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com
Cardiovascular
II
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Donald J. Sefcik is the Associate Dean at the chicago college of osteopathic Medicine (ccoM), Midwestern university (MWU), in Downers Grove, IL. He is a tenured professor and board certified in both Emergency Medicine and Family Medicine. From June L997 through May 2000, Dr. Sefcik served as Medical Director for the Physician Assistant Program, College of Health Sciences (CHS), at MWIJ. Dr. Sefcik,s lectures are based upon his experiences as a clinician and preceptor, tenure as a medical school faculty rnembero and his student assessment research.
Dr. Sefcik has practiced with physician assistants since 1988 and been involved in the clinical training of physician assistants since 1990. Prior to joining Midwestern University's faculty, Dr. Sefcik was a faculty member in
the Pharmacology Deparfinent at Butler University and in the Nursing Depaitment at Marian College, both in Indianapolis, Indiana. Dr. Sefcik has a Bachelor of Science in Pharmacy (1981), a Master of Science in Pharmacology (1994), both from Butler university, illd an MBA (May 2004) from Purdue University.
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Learning Objectives
Upon completion of this portion of the review course, the participant should be able to:
2. Present an overview of aortic aneurysms and dissection. 3. Define ischemic heart disease (II{D) and coronary artery disease (CAD). 4. List several risk factors associated with CAD and IHD. 5. Compare and contrast stabie angina, unstable angina and Prinzmetal's angina. 6. Discuss diagnostic modalities utilized in the evaluation of IHD. 7. Describe the events culminating in a myocardial infarction (MI). 8. Discuss EKG manifestations of myocardial ischemia/infarction. 9. IdentiSr high-risk patients for acute MI.
10. Describe how a myocardial infarction is definitively diagnosed. 1. Discuss indications for acute coronary thrombolysis. 12. Describe therapeutic options for an acute MI. 13. Describe the rationale for IIID drug therapy.
1
1.
14. Identify potential complications of myocardial infarction. 15. Describe pericarditis: etiologies, manifestations & management. 16. Cornpare and contrast puhnonary edema and heart failure. 17. Differentiate left-sided and right-sided heart failure. 18. Conpare and contrast systolic and diastolic heart failure. 19. Prescribe appropriate heahnent for acute pulmonary edema. 20. Prescribe appropriate therapy for left ventricular dysfunction.
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Case
A 44 year-old male presents for a "checkup". He denies any health problems. He discloses to you that he drinks "regularly", smokes 1.5 packs of cigarettes a day and doesn't exercise ever. His BMI is 33, His blood pressure is 168/102 mrn Hg. His fundoscopic examination is unremarkable. You do note that his PMI (point of maximal impulse) is located in the fifth, left intercostal space, near the midclavicular line.
Case 1.1 Which one of the following therapeutic regimens is the optimal choice for this patient?
A. metoprolol B, hydrochlorothiazide Sg
C, D.
enalapril
diltiazem
&l
lr:c-
:-!cr.irA
e \ J,w$t
E. lifestylemodification
e -\Z t^ v'5
Case 1.2 Eventually, you add propranolol to this patient's therapeutic regimen. Which of the following side effects is most likely?
A. proteinuria
B.
bradycardia
c. depression
D. cephalgia
E.
.- V r .l
morbilliform rash
\,g.,* ovvs
su\
,)Ae-
c6'*^ y=ll"t'{u
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Case 2 A 48 year-old hypeftensive female transfers to your practice. She has currently discontinued all medications because she was concerned that her former clinician "prescribed too many medications", although she was happy with his bedside manner during the delivery of her five children. She has a history of depression and hypercholesterolem ia.
Case 2.1 Which one of the following is the best beta-blocker for this patient?
A. propranolol
B.
c.
D. E,
timolol
pindolol
[L.t.r"r
[c',
\n*dy
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ma& ntdl*-\
Case 2.2 Two weeks after the initiation of therapy for her hypertension, she returns complaining that when she coughs "she wets her pants". Which of the following medications was most likely started two weeks ago? A. reserprne
B.
clonidine
c. hydrochlorothiazide D. terazosin
E. diltiazem
d l\uoKpn
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Case 3 A 68 year-old hypertensive female presents complaining that her new antihypertensive medicaiion causes her to experience "skipping heart beats", swelling of her legs and headaches. Her blood pressure is 178/96 mm Hg, She has a grade lllA/l diastolic murmur,
u.,,)eneJ tr it pff,r*urt
Case 3.1 Which one of the following is the most likely cause for her murmur?
