High-yield algorithms, recognition patterns, and exam traps — built for rapid last-minute recall.
Includes: STEMI, NSTEMI, Unstable Angina (UA)
Pathology: Atherosclerotic plaque rupture → thrombus → myocardial ischemia/infarction
If you see this in the stem → Think ACS:
| Type | ECG Changes | Troponin | Key Point |
|---|---|---|---|
| STEMI | ST elevation (≥1mm limb, ≥2mm chest) in anatomical distribution | ↑ Elevated | Transmural infarction |
| NSTEMI | ST depression OR T wave inversion | ↑ Elevated | Subendocardial infarction |
| Unstable Angina | Normal OR ST depression | Normal | Pre-infarction state |
| Method | Timing | Details |
|---|---|---|
| PCI (Primary PCI) | Door-to-balloon: <90 min | PREFERRED. Best if within 12h of symptom onset. |
| Thrombolysis (tPA/TNK) | Door-to-needle: <30 min | Only if PCI unavailable. Effective within 12h (ideally <3h). |
Thrombolysis contraindications: Prior hemorrhagic stroke (ever), ischemic stroke <3 months, active bleeding, suspected aortic dissection.
Inflammation of pericardial sac → sharp pleuritic chest pain improved by leaning forward
Pericardial friction rub: High-pitched, scratchy, 3-component sound. Best heard at left sternal border, patient leaning forward. May be transient (come and go).
| Stage | ECG Finding |
|---|---|
| 1 | Diffuse ST elevation + PR depression |
| 2 | Normalization |
| 3 | T wave inversion |
| 4 | Normalization |
First-line: NSAIDs (ibuprofen 600mg TID OR aspirin high-dose) + Colchicine (0.6mg BD)
Indications for admission: High fever (>38°C), large effusion, tamponade signs, immunosuppression, trauma history, anticoagulation use.
Tear in aortic intima → blood enters media → creates false lumen → SURGICAL EMERGENCY
"Tearing/ripping chest or back pain" + any of:
Hypertension (most common), Marfan syndrome (tall, arachnodactyly), Ehlers-Danlos syndrome, bicuspid aortic valve, cocaine use, pregnancy (3rd trimester), trauma.
First test if stable: CT angiography (gold standard). If unstable: Bedside echo (TTE/TEE). CXR: Widened mediastinum (>8cm), abnormal aortic contour.
Medical management UNLESS: malperfusion (renal, mesenteric, limb), rupture, uncontrolled pain/HTN, progression of dissection. Treatment: Beta-blockers + pain control.
| Condition | Pain Quality | Key Features | First Test |
|---|---|---|---|
| Costochondritis | Sharp, stabbing | Reproducible on palpation, localized tenderness | Clinical diagnosis |
| GERD | Burning | After meals, relieved by antacids | Clinical, PPI trial |
| Esophageal spasm | Squeezing | May mimic ACS, triggered by swallowing | Barium swallow, manometry |
| Pneumonia | Pleuritic | Fever, cough, crackles | CXR |
| Pneumothorax | Sharp, pleuritic | Sudden onset, ↓ breath sounds | CXR (upright) |
| Pulmonary embolism | Pleuritic | Sudden dyspnea, risk factors (DVT, surgery) | D-dimer → CT-PA |
| Anxiety/Panic | Tightness | Palpitations, hyperventilation, paresthesias | Diagnosis of exclusion |
Even if pain seems "atypical," consider ACS if:
Heart's inability to meet metabolic demands → fluid overload + low cardiac output
| Feature | HFrEF (Systolic) | HFpEF (Diastolic) |
|---|---|---|
| Ejection Fraction | <40% | ≥50% (preserved) |
| Pathophysiology | Weak contraction (dilated heart) | Stiff ventricle (can't relax) |
| Physical Exam | S3 gallop (ventricular filling) | S4 gallop (atrial contraction against stiff ventricle) |
| Patient Profile | Post-MI, dilated cardiomyopathy | Elderly, hypertensive, diabetic women |
| CXR | Cardiomegaly (↑ heart size) | Normal heart size |
| Mortality Rx | ACE-I/ARB + BB + MRA + SGLT2i | No proven mortality benefit |
| Symptom Rx | Diuretics for volume | Diuretics + BP control |
CXR signs of pulmonary edema (ABCDE): Alveolar edema (bat-wing), B lines (Kerley B), Cardiomegaly (>0.5), Dilated upper lobe vessels (cephalization), Effusions (pleural).
ECG: Irregularly irregular rhythm + No P waves + Narrow QRS (usually)
"Irregularly irregular" = AFib until proven otherwise
| Criterion | Points |
|---|---|
| CHF | 1 |
| Hypertension | 1 |
| Age ≥75 | 2 |
| Diabetes | 1 |
| Stroke/TIA/thromboembolism | 2 |
| Vascular disease (MI, PAD, aortic plaque) | 1 |
| Age 65-74 | 1 |
| Sex (Female) | 1 |
Score ≥2 (men) or ≥3 (women) → Anticoagulate (DOAC preferred over warfarin)
ECG: Narrow QRS tachycardia + Sudden onset/offset + Rate 150-250
Management (stable): Vagal maneuvers first → Adenosine 6mg rapid IV push (↑ to 12mg ×2 if needed; warn patient: "chest tightness, sense of doom for 10 seconds"; contraindicated in asthma) → If recurrent: BB or non-DHP CCB → Definitive: Catheter ablation.
If UNSTABLE → Synchronized cardioversion.
ECG: Wide QRS (>120ms) + Rate >100
ECG: Chaotic, no organized QRS. Management: Immediate CPR + Defibrillation.
| Type | ECG | Management |
|---|---|---|
| 1st Degree | Prolonged PR (>200ms), all P waves conducted | Observation only |
| 2nd° Mobitz I (Wenckebach) | Progressive PR lengthening until dropped QRS | Usually benign, observe |
| 2nd° Mobitz II | Fixed PR, sudden dropped QRS | HIGH RISK → Pacemaker |
| 3rd Degree (Complete) | P waves and QRS completely dissociated | Pacemaker immediately |
Key distinction: Mobitz I: Usually AV node → Benign. Mobitz II: Usually His-Purkinje → Dangerous, high risk of progressing to complete block.
| Type | Clinical Features | Hemodynamics | Management |
|---|---|---|---|
| Cardiogenic | Hypotension, cold/clammy, ↑JVP, crackles | ↓CO, ↑PCWP, ↑SVR | Inotropes (dobutamine), treat MI, minimal fluids |
| Obstructive | Tamponade: Beck's triad; Tension PTX: tracheal deviation, ↓breath sounds | ↓CO, ↑CVP | Pericardiocentesis / Needle decompression |
| Septic | Warm skin (early), fever/hypothermia, AMS | ↓SVR, ↑CO (early) | IV fluids 30mL/kg + antibiotics + norepinephrine |
| Hypovolemic | Cold/clammy, ↓JVP, tachycardia | ↓CO, ↓CVP, ↑SVR | Aggressive IV fluids, blood products |
"Post-MI patient, cold extremities, lung crackles, BP 80/50." JVP elevated. Key: Pump failure → fluid backing up into lungs.
