from 1976, refer to feline cardiomyopathy and propose classifications of

Department of Small Animal Clinical Sciences, Virginia-Maryland Regional College of Veteri-

nary Medicine, Virginia Polytechnic Institute and State University, Duck Pond Drive, Blacksburg,
VA 24061-0442, USA
E-mail address: abbottj@vt.edu

Vet Clin Small Anim 40 (2010) 685–700

doi:10.1016/j.cvsm.2010.04.004 vetsmall.theclinics.com
0195-5616/10/$ – see front matter ª 2010 Elsevier Inc. All rights reserved.
686 Abbott

this entity.14 Tilley and Liu proposed the possibility that feline HCM might represent
a model of the human disease in 1980, and the echocardiographic features of feline
myocardial disease were defined later during that decade.15,16

ETIOPATHOGENESIS

It is now established that HCM in human beings is a genetic disease.8,17 Several

hundred distinct genetic mutations have been associated with HCM; genetic testing
together with pedigree analyses have demonstrated that these mutations are casually
related to the HCM phenotype.18–20 Although exceptions have recently been identi-
fied, causative mutations primarily affect genes that encode proteins that are incorpo-
rated into the contractile elements, or sarcomeres, of the myocyte.21
Among feline patients, familial occurrence of HCM has been observed in mix-breed,
Persian and American shorthair cats, and a mutation responsible for HCM in Maine
coon cats has been identified.3,22–24 The occurrence of HCM in Maine coon cats lack-
ing this mutation has been reported, suggesting that other causative mutations exist in
the gene pool of this breed or that there is a nongenetic cause of HCM in some Maine
coon cats. A genetic mutation associated with HCM in ragdoll cats also has been
recently identified.4 Although other etiologic factors cannot be excluded, available
evidence suggests that feline HCM probably has a genetic basis.
The precise mechanism by which genetic mutations lead to the development of
hypertrophy has not been established. It is thought that altered sarcomeric proteins
are responsible for myofiber dysfunction. Indeed, there are data acquired from in vitro
investigations that provide evidence of diminished contractile function in HCM despite
the finding that most affected patients have normal or enhanced ventricular
emptying.25,26 Why impaired systolic myocardial function should result in compensa-
tory hypertrophy has not yet been determined. Activation of signaling pathways asso-
ciated with trophic factors, such as angiotensin II, aldosterone, and insulin-like growth
factor, may ultimately be responsible for the development of hypertrophy.27,28
In human beings with HCM, the phenotypic expression of causative mutations is
highly diverse. The pathogenic potential of the various mutations is variable, but other
factors also determine the consequences of abnormal genotype. Indeed, family
members that share a causative mutation may differ markedly in clinical outcome
and severity of myocardial hypertrophy.20 It is likely that variable genetic expressivity
observed in human HCM is related to factors that include the pathogenic heteroge-
neity of causative mutations; the presence of genetic co-modifiers; and epigenetic
influences, possibly including the environment.20 It is possible that feline HCM shares
these features and, despite considerable progress, more complete characterization of
this disease will therefore present challenges.

EPIDEMIOLOGY

Population characteristics of feline HCM have been retrospectively evaluated.29,30 A

sex predisposition for males is consistent and the mean age at diagnosis is close to
6 years.29–31 Despite the fact that these data were obtained from referral populations,
a substantive proportion, between 33% and 55%, were subclinical (asymptomatic)
when the disease was identified.29–31 One of these investigations identified the admin-
istration of corticosteroids as a historical antecedent to the development of heart
failure.30 The association between administration of glucocorticoids and development
of heart failure in cats was also addressed in a separate retrospective investigation.32
The design of the latter study does not allow conclusions regarding causality, but
evidence was provided demonstrating that the development of heart failure
 Feline Hypertrophic Cardiomyopathy 687

associated with glucocorticoid administrations is a distinct clinical entity; specifically,

patients that survive acute decompensation may have improved survival relative to
cats that have not received glucocorticoids.32
Disease prevalence and identification of physical findings that represent markers of
disease have been the focus of recent investigations.33–36 Most studies have used
a cross-sectional or retrospective study design, and therefore inferences regarding
the causes of HCM are limited. However, prevalence (the instantaneous disease
burden of a population) is potentially useful because it provides an a priori or pretest
probability of disease in specific populations. This information has clinical relevance
because it has a bearing on potential value of diagnostic screening and the interpre-
tation of diagnostic tests.
The prevalence of cardiac murmurs in a sample of 103 cats recruited for participa-
tion in a blood donor program in New England was reported to be 21%.33 Cats
included in this investigation were between 1 and 9 years of age and, in the opinion
of the pet owner, healthy. Murmurs were generally of low intensity and, in some
cats, the intensity of murmurs varied in association with changes in heart rate. Quan-
titative echocardiographic variables were not reported but left ventricular hypertrophy
or equivocal septal hypertrophy was identified in six of the seven cats that were echo-
cardiographically examined. Systemic arterial blood pressure was not reported so it is
possible that hypertrophy identified during this study was associated with systemic
disease and did not reflect HCM.
Of 42 healthy purebred Maine coon cats subject to screening examinations in
Scandinavia, only one had a cardiac murmur.34 And indeed, this murmur was
thought to be associated with pregnancy because it was not identified during
reexamination performed after queening. Echocardiographic evidence of LVH
was detected in 9.5% of these 42 cats. Reported follow-up data for some of these
cats provide indirect evidence that noncardiac disorders were not responsible for
the finding of LVH but blood pressure was not determined. Two cats that did not
have LVH had echocardiographic evidence of systolic anterior motion of the mitral
valve (SAM) suggesting an incipient or variant form of HCM. When these cats
were included in the affected group, the prevalence of echocardiographic findings
compatible with HCM was 14.3%.
Echocardiographic data obtained during pre-breeding evaluation of purebred cats
thought to be at risk for heritable heart disease have also been retrospectively evalu-
ated.35 Of 144 cats, the majority were Maine coon cats but sphinx, British shorthair,
Bengal, and Norwegian forest cats were also represented. Physical examination find-
ings were not reported but echocardiographic evidence of HCM was detected in 8.3%
of the cohort. In a recent investigation, the results of which have been presented in
abstract form but not yet published, 34% of 199 apparently healthy cats had murmurs
during at least one examination. Of cats with murmurs that were subject to echocar-
diographic examination, 50% had left ventricular hypertrophy.37
The author and colleagues recently reported the results of a community-based
echocardiographic survey of apparently healthy cats.36 One hundred three healthy
cats were recruited from the pet-owning population of a veterinary college in the
Southeastern United States. The echocardiographer was unaware of the physical find-
ings and subjects with noncardiac disorders, including systemic hypertension and
hyperthyroidism, were excluded. Of 103 cats, 16% had cardiac murmurs while at
rest, during routine auscultatory examination. Dynamic auscultation was also per-
formed during this study; the prevalence of murmurs in cats subject to a provocative
maneuver that consisted of lifting the cat quickly in the air, was 27%. Of cats that had
a murmur during dynamic auscultation, 46% did not have a murmur during routine
688 Abbott

auscultation. HCM was echocardiographically identified in 15% of the study popula-

tion, but of cats with HCM, only 33% had heart murmurs.
The echocardiographic criteria used for diagnosis of HCM in this study are relevant to
interpretation of the results. Two-dimensional echocardiography, not M-mode, was
exclusively used for evaluation of ventricular wall thickness. Systematic quantitative
assessment of wall thickness was made in short- and long-axis images. HCM was iden-
tified when any region of the left ventricular wall was equal to or exceeded 6 mm at end
diastole. This method is apt to be more sensitive than the use of M-mode echocardiog-
raphy for identification of hypertrophy. The majority of affected cats had mild and
segmental hypertrophy and none had atrial enlargement. The diagnostic criteria used
in this study were based on those that have been used for identification of HCM in
humans and similar to those used in a published veterinary investigation.31,38 The prev-
alence was seemingly high, but it is consistent with current understanding, as it is now
accepted that HCM in humans is a disease that has a broad spectrum of phenotypic
expression, occurs in a subclinical form, and is not inevitably associated with progres-
sion and poor outcome. To place the findings in perspective, the prevalence of HCM
characterized by diffuse hypertrophy or marked SAM was 4%.
The various reported estimates of murmur and disease prevalence likely differ
because of geographic variability and differences in methodology. However, it is clear
that cardiac murmurs are often detected in apparently healthy cats, that murmurs in
cats vary in intensity in association with environmental stimuli, and that the finding
of a cardiac murmur is not consistently associated with echocardiographic abnormal-
ities. The prevalence of mild, subclinical HCM in cats is probably close to 15%. HCM is
the most common genetic heart disease in humans and has a reported prevalence of
0.2%.38 Based on available data, the prevalence of HCM in cats is considerably
higher, but this is credible if it is accepted that clinical signs are not the inevitable
consequence of this disease. In humans, clinically evident HCM is rare.8,39,40 In
contrast, feline HCM is the disease most commonly responsible for heart failure in
this species. In clinical studies that have evaluated biomarkers in feline subjects
with respiratory distress, more than 50% of subjects with heart failure had
HCM.41,42 When echocardiographic case records are considered independent of clin-
ical signs, HCM is identified in approximately 30% of patients.43

