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FoEM CBR22- Cardiology Exam

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FoEM CBR22- Cardiology Exam What underlying pathologic process distinguishes myocardial infarction from angina/unstable angina? Atherosclerotic plaque rupture → exposed endothelium → clot attaches → reduced blood flow; if cell death occurs (usually due to complete vascular obstruction) then positive trop and MI; if no cell death occurs then negative trop and angina/unstable angina. What is the difference between transmural and nontransmural infarction? Transmural: usually STEMI, large vessel affected, benefit from thrombolytics/PCI; Non-Transmural: usually NSTEMI, smaller subendocardial artery, may benefit from PCI but no thrombolytics. What defines Unstable Angina? Stable Angina + pain at rest, new pain, increasing pain severity, hemodynamic changes with pain. Acute chest pain at night, EKG with STEMI, all symptoms and EKG changes resolve with nitro? Prinzmetal's Angina (coronary spasm, most do not have CAD). Treat with CCB. What are early to late EKG changes with ACS? Hyperacute T's and Giant R (very early and transient), ST Elevations, ST Depression (ischemia or reciprocal), Q waves (1 square wide, 1/3 height QRS), T wave inversions. What syndrome associated with Biphasic T-wave in V2/V3? Wellens Syndrome: biphasic (type A) or deeply inverted, symmetric (type B) T wave in septal leads = early signal of proximal LAD lesion. Chest Pain with STE V1-V4 with STD II, III, aVL Anterior MI 2/2 LAD occlusion, may affect large territory of LV, septum and conduction system (high grade blocks, wide complex bradycardias), commonly have shock, possible ruptures Chest Pain with STE I, aVL, V5, V6 with STD V1 Lateral MI 2/2 LAD vs LCx occlusion, may affect LV Chest Pain with STE II, III, aVF with STD V1-V4 Inferior MI 2/2 occlusion of PDA (RCA LCx), may affect AV node (usually transient narrow complex bradycardias), may cause papillary muscle rupture Chest Pain with STE III II and V1 V2 Right Ventricular MI, should get R-sided leads (STE in V4R, V5R), 2/2 proximal RCA lesion, associated with Inferior MI. Chest Pain with STD V1-3 Posterior MI, get posterior leads to dx (req only 0.5 mm elevation for STEMI dx), 2/2 occlusion of Posterior Descending (RCA L circ) What meets STEMI criteria for leads V2-V3 versus all other leads? V2-V3: ≥2mm in MEN ≥ 40yrs, ≥2.5mm in MEN 40yrs, or ≥ 1.5mm in WOMEN; All other leads: STE at the J-point of ≥ 1 mm in two contiguous lead What distinguishes Type I-Type V MI? Type I: MI caused by acute atherothrombotic CAD, usually due to plaque rupture or erosion; Type II: MI 2/2 mismatch of oxygen supply and demand; Type III: typical MI presentation but death before biomarkers obtained; Type IV: MI 2/2 PCI; Type V: MI 2/2 CABG How can you detect MI in patients with paced rhythm or old LBBB Sgarbossa Criteria: a) STE 1mm with concordant (same direction) QRS, b) concordant STD 1mm V1-V3, c) STE 5mm with discordant (opposite direction) QRS (modified Sgarbossa changes this last rule to discordant STE 25% preceding S wave) What is unique about the management of Inferior MIs? With Inferior MI, always consider RV involvement and get right-sided ECG leads What is unique about the management MI with right-ventricular involvement? They are preload dependent and will become very hypotensive with nitroglycerin - avoid this, give IVF for hypotension What are potential early complications (24hr) of MI? Arrhythmia (most common), shock 2/2 pump failure or valve dysfunction (valve rupture).

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FoEM CBR22- Cardiology Exam
What underlying pathologic process distinguishes myocardial infarction from angina/unstable angina?
Atherosclerotic plaque rupture → exposed endothelium → clot attaches → reduced blood flow; if cell
death occurs (usually due to complete vascular obstruction) then positive trop and MI; if no cell death
occurs then negative trop and angina/unstable angina.


What is the difference between transmural and nontransmural infarction?
Transmural: usually STEMI, large vessel affected, benefit from thrombolytics/PCI; Non-Transmural:
usually NSTEMI, smaller subendocardial artery, may benefit from PCI but no thrombolytics.


