Myocardial Infarction Flashcards
Definition, Causes and Risk Factors
An occlusion or spasm causing myocardial ischemia and subsequent myocardial tissue death.
Most commonly caused by acute thrombus formation on a ruptured atherosclerotic plaque.
Risk factors are the same as in ischemic heart disease.
Symptoms
Acute-onset chest pain that may radiate to the left arm, jaw, neck, and shoulder
Diaphoresis
Dyspnea
Nausea/vomiting
Lightheadedness/dizziness
Be aware of silent MIs: biggest concern in the elderly, post-menopausal women, and diabetics
Physical Exam
Tachycardia
New mitral regurgitation via ruptured papillary muscle
S4
Hypotension secondary to cardiogenic shock from decreased cardiac output
Crackles from pulmonary edema caused by backflow secondary to decreased cardiac output
Evaluation
Diagnosis made by demonstrating at least 2 out of 3 of the following signs, symptoms, and risk factors
ST-elevation or ST-depression
reflects transmural ischemia or subendothelial ischemia, respectively occurs within minutes and resolves after 24-48 hours
T-wave inversion reflects transmural infarction
occurs within hours, returns to upright after weeks
Q-waves reflect transmural infarction occur within hours can be a sign of an old infarction new-onset left bundle branch block
Positive cardiac enzymes
troponin is standard in first 8 hours
CK-MB standard in the first 24 hours
LDH1 is best for 2-7 days after symptoms
diagnosis of re-infarction made if CK-MB rises four days after the initial presentation
Differential
Angina, PE, aortic disection, pneumothorax, pericarditis, PUD, GERD, cholecystitis, esophageal spasm, aortic dissection
Treatment
All patients with suspected MI are to be:
Hospitalized in CCU or cardiac step-down unit and
Not to be discharged home until ruling out-MI
24-hr cardiac enzymes and serial EKGs
Acute Management
Morphine
Oxygen
Nitroglycerin
ACEI
Aspirin
Beta-blockers (if no hypotension, bradycardia, or pulmonary edema)
Heparin
In first 6 hours
Can use thrombolytics
Heparin (give 48 hours post infarct if TPA has not been used to lyse clot)
Streptokinase
PTCA is more effective if available
5 days following episode
If stress test is positive then order cardiac catherization
Long term therapy
Aspirin
Beta-blockers
Lipid-lowering drugs HMG-CoA reductase inhibitors decrease mortality post-MI
ACEIs
Reduction of social habit risk factors smoking cessation
Potentially schedule for CABG or stenting procedures if needed
Prognosis, Prevention, and Complications
Time to restoration of coronary blood flow is the strongest predictor of long-term prognosis
Cardiac arrythmias (90%) are the most common cause of death
LV failure and pulmonary edema (60%)
Thromboembolism
Cardiogenic shock via decreased cardiac output
Ventricular wall rupture leading to cardiac tamponade if pericardium intact or massive intrathoracic blood loss and death
Papillary muscle rupture with mitral regurgitation
Fibrinous pericarditis results in friction rub 3-5 days post MI
Dressler’s Syndrome autoimmune disease leads to fibrinous pericarditis several weeks post-MI
High Yield
Presentation
an elderly, obese, diabetic patient presents with crushing, substernal chest pain that radiates to the left arm
High Yield
Management
Best next step in management: aspirin
aspirin, nitrates, oxygen and morphine is another acceptable answer
aspirin is the only treatment that decreases mortality
ADP antagonists (clopidogrel) can be used in conjunction with aspirin
Treatment is a better next step instead of diagnostic testing with a clear and classic presentation
Best initial test: EKG
look for ST elevation, if no ST elevation consider NSTEMI and order enzymes
Next test: cardiac enzymes
cardiac troponins are the most specific
CK-MB is very specific and only stays elevated for 1-2 days => can diagnose reinfarction
Myoglobin is the first marker to rise but is non-specific
Other diagnostic tests
Stress test
Used in non-acute setting if EKG and enzymes are not revealing
Dipyidamole/adenosine thallium stress test and dobutamine echo
Useful if patient can’t exercise to 85% of max heart rate (COPD, disability, dementia)
Exercise thallium testing and stress echocardiography used if EKG is not readable (left bundle branch block, digoxin, pacemaker, or baseline EKG abnormality that makes it unreadable)
Most accurate test: angiography down prior to ultimate treatments
Ultimate treatment
PCI - preferred, and must be done within 90 minutes
Tthrombolytics - used if PCI can’t be administered in a timely manner - should be done within 30 minutes
Long-term treatment - post MI
Beta-blockers
ACE inhibitors/ARBs
Statins
these therapies decrease mortality in the long run but are usually not necessary in the acute episode
Spironolactone
only lowers mortality in certain fluid overloaded states
NSTEMI
the key difference in management of NSTEMI vs. STEMI
low molecular weight heparin is used routinely
Thrombolytics are not used
Gp IIb/IIIa inhibitors are used
Complications