PATHOPHYSIOLOGY OF HYPERTROPHIC CARDIOMYOPATHY

Diastolic Dysfunction
It has generally been accepted that diastolic dysfunction is the pathophysiologic
mechanism that is primarily responsible for the clinical manifestations of HCM. That
systolic function contributes prominently to cardiac performance is readily evident
but the importance of diastolic function is less obvious. Diastolic function (the ability
of the ventricle to fill at low pressure) is complex but depends on the energy-depen-
dent process of myocardial relaxation and mechanical properties of the ventricle
that determine chamber stiffness. In most patients with HCM, global systolic perfor-
mance is normal or hyperdynamic but delayed myocardial relaxation and diminished
ventricular compliance potentially result in elevated filling pressures when ventricular
volumes are normal or small.43 Rises in ventricular filling pressures can result in pulmo-
nary venous congestion and edema. Chronic elevation of ventricular filling pressures
contributes atrial enlargement.
Dynamic Left Ventricular Outflow Tract Obstruction
The phenomenon of dynamic left ventricular outflow tract (LVOT) obstruction (LVOTO)
has generated considerable interest and has been a subject of debate. Usually
 Feline Hypertrophic Cardiomyopathy 689

dynamic, as opposed to fixed or anatomic, obstruction of left ventricular outflow results

from systolic motion of the mitral valve leaflets toward the interventricular septum
(IVS).17,31 Because the IVS represents the anterior boundary of the subvalvular LVOT
and because of the parallel anatomic arrangement of left ventricular inflow and outflow,
the displaced leaflets cause a mechanical impediment to ventricular ejection. As
a consequence, a systolic pressure gradient develops across the LVOT. Mitral valve
regurgitation usually accompanies SAM because the abnormal orientation of the valve
apparatus results in incomplete leaflet apposition during systole (Fig. 1). The cause of
SAM has been the subject of considerable speculation. The notion that SAM was a result
of the Venturi effect was initially favored.44 Venturi forces develop when narrowing of
a conduit results in the acceleration of flow and the development of a pressure gradient.
In the context of HCM, the development of lower systolic pressures distal to the site of
leaflet-septal apposition results in lift, or Venturi, forces that act perpendicular to flow,
pulling the mitral leaflets toward the septum. More recently it has been recognized that
SAM may begin in early systole, even before ejection, at a time when Venturi forces are
apt to be negligible.45 Current evidence suggests that the hydrodynamic pushing force,
or drag, is primarily responsible for anterior movement of the leaflets.44 Abnormal
geometry of the mitral valve apparatus, with or without structural abnormalities, likely
plays a predisposing role. In fact, in a canine model, experimental displacement of
the left ventricular papillary muscles toward the geometric center of the ventricle results

Fig. 1. Echocardiographic images obtained from a cat with hypertrophic cardiomyopathy.

Left ventricular outflow tract obstruction and mitral valve regurgitation caused by systolic
anterior motion of the mitral valve are evident. (A) Systolic right parasternal long-axis image
that includes the left ventricular outflow. Arrow indicates point of mitral leaflet-septal
contact. (B) M-mode image of the mitral valve. Arrow indicates point of mitral leaflet-septal
contact. (C) Systolic right parasternal long-axis image that includes the left ventricular
outflow with superimposed color Doppler map; there is caudally detected jet of mitral valve
regurgitation. Disturbed flow is evident within the subvalvular left ventricular outflow tract.
(D) Continuous-wave Doppler spectrogram of the left ventricular outflow tract. The peak
velocity exceeds 3 ms/s. There is late-systolic acceleration, which provides evidence of
dynamic obstruction.
690 Abbott

in SAM.46 It is probable that the cause of SAM is multifactorial. Abnormalities of the

mitral apparatus that result in chordal laxity together with hyperdynamic systolic perfor-
mance result in a substrate in which drag forces cause anterior displacement of the
mitral valve leaflets. SAM is not an intrinsic feature of HCM and has been observed in
other clinical and experimental scenarios in which there is absolute or relative redun-
dancy of the mitral leaflets or chordae in the setting of hyperdynamic systolic perfor-
mance.47 Therefore, echocardiographic identification of SAM is not necessarily
a specific echocardiographic marker of feline HCM but in most cases, it is finding
that is highly suggestive of the diagnosis. It is clinically relevant that the tendency to
develop SAM is load dependent and highly labile. Decreases in preload and afterload,
and increases in contractile state can all induce or augment SAM in susceptible individ-
uals. As a result, the pressure gradient and resulting heart murmur associated with SAM
can vary markedly during brief time intervals.
The clinical importance of SAM has been debated, and indeed whether or not SAM
results in actual obstruction was once questioned.48 It is now accepted that SAM not
only results in a systolic pressure gradient across the LVOT but also causes an imped-
iment to ventricular ejection.8 The pathophysiologic consequences of this obstruction
are reported to include increased wall stress.8,49 Wall stress, or the tension borne by
the ventricle, is determined by intracavitary pressure, chamber volume, and wall thick-
ness; it is directly proportional to the first two factors and inversely related to the last.
The prevalence of asymmetrical ventricular geometry in patients with HCM makes it
difficult to accurately define global wall stress and unsurprisingly, there are few
reported, relevant data. However, in one study of human patients with HCM, global
wall stress was not different when patients with obstructive and nonobstructive
HCM were compared.50 It is relevant that the supraphysiologic intraventricular pres-
sures in HCM develop during late systole. During this phase of the cardiac cycle,
ventricular wall thickness and radius are high and low, respectively, which are factors
that limit the development of high wall stress.
As increase in wall thickness can serve to normalize wall stress, and therefore, even
if wall stress is not increased in patients with HCM, the pressure gradient resulting
from SAM might be an additional stimulus for hypertrophy. Indeed there are observa-
tional data obtained from cohorts of human subjects with obstructive HCM who have
been subject to surgical treatment that decreases systolic pressure gradient that
suggest regression of hypertrophy.51 Still, it is difficult to reconcile the notion of
SAM as a cause of hypertrophy with the prevalence of asymmetric septal hypertrophy
in people with HCM. Presumably, if SAM were the cause of hypertrophy it would affect
the free wall and septum equally.50
Structural and functional coronary artery abnormalities are associated with HCM.
Intramural coronary arteries are narrowed because of medial hypertrophy and,
although there are inconsistencies in the published literature, perfusion abnormalities
have been associated with pressure gradients across the LVOT.52–55
The presence of dynamic LVOTO in human patients with HCM has been associated
with poor outcome and particularly with sudden unexpected death.49 This association,
however, has been questioned.56 The risk for poor outcome reported in one influential
publication was not statistically related to magnitude of pressure gradient. Instead, it
was simply the presence of obstruction at rest (treated as a yes/no binary variable) that
was associated with poor outcome.49 When this is considered in light of the marked
lability of pressure gradient in human HCM (a day-to-day change of as much as 32
mmHg can apparently reflect random variation) and the prevalence of LVOTO in
human beings that are subject to provocations, including exercise, it raises questions
regarding the association between LVOTO and poor prognosis.56–59
 Feline Hypertrophic Cardiomyopathy 691

Ultimately, uncertainty persists. SAM is undoubtedly the cause of LVOTO obstruction

and mitral valve regurgitation, abnormalities that may be responsible for rises in filling
pressures, altered coronary perfusion, and therefore perhaps the development of
myocardial fibrosis. Furthermore, in human beings, clinical signs that are not responsive
to medical therapy and are associated with LVOTO are successfully treated by surgery.8
Still, it is possible that resting obstruction is a confounding variable that is associated with
malignant phenotype but is not the proximate cause of mortality. Although inherently
limited by the retrospective nature of the observations, it is interesting that SAM in feline
patients has been associated with better rather than worse survival.30,31 In the cat, the
effect of obstruction on clinically relevant end points, including morbidity and mortality,
is unclear and the suitability of SAM as therapeutic target can therefore be debated.

CLINICAL PRESENTATION

Feline HCM is usually identified when auscultatory findings, such as arrhythmias,

gallop sounds, or murmurs, are incidentally detected during routine veterinary exam-
inations or when clinical signs result from heart failure or embolism.29,30 In a few
affected cats, sudden unexpected death is the first clinical manifestation of the
disease. Respiratory distress related to pulmonary edema or sometimes, pleural effu-
sion, is the most common clinical manifestation of heart failure in feline HCM. Clinical
signs of feline heart failure typically have a sudden onset and, in contrast to canine
patients with heart failure, cough is rarely observed. In some cats with heart failure,
clinical signs of low cardiac output, including hypothermia and pre-renal azotemia
are observed. In cats, tachycardia is not consistently associated with heart failure
and in some cases, bradycardia is evident.
Murmurs in patients with HCM have been associated with SAM, which results in
LVOTO and mitral regurgitation (MR), as well as with MR caused by hypertrophic
remodeling and distortion of the mitral apparatus.43 It appears that murmurs in cats
with or without cardiomyopathy are commonly associated with dynamic and labile
phenomena. Fairly often, the intensities of murmurs heard in cats vary from moment
to moment. The lability of SAM no doubt accounts for this observation in some
cats. Additionally, dynamic right ventricular outflow tract obstruction has been identi-
fied as a cause of murmurs in healthy cats and cats with noncardiac disease.60 In an
echocardiographic survey of apparently healthy cats, the prevalence of cardiac
murmurs was 16%, of which only 31% had echocardiographically identified structural
heart disease.36 However, the Doppler finding of late-systolic acceleration of either
right or left ventricular outflow in apparently healthy cats was statistically associated
with the finding of a murmur independent of the presence of structural heart disease.
Some cats had late-systolic acceleration that was anatomically localized to the prox-
imal LVOT. Dynamic mid-LVOT obstruction perhaps related to sympathetic activation,
but not obviously associated with HCM, may therefore cause murmurs in some cats
that do not have structural cardiac disease. The statistical association between
murmurs and late-systolic acceleration of ventricular ejection was stronger when
provoked murmurs were included in the analysis.36 Auscultation and echocardiog-
raphy were performed by different examiners at different times so the association is
not necessarily causal, but it is plausible that sympathetic activation causes dynamic
outflow tract obstruction that explains some apparently physiologic feline murmurs.
Echocardiography
Feline HCM has been echocardiographically defined by end-diastolic measurements
of ventricular wall thickness that equal or exceed 6 mm.31 Hypertrophy is commonly
692 Abbott

asymmetric and in Maine coon cats with HCM, it is often the left ventricular posterior
wall and papillary muscles that are most affected.61 Ejection phase indices of left
ventricular systolic performance such as %fractional shortening are usually normal
or reflect hyperdynamic ventricular emptying. Left atrial size in cats with HCM is gener-
ally greater than in healthy cats, but left atrial enlargement is not an intrinsic feature of
the disease nor required for its diagnosis.62 However, left atrial size is a surrogate
measure of hemodynamic burden and left atrial enlargement has been associated
with poor outcome in people and cats with HCM.30,63 Furthermore, left atrial enlarge-
ment is a clinically important finding and is almost always present when clinical signs
of respiratory distress result from feline myocardial disease. As previously described,
SAM is commonly identified in cats with HCM and associated with SAM are Doppler
findings of a labile, late-systolic pressure gradient across the LVOT and usually
concurrent MR.
Progressive decline in systolic myocardial function is observed in some affected
cats and presumably this is caused by ischemia related to small vessel disease or
LVOTO.64 Feline myocardial disease sometimes defies simple classification even after
echocardiographic examination. Indeed, some examples of unclassified cardiomyop-
athy may represent progression of long-standing HCM. Restrictive cardiomyopathy
(RCM) is generally considered to be a distinct disorder, which is characterized by atrial
enlargement in association with normal, or nearly normal, ventricular wall thickness.
Although some forms of RCM may represent the sequela of endomyocardial fibrosis,
it is interesting that a restrictive phenotype has been documented in people who have
sarcomeric mutations that are known to result in HCM.65
Early echocardiographic descriptions suggested that outflow tract obstruction was
infrequently observed in feline HCM.16 However, more recent data suggest that the
prevalence is as high as 67%.31 This figure is considerably higher than that reported
from humans in which approximately 30% of the those affected manifested LVOT
obstruction at rest.59 However, current data suggest that the classification of obstruc-
tive and non-obstructive HCM may represent a false dichotomy. When human
subjects with HCM are echocardiographically evaluated immediately after exercise
or after provocations known to induce LVOTO, the proportion of those subjects that
have obstruction exceeds 60%.59,66,67 It is clear that the phenomenon of SAM is labile
and highly dependent on functional state. The high prevalence of SAM in cats might
reflect sympathetic activation associated with a ‘‘white-coat effect’’ in hospitalized
cats; in a sense all echocardiographic examinations of non-sedated cats are per-
formed in a state that is analogous to that immediately after exercise.

