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44 Cards in this Set

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The ischemic cascade ?
increased lvedp→
wall motion abnormality→
st segment changes→
angina
Clinical coronary ischemic events (MI, angina) almost always implies _______.
LV ischemia

--May have concomitant RV and/or atrial infarction also
As a general rule, which wall MI has a higher morbidity and mortality?
anterior
muscles-infarcted mitral papillary muscles can result in mitral regurgitation
More common in ______ wall MI (pm papillary muscle)
inferior
Septal MI can result in ____
VSD
Symptoms of ischemia
Angina (Greek: choking)
Dyspnea
Diaphoresis
Nausea
Fatigue/weakness/faintness
Arrhythmia symptoms
Radiation of angina pectoris
Left arm, possible right or both, throat, jaw, intrascapular
Duration of angina pectoris
Classic is 2 to 5 minutes. Remember, pt’s perception of time is distorted. Rarely if ever less than a minute.
Relief of angina pectoris
Rest, nitroglycerine (ntg relief is very fast; pts relieved by ntg in 10 or 15 minutes is not a ntg effect)
Prinzmetal’s Angina is Chest pain secondary to _____.
coronary artery spasm
is there atherosclerotic obstructive disease in Prinzmetal’s Angina?
Usually no significant atherosclerotic obstructive disease
ECG finding in Prinzmetal’s Angina
Hallmark is ST segment elevation during an occurrence of chest pain
When does Prinzmetal's angina occur?
Occurs at rest
Usually early AM hours
Segmental or global wall motion abnormalities secondary to acute, relatively short occurring ischemia. Viable myocardium with potential for reversibility
Myocardial Stunning
Segmental or global wall motion abnormalities secondary to chronic ischemia. Viable myocardium with potential for reversibility. Differentiate from CMO and infarcted tissue (PET scan)
Myocardial Hibernation
How to reverse wall motion abnormalities?
Revascularization will usually result in improved or complete recovery of wall motion abnormalities
May take several months to reverse
CMO?
cardiomyopathy
Stress testing
Treadmill only

Comment on sensitivity and specificity
Sensitivity and specificity low. High false positives in women
Nuclear Stress testing -

comment on sensitivity and specificity
Highly sensitive and specific
Can assess LVEF response to exercise

a) treadmill stress test
b) nuclear stress test
nuclear stress test
Downside to nuclear stress test
Expensive, time consuming, requires pt cooperation, radiation exposure
Stress Testing For patients unable to walk adequately on a treadmill
Pharmacologic Stress Testing
Agents “stress” the heart and can provide equal assessment to exercise testing for ischemia
Adenosine, dipyrimidole with nuclear
Pharm Stress test type:
Chronotropic/inotropic stress, also provides equally good assessment of ischemia
Dobutamine with nuclear or Echo
Stress test type:
Evaluation of new wall motion abnormalities compared to rest as a sign of ischemia
Equal sensitivity and specificity to nuclear stress testing
Echocardiographic stress test
Same quality, location, related symptoms, etc as stable angina but occurs with little or no exertion, or represents a marked change in pattern from the pts stable condition (occurring with less activity, more frequent, more intense, persists for longer periods of time)
Unstable Angina Pectoris
Unstable symptoms with positive enzyme elevation and no st segment elevation on the ECG
Old names include sub-endocardial MI, and non-Q wave MI
Early mortality and morbidity less than STEMI but 1 year M&M begins to catch up
Non ST segment elevation MI
what differentiates NSTEMI and unstable angina pectoris?
Elevation of cardiac enzymes differentiates NSTEMI and UAP
Consider these entities as a continuum
As the name states, must have ECG st segment elevation criteria for diagnosis, along with cardiac enzyme elevation
ST Segment MI
Not all st segment elevation on an ECG constitutes infarction (consider pericarditis, early repolarization, _______.)
bundle branch blocks, hypertrophy, spasm
Usually means transmural injury, old names transmural MI, Q wave infarct
ST Segment MI
Physical Findings of MI
Persistent anginal pain, dyspnea, diaphoresis
Acute distress, clammy skin, exam may be normal, or may include S4 or S3 gallop, murmur of MR or VSD, neck vein distention, pulmonary rales, low blood pressure
ECG findings of MI
Classic st segment elevation (fireman’s hat), st segment depression and/or t wave inversion, arrhythmias, heart block, tachy or bradycardia
Echo findings of MI
Wall motion abnormality, MR, VSD
CXR of MI
Look for CHF (edema)
Cardiac catheterization of MI
LV wall motion abnormality, occluded, or near occluded vessel
STEMI usually results from total vessel occlusion
NSTEMI and UAP usually results from sub total occlusion, or total occlusion with collaterals
Labs of MI
Cardiac marker enzymes are the mainstay of diagnosis
Troponin I and T are the most specific, very sensitive (false elevations occur
Elevation of CK, SGOT, LDH-much less clinical utility
Myocardial Infarction Treatment

(ins company is watching you!)
Oxygen
Rest
Pain management
Anxiolytic
Blood pressure control
Anti-platelet (ASA is mainstay, plavix, IIb-IIIa agents)
B blockers, if no contra-indications
Nitroglycerine
Heparin (unfractionated)
ST segment MI, or new LBBB: fibrinolytic, if no contra, and no plan for immediate cath and intervention
Non ST segment MI: Glycoprotein IIb-IIIa agent
Intensive care unit
Potential additional pharm agents: Plavix, ACE-I, coumadin, statin, anti-arrhythmics
The ultimate predictor of morbidity and mortality is infarct size: often reflected as what heart parameter
ejection fraction.
Acute Coronary Revascularization
treatments
PTCI: balloon angioplasty, stents
treatment of Ventricular Arrhythmias post-MI
Lidocaine, amiodarone
Polymorphic VT usually indicates ________ mediated
ischemia
Monomorphic VT usually secondary to __________
scar tissue
Treatment of CHF post-MI
diuresis, morphine, afterload reduction, possible need for positive inotrope