Additional: Pulsus paradoxus (SBP drop >10mmHg on inspiration), electrical alternans on ECG, echo: diastolic collapse of RA/RV.
Sudden onset, unilateral ↓breath sounds, tracheal deviation AWAY, hypotension + ↑JVP. DON'T wait for CXR → Clinical diagnosis → Immediate needle decompression.
Sound: Harsh crescendo-decrescendo ("ejection murmur"). Location: Right 2nd ICS. Radiation: To carotids. Timing: Midsystolic.
Classic Triad (Severe AS) — SAD mnemonic: Syncope (exertional), Angina (exertional), Dyspnea (HF symptoms).
Physical Exam: Delayed carotid upstroke ("pulsus parvus et tardus"), narrow pulse pressure, S4 gallop, paradoxical splitting of S2.
Causes: Senile calcific (>70yo), bicuspid valve (younger), rheumatic fever.
Severity: Valve area <1.0 cm² = severe | Mean gradient >40 mmHg = severe.
Mgmt: Valve replacement (surgical or TAVR). Once symptoms develop, survival 2-3 years without surgery.
Sound: Holosystolic (blowing). Location: Apex. Radiation: To axilla.
Causes: Acute — papillary muscle rupture (post-MI), endocarditis, chordae rupture. Chronic — MVP, rheumatic, dilated cardiomyopathy.
Physical Exam: Displaced apex, S3 gallop, hyperdynamic apex.
Mgmt: Acute severe MR → Emergency surgery. Chronic → Surgery if symptomatic or EF <60%.
Sound: Mid-systolic click ± late systolic murmur. Key Feature: Click-murmur complex.
Maneuvers: Valsalva/standing → click earlier, murmur longer (↓venous return). Squatting/leg raise → click later, murmur shorter (↑venous return).
Associated with: Marfan, Ehlers-Danlos, thin young females. Usually benign.
Sound: Harsh holosystolic at LLSB. Paradox: Small VSD = louder murmur (high-velocity jet). Large VSD = softer murmur + HF symptoms.
Mgmt: Small → Observe. Large → Surgical repair.
Sound: High-pitched, blowing, early diastolic. Location: Left 3rd-4th ICS. Best heard: Patient sitting forward, breath held in expiration.
Chronic AR signs: Wide pulse pressure (>60), bounding "water-hammer" pulses (Corrigan), head bobbing (de Musset), capillary pulsations (Quincke), pistol-shot femorals (Traube).
Causes: Chronic — bicuspid, rheumatic, connective tissue. Acute — endocarditis, dissection, trauma → SURGICAL EMERGENCY.
Sound: Low-pitched rumbling, diastolic. Location: Apex. Best heard: Left lateral position, bell.
Cause: Almost always rheumatic heart disease (history 10-20 years prior).
Physical Exam: Loud S1, opening snap, diastolic rumble, accentuation with exercise.
Complications: AFib (LA enlargement), pulmonary hypertension, thromboembolism.
Mgmt: Mild → Medical (rate control if AF, anticoagulation). Severe → Balloon valvuloplasty or surgery.
| Murmur | Timing | Location | Radiation | Key Feature |
|---|---|---|---|---|
| AS | Systolic | R 2nd ICS | Carotids | Crescendo-decrescendo, delayed carotid pulse |
| MR | Holosystolic | Apex | Axilla | Blowing |
| MVP | Mid-late systolic | Apex | — | Click before murmur |
| VSD | Holosystolic | LLSB | — | Loud if small defect |
| AR | Early diastolic | L 3rd ICS | — | High-pitched, blowing, wide pulse pressure |
| MS | Diastolic | Apex | — | Opening snap, rumbling, loud S1 |
| TR | Holosystolic | LLSB | — | ↑ with inspiration (Carvallo sign) |
Increase with Valsalva/Standing (↓ preload):
Decrease with Valsalva/Standing:
Increase with Squatting/Hand grip (↑ afterload):
Decrease with Hand grip:
Increase with Inspiration (↑ venous return to RV):
The 4 Defects:
Presentation: Cyanosis (degree depends on severity of PS). "Tet spells" — crying/feeding → ↑O₂ demand → ↑cyanosis → irritability → more crying (vicious cycle). Squatting posture (↑SVR → ↓R→L shunt → ↑pulmonary flow).
CXR: "Boot-shaped heart" (upturned apex from RVH). ECG: RVH (right axis deviation).
Other Cyanotic Defects: Transposition of Great Arteries (most common cyanotic in newborns, "egg-on-string" CXR), Truncus arteriosus, Tricuspid atresia, TAPVR.
Key Feature: Fixed splitting of S2. S2 normally splits with inspiration; in ASD: split is wide and FIXED (doesn't change with breathing). Mechanism: ↑RA volume → delays RV emptying → delayed P2.
Murmur: Systolic ejection murmur at pulmonic area (↑flow across normal pulmonary valve).
Types: Ostium secundum (most common, 70%) | Ostium primum (associated with Down syndrome).
Complications: Atrial arrhythmias, paradoxical embolism.
Murmur: Harsh holosystolic at LLSB. Paradox: Smaller defect = louder murmur.
Small VSD (Roger disease): Loud murmur, no symptoms, many close spontaneously.
Large VSD: Softer murmur, HF symptoms, Eisenmenger syndrome risk.
Murmur: Continuous "machinery" murmur (systole + diastole). Location: Left infraclavicular. Associated: Bounding pulses, wide pulse pressure.
Risk factors: Prematurity, high altitude, maternal rubella.
Mgmt: Indomethacin/ibuprofen (closes PDA in neonates by inhibiting PGE2) | Surgical ligation if medical fails.
Atherosclerotic narrowing of peripheral arteries (usually lower extremity)
Classic: Intermittent claudication — calf pain with walking, relieved by rest. Progression: Asymptomatic → Claudication → Rest pain → Tissue loss (ulcers, gangrene).
Physical Exam: Diminished/absent pulses, cool extremity, hair loss, shiny atrophic skin, pallor on elevation, rubor on dependency.
Diagnosis — Ankle-Brachial Index (ABI):
Mgmt: Smoking cessation (MOST IMPORTANT) + statin + BP/diabetes control → Antiplatelet (aspirin/clopidogrel) → Exercise rehabilitation → Cilostazol (if lifestyle fails; contraindicated in HF) → Revascularization if severe.
Definition: ≥140/90 mmHg (general) | ≥130/80 mmHg (diabetes, CKD, age >65)
| Stage | BP Range |
|---|---|
| Stage 1 | 130-139 / 80-89 |
| Stage 2 | ≥140/90 |
| Hypertensive urgency | >180/120, no end-organ damage |
| Hypertensive emergency | >180/120 + end-organ damage |
End-organ damage: CNS (encephalopathy, ICH), Cardiac (ACS, pulmonary edema), Renal (AKI), Vascular (dissection).
Mgmt: IV antihypertensive (reduce BP 10-20% in first hour) — Nicardipine/clevidipine, Labetalol, Nitroprusside (avoid in renal failure). Monitor in ICU. Avoid rapid BP reduction (except aortic dissection).
