Week 2: Acute coronary syndrome Flashcards
Define acute coronary syndrome.
-group of clinical symptoms/signs compatible with acute myocardial ischemia and include: sudden death, unstable angina, non-ST elevation MI (Non-Stemi), ST elevation MI (STEMI)
Describe the mechanism of coronary thrombosis.
Atherosclerosis leading to:
- plaque rupture:
- interplaque hemorrhage leads to decreased vessel diameter
- release of tissue factor, activation of of coagulation cascade
- exposure of sub endothelial collagen/turbulent blood flow leading to platelet activation and aggregation–>further vasoconstriction, and activation of coag cascade - Dysfunctional endothelium
- decreased vasodilator effect
- decreased antithrombotic effect
What are the consequences of coronary thrombosis?
- small thrombus: non flow limiting
- no ECG changes
- healing and plaque enlargement
- stable angina - Partially occlusive thrombus
- ST segment depression and/or T wave inversion–>
- unstable angina if no serum biomarkers
- non-ST segment elevation MI if +serum biomarkers - occlusive thrombus
- can have ST segment depression and/or T wave inversion (like above) if it recanalizes or has collateral flow.
- reperfusion in less than 20mins–>unstable angina
- reperfusion after 20min and before 2hrs->NSTEMI
- can have ST elevation which w/ serum biomarkers indicates ST elevation MI
Other uncommon causes of ACS.
-suspected when ACS is in young person or person with no coronary risk factors
Severe coronary artery spasm ( primary or cocaine induced)
Coronary emboli ( endocarditis, prosthetic valves)
Coronary trauma
Increased blood viscosity ( polycythemia vera, thrombocytosis)
Markedly increased myocardial oxygen demand ( severe aortic stenosis or acute aortic regurgitation)
Vasculitis syndromes
Congenital coronary artery anomalies
Describe the clinical presentation of Unstable Angina.
- crescendo pattern in which a patient with chronic stable angina experiences a sudden increase in frequency, duration, and/or intensity of ischemic episodes
- episodes of angina that occur at rest, without provocation
- new onset of anginal episodes, severe class III severity, without previous CAD symptoms
Describe the clinical presentation of myocardial infarction.
- rapid in onset, rapid crescendo to feeling of doom
- pain doesn’t go away with rest
- maybe be little response to nitroglycerin
- systemic signs from sympathetic response: sweating (diaphoresis), tachycardia, cool and clammy skin due to vasoconstriction
- dyspnea (due to reduced LV contractility, causes decreased SV, rise in pressure in LV and EDV, conveyed to left atrium and pulmonary veins)
Describe ECG findings in ACS.
Unstable Angina and NSTEMI
-ST segment depression and/or T wave inversions. May be transient, occurring just during chest pain in UA, or may persist in patients with NSTEMI
STEMI
-acute: initial ST segment elevation
-hours: ST elevation, Q wave begins, decreased R wave
-1-2days: T wave inversion, Q wave deeper
-Days: ST normalizes, T wave inverted
-Weeks: ST and T normal, Q wave persists.
Assessment of ACS
- ECG
- cardiac biomarkers: Troponin is more sensitive than ck-mb. Onset 3-4 hrs, peak 18-36 hrs, persist up to 10-14 days
- Clinical hx and symptoms: chest pain
If still uncertain, echocardiogram useful for assessing wall motion abnormalities in suspected region of ischemia or infarction
Approach to management after EKG, history, and physical exam of ACS.
ALL patients
1. anti-ischemic meds: beta blocker, nitrates, +/-Ca2+ channel blocker
2. General measures: oxygen, pain control
3. additional therapies: ACE inhibitor, statins
STEMI–Reperfusion approach
1. Aspirin
2. heprain
3. clopidogrel
4. reperfusion method: fibronlytic drug or primary PCI w/ GP iib/iiia inhibitor
NSTEMI/UA–antithrombotic approach
1. aspirin
2. heparin
3. clopidogrel
4. high risk patients: GP IIb/IIIa inhibitor, proceed to cardiac cath
Treatment goals and pharmocologic management after ACS.
- relief is ischemia not just chest pain
- prevent propagation of intracoronary thrombosis
- ID high risk patients
- cardiac cath and revascularization in high risk patients who fail medical therapy
- Standard pharmacologic therapy following discharge from the hospital includes measures to reduce the risks of thrombosis (aspirin and clopidogrel), recurrent ischemia (a
Describe treatment strategies for ACS
- Conservative
- stabilized by meds only initially
- cardiac angiography done only if patients fail medical therapy or noninvasive risk assessment indicate high risk features - early invasive strategy
- diagnosis angiography with intent to revascularize
- patients with high risk features
- advantage of early ID and revascularization for high risk anatomy
- but costly and potentially risky