SCREENING FOR HCM

Recent interest in the epidemiology of feline heart disease raises questions regarding
screening for this disease. The cost-benefit ratio of screening for clinically occult
disease is favorable if an affordable test can identify a disease that is serious and treat-
able. Feline HCM, in its severe form, is undoubtedly serious and is clearly an important
cause of morbidity and mortality in cats. Unfortunately, there is little known of the
natural history of feline HCM; the rate at which subclinical HCM progresses to a clinical
stage and indeed, the proportion of subclinically affected patients that ultimately
develop clinical signs is not known. There is also little known regarding the efficacy
of treatment for HCM. Several therapeutic strategies intended to prevent the develop-
ment of congestion and the occurrence of embolism have been employed but none
systematically evaluated. For purebred cats with a known or presumed genetic basis
for HCM, screening can be justified because genetic counseling might reduce the
 Feline Hypertrophic Cardiomyopathy 693

prevalence of disease in specific populations. The question of screening for HCM

might also be relevant for populations subject to elective procedures, such as dental
cleaning, that require anesthesia.
In apparently healthy cats, auscultation is an insensitive diagnostic marker of HCM,
meaning that few cats with subclinical HCM have murmurs. The positive predictive
value of a test (the proportion of individuals that have the disease among those that
have a positive test) is dependent on the prevalence of the disease. If the prevalence
of subclinical HCM is close to 15%, the positive predictive value of a murmur in appar-
ently healthy cats is only 31%. The negative predictive value of a cardiac murmur
might be more diagnostically useful; it can be anticipated that 87% of cats that do
not have murmurs do not have cardiomyopathy. In practical terms, echocardiographic
examination of outwardly healthy cats with heart murmurs is advisable, but it should
be recognized that many murmurs are apt to represent false positives; that is, echo-
cardiographic examination prompted by identification of a cardiac murmur will
disclose a sizable proportion of cats that are free of structural cardiac disease.
Echocardiographic screening, without regard to physical findings, for HCM can be
justified in populations subject to the development of familial HCM. Otherwise, the
cost of the examination might be excessive given the prevalence of the disease and
the lack of proven therapies. In the absence of a hypothetical and flawless molecular
or genetic test, there is no definitive, gold-standard test for HCM. Even postmortem
examination is likely to have diagnostic limitations given the interindividual variability
in cardiac mass among normal cats; the potential subjectivity of the examination; and
the fact that histologic abnormalities, such as myofiber disarray, are not necessarily
diffuse.68 Although the sensitivity and specificity of echocardiography for diagnosis
of HCM has not been evaluated, echocardiographic examination is, for all intents and
purposes, the gold standard. Even then, the accuracy of echocardiographic identifica-
tion of HCM depends on not only technical factors, including the experience of the
examiner, but also on the cut point of wall thickness that is used as the diagnostic crite-
rion. Many, but not all, clinical investigations of feline HCM have used an end-diastolic
wall thickness equal to or exceeding 6 mm as the primary diagnostic criterion.30,31,61
Provided metabolic and hemodynamic causes of hypertrophy are excluded, this
dimension (6 mm) likely represents a specific, but not necessarily sensitive, marker of
HCM. In fact, reference intervals defined by published normative echocardiographic
data have upper limits that are generally less than 5.5 mm and less than 5 mm for
two.43 The feline study that included the largest number of subjects suggests that
95% of healthy cats have septal and free wall dimensions that are less than 5.6
mm.69 Although it is not generally taken into account, end-diastolic ventricular wall
thickness is weakly related to body weight, which might be relevant to the evaluation
of exceptionally heavy cats. The results of studies of healthy Maine coon cats, a breed
which tends to have a large body size, refute this because unaffected individuals of this
breed have end-diastolic measurements of wall thickness that are similar to mixed-
breed cats.70 Indeed, statistical analysis of echocardiographic data obtained during
screening examinations of Maine coon cats suggests that 6 mm might be overly conser-
vative as a marker of ventricular hypertrophy. Evaluation of jackknife distances, which
statistically identify extreme observations or outliers, suggested the possibility that
a measurement of wall thickness that exceeds 5 mm is outside the normal range.34
Biomarkers, specifically B-type natriuretic peptide (BNP), have been evaluated as
screening strategies and this subject is more completely addressed in another article
by David J. Connolly elsewhere in this issue. Although differences in criteria used to
define the severity of HCM make the data difficult to interpret, the sensitivity of raised
BNP for the identification of subclinical HCM may be as high as 94% or even
694 Abbott

100%.71–73 However, sensitivity (the proportion of patients with the disease that have
a positive test) is an intrinsic feature of the test. In contrast, positive predictive value
is highly dependent on disease prevalence. Because of the dependence on preva-
lence, even a test with 95% sensitivity and 95% specificity has only a 77% positive
predictive value when prevalence is 15%. Because of this and other factors, the suit-
ability of BNP measurement as a screening test is uncertain at this time.74

THERAPY
Subclinical HCM
Optimally, it would be possible to identify patients that have a subclinical form of HCM
that is destined to worsen and to intervene in a way that would slow or prevent
progression of disease. Unfortunately, there is little known of the natural history of
feline HCM and as yet no published evidence that medical therapy can alter the course
of subclinical disease. The use of beta-blockers, such as atenolol, is often advocated
particularly in patients that have resting LVOTO, but the efficacy of this intervention
has not been determined. In cats, a causal relationship between LVOTO and poor
outcome has not been established, and as noted, retrospectively evaluated case
series have associated LVOTO with improved outcome in cats.30,31 However, the
latter argument must be viewed with circumspection. Cases of HCM associated
with LVOTO generally have murmurs and therefore are apt to be identified when
patients are subclinical. Furthermore, if progression to clinical disease is associated
with a decrease in systolic myocardial function, a notion for which there is some
evidence, cross-sectional or retrospective studies might associate poor outcome
with lack of LVOTO.75 The role of LVOTO is presently inconclusive. However, there
is evidence that beta-blockade may hasten the recurrence of pulmonary edema in
cats that have developed heart failure caused by HCM or RCM and, in the absence
of evidence to the contrary, this raises the possibility that beta-blockade might
harm cats with subclinical disease.76 The occurrence of pulmonary edema caused
by HCM is an objective marker that is a suitable inclusion criterion for clinical trials
but it is a factor without an established relationship to characteristics that might
predispose patients with HCM to adverse outcome in response to beta-blockade. If
beta-blockade does indeed harm cats that have developed edema, the absence of
data makes it impossible to determine precisely when, during the natural history of
HCM, patients are at risk for these adverse effects.
Because there are data that suggest a role for abnormal response to hormones in
the pathogenesis of HCM, the possibility that neuroendocrine modulating drugs might
favorably affect the natural history of the disease has been investigated.77,78 Evidence
obtained from studies of transgenic mice suggests that aldosterone may be relevant
to the pathogenesis of HCM insofar as spironolactone attenuates the development of
myocardial fibrosis and myofiber disarray.28 Based on these experimental findings,
there may be a role for the use of spironolactone in cats with cardiac disease.
However, relative to placebo, 4-months therapy with oral spironolactone did not alter
echocardiographic indices of diastolic function in a colony of Maine coon cats with
HCM.79 The same group also evaluated the effect of angiotensin-converting enzyme
inhibition.77 Maine coon cats with HCM but without heart failure were randomly
assigned to receive placebo or ramipril. Evidence that the circulating renin angiotensin
system was suppressed was presented, but despite this, echocardiographic and
magnetic resonance indices of myocardial mass and diastolic function were unaf-
fected. Given the genetic heterogeneity that probably exists in feline HCM, it is
possible that these agents or others might slow progression of HCM in other breeds
 Feline Hypertrophic Cardiomyopathy 695

of cats. And of course, it is possible that longer duration of therapy and the evaluation
of clinically relevant outcome measures, such as time to onset of heart failure or
mortality, might have disclosed benefit. At this time, however, evidence that medical
therapy favorably alters the course of subclinical feline HCM is lacking.
Heart Failure
Other than furosemide, for which efficacy is assumed, there are no medical interven-
tions that have demonstrated efficacy in the management of feline heart failure.
Attempts to improve diastolic function have been made through interventions that
are thought to speed myocardial relaxation or slow heart rate. Diltiazem is a calcium
channel blocker that has been widely used in the therapy of feline HCM. The effect
of diltiazem on heart rate is modest.80 However, there is evidence to suggest that
this drug has a positive lusitropic effect; that is, it improves ventricular filling through
a salutary effect on myocardial relaxation.81 The presumed favorable effects of
beta-blockers on diastolic function are primarily indirect and result from decreases
in heart rate. In an open-label clinical trial, the effects of diltiazem, propranolol, and
verapamil on cats with pulmonary edema caused by HCM were compared. Of the
three, diltiazem was the most efficacious.81 However, this trial did not include a nega-
tive control in the form of a placebo group. Ace inhibition has also been used in the
management of heart failure due to feline HCM.82 These drugs are apparently safe
and the concern that vasodilation due to ACE inhibition might result in adverse effects
related to worsening LVOTO may not be valid.82 However, conclusive evidence of effi-
cacy is lacking.
The results of a multicenter, randomized, placebo-controlled trial that had been
designed to evaluate the relative efficacy of atenolol, diltiazem, and enalapril in feline
patients with congestive heart failure caused by HCM or RCM have been presented at
a national meeting, but not yet published.76 The primary outcome variable was time
until recurrence of congestive signs and none of the agents was superior to placebo
in this regard. Patients that received enalapril remained in the trial longer than those
receiving the alternatives, although this result was not statistically significant. Patients
receiving atenolol fared less well than did those in the placebo group.83 The finding
that atenolol may harm cats with pulmonary edema was possibly unexpected but is
consistent with the result of the only comparable study in which administration of
propranolol was associated with decreased survival.81 Based on the results of the
aforementioned randomized clinical trial,76 the use of enalapril together with furose-
mide seems a reasonable approach to the management of feline patients with conges-
tive heart failure caused by diastolic dysfunction.