Specific situations:
Infection of endocardial surface → vegetations (platelet-fibrin + bacteria) on valve leaflets
Acute: S. aureus on normal valve | Subacute: S. viridans on abnormal/prosthetic valve
Definite IE = 2 Major OR 1 Major + 3 Minor OR 5 Minor
Major: (1) Positive blood cultures with typical organisms ×2 (2) Positive echo (vegetation/abscess/dehiscence) or new regurgitation.
Minor: Predisposition, fever ≥38°C, vascular phenomena (Janeway), immunologic (Osler/Roth), positive cultures not meeting major.
| Scenario | Organism | Key Point |
|---|---|---|
| Native (acute) | S. aureus | Most common overall |
| Native (subacute) | S. viridans | Post-dental |
| IVDU | S. aureus | Tricuspid, septic pulmonary emboli |
| Prosthetic early | S. epidermidis | Biofilm former |
| Colon cancer link | S. bovis | Always colonoscopy! |
| Culture-negative | HACEK group | Prolonged incubation |
Empiric: Vancomycin + Gentamicin (add Rifampin if prosthetic).
Prophylaxis (before dental): Amoxicillin 2g PO 1h before. Who: Prosthetic valves, prior IE, unrepaired cyanotic CHD, transplant with valvulopathy.
Thrombus (usually from DVT) embolizes to pulmonary vasculature → V/Q mismatch → hypoxemia → RV strain
Virchow's Triad: (1) Stasis (2) Endothelial injury (3) Hypercoagulability (cancer, OCP, Factor V Leiden)
| Criteria | Points |
|---|---|
| Clinical signs of DVT | 3 |
| PE most likely diagnosis | 3 |
| Heart rate >100 | 1.5 |
| Immobilization/surgery in prior 4 weeks | 1.5 |
| Previous DVT/PE | 1.5 |
| Hemoptysis | 1 |
| Active cancer | 1 |
Score ≤4: D-dimer → if negative, PE excluded. Score >4: CTPA directly (gold standard).
Anticoagulation: Initial: LMWH, UFH, or fondaparinux → Long-term: DOAC preferred or warfarin (INR 2-3).
Duration: Provoked: 3 months | Unprovoked: ≥3 months/indefinite | Cancer: indefinite.
Massive PE (hemodynamically unstable):
Elevated LDL = causal risk factor for ASCVD. Treatment guided by overall CV risk, not just lipid numbers.
| Component | Desirable | Borderline | High Risk |
|---|---|---|---|
| Total Cholesterol | <200 | 200-239 | ≥240 |
| LDL | <100 | 130-159 | ≥160 |
| HDL | ≥60 (protective) | 40-59 | <40 (risk) |
| Triglycerides | <150 | 150-199 | ≥200 |
Friedewald: LDL = Total − HDL − (TG/5) | Invalid if TG >400
4 Major Statin Benefit Groups:
| Intensity | LDL ↓ | Examples |
|---|---|---|
| High | ≥50% | Atorvastatin 40-80mg, Rosuvastatin 20-40mg |
| Moderate | 30-49% | Atorvastatin 10-20mg, Rosuvastatin 5-10mg, Simvastatin 20-40mg |
| Low | <30% | Simvastatin 10mg, Pravastatin 10-20mg |
Add-ons if not at goal: Ezetimibe (↓LDL 15-20%) → PCSK9i (↓LDL 50-60%) → Bempedoic acid (statin-intolerant).
TG ≥500: Fibrates FIRST (prevent pancreatitis) | Icosapent ethyl (EPA) ↓ CV events.
If you see this phrase → Think this diagnosis:
| Parameter | Value |
|---|---|
| Normal EF | 55-70% |
| HFrEF | EF <40% |
| Severe AS | Valve area <1 cm², gradient >40 mmHg |
| Troponin rise | 3-4 hours post-MI |
| Door-to-balloon (STEMI) | <90 minutes |
| Door-to-needle (tPA) | <30 minutes |
| ABI normal | 1.0-1.4 |
| ABI PAD | <0.9 |
| CHA₂DS₂-VASc threshold | ≥2 (men) or ≥3 (women) → Anticoagulate |
| Hypertensive emergency | >180/120 + end-organ damage |
| Normal PR interval | 120-200 ms |
| Normal QRS | <120 ms |
| VT definition | ≥3 consecutive ventricular beats at >100 bpm |
Correct: C) Aspirin 300mg chewed
Concept: STEMI first-10-minutes algorithm Recall
Why C: TIME = MUSCLE. Chewed aspirin cuts mortality by 23% and is given BEFORE the ECG — drug first, then diagnostics.
Discriminator: crushing pain + anterior ST elevation = STEMI in progress.
| A) ECG | Mandatory within 10 minutes, but aspirin goes first — that is the exam point |
| B) Troponin | Diagnostic support only; waiting for it delays reperfusion decisions |
| D) Morphine | Analgesia, but delays platelet effect of antiplatelets — use sparingly |
Trap: Sequence trap — running diagnostics before giving the mortality drug.
Future alert: Suspected STEMI → aspirin 300mg chewed precedes everything, even the ECG.
Correct: B) Anticoagulation (DOAC or warfarin)
Concept: CHA₂DS₂-VASc-driven anticoagulation in AFib Recall
Why B: Score ≥2 in men mandates anticoagulation; DOAC is preferred over warfarin. AFib carries a 5× stroke risk.
| A) Aspirin | Inadequate stroke protection at this score — not an alternative to anticoagulation |
| C) Observation | Ignores a clear anticoagulation indication |
| D) Cardioversion | Patient is stable; if done >48h or unknown onset it needs TEE or 3 weeks of anticoagulation first |
Trap: Undertreatment trap — offering aspirin where a DOAC is indicated.
Future alert: CHA₂DS₂-VASc ≥2 (men) / ≥3 (women) → anticoagulate.
Correct: B) Pericarditis
Concept: Pericarditis ECG vs STEMI Interpretation
Why B: Sharp pain better sitting forward + diffuse ST elevation + PR depression + NO reciprocal changes + normal troponin = the pericarditis signature.
Discriminator: PR depression with diffuse (non-anatomical) ST elevation.
| A) STEMI | ST elevation in ONE anatomical territory WITH reciprocal depression; troponin rises 3-4h |
| C) Dissection | Tearing pain, pulse/BP differential, widened mediastinum — none present |
| D) PE | Pleuritic pain with hypoxia and risk factors, not diffuse ST elevation with PR depression |
Trap: Recognition trap — any ST elevation reflexively labelled STEMI.
Future alert: Diffuse ST↑ + PR↓ + no reciprocal changes = pericarditis, not STEMI.
Correct: C) Assume VT, give amiodarone
Concept: Wide-complex tachycardia rule Analysis
Why C: In known heart disease, wide-complex tachycardia is VT until proven otherwise — treating as VT is the safe default. Stable VT → amiodarone 150mg IV over 10 min.
| A) Adenosine | An SVT tool; useless in VT and misleading as a diagnostic trial here |
| B) Verapamil | DANGEROUS — non-DHP CCB in VT can cause hemodynamic collapse |
| D) Observation | Untreated VT can degenerate into V-fib |
Trap: Misclassification trap — hoping the wide complex is just SVT with aberrancy.
