Flashcards in Acute Coronary Syndromes Deck (62)
Non q-wave MI.
Subendocardial ischemia -- few collaterals there and exposed to highest pressures from ventricle
Presentation of ACS?
Ischemic discomfort at rest
Sign of ACS
Either ST segment elevation or non ST segment elevation
Non ST segment elevation ACS
Can be unstable angina, Non-q wave MI, or even a Q wave MI (very rarely)
ST segment elevation ACS
Generally a q-wave MI, but sometimes (rare) can be a non-q wave MI.
Nonocclusive ruptured plaque leading to thrombus causes
Unstable angina, NSTEMI
Occlusive ruptured plaque leading to thrombus causes
Increasing severity of ACS
Unstable angina -> NSTEMI -> STEMI
Most critical distinction to make
NSTEMI or STEMI
Clinical symptoms of MI
Chest pain more severe, longer duration, with greater radiation than normal. Does not improve with rest or nitroglycerin.
Sympathetic discharge (diaphoresis, tachycardia, nausea, clammy skin)
Shortness of breath (LV volume rises, so backs up to lungs)
Who is likely to have an MI without symptoms?
Physical findings of MI
S4 (noncompliant LV)
S3 (volume overload and systolic dysfunction)
Systolic murmur (may come from papillary muscle dysfunction leading to MR)
Why can an MI cause MR?
Because papillary muscle doesn't function properly.
Differential for MI
Pericarditis, pleuritis (pain w/inspiration and diffuse ST ele)
Aortic dissection (ripping pain, BP asymmetry, widened mediastinum on CXR)
ECG findings of USA or NSTEMI
T wave inversion, ST depression or normal
Are biomarkers elevated in USA?
Are biomarkers elevated in NSTEMI
ECG evolution with STEMi
Definition of STEMI
Prolonged chest discomfort unrelieved by nitroglycerin with ST segment elevation on EKG and rise in cardiac markers
Definition of NSTEMI
Angina at rest for longer than 20 minutes without ST segment elevation but with cardiac biomarkers.
Pathophysiology of STEMI
Total or near total occlusion of coronary artery
Pathophys of NSTEMI
Abrupt decrease in myocardial O2, thrombus formation or an atherosclerotic plaque
Management of STEMI
Immediate reperfusion with a preferred door to balloon time of <90 minutes
Management of NSTEMI
Depends on TIMI score
Troponin (T, I, or C)
Creatine Kinase Myocardial Band (CK-MB)
Control calcium mediated interactions between actin and myosin that are released into circulation from muscle and cytosolic reserves during necrosis. TNI and TNT are highly sensitive and specific for myocardial necrosis.
Where is troponin released from first?
Cytosolic pool, but if injury persists, then muscular pool
When do levels of troponin rise and peak?
Rise within 3-4 hours. Peak at 18-36 and decline slowly