PROGNOSIS/NATURAL HISTORY

Survival data obtained from retrospective evaluation of teaching hospital records have
been reported by two groups of investigators.29,30 Survival times for the entire study
samples were similar for both studies and were close to 700 days. Median survival
times of 92 days and 563 days were reported for patients with heart failure. The retro-
spective nature of the studies makes it difficult to interpret these differences but it
seems that patients with heart failure in general, fare poorly. However, both groups
of investigators reported median survival for subclinical HCM that was in excess of
3 years.29,30
Much of the early clinical literature that relates to HCM in human beings originated
from a small number of tertiary, HCM centers and was therefore subject to referral
bias. This bias contributed to the notion that HCM was generally associated with an
696 Abbott

ominous prognosis.8 It is now recognized that human HCM is a disorder that exhibits
a broad spectrum of severity. In fact, in a recent review, human HCM was described as
a ‘‘relatively benign disease’’; the finding that survival times of non-selected cohorts
are similar to those of the general population supports this view.20 Little is known of
the natural history of feline HCM. However, it is possible that referral bias has similarly
shaped perception of this disease and it may be that the feline disorder is also char-
acterized by genetic heterogeneity and a broad spectrum of phenotypic expression
that includes mild, non-progressive disease and lethal variants that cause congestive
failure, embolism, and death.

REFERENCES

1. Maron BJ, Towbin JA, Thiene G, et al. Contemporary definitions and classification
of the cardiomyopathies: an American Heart Association Scientific Statement
from the Council on Clinical Cardiology, Heart Failure and Transplantation
Committee; Quality of Care and Outcomes Research and Functional Genomics
and Translational Biology Interdisciplinary Working Groups; and Council on
Epidemiology and Prevention. Circulation 2006;113:1807–16.
2. Thiene G, Corrado D, Basso C. Cardiomyopathies: is it time for a molecular clas-
sification? Eur Heart J 2004;25:1772–5.
3. Meurs KM, Sanchez X, David RM, et al. A cardiac myosin binding protein C muta-
tion in the Maine Coon cat with familial hypertrophic cardiomyopathy. Hum Mol
Genet 2005;14:3587–93.
4. Meurs KM, Norgard MM, Ederer MM, et al. A substitution mutation in the myosin
binding protein C gene in ragdoll hypertrophic cardiomyopathy. Genomics 2007;
90:261–4.
5. Richardson P, McKenna W, Bristow M, et al. Report of the 1995 World Health
Organization/International Society and Federation of Cardiology Task Force on
the Definition and Classification of cardiomyopathies. Circulation 1996;93:
841–2.
6. Maron BJ, McKenna WJ, Elliott P, et al. Hypertrophic cardiomyopathy. JAMA
1999;282:2302–3.
7. Maron BJ, Epstein SE. Hypertrophic cardiomyopathy: a discussion of nomencla-
ture. Am J Cardiol 1979;43:1242–4.
8. Maron BJ, McKenna WJ, Danielson GK, et al. ACC/ESC Clinical expert document
on hypertrophic cardiomyopathy: a report of American College of Cardiology
Foundation Task Force on Clinical Expert Consensus Documents and European
Society of Cardiology Committee for Practice Guidelines. J Am Coll Cardiol
2003;42:1687–713.
9. Roberts WC. Fifty years of hypertrophic cardiomyopathy. Am J Cardiol 2009;103:
431–4.
10. Buchanan J, Baker G, Hill J. Aortic embolism in cats: prevalence, surgical treat-
ment and electrocardiography. Vet Rec 1966;79:496–506.
11. Holzworth J. University of Pennsylvania Veterinary Extension Quarterly.
1958;151:101.
12. Liu SK. Acquired cardiac lesions leading to congestive heart failure in the cat. Am
J Vet Res 1970;31:2071–88.
13. Harpster N. Acquired heart disease in the cat. In: 40th Annual Meeting of the
American Animal Hospital Association. San Antonio (TX), April 8–13, 1973. South-
bend (IN): American Animal Hospital Association. p. 118.
14. Tilley L. Feline cardiology. Vet Clin North Am 1976;6:415–32.
 Feline Hypertrophic Cardiomyopathy 697

15. Liu SK, Tilley LP. Animal models of primary myocardial diseases. Yale J Biol Med
1980;53:191–211.
16. Moise NS, Dietze AE, Mezza LE, et al. Echocardiography, electrocardiography,
and radiography of cats with dilatation cardiomyopathy, hypertrophic cardiomy-
opathy, and hyperthyroidism. Am J Vet Res 1986;47:1476–86.
17. Maron BJ. Hypertrophic cardiomyopathy: a systematic review. JAMA 2002;287:
1308–20.
18. Jarcho JA, McKenna W, Pare JA, et al. Mapping a gene for familial hypertrophic
cardiomyopathy to chromosome 14q1. N Engl J Med 1989;321:1372–8.
19. Geisterfer-Lowrance AAT, Kass S, Tanigawa G, et al. A molecular basis for familial
hypertrophic cardiomyopathy: a [beta] cardiac myosin heavy chain gene
missense mutation. Cell 1990;62:999–1006.
20. Marian AJ. Hypertrophic cardiomyopathy: from genetics to treatment. Eur J Clin
Invest 2010;40:360–9.
21. Bos JM, Ommen SR, Ackerman MJ. Genetics of hypertrophic cardiomyopathy:
one, two, or more diseases? Curr Opin Cardiol 2007;22:193–9.
22. Kraus MS, Calvert CA, Jacobs GJ. Hypertrophic cardiomyopathy in a litter of five
mixed-breed cats. J Am Anim Hosp Assoc 1999;35:293–6.
23. Marin L, VandeWoude S, Boon J, et al. Left ventricular hypertrophy in a closed
colony of Persian cats [abstract]. J Vet Intern Med 1994;8:143.
24. Meurs KM, Kittleson MD, Towbin J, et al. Familial systolic anterior motion of the
mitral valve and/or hypertrophic cardiomyopathy is apparently inherited as an
autosomal dominant trait in a family of American shorthair cats. J Vet Intern
Med 1997;11:138.
25. Nicol RL, Frey N, Olson EN. From the sarcomere to the nucleus: role of genetics
and signaling in structural heart disease. Annu Rev Genomics Hum Genet 2000;
1:179–223.
26. Tardiff J. Sarcomeric proteins and familial hypertrophic cardiomyopathy: linking
mutations in structural proteins to complex cardiovascular phenotypes. Heart
Fail Rev 2005;10:237–48.
27. Roberts R, Sigwart U. Current concepts of the pathogenesis and treatment of
hypertrophic cardiomyopathy. Circulation 2005;112:293–6.
28. Tsybouleva N, Zhang L, Chen S, et al. Aldosterone, through novel signaling
proteins, is a fundamental molecular bridge between the genetic defect and
the cardiac phenotype of hypertrophic cardiomyopathy. Circulation 2004;109:
1284–91.
29. Atkins CE, Gallo AM, Kurzman ID, et al. Risk factors, clinical signs, and survival in
cats with a clinical diagnosis of idiopathic hypertrophic cardiomyopathy: 74
cases (1985–1989). J Am Vet Med Assoc 1992;201:613–8.
30. Rush JE, Freeman LM, Fenollosa NK, et al. Population and survival characteris-
tics of cats with hypertrophic cardiomyopathy: 260 cases (1990–1999). J Am
Vet Med Assoc 2002;220:202–7.
31. Fox PR, Liu S-K, Maron BJ. Echocardiographic assessment of spontaneously
occurring feline hypertrophic cardiomyopathy: an animal model of human
disease. Circulation 1995;92:2645–51.
32. Smith SA, Tobias AH, Fine DM, et al. Corticosteroid-associated congestive heart
failure in 12 cats. Int J Appl Res Vet Med 2004;2:159–70.
33. Cote E, Manning AM, Emerson D, et al. Assessment of the prevalence of heart
murmurs in overtly healthy cats. J Am Vet Med Assoc 2004;225:384–8.
34. Gundler S, Tidholm A, Haggstrom J. Prevalence of myocardial hypertrophy in a pop-
ulation of asymptomatic Swedish Maine coon cats. Acta Vet Scand 2008;50:22.
698 Abbott

