Foundations CBR20 – Cardiology Exam Questions With Answers
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Foundations CBR20 – Cardiology Exam Questions With Answers
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 co...
Foundations CBR20 – Cardiology Exam
Questions With Answers
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 non-transmural 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?
Prinzmental's Angina (coronary spasm, most do not have CAD; treat with CCBs)
What are early to late EKG changes with ACS?
Hyperacute T's and Giant R (very early and transient), STE, STD (ischemia or reciprocal), Q waves (1
square wide, 1/3 height QRS), TWI
Biphasic T-wave in V2/V3
Wellen's Syndrome: biphasic (type A) or deeply inverted, symmetric (type B) TW 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 sysytem (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 ≥ 1mm 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: STE >1mm with concordant (same direction) QRS, concordant STD >1mm V1-V3,
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 EKG 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, shock 2/2 pump failure or valve dysfunction
What are potential late complications (>24hr) of MI?
Thromboembolism, myocardial rupture, valve rupture, CHF, pericarditis
Pleuritic chest pain 4wks after MI?
Dressler's syndrome: autoimmune pericarditis, typically 2-6wks s/p MI. Tx it with NSAIDs like any
other pericarditis
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
Cardiac Tamponade after MI
Myocardial wall rupture, give IVF and dispo to OR
What EKG finding is classic in Cardiac Tamponade?
Electrical Alternans
Shock + new murmur after recent MI
Papillary muscle rupture, 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)
, What is the only contraindication to aspirin in ACS?
True aspirin allergy (anaphylaxis)
What is better for treatment of STEMI, thrombolytics or PCI?
PCI is better. Thrombolytics should only be considered if PCI is not available at center within 90min or
after transfer within 120min
What EKG changes are included under indications for thrombolysis?
STEMI (STE >2mm for men, >1.5mm for women in V2-3, STE >1mm in 2+ other leads), STD V1-3
(posterior MI), old LBBB + Sgarbossa
What are absolute contraindications for thrombolysis?
Any previous brain bleed or known mass, ischemic stroke or closed head injury within 3mo, known
bleeding disorder, current active bleeding, major surgery in the last 2 months, BP > 180/110 *after
treatment, suspected aortic dissection
What are concerning complications of thrombolysis and how often do they occur?
Intracranial hemorrhage (1/70 to 1/100, >50% mortality), major bleeding (e.g. GI bleed) in 5%
What EKG changes may occur with reperfusion?
Accelerated idioventricular rhythm, NSVT, PVCs; these should be transient, are overall benign and do
not require additional treatment
What is the appropriate treatment of ST elevation after cocaine use?
First treat with benzos, aspirin, nitrates, calcium channel blockers or alpha blockers (e.g.
phentolamine) for HTN, thrombolysis only if ST does not return to baseline after these treatments
What is the appropropriate treatment for HTN after cocaine use?
Benzos, CCBs or phentolamine; NO Beta Blockers (may theoretically lead to unopposed alpha
stimulation and worsened HTN)
What are key risk factors for Infective Endocarditis?
Diseased valves, artificial valves, IV drug use, dental extractions
What heart valve and what organism is most common in Infective Endocarditis?
Left sided (mitral most common valve affecred overall) > right sided (tricuspid > pulmonary); Staph
aureus is most common pathogen but viridans strep if s/p tooth extraction); Tricuspid is most
common with IV drug use (Staph aureus)
Describe the classic physical exam findings in Infective Endocarditis?
Osler Nodes (painful nodules on fingertips), Janeway Lesions (nontender hemorrhagic lesions on
palms/soles), Roth Spots (retinal hemorrhages), Splinter hemorrhages (linear on nails), Petechiae,
New Murmur
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