Emergency Medicine R E S P I R ATO RY

Peer Reviewed

Stacey Leach, DVM, & Deborah Fine, DVM, MS, Diplomate ACVIM
University of Missouri

Acute Respiratory
Distress:
The Blue Patient

PROFILE and respiratory rate and effort, as well as ausculta-

Acute respiratory distress is a serious and com- tion of the thorax. Evaluation of the mucous
mon emergency presentation. Respiratory distress membranes may reveal cyanosis, suggestive of
occurs for various reasons, and prompt recogni- hypoxemia.
tion of the underlying source is essential to
providing appropriate therapy. Anemic animals may have pale mucous mem-
branes, and cyanosis may not be apparent, even
Acute respiratory distress can be broadly divided with severe hypoxemia. The pattern of respiration
into 8 categories based on anatomic localization. can help localize the problem and guide further Prompt recognition
Several of these can be distinguished by simple diagnostics and treatments.
of the underlying rea-
observation and physical examination, whereas
son for respiratory
others require additional diagnostics. Categorical causes of hypoxemia include:
● Upper airway obstruction ● Ventilation-perfusion mismatch (pulmonary distress is essential
● Lower airway obstruction parenchymal disease) to providing appro-
● Thoracic wall disorders ● Diffusion impairment (edema, fibrosis, neoplasia) priate therapy.
● Pleural space disorders ● Alveolar hypoventilation (airway obstruction,
● Pulmonary parenchymal disease pleural space disorders)
● Pulmonary vascular disorders ● Vascular shunts (right-to-left shunts)
● Abdominal distension ● Decreased fraction of inspired oxygen or
● Nonrespiratory disorders (mimics) oxygen concentration (high altitudes).

INITIAL ASSESSMENT & DIAGNOSIS Upper airway obstructions can lead to inspiratory
Initial assessment of these patients involves dypsnea and stridor. Examples of such obstruc-
observation of the patient’s mentation, posture, tions include laryngeal paralysis, extrathoracic

CONTINUES

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Emergency Medicine CONTINUED

A B
1
Right lateral (A) and ventrodorsal (B) radiographic projections of the thorax of a dog presenting with acute respira-
tory distress. An alveolar lung pattern is present in the right cranial, middle, and caudal lung lobes, a pattern consis-
tent with aspiration pneumonia. Megaesophagus is present (black arrows), likely leading to chronic regurgitation
and secondary aspiration.

tracheal collapse, compressive masses, foreign
bodies, and brachycephalic syndrome.
Lower airway obstructions result in expiratory
dyspnea with auscultable expiratory wheezes.
Causes of such obstructions include bronchocon-
MORE striction/spasms, inflammation of the bronchial
walls (feline asthma, chronic bronchitis), intralu-
Go to cliniciansbrief.
minal exudative/mucoid debris, intrathoracic tra-
com/journal to view
cheal collapse and bronchomalacia, or bronchial
and download the compression secondary to left atrial enlargement.
algorithm Acute
Breathing Difficulty: Thoracic wall disorders (eg, flail chest, “sucking”
Initial Management chest wounds) can lead to paradoxical respiration
(in the January 2005 with the affected area of the thorax collapsing
issue of Clinician's inward on inspiration and forced outward on
Brief ). expiration.
Pleural space disorders, such as pleural effusion
or pneumothorax, can lead to rapid, shallow
breathing patterns with inspiratory distress.
Pulmonary parenchymal disorders, such as pneu-
monia (Figure 1), edema (cardiogenic or noncar-
diogenic), pulmonary contusions, interstitial lung
disease, and neoplastic or fungal infiltration (Fig-
ure 2), can lead to both inspiratory and expiratory
difficulty. The presence of heart murmurs, gallops,
or arrhythmias may suggest underlying heart dis-
ease but not necessarily congestive heart failure.
Congestive heart failure can lead to activation of
the sympathetic nervous system, which almost
invariably results in tachycardia. Primary respira-
tory disease often induces a vagal response lead-
ing to normal sinus rhythms, sinus arrhythmias,
or sinus bradycardias.
Pulmonary vascular disorders are most com-
monly pulmonary thromboembolism and heart-
worm disease. Clinical signs of pulmonary
vascular diseases are variable and include hemopt-
ysis, coughing, dyspnea, and syncope. Other clini-
cal signs may be noted and attributed to the
predisposing disease process.1 Split heart sounds
may be heard due to concurrent pulmonary
hypertension.
Severe abdominal distension can impair
diaphragmatic contraction, leading to inspiratory
distress that is typically characterized by a slow