A.
aortic stenosis
Case 3.2 Assuming that this patient was prescribed a calcium channel blocker, which of the following is LEAST likely the agent she was taking?
A.
;: i;ffiil; \ C. amlodipine
-
nifedioine
,/
r:u\o.\
'
rr,+l"c),\^d^rt
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Case 4
A 51 year-old male presents to your office after being discharged for a heart attack. He is currently taking one aspirin a day. You review his charts and note that he has a history of hypertension, gout and diabetes type 2. His echocardiogram in the hospital, prior to discharge, revealed an ejection fraction of 52%.
Case 4.1 Which one of the following antihypertensive agents is the best choice for this patient?
A. B.
hydrochlorothiazide
lisinopril
Ou-:\
nn
T.
Case 4.2 Which one of the following agents would most likely worsen his gout?
A. hydrochlorothiazide '-T\n;r.,,:flC C^ur<: h 1p"*t-,"-" B. clonidine C. methyldopa D. verapamil E. propranolol t)*,clu;'*- AgA =
\o^
T
o"J'
tI
t! ' Jta+ tt
d- t..-
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Gase 5
A 54 year-old male presents with a sudden loss of vision that began 30 minutes prior to arrival' He denies any trauma prior toirre visual ror.. i" oenies pain. Examination of his visual acuity reveals that,he r'trr iigl'rt perception oniy. L*"rination of the ipsilateral ?il::::::,:"":"3["j::]fifl?y 991eit a1o ,ignifi.rni ,ia,rowins of the retinar arreriores rhere are no cotton-woor
ipots oin"mo"rr.s;.
;p;,;;i;i;:"'r;.:'j:,:'??ffi:i,B
o,
crorni.r,,
Case 5,1 which one of the following, fundoscopic findings would be most supportive of the diagnosis that you suspeCt?
A. macular B. tortuous and dilated retinal veins c. retinal at"rilf" r"-grentation of blood D. an,increased cup:disc ratio (greaterihan E. isolated hyperemia of the naial naft of tne fundus
edema
4,,.-la
-:
-
lBoxcc.m.\) J 0.6)
which one of the following diagnostic study combinations would most likely reveal the etiology for this patient,s ophthZtmic
piobtem?
A.
D' E.
? c'
complete blood count and INR echocardiogram and carotid doppler studies cr scan of the brain and intraocrt.r pr"rrrre measurements fluoroscein staining and intraocur.i pr"rrrre measure,";;i; MRI scan of the briin and ,ortogrm
"n
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Case 6 A 62 year-old male presents complaining of shortness of breath on exerlion for the past several weeks. He states that his "heart races in his chest" because he gets so short of breath. His chest x-ray is unremarkable. ljs-Hemoccult is negative. r unremarkable. His hemoglobin is 9.4 Gm/dL; McV is Tp fL; RDW is(0.8)
\!",,, r.x.r$n,. *" ,. cldr"''r'*r'''s {L^l "trln r ci. ,-., .,. {}^tt""t$' ,"N ,{ RDiq-' l-Case 6.1 Which one of the following is the most appropriate at this time? Tn^*,[dfr,
A. order a serum ferritin level, TIBC and reticulocyte count B. order a hemoglobin electrophoresis C. order both serum 812 and folate levels D. prescribe vitamin 812 E. prescribe a multivitamin supplement with vitamins A, B, C, E, and iron
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\Case 7
c.
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loii *f
Ten days after an acute myocardial infarction, a 56 year-old female presents complaining of chest pain. The pain is worsened with inspiration. She denies shortness of breath. Physical examination revels a low-grade fever, bilaterally clear lungs, and a normal sinus rhythm without gallops, murmurs or rubs. An EKG reveals inferior q-waves, without evidence of ST segment displacement.
Drc*-$nr> -s/nulfo? =
Case 7.1 Which one of the following therapies is the most likely to be effective?