35. Riesen SC, Kovacevic A, Lombard CW, et al. Echocardiographic screening of

purebred cats: an overview from 2002 to 2005. Schweiz Arch Tierheilkd 2007;
149:73–6.
36. Paige CF, Abbott JA, Pyle RL, et al. Prevalence of cardiomyopathy in apparently
healthy cats. J Am Vet Med Assoc 2009;234:1398–403.
37. Wagner T, Luis Fuentes V, McDermott N, et al. Association between cardiac
murmurs and left ventricular hypertrophy in 199 healthy adult cats. J Vet Intern
Med 2009;23:1332 [abstract #29].
38. Maron BJ, Gardin JM, Flack JM, et al. Prevalence of hypertrophic cardiomyop-
athy in a general population of young adults. Echocardiographic analysis of
4111 subjects in the CARDIA Study. Coronary Artery Risk Development in
(Young) Adults. Circulation 1995;92:785–9.
39. Goda A, Yamashita T, Suzuki S, et al. Prevalence and prognosis of patients with
heart failure in Tokyo: a prospective cohort of Shinken Database 2004–5. Int Heart
J 2009;50:609–25.
40. Maron BJ, Peterson EE, Maron MS, et al. Prevalence of hypertrophic cardiomyop-
athy in an outpatient population referred for echocardiographic study. Am J Car-
diol 1994;73:577–80.
41. Connolly DJ, Soares Magalhaes RJ, Fuentes VL, et al. Assessment of the diag-
nostic accuracy of circulating natriuretic peptide concentrations to distinguish
between cats with cardiac and non-cardiac causes of respiratory distress.
J Vet Cardiol 2009;11:S41–50.
42. Fox PR, Oyama MA, Reynolds C, et al. Utility of plasma N-terminal pro-brain natri-
uretic peptide (NT-proBNP) to distinguish between congestive heart failure and
non-cardiac causes of acute dyspnea in cats. J Vet Cardiol 2009;11:S51–61.
43. Fox P. Feline cardiomyopathies. In: Fox PR, Sisson D, Moise NS, editors. Textbook
of canine and feline cardiology: principles and practice. 2nd edition. Philadel-
phia: WB Saunders Co; 1999. p. 621–78.
44. Sherrid MV. Pathophysiology and treatment of hypertrophic cardiomyopathy.
Prog Cardiovasc Dis 2006;49:123–51.
45. Sherrid MV, Gunsburg DZ, Moldenhauer S, et al. Systolic anterior motion begins
at low left ventricular outflow tract velocity in obstructive hypertrophic cardiomy-
opathy. J Am Coll Cardiol 2000;36:1344–54.
46. Levine RA, Vlahakes GJ, Lefebvre X, et al. Papillary muscle displacement causes
systolic anterior motion of the mitral valve. Experimental validation and insights
into the mechanism of subaortic obstruction. Circulation 1995;91:1189–95.
47. Paige CF, Abbott JA, Pyle RL. Systolic anterior motion of the mitral valve associ-
ated with right ventricular systolic hypertension in 9 dogs. J Vet Cardiol 2007;9:
9–14.
48. Maron BJ, Maron MS, Wigle ED, et al. The 50-year history, controversy, and clin-
ical implications of left ventricular outflow tract obstruction in hypertrophic cardio-
myopathy: from idiopathic hypertrophic subaortic stenosis to hypertrophic
cardiomyopathy. J Am Coll Cardiol 2009;54:191–200.
49. Maron MS, Olivotto I, Betocchi S, et al. Effect of left ventricular outflow tract
obstruction on clinical outcome in hypertrophic cardiomyopathy. N Engl J Med
2003;348:295–303.
50. Blanksma PK. Is regional wall stress a stimulus for myocardial hypertrophy in
hypertrophic cardiomyopathy? Z Kardiol 1987;76(Suppl 3):57–60.
51. Deb SJ, Schaff HV, Dearani JA, et al. Septal myectomy results in regression of left
ventricular hypertrophy in patients with hypertrophic obstructive cardiomyopathy.
Ann Thorac Surg 2004;78:2118–22.
 Feline Hypertrophic Cardiomyopathy 699

52. Knaapen P, Germans T, Camici PG, et al. Determinants of coronary microvascular

dysfunction in symptomatic hypertrophic cardiomyopathy. Am J Physiol Heart
Circ Physiol 2008;294:H986–993.
53. Celik S, Dagdeviren B, Yildirim A, et al. Comparison of coronary flow velocities
between patients with obstructive and nonobstructive type hypertrophic cardio-
myopathy: noninvasive assessment by Transthoracic Doppler Echocardiography.
Echocardiography 2005;22:1–7.
54. Maron MS, Olivotto I, Maron BJ, et al. The case for myocardial ischemia in hyper-
trophic cardiomyopathy. J Am Coll Cardiol 2009;54:866–75.
55. Liu SK, Roberts WC, Maron BJ. Comparison of morphologic findings in spontane-
ously occurring hypertrophic cardiomyopathy in humans, cats and dogs. Am J
Cardiol 1993;72:944–51.
56. Efthimiadis GK, Parcharidou DG, Giannakoulas G, et al. Left ventricular outflow
tract obstruction as a risk factor for sudden cardiac death in hypertrophic cardio-
myopathy. Am J Cardiol 2009;104:695–9.
57. Kizilbash AM, Heinle SK, Grayburn PA. Spontaneous variability of left ventricular
outflow tract gradient in hypertrophic obstructive cardiomyopathy. Circulation
1998;97:461–6.
58. Geske JB, Sorajja P, Ommen SR, et al. Left ventricular outflow tract gradient vari-
ability in hypertrophic cardiomyopathy. Clin Cardiol 2009;32:397–402.
59. Maron MS, Olivotto I, Zenovich AG, et al. Hypertrophic cardiomyopathy is
predominantly a disease of left ventricular outflow tract obstruction. Circulation
2006;114:2232–9.
60. Rishniw M, Thomas WP. Dynamic right ventricular outflow obstruction: a new
cause of systolic murmurs in cats. J Vet Intern Med 2002;16:547–52.
61. Kittleson MD, Meurs KM, Munro MJ, et al. Familial hypertrophic cardiomyopathy
in Maine coon cats: an animal model of human disease. Circulation 1999;99:
3172–80.
62. Abbott JA, MacLean HN. Two-dimensional echocardiographic assessment of the
feline left atrium. J Vet Intern Med 2006;20:111–9.
63. Nistri S, Olivotto I, Betocchi S, et al. Prognostic significance of left atrial size in
patients with hypertrophic cardiomyopathy (from the Italian registry for hypertro-
phic cardiomyopathy). Am J Cardiol 2006;98:960–5.
64. Fox PR. Hypertrophic cardiomyopathy. Clinical and pathologic correlates. J Vet
Cardiol 2003;5:39–45.
65. Kubo T, Gimeno JR, Bahl A, et al. Prevalence, clinical significance, and genetic
basis of hypertrophic cardiomyopathy with restrictive phenotype. J Am Coll Car-
diol 2007;49:2419–26.
66. Nishimura RA, Ommen SR. Hypertrophic cardiomyopathy: the search for
obstruction. Circulation 2006;114:2200–2.
67. Shah JS, Esteban MT, Thaman R, et al. Prevalence of exercise-induced left
ventricular outflow tract obstruction in symptomatic patients with non-obstructive
hypertrophic cardiomyopathy. Heart 2008;94:1288–94.
68. Liu S-K, Maron BJ, Tilley LP. Feline hypertrophic cardiomyopathy: gross anatomic
and quantitative histologic features. Am J Pathol 1981;102:388–95.
69. Sisson DD, Knight DH, Helinski C, et al. Plasma taurine concentrations and M-
mode echocardiographic measures in healthy cats and in cats with dilated
cardiomyopathy. J Vet Intern Med 1991;5:232–8.
70. Drourr L, Lefbom BK, Rosenthal SL, et al. Measurement of M-mode echocardio-
graphic parameters in healthy adult Maine Coon cats. J Am Vet Med Assoc 2005;
226:734–7.
700 Abbott

71. Connolly DJ, Soares Magalhaes RJ, Syme HM, et al. Circulating natriuretic
peptides in cats with heart disease. J Vet Intern Med 2008;22:96–105.
72. Wess G, Daisenberger P, Hirschberger J, et al. The utility of NT-proBNP to detect
early stages of hypertrophic cardiomyopathy in cats and to differentiate disease
stages. J Vet Intern Med 2009;23:687 [abstract 9].
73. Fox PR, Oyama MA, MacDonald KA, et al. Assessment of NT proBNP concentra-
tion in asymptomatic cats with cardiomyopathy. J Vet Intern Med 2008;22:759
[abstract 191].
74. Hsu A, Kittleson MD, Paling A, Investigation into the use of plasma NT-proBNP
concentration to screen for feline hypertrophic cardiomyopathy. J Vet Cardiol
2009;11(Suppl 1):S63–70.
75. Baty CJ, Malarkey DE, Atkins CE, et al. Natural history of hypertrophic cardiomy-
opathy and aortic thromboembolism in a family of domestic shorthair cats. J Vet
Intern Med 2001;15:595–9.
76. Fox PR. Prospective, double-blinded, multicenter evaluation of chronic therapies
for feline diastolic heart failure: interim analysis [abstract]. J Vet Intern Med 2003;
17:398.
77. MacDonald KA, Kittleson MD, Larson RF, et al. The effect of ramipril on left
ventricular mass, myocardial fibrosis, diastolic function, and plasma neurohor-
mones in Maine Coon cats with familial hypertrophic cardiomyopathy without
heart failure. J Vet Intern Med 2006;20:1093–105.
78. Amberger CN, Glardon O, Glaus T, et al. Effects of benazepril in the treatment of
feline hypertrophic cardiomyopathy: results of a prospective, open-label, multi-
center clinical trial. J Vet Cardiol 1999;1:19–26.
79. MacDonald KA, Kittleson MD, Kass PH. Effect of spironolactone on diastolic func-
tion and left ventricular mass in Maine Coon cats with familial hypertrophic
cardiomyopathy. J Vet Intern Med 2008;22:335–41.
80. Johnson LM, Atkins CE, Keene BW, et al. Pharmacokinetic and pharmacody-
namic properties of conventional and CD-formulated diltiazem in cats. J Vet
Intern Med 1996;10(5):316–20.
81. Bright JM, Golden AL, Gompf RE, et al. Evaluation of the calcium channel-block-
ing agents diltiazem and verapamil for treatment of feline hypertrophic cardiomy-
opathy. J Vet Intern Med 1991;5:272–82.
82. Rush JE, Freeman LM, Brown DJ, et al. The use of enalapril in the treatment of
feline hypertrophic cardiomyopathy. J Am Anim Hosp Assoc 1998;34:38–41.
83. Fox PR. Newest developments: feline heart disease and management. In:
Proceedings of the North American Veterinary Conference. Orlando (FL),
January 17–21, 2004. Gainesville (FL): Eastern States Veterinary Association.
p. 133–5.
 ANESTHETIC MANAGEMENT OF SPECIFIC CARDIOVASCULAR DISEASES
Luisito S. Pablo, DVM, MS, DACVA
University of Florida, Gainesville, Florida

Small animal patients that need general anesthesia may have preexisting cardiovascular
diseases. To ensure oxygen delivery to the tissue, the cardiac output and oxygen content of the
blood should be optimized. Cardiac output is the product of stroke volume and heart rate.
Patients with cardiovascular diseases may have reduced cardiac output due to decreased stroke
volume. The determinants of stroke volume are preload, afterload, and myocardial contractility.
The hemodynamic goals for patients with cardiovascular diseases involve targeting these factors
with the ultimate objective of providing adequate cardiac output to the anesthetized patients.
The main objective of this presentation is to present the anesthetic management of
specific cardiovascular diseases. The cardiovascular conditions that will be discussed in this
presentation are the more commonly encountered problems in practice.