Future alert: Wide QRS + structural heart disease = VT. Amiodarone, not verapamil.
Correct: B) IV fluids
Concept: RV infarction complicating inferior MI Analysis
Why B: Inferior MI + hypotension + elevated JVP + CLEAR lungs = RV infarction. The RV is preload-dependent — volume loading restores output.
Discriminator: hypotension with clear lungs — the pump works, the right side fails.
| A) Diuretics | Drop preload — exactly the wrong direction in RV infarction |
| C) Inotropes | Second-line here; volume first, inotropes if fluids fail |
| D) Nitrates | Forbidden — venodilation kills preload; check V4R before any nitrate in inferior MI |
Trap: Treatment trap — treating the ECG territory instead of the hemodynamics.
Future alert: Inferior MI + hypotension + clear lungs → fluids first, nitrates never.
Correct: B) ASD
Concept: Fixed split S2 buzzword Recall
Why B: ↑RA volume delays RV emptying → delayed P2 that does not vary with respiration — fixed splitting is pathognomonic for ASD.
| A) VSD | Harsh holosystolic murmur at LLSB, not a fixed split |
| C) PDA | Continuous "machinery" murmur, left infraclavicular |
| D) PS | Delay P2 but the split stays physiologic, not fixed |
Trap: Buzzword trap — fixed split has one owner.
Future alert: Fixed split S2 = ASD until proven otherwise (secundum >70%).
Correct: C) CT angiography
Concept: Aortic dissection diagnostic pathway Interpretation
Why C: Tearing pain + BP differential between arms = dissection; in a STABLE patient CT angiography is the gold standard.
| A) ECG | May show inferior changes from RCA ostium involvement — misleading, not diagnostic |
| B) Troponin | May be normal in dissection; cannot exclude it |
| D) Echo | Bedside TTE/TEE is for the UNSTABLE patient, not the stable workup |
Trap: Next-step trap — reaching for troponins in a dissection story.
Future alert: Stable + dissection suspicion → CTA. Unstable → bedside echo and the OR.
Correct: A, B, C and E (multi-select)
Concept: HFrEF mortality-reduction drugs ("ABCD" + SGLT2i) Recall
Why: The mortality quartet in HFrEF is ACEi/ARB, evidence-based beta-blockers, aldosterone antagonists (EF <35%), and SGLT2 inhibitors (↓ mortality ~30%).
| D) Digoxin | Symptom control and rate control only — NO mortality benefit |
Trap: Select-all trap — digoxin rides along in every HFrEF list but never earns a mortality claim.
Future alert: Mortality drugs = ACEi/ARB + BB + MRA + SGLT2i. Everything else is symptom care.
Correct: B) Worsened
Concept: Beta-blocker initiation timing in HF Interpretation
Why B: Beta-blockers are negative inotropes — starting one during acute decompensation worsens congestion and can precipitate shock. Wait until euvolemic.
| A) Improved | The long-term mortality benefit does not apply during acute decompensation |
| C) No change | A negative inotrope on a failing, congested ventricle has real consequences |
Trap: Timing trap — right drug, wrong moment.
Future alert: Never INITIATE a beta-blocker in acute decompensated HF — stabilize first.
Correct: B) Beta-blocker
Concept: Cocaine-induced MI pharmacology Interpretation
Why B: Beta-blockade leaves alpha-mediated vasoconstriction unopposed → worsened coronary vasospasm and hypertension.
| A) Aspirin | Appropriate — standard ACS care |
| C) Benzodiazepines | First-line — they calm the sympathetic drive |
| D) Nitrates | Appropriate — vasodilation counters the spasm |
Trap: Substance-specific trap — applying routine ACS care without adjusting for cocaine.
Future alert: Cocaine MI → benzodiazepines + nitrates + CCB. Beta-blockers never.
Correct: B) IV isotonic fluids
Concept: RV infarction — preload-dependent failure Analysis
Why B: Inferior STEMI (II, III, aVF) with reciprocal I/aVL changes, hypotension, raised JVP and CLEAR lungs is RV infarction until proven otherwise (confirm ST↑ in V4R). The RV fails as a volume conduit — output depends on preload, so fluids restore cardiac output.
Discriminator: hypotension + congested neck veins + clear lungs.
| B) Fluids | Correct — volume loading is first-line in RV infarct |
| A) Nitrates | Drop preload — can precipitate profound collapse; contraindicated here |
| C) Furosemide | Same preload crime as nitrates, worse — the lungs are already clear |
| D) Morphine and observe | Analgesia without hemodynamic rescue; delays definitive care |
| E) Cardioversion | No arrhythmia to cardiovert — the problem is preload, not rhythm |
Trap: Treatment trap — reflexively treating any MI with nitrates.
Future alert: Before nitrates in ANY inferior MI, check V4R and the lungs.
Correct: B) Aspirin 300mg chewed
Concept: STEMI first-10-minutes sequencing Recall
Why B: Aspirin is the first drug in the algorithm — chewed for buccal absorption, given before the ECG is even repeated. 23% mortality reduction.
| A) Morphine | Relieves pain but delays antiplatelet absorption — after aspirin, sparingly |
| C) Clopidogrel | Part of dual antiplatelet therapy but follows aspirin, not before it |
| D) Nitroglycerin | After aspirin; and only if BP adequate and no RV infarct |
| E) Heparin | Anticoagulation follows antiplatelet loading in the sequence |
Trap: Order trap — all five are "given in STEMI," the exam tests the ORDER.
Future alert: First drug in STEMI = chewed aspirin. Everything else lines up behind it.
Correct: E) Metoprolol
Concept: Cocaine-induced MI — unopposed alpha Analysis
Why E is contraindicated: Beta-blockade removes beta-2 vasodilation, leaving alpha vasoconstriction unopposed → worsening coronary spasm and BP.
| A) Aspirin | Correct therapy — standard ACS antiplatelet |
| B) Lorazepam | First-line — cuts sympathetic drive, often resolves pain and hypertension alone |
| C) Nitroglycerin | Correct — counters coronary vasospasm |
| D) Verapamil | Acceptable alternative if benzos + nitrates fail — CCB, no unopposed alpha problem |
Trap: Recognition trap — young patient + MI + drug history; missing the cocaine context makes BB look routine.
Future alert: Cocaine + chest pain → benzos + nitrates (+CCB). Beta-blockers are the forbidden fruit.
Correct: B) Dressler syndrome
Concept: Post-MI pericarditis timing Interpretation
Why B: Weeks (2-10) after MI + fever + pleuritic pain + friction rub = autoimmune (Dressler) pericarditis. Early post-MI pericarditis is 1-3 days and direct inflammation.
