Acute Coronary Syndromes Flashcards
acute coronary syndromes are associated with…
acute plaque changes - either severe partial occlusion or complete occlusion
often due to plaque rupture - lipid core is highly thrombogenic, activates platelet adhesion and clotting cascade —> vessel occlusion —> dramatic decrease in blood supply
what causes atherosclerotic plaques to rupture, leading to acute coronary syndromes?
thinning of cap due to inflammation within and metalloprotease activity
plaques with thin caps or large amounts of lipids are prone to rupture
this exposes the lipid core which is highly thrombogenic - platelets and clotting cascade are activated, and clot causes occlusion of vessel
how long can severe ischemia generally last until irreversible necrosis occurs?
20-30 mins, after that irreversible necrosis occurs
preceded by cell/mitochondrial swelling, glycogen depletion, myofibril relaxation, ATP depletion (within minutes)
recall that necrotizing myocardium releases cardiac biomarkers - troponin I/T (specific, prolonged) and CK-MB (less specific, transient)
describe the cause of NSTEMI/ how it presents
NSTEMI = NON-ST elevated MI = unstable angina
due to severe partial coronary occlusion —> sudden increase in frequency/duration/intensity of symptoms in patient with stable angina, occurring unexpectedly at rest, or new onset of severe anginal symptoms
associated with plaque disruption and thrombus formation with vasospasm
which area of the heart is most affected by NSTEMI?
NSTEMI = NON-ST elevated MI = unstable angina
sub-endocardium (innermost) is most vulnerable to ischemia because it is farthest away from coronary blood supply
how do the symptoms of NSTEMI/unstable angina differ from those of chronic stable angina?
chronic stable angina - predicable, brief, non-progressive symptoms
unstable angina - sudden increase in frequency/duration/intensity of symptoms in patient with stable angina, occurring unexpectedly at rest, or new onset of severe anginal symptoms
what changes may be seen on ECG with unstable angina/NSTEMI? (2)
- new ST segment depression*
- new T wave inversion
*recall ST depression = incomplete occlusion/subendocardial ischemia, while ST elevation = total occlusion/ transmural ishcemia
what can be used to distinguish between unstable angina and NSTEMI, which have the same clinical presentation and ECG?
ECG will show ST depression + T wave inversion
to determine if there is infarction, you need to measure cardiac biomarkers (esp. troponin I/T)
neg. for troponins = unstable angina
pos. for troponins = NSTEMI (non-ST elevation myocardial infarction)
How are unstable angina and NSTEMI medically managed?
want to address symptoms, prevent thrombosis, and reduce remodeling
anti-anginal drugs:
1. nitrates - decrease EDV, wall tension
2. beta blockers - decrease O2 demand
anti-thrombotic drugs:
1. aspirin
2. anticoagulants
reduce remodeling:
1. ACE inhibitors - reduce mortality
2. high intensity statin - reduce mortality
what are the contraindications for the following drugs used to manage unstable angina or NSTEMI?
a. nitrates
b. beta blockers
c. aspirin/anticoagulants
a. nitrates - patients with RV infarct (nitrates reduce preload, exacerbates condition)
b. beta blockers - patients with bradycardia, bronchospasm, heart failure, hypotension
c. aspirin/anticoagulants - patients with bleeding disorders
when does STEMI occur?
STEMI = ST elevation myocardial infarction
symptoms occur due to abrupt cessation of coronary blood flow due to thrombosis (esp. vulnerable plaques) —> progressively (moves inward to outward) transmural injury
*recall ST elevation occurs with total occlusion (transmural), while ST depression occurs with partial occlusion
what histological changes occur following STEMI?
give time frame for >24hours, 2-5days, 7-10days, 2 weeks, and up to 2 months
STEMI = ST elevation myocardial infarction
<24hours: edema creates spaces between cells, lactate dehydrogenase leakage, mitochondrial swelling, marginal contraction band necrosis
2-5days: neutrophils infiltrate and cause degradation
7-10days: macrophages infiltrate to phagocytose debris and necrotic myocytes
2weeks: granulation tissue forms
up to 2 months: collagen deposition and scar formation
what causes marginal contraction band necrosis, a histological change observed in the first 24 hours following STEMI?
typically seen if there has been some re-perfusion to the necrotic area
increased calcium (from blood) causes contraction, and oxygen exposure causes ROS-mediated damage
how do patients with STEMI present?