Dogs with Mitral Regurgitation (MR)

MR in dogs is due mainly to endocardiosis. The clinical consequences of mitral valve
endocardiosis are seen in elderly small-breed dogs. The anesthetic risk associated with MR
depends on its severity. Mild MR does not have hemodynamic consequence. Dogs with
untreated congestive heart failure will have the highest risk. Dogs being treated with an ACE
inhibitor and diuretics for congestive heart failure can be anesthetized but extreme care should be
taken. Anesthesia should not be performed in dogs with untreated congestive heart failure.
With MR, part of the left ventricular stroke volume is ejected through the incompetent
mitral valve into the left atrium. It creates a volume load on the left atrium and left ventricle
resulting in increased pressure in those chambers. With these increased pressures, the LA and LV
dilate and develop hypertrophy. Later in the disease process, the increased pressures will be
reflected back upon the pulmonary venous circulation and ultimately results in pulmonary
edema.
The hemodynamic goals for MR include: (1) reduce preload slightly to reduce regurgitant
flow (preload); (2) avoid acute increases in afterload; (3) maintain contractility; (4) avoid
bradycardia; (5) maintain sinus rhythm; and (6) do not increase myocardial oxygen requirement
by avoiding severe tachycardia and hypotension.
To accomplish the above mentioned goals, there are specific steps that can be done. Do
not overload the patient with fluids. Do not use fluid boluses to treat hypotension during
anesthesia. Fluid should be given at a lower rate of 3.0-5.0 ml/kg/hour. Those patients with
compensated CHF should receive fluid with lower sodium load like 2.5% dextrose and half-
strength LRS. Avoid sinus bradycardia. Maintain normal heart rate. Slight tachycardia is
acceptable. Atropine (0.02 mg/kg IV) or glycopyrrolate (0.01 mg/kg IV) should be given to
correct sinus bradycardia. Maintain myocardial contractility. Treat hypotension using beta-1
agonist like dobutamine or dopamine. Dobutamine and dopamine can be given at 5.0-10.0
μg/kg/min. Slight vasodilation is acceptable. Avoid peripheral vasoconstriction. Alpha2-agonists
should not be used in dogs with MR. Minimize excitement. Increased catecholamine release may
cause vasoconstriction.

452
Anesthetic Considerations
Premedication: Low dose of acepromazine is acceptable. This will reduce the afterload. It
will provide sedation and minimize catecholamine-induced dysrhythmias. It can be administered
at 0.01-0.02 mg/kg IM, SC. Opioids are indicated if there will be pain involved. Most opioids
maintain cardiac contractility. However, they may cause sinus bradycardia. An anticholinergic
(atropine or glycopyrrolate) can be added to the preanesthetic protocol if the patient has
preexisting bradycardia or if a relatively high dose of an opioid is used. The opioids that are
commonly used for premedication are morphine, hydromorphone, butorphanol, and
buprenorphine. These are the recommended dosages for the different opioids: (1) morphine: 0.2-
0.5 mg/kg IM, SC, (2) hydromorphone: 0.05-0.1 mg/kg IM, SC, (3) butorphanol: 0.2-0.4 mg/kg
IM, SC, and (4) buprenorphine: 0.01-0.02 mg/kg IM, SC. Benzodiazepines are acceptable
premedicants for MR. They produce minimal cardiopulmonary depression. They can produce
paradoxical agitation in dogs if given alone or with an opioid. Instead of sedation, the dog may
show restlessness and dysphoria. It is best to avoid the use of benzodiazepines in dogs that are
not depressed. Diazepam and midazolam are the two most commonly used benzodiazepines in
dogs. Midazolam is water soluble and can be administered IM, SC or IV. Diazepam is not water
soluble and when given IM will result in unpredictable absorption. These are the dosages for the
benzodiazepines: (1) diazepam: 0.2-0.4 mg/kg IV and (2) midazolam: 0.2-0.4 mg/kg IM, SC, IV.
Induction: Propofol is an acceptable choice for dogs with mitral regurgitation. It causes some
degree of vasodilation, which will be beneficial for this heart condition. When used in these
cases, it should be given slowly following premedication. The dose of propofol is 4.0 mg/kg IV;
half of the dose should be given over 40-60 seconds and the remaining dose is given to effect.
A combination of diazepam-ketamine or midazolam-ketamine can be used in MR. The
combination will result in transient sinus tachycardia. Ketamine, by itself, does not result in
significant increase in peripheral vascular resistance. Diazepam is given at 0.25 mg/kg IV and
ketamine at 5.0 mg/kg IV. Lower doses should be used in dogs that have profound sedation from
the premedicants and are depressed. Etomidate is the most heart-friendly induction agent.
However, it is still expensive. It is the drug of choice in patients with enlarged heart and showing
signs of congestive heart failure before presentation. The dose of etomidate is 0.5-1.0 mg/kg IV.
If etomidate is not available, a neuroleptanalgesic combination can be used. This combination
maintains myocardial function. Bradycardia may occur due to the opioid’s effect on the vagal
tone. Anticholinergic can be added to the protocol to prevent sinus bradycardia. The two most
common combinations used in practice are diazepam-hydromorphone and diazepam-fentanyl.
The doses for diazepam and hydromorphone are 0.25 mg/kg IV and 0.2 mg/kg IV, respectively.
When fentanyl is chosen, instead of hydromorphone, the dose is 10 ug/kg IV.
Maintenance: Anesthesia should be maintained with either isoflurane or sevoflurane.
Dogs that develop hypotension and tend not to respond to the positive inotrope should be
managed by “balancing” the anesthetic technique. A fentanyl CRI at 0.2-2 ug/kg/min can be
added to the inhalant administration. This will allow the use of the lower concentration of the
inhalant.
The drugs that need to be avoided in dogs with MR are xylazine, medetomidine,
dexmedetomidine, and phenylephrine (vasoconstrictor).
Postoperative: Provide external heat support. Hypothermia can result in increased oxygen
demand. Provide oxygen until the patient is ventilating adequately. Hypoventilation will result in
hypoxemia when breathing room air. Provide optimal recovery conditions. Minimize stress,
which can increase catecholamine release. Provide pain control when painful procedure is

453
performed. It is not recommended to give NSAID in patients with compensated congestive heart
failure.

Cats with Hypertrophic Cardiomyopathy

Many cats with hypertrophic cardiomyopathy may be asymptomatic. These cats can have
mild to severe left ventricular thickening. Cats with hypertrophic cardiomyopathy can live longer
than two years after a bout of pulmonary edema. Anesthesia should not be performed in cats with
definite signs of congestive heart failure due to hypertrophic cardiomyopathy.
Left ventricular myocardium thickens (concentric hypertrophy). This results in stiff
chamber. The basic problem in hypertrophic cardiomyopathy is the diastolic dysfunction of the
left ventricle. It is characterized by delayed or incomplete myocardial relaxation and reduced
compliance of the left ventricle. The stiff chamber leads to increased diastolic intraventricular
pressure and then left atrial enlargement. The increased pressure in left atrium will be transmitted
to the pulmonary veins and pulmonary edema will follow. Mitral regurgitation will develop as a
result of the distortional change in the mitral valve apparatus caused by the hypertrophy of the
left ventricle. In those cats with asymmetric hypertrophic cardiomyopathy, left ventricular
outflow obstruction can develop when the anterior leaflet of the mitral valve moves to contact
the septum during systole.
Hemodynamic goals for hypertrophic cardiomyopathy include: (1) maintain preload in
cats without congestive heart failure; (2) increase afterload, if possible; (3) do not increase
myocardial contractility; (4) maintain normal heart rate and avoid sinus tachycardia; (5) maintain
sinus rhythm; and (6) avoid increase in myocardial oxygen consumption. To accomplish these
goals, there are specific steps that should be considered. Adequate diastolic filling can be
accomplished by large ventricular volume and sinus rhythm. Increased contractility, reduced
afterload and preload will decrease the ventricular volume. Ketamine should be avoided because
it increases contractility and heart rate. It also increases the myocardial oxygen demand.
Acepromazine at the higher dose will cause vasodilation resulting in augmentation of the outflow
obstruction. Dysrhythmias should be controlled before anesthesia. Minimize stress and
excitement because of the catecholamine release that will increase heart rate and contractility.
The drugs (beta blocker or calcium channel blocker) being taken by the patient for hypertrophic
cardiomyopathy should be administered up to and including the day of anesthesia.

Anesthetic considerations
Premedication: Opioids are considered good choices because they have minimal effects on
myocardial contractility, preload and afterload. The opioids that are commonly used for
premedication are hydromorphone, morphine, methadone, butorphanol, and buprenorphine. The
premedicant doses for the opioids are as follows: hydromorphone (0.03-0.05 mg/kg IM SC),
morphine (0.1 mg/kg IM SC), methadone (0.1 mg/kg IM SC), butorphanol (0.2 mg/kg IM SC),
and buprenorphine: (0.01-0.02 mg/kg IM SC).
Benzodiazepines are also suitable for these cases. They produce minimal cardiopulmonary
depression. However, they can produce paradoxical agitation and restlessness in cats. To
minimize these side effects, midazolam or diazepam can be given with the IV induction agent.
Small amount of the induction agent is given first. The dose of midazolam or diazepam is given
next. The induction is completed with the primary induction agent given to effect. The dose for
diazepam and midazolam is 0.2-0.4 mg/kg. Diazepam is preferably given IV while midazolam
can be given by IM, SC, or IV route.