Discriminator: the calendar — 3 weeks = late = autoimmune.
| A) Early pericarditis | Wrong time window — that is 1-3 days post-MI |
| C) Recurrent MI | Would show new ST changes and rising troponin, not a friction rub at 3 weeks |
| D) Endocarditis | Fever + new murmur + vegetation story, not pleuritic pain with a rub |
| E) Pneumonia | Cough, sputum, consolidation — not a pericardial rub |
Trap: Timing trap — both post-MI pericarditids exist; the calendar separates them.
Future alert: Post-MI + weeks + friction rub = Dressler (NSAIDs + colchicine).
Correct: C) Hemorrhagic stroke 6 years ago
Concept: Thrombolysis contraindications Recall
Why C: Any PRIOR hemorrhagic stroke (ever) is an absolute contraindication — re-bleeding risk is prohibitive.
| A) BP 165/95 | Elevated but below the treatment-refractory >180/110 threshold — treat BP, not a contraindication |
| B) Ischemic stroke 8 months | Relative concern only within <3 months — 8 months clears it |
| D) Dental extraction | Minor bleeding risk, not a contraindication |
| E) Aspirin use | He is supposed to get aspirin anyway |
Trap: List trap — exam swaps "ischemic <3 months" for "hemorrhagic ever" and hopes you blur the two.
Future alert: Hemorrhagic stroke EVER = never thrombolyze. Ischemic stroke = only <3 months blocks.
Correct: B) NSTEMI
Concept: ACS troponin-based differentiation Analysis
Why B: Ischemic rest pain + ST depression + ELEVATED troponin = subendocardial infarction = NSTEMI. UA is the identical picture with NORMAL troponin.
| A) UA | That was the diagnosis one troponin ago — elevation upgrades it to NSTEMI |
| C) STEMI | Requires ST ELEVATION; depression + troponin is NSTEMI territory |
| D) Pericarditis | Diffuse ST↑, PR↓, no troponin rise |
| E) Takotsubo | Stress trigger + apical ballooning on echo, not this pattern |
Trap: Definition trap — UA vs NSTEMI is ONLY the troponin.
Future alert: ST depression + troponin↑ = NSTEMI. Same picture + normal troponin = UA.
Correct: A) NSAIDs + colchicine
Concept: Acute pericarditis treatment Recall
Why A: First-line is NSAIDs (ibuprofen 600mg TID or high-dose aspirin) + colchicine 0.6mg BD for 3 months minimum — colchicine cuts recurrence by 50%.
| B) Heparin + PCI | That is the STEMI pathway — this is pericarditis (no troponin, diffuse ST↑ + PR↓) |
| C) Steroids | Reserved for refractory/autoimmune cases — first-line steroids increase recurrence |
| D) Antibiotics | Purulent pericarditis only — this is post-viral |
| E) Digoxin | No role in pericarditis |
Trap: Treatment trap — the ECG scares you into the cath lab.
Future alert: Pericarditis Rx = NSAID + colchicine, 3 months, not steroids.
Correct: B) Uremic pericarditis
Concept: Pericarditis etiology by context Interpretation
Why B: ESRD + friction rub + NO fever is the uremic signature — it classically lacks the fever of infectious causes.
| A) Viral | Post-viral prodrome + fever expected |
| C) Dressler | Needs a prior MI weeks ago |
| D) TB pericarditis | Chronic course, systemic symptoms, high-risk epidemiology |
| E) Tamponade | Beck's triad (hypotension, ↑JVP, muffled sounds) — a complication, not the diagnosis here |
Trap: Context trap — the dialysis chair was the diagnosis.
Future alert: Friction rub + afebrile + renal failure = uremic pericarditis.
Correct: B) CT angiography of the chest
Concept: Dissection recognition + imaging choice Analysis
Why B: Tearing pain maximal at onset + inter-arm BP differential >20mmHg + new AR murmur + widened mediastinum = dissection. Stable patient → CTA is the gold standard.
| A) Troponins | May be normal; cannot exclude dissection — a normal troponin here is a trap |
| C) TTE in lab | Bedside echo is the UNSTABLE pathway; he is stable |
| D) D-dimer | Useless — dissection and many comorbidities elevate it; not a dissection rule-out tool |
| E) Aortography | Historical gold standard — invasive, replaced by CTA |
Trap: Anchor trap — anchoring on "chest pain" and ordering cardiac enzymes.
Future alert: Tearing pain + BP differential → CTA. Troponin will betray you.
Correct: A) IV esmolol or labetalol
Concept: Type A dissection management sequence Analysis
Why A: Beta-blockade FIRST to cut dP/dt (shear stress), THEN vasodilator. Target SBP 100-120, HR <60, and emergency surgical repair.
| B) Nitroprusside first | Reflex tachycardia increases shear stress — vasodilator only AFTER beta-blockade |
| C) Nifedipine | Uncontrollable sublingual hypotension — not for dissection |
| D) Heparin | Anticoagulating a dissection invites fatal hemorrhage |
| E) Thrombolysis | Lethal — the never-do of this section |
Trap: Sequence trap — the drugs are right, the order is fatal.
Future alert: Type A: BB first, vasodilator second, surgeon third. Never delay surgery for imaging.
Correct: A) Costochondritis — clinical diagnosis
Concept: Musculoskeletal chest pain Interpretation
Why A: Sharp, localized, REPRODUCIBLE ON PALPATION after exertion with normal vitals and ECG — the textbook costochondritis cluster. Reproducibility excludes ACS.
| B) PE | Needs dyspnea/hypoxia/risk factors — none present |
| C) Pneumothorax | Sudden onset + ↓breath sounds — exam is normal |
| D) GERD | Burning, postprandial, NOT reproducible on palpation |
| E) Myocarditis | Would have troponin rise, arrhythmias, systemic symptoms |
Trap: Over-investigation trap — ordering tests for a clinical diagnosis.
Future alert: Reproducible on palpation = chest wall. Do not burn a D-dimer on it.
Correct: B) HFpEF — diuretics, BP control, SGLT2 inhibitors
Concept: HFpEF vs HFrEF classification and treatment Analysis
Why B: EF ≥50% + S4 + elderly hypertensive diabetic woman = HFpEF. Symptom control: diuretics for volume, BP <130/80, SGLT2i (recent benefit); NO proven mortality benefit from neurohormonal blockade.
| A) HFrEF regimen | Wrong EF category — the mortality quartet is for EF <40% |
| C) Digoxin | No mortality benefit anywhere in HF |
| D) Proven mortality for HFpEF | The trap — ACEi/BB/MRA lack mortality proof in HFpEF |
| E) No treatment | Symptoms are real — treat congestion and comorbidities |
Trap: Category trap — treating HFpEF with the HFrEF mortality quartet and claiming benefit.
Future alert: EF ≥50% + S4 + elderly female = HFpEF. Diuretics + BP + SGLT2i.
Correct: B) Spironolactone
Concept: HFrEF mortality add-on therapy Analysis
Why B: EF <35% + symptoms despite ACEi + BB = add aldosterone antagonist (spironolactone/eplerenone) — mortality benefit. Monitor K⁺; avoid if CrCl <30.
| A) Digoxin | Symptom/rate control only — no mortality benefit |
| C) Amlodipine | Neutral DHP — safe but no mortality claim |
| D) Furosemide | Symptom-only diuresis — the "D" is for symptoms ONLY |
| E) Amiodarone | Arrhythmia suppression, no mortality benefit, toxic load |
Trap: Benefit trap — three of these drugs are routinely given; only one claims mortality.