What defines Unstable Angina?
Stable Angina + pain at rest, new pain, increasing pain severity, hemodynamic changes with pain.


Acute chest pain at night, EKG with STEMI, all symptoms and EKG changes resolve with nitro?
Prinzmetal's Angina (coronary spasm, most do not have CAD). Treat with CCB.


What are early to late EKG changes with ACS?
Hyperacute T's and Giant R (very early and transient), ST Elevations, ST Depression (ischemia or
reciprocal), Q waves (1 square wide, 1/3 height QRS), T wave inversions.


What syndrome associated with Biphasic T-wave in V2/V3?
Wellens Syndrome: biphasic (type A) or deeply inverted, symmetric (type B) T wave in septal leads =
early signal of proximal LAD lesion.


Chest Pain with STE V1-V4 with STD II, III, aVL
Anterior MI 2/2 LAD occlusion, may affect large territory of LV, septum and conduction system (high
grade blocks, wide complex bradycardias), commonly have shock, possible ruptures


Chest Pain with STE I, aVL, V5, V6 with STD V1
Lateral MI 2/2 LAD vs LCx occlusion, may affect LV


Chest Pain with STE II, III, aVF with STD V1-V4
Inferior MI 2/2 occlusion of PDA (RCA > LCx), may affect AV node (usually transient narrow complex
bradycardias), may cause papillary muscle rupture


Chest Pain with STE III > II and V1 > V2
Right Ventricular MI, should get R-sided leads (STE in V4R, V5R), 2/2 proximal RCA lesion, associated
with Inferior MI.


Chest Pain with STD V1-3
Posterior MI, get posterior leads to dx (req only 0.5 mm elevation for STEMI dx), 2/2 occlusion of
Posterior Descending (RCA > L circ)


What meets STEMI criteria for leads V2-V3 versus all other leads?

, V2-V3: ≥2mm in MEN ≥ 40yrs, ≥2.5mm in MEN < 40yrs, or ≥ 1.5mm in WOMEN; All other leads: STE at
the J-point of ≥ 1 mm in two contiguous lead


What distinguishes Type I-Type V MI?
Type I: MI caused by acute atherothrombotic CAD, usually due to plaque rupture or erosion; Type II:
MI 2/2 mismatch of oxygen supply and demand; Type III: typical MI presentation but death before
biomarkers obtained; Type IV: MI 2/2 PCI; Type V: MI 2/2 CABG


How can you detect MI in patients with paced rhythm or old LBBB
Sgarbossa Criteria: a) STE >1mm with concordant (same direction) QRS, b) concordant STD >1mm V1-
V3, c) STE >5mm with discordant (opposite direction) QRS (modified Sgarbossa changes this last rule
to discordant STE >25% preceding S wave)


What is unique about the management of Inferior MIs?
With Inferior MI, always consider RV involvement and get right-sided ECG leads


What is unique about the management MI with right-ventricular involvement?
They are preload dependent and will become very hypotensive with nitroglycerin - avoid this, give IVF
for hypotension


What are potential early complications (<24hr) of MI?
Arrhythmia (most common), shock 2/2 pump failure or valve dysfunction (valve rupture).


What are potential late complications (>24hr) of MI?
Thromboembolism, myocardial rupture, valve rupture, CHF, pericarditis


What syndrome would you consider in someone with pleuritic chest pain 4wks after MI?
Dressler's syndrome: autoimmune pericarditis, typically 2-6wks s/p MI. Tx it with NSAIDs.


What artery typically supplies the SA node and AV node?
SA- RCA 60%, LCx 40%; AV- RCA 90%, LCx 10%; concern for bradycardias if Inferior MI


What is the cause of cardiac Tamponade after MI?
Myocardial wall rupture, give IVF, bimodal distribution first few days and 1-2 weeks, pericardial
tamponade. Dispo to OR.


What ECG finding is classic in Cardiac Tamponade?
Electrical Alternans


What could cause a new murmur and shock after MI?
Papillary muscle rupture leading to mitral regurgitation, Rx- reduce afterload and dispo to OR; same
treatment if septal wall rupture


What potential treatments for AMI have been shown to reduce mortality?
Defibrillation for VF/VT (30% mortality reduction), Aspirin (25% mortality reduction)

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