454
 Medetomidine has been shown to eliminate outflow tract obstruction in cats with dynamic
left ventricular outflow obstruction. The dose used in the study is 20 ug/kg IM. It appears that
medetomidine or now dexmedetomidine may be used in cats with HCM that are not amenable to
physical restraint during examination.
Induction: The use of propofol in cats with hypertrophic cardiomyopathy is debatable. There
is a study that showed that it impairs regional myocardial function in ischemic myocardium. It
also causes peripheral vasodilation. If used, it should be given very slowly and with a
benzodiazepine. The calculated dose is 4.0 mg/kg IV; half of the dose should be given over 40-
60 seconds and the remaining dose is given to effect.
Etomidate is the most heart-friendly induction agent. However, it is very expensive. It is the
author’s drug of choice in patients with enlarged heart and had shown signs of congestive heart
failure before presentation. The dose is 0.5-1.0 mg/kg IV. Half of the calculated dose is given as
a slow bolus and the rest of the dose given to effect.
Neuroleptanalgesic combination is another option in cats with HCM. The combination
maintains myocardial function. Diazepam and hydromorphone are given at 0.25 mg/kg IV and
0.2 mg/kg IV, respectively. The fentanyl can replace the hydromorphone and is given at 10 ug/kg
IV.
Mask induction using sevoflurane or isoflurane should be avoided because of the stress and
excitement associated with this induction method. The outflow obstruction will be worse because
of the increased heart rate and myocardial contractility due to the sympathetic stimulation.
The drugs that should be avoided are high to moderate dose of acepromazine, ketamine,
atropine, glycopyrrolate, and thiopental.
Maintenance: Anesthesia should be maintained with either isoflurane or sevoflurane. Cats
that develop hypotension should be managed by administering phenylephrine CRI at 1-5
μg/kg/min. It is advisable to avoid dobutamine and dopamine. A fentanyl CRI at 0.2-2
μg/kg/min can be added to the inhalant administration. This will allow the use of the lower
concentration of the inhalant.
The patient should be monitored closely during anesthesia. The monitoring tools should
include pulse oximetry, blood pressure measurement, capnography, ECG, and temperature
probe.
Postoperative: The measures taken postoperatively will minimize mortality and morbidity in
these cases. Provide external heat support. Hypothermia can result in increased oxygen demand.
Provide oxygen until the patient is ventilating adequately. Hypoventilation will result in
hypoxemia when breathing room air. Minimize stress, which can increase catecholamine release.
Provide pain control when painful procedure is performed. It is advisable not to give NSAID in
patients with compensated congestive heart failure.

Dilated cardiomyopathy (DCM)

DCM is common in large-breed dogs. The main concerns in this condition are the
reduction in myocardial contractility and dysrhythmias. The hemodynamic goals these patients
that need anesthesia include: (1) maintain preload, (2) avoid increases in afterload, (3) maintain
or increase contractility, (4) maintain normal heart rate, (5) control dysrhythmias, and (6) do not
increase myocardial oxygen requirement by avoiding severe tachycardia and hypotension. These
goals are almost similar to those set for mitral regurgitation. Therefore, a detailed discussion of
the management of DCM is not included in these notes.

455
References
Clutton RE: Cardiopulmonary disease, in Seymour C, Gleed R (eds): Manual of Small Animal
Anaesthesia and Analgesia. Kingsley House, UK, British Small Animal Veterinary Association,
1999, pp155-181
Skubas N, Lichtman AD, Sharma A, et al: Anesthesia for cardiac surgery, in Barash PG, Cullen
BF, Stoelting RK (eds): Clinical Anesthesia (ed 5). Philadelphia, PA, Lippincott Williams and
Wilkins, 2006, pp 886-973

456
ANESTESIA EN
CARDIOMIOPATIA
HIPERTROFICA FELINA

INTRODUCCION
• Engrosamiento CONCENTRICO del miocardio
• Relajación Alterada
• Disfunción DIASTOLICA
• IDIOPATICA o SECUNDARIA
• Consecuencias Hemodinámicas
• Aumento Presión Atrial
• Regurgitación
• Edema Pulmonar
• LVOT (Aumentos FC o Velocidad de Flujo)
• Trombos en atrio por estasis o TEP

GC = FC X VS
 MANEJO ANESTÉSICO
• Evaluación de acuerdo a SEVERIDAD
• Casos Subclínicos – poca relevancia hemodinámica

• Enfermedad LEVE, soplos y cambios estructurales menores podrían ser anestesiados con
diversas combinaciones de fármacos.
CONSIDERACION  Disociativos en Contexto de HTA es controversial…
AUMENTO estimulación simpática, FC, Contractilidad, Presión Arterial y trabajo
Cardiovascular , Consumo de O2 y LVOTO.
 MANEJO ANESTÉSICO

• OBJETIVO PRINCIPAL INDEPENDIENTE DE SEVERIDAD

OPTIMIZAR PERFUSION Y MINIMIZAR DEMANDA DE OXIGENO MIOCARDICO.

MANEJO ANESTÉSICO - PREMEDIACIÓN

• Opiodes
• Acepromacina Controversial – Efecto Dosis dependiente
• Agonistas Alfa2  Contraindicados?
• Benzodiazepinas
 MANEJO ANESTÉSICO - INDUCCION
• PROPOFOL
• ETOMIDATO
• FENTANILO – BENZODIAZEPINA
• CAJA CON ANESTESICOS INHALADOS
• KETAMINA ??

MANEJO DE HIPOTENSIÓN

• OPTIMIZACION DE FC Y RITMO ( Enfermedad leve vs grave – engrosamiento,

consumo y perfusión)
• CORRECCION DE CAM ADMINISTRADA
• FLUIDO TERAPIA Y VOLUMEN ( COLOIDES ??)
• INOTROPOS POSITIVOS??(consumo O2 – trabajo cardiaco - arritmogenicos)
• VASOPRESORES - Fenilefrina CRI at 1-5 μg/kg/min
 Anestesia en
Enfermedad
Valvular

Introducción
Enfermedad mas común en el perro

Mitral dentro del top 3 enfermedades en el gato

dMVD, la forma mas común en el perro, 30% de perros geriátricos

Endocardiosis, enfermedad degenerativa valvular, degeneración

mixomatosa

Incompetencia valvular e incluso prolapso hacia el atrio

REFLUJO
 Introducción

GC = FC X VS
 Evaluación Pre anestésica

Soplo?

No todos los pacientes con enfermedad cardiaca se tratan igual

Historia detallada (antigua y actual)

Exámenes de Sangre y Orina

Examen Físico

Radiografías de Tórax

ECG

Presión Arterial
Documentar enfermedad
Determinar el riesgo
 MANTENER
HOMEOSTASIS Y
PERFUSION TISULAR,
DO2 Y CORONARIA

Manejo Anestésico – Consideraciones Generales

Regurgitación
Mantener FC alta ?

GC = ↑FC X ↓VS Anticolinergicos ?

Opiodes ¡?

Control Hipotermia

GC = ↓ FC X VS
 Manejo Anestésico – Inducción
Pacientes Estables
Ketamina ??

Propofol ??

Gases ??

Agonistas alfa 2 ?? Regurgitación

Acepromacina??

Manejo Anestésico – Inducción

Pacientes Inestables
En riego Significativo de Insuficiencia Cardiaca
Congestiva o que hayan tenido eventos de Congestión
o Arritmias
• Requieren Estabilización Previa
Control de Hipotensión
Control de Arritmias
Control Edema Pulmonar

• Chequeo Cardiorespiratorio
Rx Tórax
Ecocardiografía
ECG
Presión Arterial
 Manejo Anestésico – Inducción
Pacientes Inestables
Objetivo Especifico : Evitar al Máximo los efectos Cardiodepresores de los
Agentes Inhalatorios

ANESTESIA BALANCEADA

Agonistas Alfa 2 ?
Opiodes ?
Benzodiacepinas ?
 Conceptos generales y
Fisiología Cardiovascular
Aplicada a la Anestesia
de Cardiopatas Dr. Paulo Mallea V.
Dipl. Anestesia y Cuidados Intensivos
Cert FCCS – Cert ABCtrauma

Introducción
• Función Sistema Cardiovascular

• Entonces ¿ Enfermedad Cardiovascular ?

• Drogas Anestésicas - Mecanismos de acción – DO2

• Metas en Anestesia Cardiovascular

Entender Mecanismos Fisiológicos y Fisiopatológicos
Mecanismos de Acción de Fármacos
Soporte del Paciente
Herramientas de Monitorización
 Fármacos

Fisiopatología

¿ Se Puede Predecir lo que ocurrirá con nuestro Paciente ?

Introducción – Riesgo Anestésico
Clasificación ACVIM
cardiopatías

Introducción – Riesgo Anestésico

Introducción – Riesgo Anestésico

Raza
+
+ ASA +
Temperamento Equipamiento
 Introducción - Mortalidad
Valores de Mortalidad varian de acuerdo al lugar
Introducción - Mortalidad

Introducción - Mortalidad
 Deshidratación
Azotemia

Luego…

Diuresis por Frío ↓ Flujo Renal

Hipervolemia Relativa ↓ TFG
↓ ADH Isquemia

↓ Actividad Enzimático
Metabólica

Mayor tiempo de
recuperacion Anestesica
 ACIDOSIS RESPIRATORIA

Lactato

ACIDOSIS METABOLICA

Escalofríos

Provea Oxigeno

Tremores aumentan el VO2 hasta 500% !!!!

Perfusión y Entrega de Oxigeno

Perfusión y Entrega de Oxigeno

Perfusión y Entrega de Oxigeno

Presión Arterial Y Gasto Cardiaco

VS
VELOCIDAD EYECCION VI
RESITENCIA ARTERIAL
VISCOSIDAD SANGUINEA

VISCOSISDAD
COMPLIANCE ARTERIAL
DURACION DEL CICLO
CARDIACO
¿ Cuando tomar medidas ?

Causas Hipotensión
 Evaluación Peri-Quirúrgica

• Diagnostico Cardiovascular
• Tratamientos Farmacológicos
• Cambios de dosis recientes
• Radiografias previas
• ECG
• Presion Arterial
• Ecocardiograma

Pacientes con enfermedad Grave

deben tener una evaluación máximo con
2 semanas de antigüedad

Evaluación Peri-Quirúrgica – Examen Físico

¿ SEDACION O ANESTESIA ?