A. cephalexin 500 mg orally four times a day B. doxycycline 100 mg orally twice a day C. nitroglycerin sublingually @ibuprofen 600 mg orally four times a day E. warfarin Smg orally every morning
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Chest Pain
Principles:
4.
1. Any chest or abdominal pain complaint may be a manifestation of heart disease. 2. Accurate diagnosis is based upon interpretation of the patient's pain perception. 3. The diagnosis, often based solely on history, can be biased and/or misperceived.
Physicalfindings/ancillary tests may not be helpful, and may be misleading.
Non-Emerqent Etioloqies
Klinkman MS, Stevens D, Gorenflo DW. Episodes of care for Chest Pain J Fam Pract 1994;38:345
A. Musculoskeletal
36
o/o
Skeletal (Costochondritis Tietze's syndrome) Commonly young women (African-American more commonly) Pain exacerbated with deep inspiration No history of repetitious activity/trauma lf NSAIDs taken - usually have reduced the symptoms Tenderness - more commonly left % costosternal margins eain is reproducible in 5 - 10 % of patients with acute cardiac ischemia
J<
B. Gastrointestinal
19 %
"-itis"
lk
Relationship to food Relief with antacids or eating G/ eocktailreso/yes pain in 5 - 10 % of patients with acute cardiac ischemia
pain/discomfort \ ! - sr'-rt,,o1.. n-ro{.k_ {V 'icu GERD - * Esophogram fcJroxr.,rf l;wt Nutcracker of Corkscrew esophagus gsopdi\{],SuS
C. Cardiac - 16 o/o Typical angina (next section) MitralValve Prolapse "Sharp" or "Dull" pain Palpitations Mid-systolic click and murmur
r .
' -
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D.Psychosocial Anxiety
-9%
. . .
F. Atypical
- 15
o/o
No etiology is clear
1.
fr*5* f:w'n*y ' S i'rrn';rr!z'Syndromes \J""aG- chest discomfort secondary to myocardiat isJfiemia .. T Stable Demand) Anqina V,3Crt,:u\ pr:'1"1"1 = t'''S\
Coronary
J+
-1*, *+^^t
.{r
q
Occurs with a fixed threshold of increased workload. Manifests as retrosternal chest discomfori, which may include radiation to the arm, back, neck or jaw, nausea, diaphoresis, shortness of breath, etc., precifitated by:
crricl '. -s a\wr"yS \ ;1'-1E"ir"5te- J Angina of new onset, angina at rest (or with less exertion), or a pattern of
l.Jnstabte (Supplv) Anqina fpreinfarction
longer
L ffr qt5 ,
-
rf\tJ6tv',ruu
.,c,k .a
ffSil:fil5ill?1 - .
L"-'S?:fiy';ffi:,?"JIii["iTI,:J:'T;:
,-+
*S,"niuJ*EA
g\.
] +U
,\c '-lrraA
pr'i.ll
Asymptomatic periods of myocardial ischemia. Silent Ml - more common in diabetics and the elderly.
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bl Myocardial lnfarq-tion
Generally secondary to coronary artery thrombosis, resembling "angina" but typically greater in severity and duration, often not relieved with rest or nitroglycerin.
SNS - diaphoresis; vasoconstriction [cool, clammy skin] PSNS - nausea; weakness [vagal effects]
C.
myocardial dysfunction: ventricular gallops (chamber compliance changes) dyskinesis (reduced cardiac output) rales (pulmonary edema) arrhythmias
Sa
A.
in cl ude :
B.
C. D.
arrhythmias [electrical - altered transmembrane ion flux] hypotension [mechanical - myocardial cellular dysfunction] embolism [mechanical - ventricular cavity thrombus formation]
pericarditis Iinflammatory] pulmonary edema/CHF [mechanical - myocardial cell dysfunction; valvular dysfunction; tamponade]
E.
A.
(,
\. -\-----
inflammation of pericardial sac pain; changes with position [reduced leaning forward]; odynophagia ,r-pleuritic pericardialfriction rub (may be intermittent) diffuse ST segment elevation
Pericarditis
----==--+
P\eotJr= T
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o pleuritic pain; pleural friction rub . SEiItGet with dyspnea triad - venostasis; hypercoagru*ilry' intimal injVry) @irchow's >-ffiAfrgradient I Al*rrl * n-:."r*l rrCo\ =T g*JF,n t .-. CXR - most commonly is normal . V/Q scan; Pulmonary angiogram - gold standard G\rut* :67rcrr .{ tt .