Future alert: EF <35% + already on ACEi/BB → next mortality drug is the MRA.
Correct: B) Carvedilol
Concept: Beta-blocker initiation timing Analysis
Why B (as the NOT-to-start): Initiating a negative inotrope while acutely congested worsens decompensation — wait until euvolemic.
| A) IV loop diuretic | Cornerstone of acute decompensation management |
| C) Sit upright | ↓preload, immediate relief |
| D) Oxygen | If hypoxic — supportive mainstay |
| E) Nitrates | ↓preload if BP permits |
Trap: Timing trap — the best chronic drug is the worst acute drug.
Future alert: BB in HF: start when EUVOLEMIC, never during the acute admission.
Correct: A) Double the dose, switch to IV, or add a thiazide
Concept: Loop diuretic resistance Interpretation
Why A: The documented options for loop resistance are exactly three: double the oral dose, switch to IV, or add a thiazide for sequential nephron blockade.
| B) Stop diuretics | He is congested — stopping worsens it |
| C) Add digoxin | Inotrope/rate drug, not a diuretic strategy |
| D) Hydralazine | Vasodilator for afterload, not volume |
| E) MRA as primary diuretic | Weak diuretic; it is a mortality drug, not a volume rescue |
Trap: Escalation trap — adding new drug classes instead of fixing the failing one.
Future alert: Loop not working? Double, IV, or thiazide — in that order of thinking.
Correct: B) Anticoagulation with a DOAC
Concept: CHA₂DS₂-VASc application Analysis
Why B: Score 4 (HTN + DM + vascular disease + age 65-74) → anticoagulate; DOAC preferred over warfarin. He is stable → rate control alongside, but anticoagulation is the scored decision.
| A) Aspirin | Not a substitute at score 4 |
| C) Rate control only | Rate control without anticoagulation leaves the 5× stroke risk open |
| D) Immediate cardioversion | Stable + unknown onset → needs TEE or 3 weeks anticoagulation first |
| E) Watchful waiting | Denies a mandatory indication |
Trap: Undertreatment trap — rate control feels like treatment but the stroke clock keeps ticking.
Future alert: Count the score first; the anticoagulation decision follows mechanically.
Correct: C) Synchronized cardioversion
Concept: Unstable tachyarrhythmia management Analysis
Why C: Hypotension + pulmonary edema = UNSTABLE. Unstable anything-tachycardia → synchronized cardioversion, no drug delays.
| A) Adenosine | A stable-patient drug — shocks first when unstable |
| B) Vagal maneuvers | Stable SVT only |
| D) IV metoprolol | Drug delay in an unstable patient — and may worsen hemodynamics |
| E) Amiodarone | For stable VT/wide-complex, not the unstable SVT pathway |
Trap: Pharmacology trap — reaching for the drug ladder when the patient already failed hemodynamically.
Future alert: Unstable + tachycardic = synchronized shock. Adenosine is for the sitting-up-and-talking patient.
Correct: B) Catheter ablation
Concept: Definitive SVT therapy Recall
Why B: Recurrent AVNRT despite medical therapy → catheter ablation is curative — it eliminates the accessory/reentrant pathway.
| A) Chronic digoxin | Second-line rate agent, not curative |
| C) Amiodarone | Toxic load for a benign rhythm — disproportionate |
| D) ICD | For malignant ventricular arrhythmias, not AVNRT |
| E) Exercise restriction | Not evidence-based management |
Trap: Palliation trap — mistaking repeated adenosine rescue for a treatment plan.
Future alert: Recurrent SVT + failed drugs = ablation. It is curative.
Correct: C) IV amiodarone — treat as VT
Concept: Wide-complex rule in structural heart disease Analysis
Why C: Prior MI + wide-complex tachycardia = VT until proven otherwise. He is STABLE → antiarrhythmic (amiodarone 150mg IV over 10 min), not shocks.
| A) Adenosine | SVT trial — wrong pathway in known heart disease |
| B) Verapamil | Potentially lethal in VT — classic kill option |
| D) Digoxin load | Slow, and digoxin toxicity itself causes VT |
| E) Carotid massage | SVT diagnostic maneuver — irrelevant in VT |
Trap: Stability trap — he is stable, so drugs not shock; and the wide complex must be read as VT.
Future alert: Stable wide-complex + old MI = amiodarone. Unstable = synchronized shock.
Correct: B) IV magnesium sulfate
Concept: Torsades de Pointes management Recall
Why B: Polymorphic VT with prolonged QT (drugs here: haloperidol, ondansetron) = torsades → IV magnesium is first-line, even with normal magnesium levels.
| A) Amiodarone | WORSENS QT prolongation — the classic wrong answer |
| C) Lidocaine | Ventricular ectopy drug, not the torsades answer |
| D) Adenosine | Narrow-complex SVT tool |
| E) Procainamide | Also prolongs QT — contraindicated here |
Trap: Reflex trap — "VT = amiodarone" fails precisely here; the QT flips the answer.
Future alert: Polymorphic VT + long QT = magnesium. Amiodarone would fuel the fire.
Correct: B) Permanent pacemaker immediately
Concept: Complete heart block management Interpretation
Why B: Complete AV dissociation + syncope = 3rd-degree block → pacemaker immediately. This is not a watch-and-wait rhythm.
| A) Atropine | A bridge at best; unreliable in complete block — the answer is the device |
| C) Amiodarone | Suppresses escape rhythms — catastrophic |
| D) Carotid massage | Diagnostic maneuver, not treatment; risky in the elderly |
| E) Reassurance | Mobitz II and 3rd-degree block progress to asystole |
Trap: Severity trap — lumping Mobitz I (benign) with Mobitz II and 3rd degree (pacemaker).
Future alert: Mobitz II or complete block → pacemaker. Observation is the wrong answer.
Correct: A) Cardiogenic shock — inotropes and urgent reperfusion, avoid excessive fluids
Concept: Cardiogenic shock after MI Analysis
Why A: Post-MI + hypotension + cold extremities + crackles + ↑JVP = pump failure. Treat the cause (reperfusion), inotropes (dobutamine), and AVOID fluid loading — the lungs are already drowning.
| B) Septic | No infection source; warm skin would be the septic tell, he is cold |
| C) Hypovolemic | Hypovolemia shows ↓JVP and clear lungs — the opposite |
| D) Tamponade | Needs Beck's triad + pulsus paradoxus + electrical alternans |
| E) PE | Would need hypoxia, risk factors, right-heart strain signs |
Trap: Fluid reflex trap — "shock = fluids" fails in cardiogenic shock.
Future alert: Cold + wet + post-MI = inotropes and reperfusion. Fluids drown the lungs.