70.............................................................................................................................................................NAVC Clinician’s Brief / February 2011 / Emergency Medicine

 2
Right lateral (A) and ven-
trodorsal (B) radiographic
projections of the thorax of
a dog presenting for progres-
sive coughing and acute
dyspnea. A diffuse structured
interstitial lung pattern is
present. Primary differentials
would include metastatic
neoplasia and fungal
disease.

A B

and exaggerated pattern. Differentials include prior to performing a physical examination or

ascites, gastric dilatation-volvulus, organomegaly,
and pregnancy.
Nonrespiratory diseases that may mimic respira-
tory distress include acidosis, anemia, pain, and
hypotension.
STABILIZATION
Oxygen supplementation is the cornerstone ther-
apy for the dyspneic patient and is often needed
diagnostic procedures (Figure 3, page 72). Several
strategies may be used for providing oxygen, with
the patient’s temperament dictating the most
appropriate method.
The clinician should ensure the airways are
patent; otherwise more invasive measures may be
indicated (eg, intubation, tracheostomy, mechani-
cal ventilation). In some cases, sedation may be
CONTINUES

Prioritizing Patient Care

● Ensure patent airway ◗ Abnormal respiratory patterns ◗ Abdominal distension
● Begin oxygen supplementation • Inspiratory distress: Upper ◗ Thoracic wall disorder
(oxygen cage, face mask, airway obstruction, pleural ◗ Thoracic findings on ausculta-
intranasal, flow-by) space disorder, abdominal tion
● Obtain vascular access distension, thoracic wall • Heart rate and rhythm
● Perform brief physical examina- disorders • Abnormal heart sounds
tion to identify • Expiratory distress: Lower • Muffled or adventitious lung
◗ Mentation changes airway obstruction sounds
◗ Abnormal mucous membrane • Mixed: Pulmonary parenchy-
color (cyanotic, pale, hyper- mal or pulmonary vascula-
emic) ture disorder

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 Emergency Medicine CONTINUED

Oxygen supple-
mentation is the
cornerstone
therapy for the
dyspneic patient.

A B

3
Oxygen therapy is the mainstay of treatment for acute respiratory distress and can be provided using a variety of methods.
Oxygen cages are the least stressful for the patient but can limit access for further treatments and diagnostic procedures.
Intranasal administration of oxygen can be supplied using a nasal prong (A) or red rubber catheters (B) and can provide a
FiO2 of 40% to 50% when using 50 to 100 mL/kg per minute of oxygen flow. Face mask and flow-by oxygen can also be used
if the patient will tolerate it.

warranted to reduce anxiety associated with ● Thoracic or cervical radiography

respiratory distress. Vascular access should be ● Echocardiography
obtained, if possible, without disrupting oxygen ● Coagulation profile, D-dimer assay
supplementation to allow intravenous administra- ● Bronchoscopy and bronchoalveolar lavage
tion of medications or fluids if indicated. ● Fine-needle aspiration of the lung
● Laryngoscopy
DIAGNOSTICS ● Serial pulse oximetry, arterial blood gas analysis.
Initial diagnostics may include:
● Blood pressure measurement
TREATMENT
● Pulse oximetry
Specific treatment is targeted to the underlying
● Blood sampling to determine packed cell vol-
cause of respiratory distress. Continued oxygen
ume, total protein, blood urea nitrogen, creati-
nine, glucose, and electrolytes supplementation and preventing stress is vital to
● Thoracocentesis if pleural disease is suspected
avoid further decompensation.
● Fluid analysis of pleural effusion (cytology, cell
counts, total protein, and triglyceride/choles- Upper Airway Obstruction
terol concentrations if chylous appearing) ● Sedation with acepromazine (eg, 0.025–0.2
● Bacterial cultures of pleural fluid. mg/kg IV or IM) or butorphanol (eg, 0.1–0.4
mg/kg IV or IM) may be needed to relieve
Once the patient has been stabilized, additional anxiety and facilitate further evaluation.
● If a patent airway cannot be maintained, intu-
diagnostics dependent on the clinical situation
may include: bation, tracheostomy, or other invasive meas-
● Complete blood count, serum biochemical ures may be required.
profile, urinalysis
FiO2 = fraction of inspired oxygen