Pulmonary embolism
- pulmonary vascular
occlusive event
C.
. Secondary
COPD; Asthma;
Pneumothorax - gas in pleural space Primary (Spontaneous) - No underlying lung disorder Young males (tall and thin); Smokers; Valsalva Maneuvers
frs| b,ant
\
p{
{s*J
Pneumonia.,..
o . r . . . r .
Simple lntrapleural space pressure is equal to atmospheric pressure Expiratory fitm rncreases visualization (loss of peripheral lung markings...) Tension Pleural defect acts as "one Way Valve" - prodUces positive pressure resulting in contralateral shifting of mediastinum; JVD; hypotension...... *** po not wait to get a chest x-ray Needle thoracostomy, zno ICS/MCL
!-
D. Pneumonia
pleuritic pain cough, sputum Produciion, fever chest x-ray and/or physical signs of consolidation
- lung consolidation
Aus"\}-- ?SaF\'\o^Y
. .
F.
begin as intimal tear - cleavage plane is within media commonly 50 - 70 year old males abrupt on - "tearing" or "ripping" - typicall(between the shoulder Classic physical features Unequal (absent) Pulses Focal neurologic deficits Signs of cardiac tamPonade **-geck's triad * fiugular venous distention, muffled heaft sounds, hypotension) Gold Standard - Aotlogram CXR (upright PA) - widened mediastinum - suggestive
Others
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1.
Definition
Myocardial cellular necrosis secondary to coronary artery occlusion, most commonly tlie result of thrombus formation upon an atherosclerotic plaque. Of acute chest pain
Entergency Department - 30 % patients = coronary ischemic event Primary Care ffice - 5 % patients coronary ischemic event
it happen
i.
Etiology
Coronary artery thrombosis (most common) Ernbolic \ lrs c\ Coronary aneritis \-ra,io.w"K, '!ea'!f
event
Cocaine use
ii. Sx/Sx
b. Who's at
risk
(
Before age70 - Male > Female After age 70 - Male = Female
L*/
hr
i.
ii.
Maleffemale
'1V'.,
,"..'
Pz:opY I LltJ Y I O
;;
Age
iii. Risk Factors - Family history premature coronary artery disease (CAD)
Hypertension Hypercholesterolemia
Cigarette smoking Diabetes mellitus
nnecl- ,,.r-,Jan5
ott;,," t^*L.*l
EKG
- 50 %o are normaVnondiagnostic
May d
fi\'n
at
AMI presentation
firt J stung
3xJ
ST Elevation - Transmural
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1.
T-Wave
Inversion:
Myocardial IschemiaAnfarction
Severe LVH or RVH with "Strain" Cardiomyopathies
i-
2.
ST Segment Elevation:
3.
Wave):
)k'
,)b
t \f .t
WBC - Often demonstrates leukocytosis Chernistries - Associated risk factors Echocardiogram May demonstrate wall motion abnormalities (hypokinesis) CXR - identifies (rules out) other pathology Cardiac En4ymes fMarkers] - May Demonstrate cellular necrosis (CK, AST, LDH; Troponin; Myoglobin)
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Myocardial ischemia results when cellular oxygen demand exceeds oxygen supply. Myocardial oxygen demand is determined by (a) gontractility [inotropic state - a measure otttre toice of contraction], (b) heart rate fdetermines ATP utilization and oxygen consumption], and (c) ventricular wall striss [a product of ventricular wall thickness and intraventricular presiure].- Myocardial oxygen supply is dependent upon oxygen,calline capacity of the blood [determined by oxygenatioo anO fremoglobin contentl and coronary blood flow [a result of vascular tone, Iumen pui"ncy *a perfusion pressures].
