Foundations CBR20 - Cardiology Test Bank Solution Manual (Rated A+)
What underlying pathologic process distinguishes myocardial infarction from angina/unstable angina? -
Answers 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? - Answers 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? - Answers 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? - Answers
Prinzmental's Angina (coronary spasm, most do not have CAD; treat with CCBs)
What are early to late EKG changes with ACS? - Answers 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 - Answers 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 - Answers 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 - Answers Lateral MI 2/2 LAD vs LCx occlusion, may affect
LV
Chest Pain with STE II, III, aVF with STD V1-V4 - Answers 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 - Answers 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 - Answers 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? - Answers 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? - Answers 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 - Answers 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? - Answers With Inferior MI, always consider RV
involvement and get right-sided EKG leads
What is unique about the management MI with right-ventricular involvement? - Answers 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? - Answers arrhythmia, shock 2/2 pump failure or
valve dysfunction
What are potential late complications (>24hr) of MI? - Answers Thromboembolism, myocardial rupture,
valve rupture, CHF, pericarditis
Pleuritic chest pain 4wks after MI? - Answers 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? - Answers SA- RCA 60%, LCx 40%; AV- RCA 90%,
LCx 10%; concern for bradycardias if Inferior MI
Cardiac Tamponade after MI - Answers Myocardial wall rupture, give IVF and dispo to OR
What EKG finding is classic in Cardiac Tamponade? - Answers Electrical Alternans
Shock + new murmur after recent MI - Answers 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? - Answers Defibrillation for
VF/VT (30% mortality reduction), Aspirin (25% mortality reduction)
What is the only contraindication to aspirin in ACS? - Answers True aspirin allergy (anaphylaxis)
What is better for treatment of STEMI, thrombolytics or PCI? - Answers 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? - Answers 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? - Answers 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? - Answers Intracranial
hemorrhage (1/70 to 1/100, >50% mortality), major bleeding (e.g. GI bleed) in 5%
What EKG changes may occur with reperfusion? - Answers 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? - Answers 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? - Answers 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? - Answers Diseased valves, artificial valves, IV drug
use, dental extractions
What heart valve and what organism is most common in Infective Endocarditis? - Answers 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? - Answers 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
What is the appropriate management and treatment of a patient with suspected Infective Endocarditis?
- Answers Blood cultures x 3 (different locations), Echo (transesophageal best), broad spectrum
antibiotics to cover staph/strep/gram negatives (Vanco + PCN + Gent)
When should a patient receive antibiotic prophylaxis for Infective Endorcarditis prior to a procedure? -
Answers High-risk procedures: dental or invasive respiratory; GI/GU procedures don't need abx. High
risk pts: Aritficial or damanged valves, ANY congnetial heart dz hx; Rx: Amoxicillin (dental procedures)
What left sided murmurs are systolic? - Answers Aortic stenosis and mitral regurg
What left sided murmurs are diastolic? - Answers Aortic insufficiency and mitral stenosis
Syncope + systolic murmur radiating to neck - Answers Aortic Stenosis, syncope is poor prognostic sign,
requires surgical consult; causes L heart strain. Patients generally present with angina, then syncope and
then heart failure.