72.............................................................................................................................................................NAVC Clinician’s Brief / February 2011 / Emergency Medicine

● Glucocorticoids (eg, dexamethasone, 0.1–0.25 Pulmonary Parenchymal Disorders
mg/kg IV) may be needed to reduce laryngeal ● Thoracic radiographs are required for defini-
and pharyngeal inflammation and edema. tive diagnosis and treatment. However, empir-
● Often these patients are hyperthermic and ical therapy may be necessary initially in
may benefit from active cooling (eg, applying extremely unstable patients.
icepacks, cooling fans, cooled IV fluids). ● If pneumonia is suspected, therapy includes
● Noncardiogenic pulmonary edema may broad-spectrum antibiotics, such as ampicillin Specific treatment
develop in patients with upper airway obstruc- (22 mg/kg IV Q 8 H) and enrofloxacin (10–20 is targeted to the
tions and will require further supportive care. mg/kg IV Q 24 H for dogs and 5 mg/kg IV Q
underlying cause of
24 H for cats), pending results of bacterial cul-
Lower Airway Obstruction tures and nebulization and coupage. respiratory distress.
● Bronchodilators (eg, terbutaline, 0.01 mg/kg ● Therapy for cardiogenic pulmonary edema
IM) may be attempted to quickly relieve bron- primarily includes a loop diuretic (furosemide,
chospasm. initially 2–6 mg/kg IV or IM) at repeated dos-
● Glucocorticoids (eg, dexamethasone, 0.1–0.25 ing intervals dependent on the patient’s clini-
mg/kg IV or IM) can also be used with acute cal response. Nitroglycerin ointment (0.25–2
asthmatic episodes in cats. inches transdermally Q 6–8 H) can be
attempted to reduce preload in congestive
Thoracic Wall Disorders heart failure but absorption is variable.
● Pain and concurrent pulmonary contusions ● No specific therapy exists for noncardiogenic
from the initiating traumatic event are the pulmonary edema and pulmonary contusions
likely main contributory factors in respiratory other than supportive care, oxygen supplemen-
distress.2 tation, and mechanical ventilation, if needed.
● Administration of parenteral opioids in com- Diuretics are generally contraindicated in this
bination with local anesthetics (intercostal context.3
nerve blocks) may provide more complete
analgesia than either alone. Nonsteroidal anti- Pulmonary Vascular Disorders
inflammatories may also be used if no con- Therapy for pulmonary thromboembolism
traindications are observed. remains largely supportive but may include a
● Stabilization of a flail segment (splinting or combination of anticoagulants, antiplatelet med-
restraining in lateral recumbency) may lead to ications, thrombolytics, bronchodilators, and
improvement in ventilation and facilitate fur- selective pulmonary arterial vasodilators (eg,
ther evaluation and treatment; however, it can sildenafil, 1 mg/kg PO Q 8–12 H; pimobendan,
also impede the patient’s inspiratory effort. 0.25 mg/kg PO Q 8–12 H) for concurrent pul-
● Intermittent thoracocentesis may be needed monary hypertension.1
initially to relieve a concurrent pneumo/hemo-
thorax until the patient has stabilized or the
placement of a chest tube is required.
See Aids & Resources, back page, for
references & suggested reading.