Myocardial hypoxia causes increased anaerobic metabolism (an innacellular acidosis develops) and an impairment of the ATPase ion pumps (resulting in altered membrane ion movement - the EKG records these changes as T wave ilversion, ST segment displacement, and,/or anhythmias; if cell death occurs, Q waves may eventually develop). Ischemia of the entire thickness of the ventricular wall is termed transmural; ischemia of the innermost layer(s) of the ventricular wall is termed subendocardial ischemia. Historically, e wave infarctions were believed to represent myocardiai necrosis of a transmural nature, while Non-e-wave infarctions were believed to be the result of subendocardial myocardial infarctions. lnterestingiy, ST segment elevation represents transmural ischemia (an injury pattern) and will probably result ini Q-wave infarction, while ST segment depression represents subendocardial ischemia and may result in u lion-q-wave infarction. The development of abnormal Q waves (over a 2 - 24 hour period after the onset of clinical symptoms) is indicative of myocardial cellular necrosis.
Finaliy, although the initial mortality is lower in patients suffering Non-Q-wave infarctions than patients having Q-wave infarctions, during the subsequent months, the reinfarction rate and risk of death is greater in the patients suffering the Non-Q-wave infarctions.
Tvpical EI(G Evolution Pattern of Mvocartlial htfsrction
Acutely
Q-wave
< 24
hrs
24 - 48 hrs
Days later
MI
sr elevation sr elevation
Non-Q-wave
MI
T wave inversion
ST depression
a. b.
upward concavity ("smiiing") - benign ??? coved (downward concavity) - acute iniury ???
;L*
--ll**,fvt*-
f+ronc-,,..1r *,,^^--J:-r :-^L^-:^ r:-r--^.:^-l Causes: [transmural] myocardial ischemia [infarction] "*,".".
Prinzmetat'sangina
acute pericardiris ventricular aneurysm twperkalemia eariy repolarization ventricular hypertrophy myocarditis Bundle-branch blocks
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ST segment
Depression:
Depressed if the ST segmett is =l> I mm below the baseline, measured at 0.08 seconds (2 mm) after the J point
Note:
a. b, c.
downsloping - most indicative (specific) horizontal - intermediate specificity upsloping - least definitive
digitaiis effects
Bundle-branch block hypokalemia; hypomagnesemia
***
A. Focal changes (Inferior, Anterior, Lateral) reflect ischemic area(s). B. Elevation and depression demonstrate 'current of injury' pattern.
EKG leads
vl -v4
V1
Inferior
Posterior
II.Itr
and aVF
Vl _V3
S
ED Interpretation
Normal Nonspecific Abnormal (nreviously documented) Abnormal (not oreviouslv documented Infarction
n^f
AU<^At\
ED EKG Diasnosis and Diagnosis upon tr'inal Hospital Discharge Emergency Medicine Reports - April 23,2001
AMI
lo/o
3o/o
Unstable Ansina
4o/o
Noncoronarv Diasnosis
95%
7 5o/o
23o/o
7%
25o/o
48Vo
43o/o
45%
32Vo
14o/o
73%
t3%
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CARDIAC MARKERS
(Variable values in Literature)
TEST
TIME
DETECTION
TIME PEAK
12
24 hours
Myogrobin
(i.*,.'
--Tlt
caA
riwory
"rfff"rf
O*^tt'
8 hours
r-+ Troponin
nL-
t^ir)r"-\
Contrsctile Protein
WA4:y>
5. Treatment Plan
a. Lifestyle changes
SpectJic Myocardial
cells
,3,.,ki',* :f t'
Stop smoking Exercise program (as indicated) Modify coexistent risk factors (Chol, Blood sugar...) Control hypertension
Minimize stress
b. Nondlug Therapy
c. Treatment -
Acutely
1. Patient Position
a. Sitting
at=/> 95Yo)
b. Nasal prongs at 2-4 liters usually adequate. c. When oxygen saturation cannot be maintained:/> 950/o, obtain ABG,
or when other clinical diagnosis/therapy requires an ABG. Avoid ABG when possible, if patient is thrombolytic candidate.
3.
fV Access
a.
10
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lnCruA\+.ll, )
4. Monitors
a. Cardiac
Relief
Nitroglycerrn ^fta=o
Morphi'e
Oi J t'^'n'A'
b.