¿ Entonces, que protocolo utilizo ?

TELEMEDICINA CARDIOIMAGEN

El servicio de telemedicina, requiere de una implementación básica para poder utilizar el servicio
en su totalidad, por ejemplo; electrocardiograma, equipo de radiografías, ecógrafo. Tener
conocimientos básicos en la obtención de imágenes, si no los tienes no te preocupes nosotros te
ayudamos con capacitación, tutoriales y material de estudio rápido y practico.

Si cuantas con uno o con todos estos equipos, estás en un muy buen momento de utilizar el
servicio en su totalidad, si aún no los tienes pero cuentas con algunos, no pasara mucho tiempo en
que te decidas complementar tu atención médica, entregar valor agregado a tus servicios.

Hoy en día con esta tecnología podemos diagnosticar el 80 % de los casos.

Estos métodos no sustituyen la atención médica presencial pero ayuda en toma de decisiones y
conducta terapéutica.

Beneficios del programa

Para el paciente/propietario:

 disminuye los costos en traslados e incomodidad en pacientes de tamaños grandes y

hospitalizados de difícil traslado.
 Aumenta la rapidez en toma de decisiones y resolución de casos.
 Evita viajes innecesarios.
 Reduce mortalidad. Muchos pacientes mueren a la espera de un especialista.

Para el médico veterinario/clínica:

 Mejora la atención de tus pacientes.

 Optimiza la formación académica, debido a que durante el uso del servicio es inevitable
no aprender sobre las enfermedades y tratamientos, y con el tiempo te darás cuenta que
cada vez puedes tomar decisiones que actualmente se te hacen complicados.
 No pierdas tiempo coordinando interconsultas, simplemente gana tiempo tomando
decisiones oportunas y resolutivas.
 Dale valor agregado a tu servicio, incrementa las ventas, fideliza a tus clientes y mejora tu
competitividad.
 Si estas lejos de los centros de especialidades, con este servicio podrás tener acceso a una
opinión especializada en corto tiempo.
 Mejora la visualización de tu clínica, cardioimagen generara campañas de marketing por
diversos medios en los cuales se promocionara la red de asociados por región, comuna o
país, de tal forma que los propietarios puedan acceder al servicio mediante tu clínica.
 Aumenta el número de clientes.
 Los integrantes de la red de diagnostico cardioimagen tendrán en un futuro acceso a
cursos de capacitación en área de medicina cardio-respiratoria a valores preferenciales e
incluso gratuitos.

Servicios: tele-radiografía, tele-electrocardiografía, tele-ecocardiografía, tele-consulta

(evaluación de casos clínicos completos), dando continuidad y seguimientos con los tele-
controles.
Los valores de los distintos servicios fueron pensados para que en tu clínica los
puedas vender a precio de mercado generando buen margen de utilidades. Sin embargo
tú decides los precios finales a propietarios.
El acceso al carro de compra es exclusivo para los médicos y clínicas asociadas,
resguardando la información económica.
Los casos estarán siempre respaldados en la nube, de esta forma podernos tener
siempre a disposición la información y poder dar continuidad a los casos.

COMO EMPEZAR.

FACIL !!! si ya tienes conocimientos en toma de imágenes ecográficas solo necesitas ver un
pequeño tutorial, revisar unos apuntes que nosotros entregamos y ya puedes comenzar a
utilizar el servicio ¡!!.

SI NO TIENES EXPERIENCIA EN ECOGRAFIA!!! Y estas comenzando en esta apasionante

área, no importa aprenderás rápido!!!!... te capacitamos!! En la obtención de las
imágenes necesarias para lograr una interpretación clínica. Como; la capacitación
consiste en la revisión de unos videos tutoriales simples y prácticos, lectura
complementaria resumida y seleccionada exclusivamente para que puedas avanzar rápido
y sin dificultad. Posteriormente terminamos la capacitación en nuestro centro con 2 días
de práctica clínica con casos reales y ya estás listo para comenzar a utilizar
TELEMEDICINA!!!
QUE COSTO TIENE: PRACTICAMENTE NO TIENE COSTO!!!, el valor de la capacitación es de
250.000 pesos que puedes cancelar con diferentes medios de pagos tarjetas de crédito,
webpay, cheques, o directamente en nuestra consulta con transbank. PERO POR QUE NO
TIENE COSTO!! TE ENTREGAMOS GRATIS LOS PRIMEROS 5 SERVICIOS DE EVALUACIÓN
DE CASOS CLINICOS que tienen un valor de mercado de 60-75 mil pesos. Por lo tanto tu
INVERSION está completamente recuperada.

Si tienes más consultas no dudes en contactarnos, estaremos felices de poder ayudar.

Whatsapp +56996219845

Me despido atentamente, un abrazo.

Nelson Pérez Ruiz MV. Director Cardioimagen.

 DR. SEBASTIÁN
BUSTAMANTE
CHILE

CHARLAS

1. Parálisis laríngea...¿qué es esto?

Operar o no operar, esa es la cuestión
Parálisis laringea: Qué es esto?
Operar o no operar?
Sebastián Bustamante B.
Primero no cagarla más…

Primum non noxere

La verdadera sabiduría está en conocer nuestra propia
ignorancia
 Parálisis Laringea
Falla de abducción de los aritenoides durante la
inspiración

Idiopática y secundaria a otras enfermedades, posible

polineuropatía

Sintomas: Tos, Estridor laringeo, tos inducida por ingesta

de alimentos o agua, cambio del ladrido e intolerancia al
ejercicio.

Diagnóstico directo por Laringoscopía

2 grandes grupos

Perros grandes y viejos: Promedio de

edad de 9 años en Labradores, Golden,
San Bernardo, Newfoundlands y Spaniel
Británico

Perros Jóvenes: Bouviers des Flandres,

Siberian Huskies, Bull Terriers y O.A.
> 30% de estos
pacientes
presentan
HipoT4
Diagnóstico

Laringoscopía PO

Laringoscopía transnasal

Ecolaringoscopía

Clínico

OJO PIOJO!!!
Movimiento paradojal de los aritenoides
Tratamiento

Quirúrgico: Unilateralización
aritenoídea, Bilateralización,
Laringectomía/Aritenoidectomía y
LaringoÞsura castellada.

Manejo mŽdico: AINES, Antitus’genos y

Broncodilatadores
Unilateralización Aritenoídea
Aritenoidectomía
 LaringoÞsura

Comparación quirúrgica

Bilateralización……………. 67% de muerte

Laringectomía……………… 30%

Unilateralización……………….14%
Traqueostom’a deÞnitiva
Article

Long-term outcome of permanent tracheostomies in dogs: 21 cases

(2000–2012)
Lindsay L. Occhipinti, Joe G. Hauptman

Abstract — This retrospective study reports long-term outcome, survival, and complications in dogs which received
a permanent tracheostomy due to upper airway obstruction. Data were collected from medical records (n = 21) in
Table Association
1. over
2 institutions ofPatients
a 12-year period. diagnosis withuntil
were followed survival time (P causes
death, complications, = 0.09)
of death, and survival approached signif
times are reported. Major complications were reported in 50% of patients with 20% of patients receiving revision
surgery. The most common complications were aspiration pneumonia andMedian days surgery. Median
need for revision
not significant, su
Diagnosis
survival time was 328 days with 25% of patients surviving 1321 days or longer.(25th, 75th)
Some (26%) patients died acutely with shortest surv
at home at various times after surgery. Permanent tracheostomy is a viable procedure for patients with end stage
Brachycephalic airway
upper airway obstruction; syndrome
however, a subpopulation of patients suffers acute1062
death at(728, 1744)
various times after surgery, paralysis, severe l
which is thought to be due to airway obstruction.
Bilateral acquired laryngeal paralysis 91 (8, 329) cervical bite wou
Laryngeal
Résumé — neoplasia
Résultat à long terme des trachéostomies chez les chiens :1399 (760, 2037)Cette étudeof patients in each
21 cas (2000–2012).
Laryngeal
rétrospective collapse
présente les of undetermined
résultats, la survie et les origin
complications à long terme628 (320,
chez les chiens937)
qui ont subi une
Severe laryngospasm
trachéostomie permanente en raison d’une obstruction des voies respiratoires 22 (11, 32)données ont été In the present s
supérieures. Les
recueillies dans les dossiers médicaux (n = 21) de 2 institutions sur une période de 12 ans. Les patients ont été
Traumatic laryngeal collapse due to bite wounds 164 (82, 245)
suivis jusqu’à la mort à la suite de complications; les causes de décès et les temps de survie sont signalés. Des
patients, which is
Laryngeal
complicationsmalformation
majeures ont été signalées chez 50 % des patients et 20 %1760 (1645,
des patients ont 2006)
subi une reprisesurgery was requir
chirurgicale. Les complications les plus fréquentes étaient la pneumonie de déglutition et le besoin de reprise
chirurgicale. Le temps de survie moyen était de 328 jours avec 25 % des patients qui ont survécu 1321 jours oureported by Hedl
Table 2. Complications
plus. Certains anddeassociation
patients (26 %) sont morts with survival
façon aiguë à la maison in days
à divers moments après la chirurgie. Une
trachéostomie permanente est une intervention viable pour les patients ayant une obstruction des voies respiratoiresrequired revision
Positive median
de stade final. Cependant, une sous-population Negative
de patients sont décédés aiguë à divers moments après latoma, which was
median
de façon
chirurgie, que l’on croit attribuable à l’obstruction des voies respiratoires.
Factor (25th, 75th) (25th, 75th) (TraduitP-value par Isabelle Vallières)viously (3). Unlik
Muchas gracias por la oportunidad a Cardioimagen!!!

Y Muchas gracias por la atención!!!!

sebaveccs@gmail.com

agenda.vetera.cl@gmal.com

Sebabustamanteb en Instagram

Sebastián Ricardo Bustamante Bustamante

En Facebook.
 Reconocimiento
Trayectoria

En el marco del curso se realizó un reconocimiento

a la trayectoria en el área cardiológica al Dr. Ramón Martínez.
Médico veterinario con dedicación a docencia y atención
clínica de la especialidad desde 1970.
Patrocina

Auspician
GRACIAS!