CONTINUES

Emergency Medicine / NAVC Clinician’s Brief / February 2011.............................................................................................................................................................73

 Stacey Leach, DVM, &
RESPIRATORY DISTRESS: Deborah Fine, DVM, MS,
DIAGNOSIS & TREATMENT AT A GLANCE Diplomate ACVIM (Cardiology)

DX AT A GLANCE
Upper Airway Obstruction Thoracic Wall Disorders • Differentials: Pneumonia, edema
•Clinical Signs: Inspiratory • Clinical Signs: Paradoxical respira- (cardiogenic or noncardiogenic),
dyspnea, stridor tion with the affected area of the tho- pulmonary contusions, interstitial
rax collapsing inward on inspiration lung disease, neoplastic or fungal
•Differentials: Laryngeal paralysis, infiltration
extrathoracic tracheal collapse, & forced outward on expiration
compressive masses, foreign • Differentials: Flail chest, “sucking”
bodies, brachycephalic syndrome chest wounds Pulmonary Vascular Disorders
• Clinical Signs: Hemoptysis,
Lower Airway Obstruction Pleural Space Disorders coughing, dyspnea, syncope; split
heart sounds possible if concur-
•Clinical Signs: Expiratory dyspnea • Clinical Signs: Rapid, shallow rent pulmonary hypertension
with auscultable expiratory breathing patterns with inspiratory
wheezes distress • Differentials: Pulmonary thrombo-
embolism, heartworm disease
•Differentials: Bronchoconstriction • Differentials: Pleural effusion,
/spasms, bronchial wall inflamma- pneumothorax
tion (feline asthma, chronic bron- Severe Abdominal Distension
chitis), intraluminal exudative/
mucoid debris, intrathoracic tra- Pulmonary Parenchymal Disorders • Clinical Signs: Inspiratory distress
cheal collapse & bronchomalacia, typically characterized by slow,
•Clinical Signs: Inspiratory & expira- exaggerated pattern
bronchial compression secondary tory difficulty; presence of heart
to left atrial enlargement murmurs, gallops, or arrhythmias • Differentials: Ascites, gastric
may suggest underlying heart dilatation-volvulus, organomegaly,
disease pregnancy

TX AT A GLANCE
Upper Airway Obstruction Pulmonary Parenchymal Disorders
• Sedation with acepromazine (eg, 0.025–0.2 mg/kg • Empirical therapy in extremely unstable patients
IV or IM) or butorphanol (eg, 0.1–0.4 mg/kg IV or IM) • Thoracic radiographs for definitive diagnosis and
• Intubation, tracheostomy, etc if patent airway treatment
cannot be maintained • Broad-spectrum antibiotics (eg, ampicillin, 22 mg/kg IV
• Glucocorticoids (eg, dexamethasone, 0.1–0.25 Q 8 H; enrofloxacin, 10–20 mg/kg IV Q 24 H for dogs &
mg/kg IV) to reduce laryngeal & pharyngeal inflam- 5 mg/kg IV Q 24 H for cats), if pneumonia suspected
mation & edema • Loop diuretic (furosemide, initially 2–6 mg/kg IV or IM)
• Active cooling for hyperthermic patients at repeated dosing intervals for cardiogenic pulmonary
edema
Lower Airway Obstruction • Supportive care, oxygen supplementation, and mechan-
ical ventilation for noncardiogenic pulmonary edema
• Bronchodilators (eg, terbutaline, 0.01 mg/kg IM) to
relieve bronchospasm
Pulmonary Vascular Disorders
• Glucocorticoids (eg, dexamethasone, 0.1–0.25
mg/kg IV or IM) for acute asthma in cats • Anticoagulants, antiplatelet medications,
thrombolytics
Thoracic Wall Disorders • Bronchodilators (eg, theophylline, 10 mg/kg PO Q 12 H)
• Pulmonary arterial vasodilators (eg, sildenafil, 1 mg/kg
• Parenteral opioids in combination with local anes- PO Q 8–12 H; pimobendan, 0.25 mg/kg PO Q 8–12 H) for
thetics; NSAIDs may be used if no contraindications concurrent pulmonary hypertension
• Stabilization of flail segment to improve ventilation
& facilitate evaluation & treatment; can impede
inspiratory effort
• Intermittent thoracocentesis to relieve concurrent
pneumo/hemothorax

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74.............................................................................................................................................................NAVC Clinician’s Brief / February 2011 / Emergency Medicine