Heparin * Unfractionated
* Low Molecular Weight Heparin (LMWII) o Less risk of bleeding r No dosage changes based on coagulation parameters IIb/IIIa Inhibitors
d,
Thrornboiytic agents (Choice ??) - Given < 70 minutes post-onset - mortality - L2 % - Given > 70 minutes post-onset- mortality - 9 % Indications
sr t"ry;3'r"Hl'J",ftre,rimb);
> 2 mm (precordial) Symptoms < 6 - 12 hours (?? beyond in "stuttering" pattern) LBBB (new onse0
r r . o o r o . r r r r
.""E
Exclusionary Criteria Hemorrhagic CVA within past 6 months Recent head trauma or known intracranial mass Uncontrolled hypertension (> 180-2001> 110-120)
Major surgery within past 2 weeks Active or recent Gastrointestinal bleeding Bleeding disorder or anticoagulation Aortic dissection or pericarditis Noncompressable vessel puncture
Prolonged CPR Previous Streptokinase use (time dependent)
l1
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e. Beta- Blockade
later
f. ACE Inhibitors
Effect on LV remodeling and recurrent ischemia Post-AMI for reduced EF; clinical CF{F; wall motion abnormalities
* Meehanissl
Pulmonary edema/Heart Failure Cardiogenic shock Pericarditis Dressler's syndrome Myocardial wall/Septal rupture LV Wall Aneurysm formation Thrombotic or embolic events
d. Surgery
a.
Patient Education Must treat coexistent conditions Stop smoking Compliance with exercise, diet, medications, etc
Future Appointments
b.
c.
Emergency Visits Recurrence of chest discomfort Pain not relieved by Nitroglycerin Any decompensation/signs of complications
t2
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PERICARDITIS
1. Definition
the heart
2. Pathophysiology
a.
i.
Idiopathic Viruses - Coxsackie, Echovirus, Adenovirus Bacteria - Haemophilus (esp. children) Fungal Uremia Neoplastic Autoimmune (SLE, Rheumatoid Arthritis.....) Dru g-induced (procainamide, hydralazine. . . ..) Post-AMI (Dressler's Syndrome) Acute Pericarditis
Chest pain
ii. Sx/Sx
usually sharp and pleuritic often reduced with sitting up/leaning forward may have associated pericardial friction rub Dyspnea, rales, tachypnea Fever, often with myalgias Odynophagia Cardiac dysrthl'rnias (often supraventricular tachycardias)
Ewart's sign
b. Who's at
risk
Male > Female Adolescents & younger adults Dependent upon etiology (see above)
13
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3. Differential Diagnosis
Acute
MI
Pneumonia
Aortic dissection
PancreatitisiCho lecystitis 4. LaboratoryD(-Ray
WBC - Leukocytosis
ESR Elevated (better to follow treatment and response) Cardiac En4,mes - may be elevated (epicarditis) CXR - may demonstrate pleural effusions/other diagnosis x large pericardial effusion - "waterbottle heart"
EKG
ntay show dffise/global ST segment elevation may show PR segment depression
5. Treatment Plan
a.
Lifestyle changes -
b. Nondrug Therapy c. Rx
d. Surgery
6. Follow Up
a. Patient Education
Up to i5% may expect recuffences Advise on signs of complications (pericardial effi.rsion) Compliance with Rx regimen
b.
Future Appointments
c.
Respiratory/Cardiovascular dysfunction + Progressive/Acute dyspnea * Worsening chest pain * Dizzinessllightheadedness (signs of hypotension)
t4
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Dyspnea
Orthopnea PND
Rales Wheezes Frothy Sputum
lvarvn L_--.-__
[oRirc
*l
i i
Fatigue 'Wealness
LT]NGS
Hepatic Congestion
IVD
Hepatojugular Reflux RUQ Pain
B
loating/As cites/Anorexia
Fatigue
Weakness
15
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HEART FAILIIRE
1.
Definition
Heart Failure is a nonspecific term.
Inability of the heart to pump adequate biood to meet the metabolic needs of the body. May be the result of "heart disease" (unable to pump) or the result of "excessive demands".
May be acute or chronic. May be systolic and/or diastolic in etiology.
2. Pathophysiology
Etiology Normal ejection fraction @2/3 ventricular volume. Myocardial dysfunction (Heart Failure) reduces ejection fraction. When the result is increased diastolic filling pressures, the organs that "empty" in the respective ventricular system become congested.