Correct: C) Immediate needle decompression, right 2nd ICS midclavicular
Concept: Tension pneumothorax — clinical diagnosis Analysis
Why C: Hypotension + distended neck veins + unilateral absent breath sounds + tracheal deviation AWAY = tension pneumothorax. It is a CLINICAL diagnosis — decompress before any imaging.
| A) CXR first | Kills the patient — never wait for film |
| B) CT chest | Even slower — same fatal error dressed up |
| D) Chest tube first | Correct definitive step but AFTER needle decompression |
| E) Intubation | Positive pressure WORSENS tension physiology |
Trap: Imaging trap — the most testable single line: DON'T wait for CXR.
Future alert: Tension PTX = needle first, tube second, imaging never first.
Correct: C) Valve replacement — surgical or TAVR
Concept: Severe AS triad and definitive treatment Analysis
Why C: SAD triad (Syncope + Angina + Dyspnea) means severe symptomatic AS; valve area 0.8cm² (<1.0) confirms severe. Once symptoms develop, survival without valve replacement is 2-3 years — replacement (SAVR or TAVR if high-risk) is the treatment.
| A) Medical only | Just delays the inevitable — symptoms drive surgery |
| B) Balloon valvuloplasty | Bridge/palliative only — restenoses; that is the MS answer, not AS |
| D) Diuretics only | Symptom care while the valve strangles output |
| E) ACEi | Afterload reduction is poorly tolerated in severe AS |
Trap: Medical-therapy trap — the exam wants you to know symptoms + severe valve = replace.
Future alert: Symptomatic severe AS: 2-3 years without surgery. Replace, do not medicate.
Correct: C) Chronic aortic regurgitation
Concept: Chronic AR volume-overload signs Interpretation
Why C: Wide pulse pressure + water-hammer (Corrigan) pulse + de Musset head-bobbing + early diastolic blowing murmur at L3-4ICS, best heard sitting forward in expiration — the full chronic AR constellation.
| A) MS | Diastolic RUMBLE + opening snap + loud S1 — low-pitched, not blowing |
| B) AS | Systolic ejection murmur radiating to carotids, DELAYED pulses (opposite of bounding) |
| D) MVP | Mid-systolic CLICK ± late systolic murmur |
| E) TR | Holosystolic LLSB, louder with inspiration (Carvallo) |
Trap: Sign-matching trap — the named signs (Corrigan, de Musset, Quincke, Traube) all point to one valve.
Future alert: Wide pulse pressure + any eponymous pulsing sign = chronic AR.
Correct: A) Mitral stenosis — AFib and thromboembolism
Concept: Rheumatic MS recognition and complications Interpretation
Why A: Rheumatic history + opening snap + diastolic rumble + loud S1 = MS (almost always rheumatic, 10-20 year lag). LA enlargement → AFib → thromboembolism — the feared complications.
| B) AS | Systolic, R 2nd ICS, to carotids |
| C) AR | Early diastolic blowing, no opening snap |
| D) MVP | Click, not an opening snap |
| E) VSD | Congenital, holosystolic LLSB |
Trap: Timing trap — childhood rheumatic fever reappearing decades later as MS.
Future alert: Opening snap + apical rumble = MS; watch for AFib and emboli.
Correct: A) Knee-chest position and oxygen
Concept: TOF tet spell management Analysis
Why A: Boot-shaped heart + squatting = TOF. The spell cycle: ↑SVR by knee-chest breaks the R→L shunt; then oxygen, morphine, IV fluids, phenylephrine.
| B) Digoxin | No role in the acute spell |
| C) Furosemide | ↓preload — worsens the R→L shunt |
| D) Aspirin | Irrelevant here |
| E) Antibiotics | No infection in a spell |
Trap: Physiology trap — treating the cyanosis as a lung problem when it is a shunt problem.
Future alert: Tet spell: knee-chest → O₂ → morphine → fluids → phenylephrine. Definitive: repair at 6-12 months.
Correct: A) Paradoxical embolism
Concept: ASD complications Recall
Why A: The ASD defect lets venous clots cross to the systemic circulation — paradoxical embolism — plus atrial arrhythmias from RA overload.
| B) Subaortic stenosis | Not an ASD association |
| C) AR | Bicuspid valve disease, not ASD |
| D) Coarctation | Separate congenital lesion; Turner association |
| E) Never complicated | False — arrhythmias and embolism are the reason to close significant shunts |
Trap: Benign-bias trap — assuming a "small" ASD means no consequences.
Future alert: ASD = fixed split S2 + paradoxical emboli. Device closure if significant shunt.
Correct: A) Indomethacin
Concept: PDA recognition and closure Recall
Why A: Machinery murmur + bounding pulses in a preterm neonate = PDA. Indomethacin/ibuprofen inhibits PGE2 → closes the ductus.
| B) Prostaglandin E1 | The OPPOSITE — PGE1 KEEPS the ductus OPEN (used in duct-dependent lesions) |
| C) Digoxin alone | Does not close the ductus |
| D) Surgery first-line | Ligation only if medical therapy fails |
| E) Wait indefinitely | Risks HF, endocarditis, Eisenmenger |
Trap: Direction trap — indomethacin CLOSES, prostaglandin KEEPS OPEN. The exam loves flipping these.
Future alert: Close PDA = indomethacin. Keep ductus open = PGE1.
Correct: B) Smoking cessation
Concept: PAD risk-factor hierarchy Interpretation
Why B: Claudication + ABI 0.68 (<0.9) = PAD; the single most important intervention across the disease course is smoking cessation — it beats every drug and procedure in impact.
| A) Cilostazol | Second-line after lifestyle; contraindicated in HF |
| C) Angioplasty now | For lifestyle-refractory or severe/critical disease — not first |
| D) Aspirin alone | Antiplatelet is part of care but does not address the driver |
| E) Bypass first | Revascularization is for severe disease/critical limb ischemia |
Trap: Pharmacy trap — the exam tempts with drugs when the answer is the cigarette.
Future alert: PAD management ladder starts and ends with smoking cessation at the top.
Correct: B) Hypertensive urgency — oral agents, BP reassessment
Concept: Urgency vs emergency line Analysis
Why B: BP >180/120 WITHOUT end-organ damage = urgency. No IV drugs, no ICU — oral agents and reassessment. The absence of findings is the diagnosis.
| A) Emergency | Requires end-organ damage — explicitly absent here |
| C) Stroke | No focal deficits |
| D) Dissection | No tearing pain, no pulse differential |
| E) Dialysis | Normal creatinine |
Trap: Number trap — the BP value looks terrifying; the ORGANS decide the answer.
Future alert: >180/120 + no organ damage = oral meds. The exam's favorite distinction.
Correct: B) IV nicardipine or clevidipine in ICU, reduce BP by 10-20% in the first hour
Concept: Hypertensive emergency management Analysis
Why B: >180/120 + encephalopathy = emergency. IV titratable agents (nicardipine/clevidipine, labetalol), ICU monitoring, and a DELIBERATE 10-20% reduction in the first hour — rapid normalization causes hypoperfusion strokes.
| A) Oral at home | That is the urgency pathway — she has encephalopathy |
| C) Normalize in minutes | Hypoperfusion → watershed stroke/MI |
| D) Sublingual nifedipine | Uncontrollable drop — abandoned for good reason |
| E) Observation | Active end-organ damage — ICU now |
Trap: Speed trap — treating the number fast instead of the organs safely.