STEMI = ST elevation myocardial infarction
pain described as heavy, squeezing, crushing which is severe and longer-lasting (>30mins) - centralized to central portion of chest, inner aspect of arms/shoulders/neck/jaw
associated with weakness, sweating, nausea, diaphoresis, “sense of impending doom”
high SNS tone —> pallor with cool skin, high HR/BP
for each location of myocardial infarction, give the artery that was most likely occluded and the ECG leads that would indicate damage here:
a. left anterior surface of heart
b. left lateral surface of heart
c. posterior and inferior surface of heart
a. left anterior surface of heart: LAD - V1-4 (anterior leads)
b. left lateral surface of heart: L circumflex - V5-6 (anterior/lateral leads), I, aVL
c. posterior and inferior surface of heart: right coronary/PDA - II, III, aVF
for each set of leads showing activity indicative of myocardial infarction, name the coronary artery most likely occluded:
a. V1-4
b. V5-6, I, aVL
c. II, III, aVF
a. V1-4: anterior leads, most likely LAD
b. V5-6, I, aVL: left lateral heart, most likely left circumflex
c. II, III, aVF: posterior/inferior heart, most likely right coronary/PDA
what is reperfusion therapy in the context of STEMI
STEMI = ST elevation myocardial infarction = transmural occlusion
repurfusion therapy means opening up the artery and placing a stent
describe the initial pharmacological management of STEMI
- anti-anginal drugs: nitrates (except for RV infarction!), beta blockers (lower O2 demand)
- reduce remodeling: ACE inhibitors (within 24 hours), high intensity statins (reduce mortality)
- anti-thrombotic drugs: aspirin, anticoagulants
*note STEMI should be managed with stent automatically, but if facilities are not capable of this procedure, fibrinolytic therapy can be given also to dissolve the clot
what causes stunned myocardium?
following an acute ischemic event and reperfusion, a portion of myocardium does not respond right away (the muscle is “stunned” by the ischemic event)
can return to normal over time
hibernating vs stunned myocardium
hibernating: heart has reduced its level of activity due to chronic inadequate blood supply
stunned: following acute ischemic event and reperfusion, a portion of myocardium doesn’t respond right away (it’s “stunned”)
in both situations, gradually can return to normal following reperfusion
what is usually the earliest complication of acute MI?
ventricular arrhythmia (fibrillation or tachycardia) - most common cause of sudden cardiac death following acute MI
can be primary (due to ischemia) - onset within 4 hours
or secondary (due to remodeling or scar) - onset within 48 hours
when are bradyarrhythmias or heart block most commonly seen following acute MI?
common, especially with inferior MI (right coronary artery occlusion)
often resolve spontaneously if onset is within 24 hours
inferior MI (RCA) —> sinus bradycardia (SA nodal artery), Mobitz Type I and complete heart block (AV nodal artery)
anterior MI (LAD) —> Mobitz Type II block, bundle branch block
what factor is the development of cardiogenic shock following acute MI most dependent on?
cardiogenic shock following acute MI is strongly dependent on infarct size, occurs 5-7 hours post-MI
leading cause of death for patients with acute MI, half within 48 hours (not sudden cardiac death as with V-tach/fib)
heart cannot recover systolic function —> low CO, BP, pulmonary edema, cool/clammy/cyanotic extremities, agitation/confusion, soft heart sounds + S3, etc, etc, etc
when is peri-infarction pericarditis most common following acute MI?
peri-infarction pericarditis is most common with transmural infarcts
occur within first week, associated with epicardial hemorrhage
resolve spontaneously
how does cardiogenic shock progress following acute MI? (what are the clinical findings)
heart cannot recover systolic function —> low CO, BP, pulmonary edema, cool/clammy/cyanotic extremities, agitation/confusion, soft heart sounds + S3, etc, etc, etc
how does pericardial inflammation present as a post-MI complication? (symptomatically)
chest pain (sharp, centrally located) that is improved by sitting up/leaning forward and pericardial friction rub
contrast peri-infarction pericarditis with Dressler syndrome
both can occur following acute MI
peri-infarction pericarditis: early (within 1 week), inflammation causes blood to pool in pericardium, resolves with NSAIDS, does not affect prognosis
Dressler syndrome: within 2 weeks, autoimmune response to heart antigens released from necrotic cells, ECG shows diffuse ST elevation
ischemic mitral regurgitation and papillary muscle rupture following acute MI most often affects which papillary muscle? what can this lead to?
most often affects posterior papillary muscle (supplied by dominant artery - usually PDA of RCA), occurs 3-5 days post MI
recall posterior papillary muscle has single blood supply, while anterolateral papillary muscle has dual blood supply from LAD and circumflex
can lead to pulmonary edema, followed by cardiogenic shock
can be accompanied by acute mitral regurgitation (early systolic murmur)
when is ventricular septal rupture most common following acute MI? what signs are indicative of this?
ventricular septal return most common with anterior MI (LAD supplies anterior 2/3 of septum), occurs 3-5 days post-MI
accompanied by holosystolic murmur at lower left sternal border (ventricular shunt), pain, dyspnea, signs of pulmonary congestion
when does ventricular free wall rupture typically occur following acute MI, and what is the clinical outcome of this?
ventricular free wall rupture occurs within 1 week
complete rupture causes rapid/sudden death from cardiac tamponade —> hypotension, JVD, muffled heart sounds
what are the signs of ventricular septal rupture following acute MI?
ventricular septal return most common with anterior MI (LAD supplies anterior 2/3 of septum), occurs 3-5 days post-MI
accompanied by holosystolic murmur at lower left sternal border (ventricular shunt), pain, dyspnea, signs of pulmonary congestion
explain how LV aneurysm can be a complication of acute MI
LV aneurysm can be delayed complication, via mural (read: wall) thrombus formation and worsening heart failure or ventricular tachyarrhythmia