* Congestive Heart Failure (CHF)
a.
Primaty Hemt Disorders - usually result in contractile abnonnality - Coronary Heart Disease - Valvular Heart Disease - Cardiomyopathies
b. Excessiye Demands
- Increased pressure (afterload) - Increased volume (preload) - Increased tissue oxygen requirements (perfusion)
Staqe
High Risk -for LVD
I
Patient Variables
HTN; CAD; DM Familv Historv Previous Ml; LVD Valvular Heart Disease Dyspnea and Fatigue Reduced exercise tolerance Marked symptoms at rest Maximaltherapv
NYHA
eft
ve
Asymptomatic LVD
c
D
Symptomatic LVD
llIV
ilt
Refractory end-stage HF
16
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D;rr'$'Jd*
Pathology
Reduced Ejection Fraction (EF) Dilated Ventricle Looks large on chest x-ray
Often Normal/Supranormal EF Altered ventricular filling Restrictive Ventricle Stiff and noncompliant ,,----."
, ,^!.Y!.{.-^F..^,*l^J
Clinical Changes
Reduced LV Elevated Pulmonary edema
EF * \r":oPCWP ,L.ru.r.{K
u
Reduced LV Prbssures "n DD.r Elevated Atrial Pressures :'l\as Pulmonary Edema DyspneaMeakness/Fatigue Rales/Peripheral Edema Sa gallop
\j
Symptomatology
Signs
Dyspn ea/Weakness/Fatig
Rales
Ssgallop
Reduced pulse pressure
Acute Tx
Vasodilators Loop Diuretics lnotropic agenis Reduced Na intake ACEIA/asodilators Diuretics (prn) Di goxin/Beta-B lockers
Chronic Tx
o ?ffe--t6;k
?rfu: c'.\\&>
*ne
*rLo:L,
?
Vroo.e v'r\bar\g
c" tc-nt e-",,*,ogr6arr1 (' '( CKu c,^-#''*r en\cgr"--t'r\ {"'tu Tu*;h,p"o=
Male > Female (ages Male = Female (> 75 years old) Note above
b.'Who's at risk
{rr** ,f
i. MalelFemale ii.
Age
40-75)
gocr$,q"*$rUr
Myocardial Infarction Hypertensive Heart Disease Negative Inotropic drugs Also note disorders listed under etiology (above)
l7
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3. Differential Diagnosis -
as:
1"
ft-;i'lr'nr'ifa Z. t DPh"l
4.
LaboratoryIX-RaY'
E-ipt
CXR EKG ABG
:{'
3 r+yp<rl)PCe'ni6\
tast
t{orr'-'
Prd&JL'{c
cBc
Serum Chemistries Drue Levels
Sear-ch for an underlYing cause
b' Lifes
Mo
dif
cati on.
- Sodium Restiction
- Cigarettes - Weight Loss - PhYsical ActivitY
- Oxygen - Diuretics
LooP - Digitaiis @igoxin ILANOXN])
-
L"giot"ntin donverting
* Nitates
- Vasodilators
- MorPhine
t gggit DYsfu,nction
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cornerstone of treatment ,Fffi-THF t'- l--Reduce afterload
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AmlodiPine
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B. Beta-Blockers Should be used in NYHA Classification ll - lll lnitiate at a loew dose lncrease dose not more often ihan every two weeks Monitor for signs of decompensation: Fluid accu mulation (congestion) Bradycardia Heart Block Hypotension
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C. Digoxin Reduces hospitalization rate, but neutral effect on mortality lncreases ejeciion fraciion - 4 - 5 % Reduce neurohormonal abnormalities Effect on baroreceptor abnormalities * Atrial fibrillation (rate unconirolled) and EF < 30 %
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D. Diuretics
May redrrcp the cardiac output (may not be the effect you want) ay cause folate rsveverrrv,rq,,rJ Spiranolactone has been shown to reduce
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6. Follow Up
a.
Patient Education Educate @ Underlying problerns Educate on reducing cardiovascular risk factors Dietary management (sodium restriction) Weight loss lnformation regarding drug side effects
b. Fuhrre Appointments
Weekly (or more frequently) as needed, until stable
c.
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