Future alert: Emergency: lower 10-20% in hour one. Dissection is the exception — SBP <120 fast.
Correct: B) ACE inhibitors
Concept: ACE-I in bilateral renal artery stenosis Interpretation
Why B: Bilateral RAS kidneys depend on efferent arteriolar constriction (angiotensin II) to hold GFR. ACE inhibition removes that → acute renal failure.
| A) Metformin | Dose-adjust/avoid in significant CKD, but the classic disaster here is the ACE-I |
| C) Statins | Indicated — atherosclerotic disease |
| D) Aspirin | Indicated — vascular protection |
| E) Beta-blockers | No specific contraindication in RAS |
Trap: Indication trap — ACE-I is the BEST drug for unilateral RAS and diabetic CKD, but poisons bilateral RAS.
Future alert: Bilateral RAS + ACE-I = acute renal failure. Check imaging before starting.
Correct: B) Staphylococcus aureus
Concept: Endocarditis organism by scenario Analysis
Why B: IVDU → right-sided (tricuspid) endocarditis with S. aureus on a NORMAL valve; CXR nodules are septic pulmonary emboli — the right-sided signature.
| A) S. viridans | Subacute, left-sided, post-dental, on abnormal valves |
| C) S. epidermidis | Early prosthetic valve (<60 days), biofilm |
| D) Enterococcus | GU/GI procedures, elderly |
| E) HACEK | Culture-NEGATIVE endocarditis, slow growth |
Trap: Organism-context trap — the lifestyle line in the stem IS the microbiology answer.
Future alert: IVDU + tricuspid + lung nodules = S. aureus right-sided IE.
Correct: A) Colonoscopy
Concept: S. bovis → colon cancer link Recall
Why A: S. bovis bacteremia is the classic marker for colonic pathology — ALWAYS colonoscopy to exclude colon cancer.
| B) Dental | S. viridans is the dental bug, not S. bovis |
| C) CT abscess | Reasonable for complications but the MANDATORY next step is the colon |
| D) EGD | Upper GI is not the S. bovis association |
| E) Antibiotics only | Treats the valve, misses the cancer |
Trap: Focus trap — treating the heart while the colon waits.
Future alert: S. bovis in blood = scope the colon. Every time.
Correct: B) Continue anticoagulation ≥3 months / indefinite
Concept: Anticoagulation duration by trigger Interpretation
Why B: Unprovoked PE → at least 3 months, commonly indefinite if bleeding risk is low. (Provoked = 3 months; cancer = indefinite.)
| A) Stop | Unprovoked means the trigger is unknown — stopping risks recurrence |
| C) Warfarin only if cancer | Backwards — cancer mandates indefinite, not unprovoked |
| D) IVC filter | Only if anticoagulation contraindicated or recurrent PE despite adequate Rx |
| E) Aspirin | Inadequate for secondary PE prevention |
Trap: Duration trap — provoked/unprovoked/cancer each carry a different clock.
Future alert: Provoked 3 months. Unprovoked ≥3/indefinite. Cancer indefinite. Memorize the trio.
Correct: B) Systemic thrombolysis with tPA
Concept: Massive PE management Analysis
Why B: Hemodynamic instability (BP 82/54) = massive PE → systemic thrombolysis is first-line; untreated mortality >50%, thrombolysis cuts it to ~25%.
| A) LMWH alone | Correct for stable PE — inadequate for massive PE |
| C) IVC filter | Prevention device, not acute rescue; for anticoagulation contraindicated/recurrent |
| D) Aspirin | Not PE therapy |
| E) Embolectomy first | Reserved for thrombolysis failure or contraindication |
Trap: Stability trap — anticoagulation is for the stable; the unstable get lytics.
Future alert: Massive PE + no contraindication = tPA. Surgery is plan B.
Correct: B) High-intensity statin — no risk calculator needed
Concept: LDL ≥190 statin rule Interpretation
Why B: LDL ≥190 (plus xanthomas/arcus suggesting familial hypercholesterolemia) mandates high-intensity statin directly — the calculator is bypassed entirely.
| A) Lifestyle only | Under-treatment of a genetic-risk pattern |
| C) Calculator first | The calculator exists for the ambiguous middle — 190 skips the queue |
| D) Ezetimibe first | Add-on therapy, not first-line |
| E) PCSK9i first | After statin + ezetimibe fail to reach goal |
Trap: Calculator trap — reaching for a tool the rule explicitly skips.
Future alert: LDL ≥190 = high-intensity statin, no calculator, no debate.
Correct: C) Adenosine 6mg rapid IV push
Concept: Stable SVT stepwise management Analysis
Why C: She is STABLE (BP 118/76, no angina, no pulmonary edema) with a regular narrow-complex tachycardia. The ladder is: vagal maneuvers → adenosine 6mg rapid push (escalate to 12mg ×2) → BB or non-DHP CCB → ablation. Vagal already failed, so adenosine is next.
Discriminator: stability — she is sitting up and talking; the Q27 patient was shocked, this one gets drugs.
| A) Cardioversion | For UNSTABLE patients (hypotension, angina, pulmonary edema) — she is stable |
| B) Metoprolol | Considered after adenosine fails or for recurrence prevention — not the immediate next step |
| D) Amiodarone | Not in the narrow-complex SVT pathway — that is VT/wide-complex territory |
| E) Digoxin load | Too slow for acute termination; reserved for sedentary/HF rate control |
Trap: Stability trap in reverse — Q27 was shocked because unstable; this patient gets the drug ladder. Warn her of the 10-second doom feeling; adenosine is contraindicated in asthma.
Future alert: Stable SVT: vagal → adenosine → BB/CCB → ablation. Unstable: shock immediately.
Correct: B) Hypertrophic obstructive cardiomyopathy
Concept: Maneuver physiology on murmurs Analysis
Why B: Standing and Valsalva ↓preload → smaller LV cavity → more outflow obstruction → murmur LOUDER. Squatting ↑preload → murmur SOFTER. Add family history of sudden death, exertional near-syncope, LLSB location without carotid radiation, and brisk upstroke — classic HOCM.
Discriminator: the murmur's direction with preload change + absence of carotid radiation.
| A) AS | OPPOSITE physiology — softer with Valsalva (less forward flow), radiates to carotids, delayed upstroke |
| C) VSD | Holosystolic at LLSB, unchanged by preload maneuvers |
| D) MVP | Also louder with standing (prolapse earlier), but identified by its mid-systolic CLICK — absent here |
| E) PS | Right-sided — louder with INSPIRATION, pulmonic area, ejection click |
Trap: Maneuver trap — AS and HOCM are both harsh systolic LLSB-ish murmurs; the Valsalva direction and carotid radiation separate them.
Future alert: Louder with Valsalva = HOCM or MVP (look for the click). AS gets QUIETER. Sudden death history → HOCM until excluded.
This MedCORE is not a medical textbook. It is only designed for rapid, last-minute recall and should be treated like a high-yield cheat sheet, not a complete learning resource. Use it to memorize critical algorithms and recognition patterns.