PA Cardiology
Bootcamp Syllabus

Every hemodynamic management question — from cardiogenic shock to ADHF — tests your understanding of preload, afterload, contractility, and the Frank-Starling mechanism. These are the physiologic levers on every exam.

• Atrial systole (atrial kick): Contributes 15–25% of ventricular filling. Critical in mitral stenosis and diastolic dysfunction.
• Isovolumetric contraction: All valves closed; pressure rises without volume change
• Ventricular ejection: Aortic/pulmonic valve opens when ventricular pressure exceeds arterial pressure
• Isovolumetric relaxation: All valves close; pressure falls without volume change
• Rapid filling: AV valves open; passive filling accounts for ~70–80% of ventricular volume

• Cardiac Output (CO) = Heart Rate × Stroke Volume. Normal: 4–8 L/min
• Cardiac Index (CI) = CO / BSA. Normal: 2.5–4.0 L/min/m²
• Preload = ventricular end-diastolic stretch. Clinically estimated by CVP/PCWP. ↑ by IV fluids, leg raise. ↓ by nitrates, diuretics.
• Afterload = resistance opposing ventricular ejection (SVR). ↑ by HTN, vasopressors. ↓ by ACE-I, vasodilators.
• Contractility = intrinsic pump strength independent of loading. ↑ by catecholamines, digoxin. ↓ by beta-blockers, ischemia, cardiomyopathy.
• Frank-Starling law: ↑ preload → ↑ stretch → ↑ force of contraction → ↑ CO — up to a physiologic limit. Beyond that, further preload causes pulmonary congestion without improving output (the "failing heart" steep part of the curve). 📈 View Curve Diagram

PA students need to recognize what Swan-Ganz findings mean clinically — not memorize normal pressures. The key PANCE application is the hemodynamic profile:

🩺 PANCE Pearl: The boards test which profile matches the clinical scenario — not the actual mmHg values. Know the pattern, not the numbers.

All diastolic murmurs and all continuous murmurs (except venous hum and mammary soufflé) are pathologic and require echocardiography. Systolic murmurs may be innocent — diastolic murmurs never are.

• 1. Timing: Systolic (during S1→S2) vs diastolic (during S2→S1) vs continuous (throughout)
• 2. Location: Aortic (RUSB), pulmonic (LUSB), tricuspid (LLSB), mitral (apex)
• 3. Radiation: AS → carotids. MR → axilla. TR → increases with inspiration.
• 4. Configuration: Crescendo-decrescendo (diamond/ejection), holosystolic (plateau), decrescendo
• 5. Intensity: Grade 1–6. Grade ≥4 = palpable thrill. Grade 6 = audible without stethoscope.
• 6. Pitch: High (diaphragm) vs low/rumbling (bell, light pressure)

• Any diastolic or continuous murmur (except venous hum/mammary soufflé)
• Holosystolic or late systolic murmurs
• Midsystolic murmurs grade ≥3
• Any murmur with associated symptoms — dyspnea, syncope, chest pain, exertional limitation
• Any murmur that increases with Valsalva or standing — suggests HCM or MVP

#1 cause of death in the US. Boards test STEMI vs NSTEMI distinction, reperfusion timing, contraindications, and post-MI medications. Every exam has multiple ACS questions.

• Classic: 58M, diabetic, smoker. Crushing substernal pressure, left arm radiation, diaphoresis, nausea. Onset 2 hours ago.
• Atypical (test favorite): Diabetics and women → jaw pain, fatigue, epigastric pain, nausea — no chest pain. Still ACS.
• Vitals: Tachycardia (sympathetic surge), possible hypotension (inferior MI with RV involvement or cardiogenic shock)

• First test: EKG within 10 minutes of presentation. Always.
• Troponin: High-sensitivity troponin rises at 1–3 hours. Repeat at 3–6 hours if initial negative. Peak at 12–24 hours.
• STEMI mimics to exclude: Aortic dissection (tearing quality + BP differential), pericarditis (diffuse + PR depression), LBBB (apply Sgarbossa)

• DAPT: Aspirin + P2Y12 inhibitor. Ticagrelor (preferred) or prasugrel. Clopidogrel if high bleeding risk.
• Anticoagulation: UFH, enoxaparin, or bivalirudin
• Post-MI four pillars: ACE-I/ARB + high-intensity statin + beta-blocker + DAPT × 12 months
• MRA (eplerenone): If LVEF ≤40% + HF symptoms or diabetes post-MI. Monitor K⁺ and renal function.

• STEMI = PCI ≤90 min (FMC to device ≤120 min)
• Troponin rises 1–3h, peaks 12–24h, normalizes 5–14 days
• Prasugrel: CONTRAINDICATED in prior stroke/TIA, age ≥75, weight <60kg
• DAPT standard duration: 12 months post-ACS
• ACEI/ARB: Start within 24h, especially anterior MI or LVEF ≤40%
• High-intensity statin (atorvastatin 80mg or rosuvastatin 20–40mg): Start in hospital, continue indefinitely

• Stable angina: Predictable chest pressure with exertion, relieved by rest or nitroglycerin within 5 minutes. NOT worsening, NOT at rest.
• Vasospastic (Prinzmetal) angina: Chest pain at REST, often nocturnal/early morning. ST elevation during episodes (transient). Normal or non-obstructive coronary arteries on cath. Triggered by cold, smoking, cocaine, triptans.
• MINOCA (MI with non-obstructive coronary arteries): Troponin positive, STEMI/NSTEMI pattern, but clean coronaries. Causes: coronary spasm, plaque erosion, SCAD, microvascular disease, Takotsubo.

• Stable angina: Beta-blocker first-line (reduces O₂ demand). CCBs or long-acting nitrates as alternatives. Ranolazine for refractory symptoms.
• Vasospastic angina: Calcium channel blockers (first-line — verapamil, diltiazem, amlodipine) + long-acting nitrates. AVOID beta-blockers — can worsen coronary spasm by leaving alpha-adrenergic tone unopposed.
• All stable CAD: Aspirin + statin + BP control + lifestyle modification

• Stress testing detects myocardial ischemia by increasing O₂ demand (exercise) or altering coronary flow (pharmacologic agents)
• Used for risk stratification in known/suspected CAD, post-MI/PCI/CABG prognosis, and preoperative cardiac risk assessment
• The PANCE tests modality SELECTION far more than raw interpretation — know which test fits which patient

🩺 PANCE Pearl: "Can the patient walk on a treadmill?" is the first branch point in every stress test question. Exercise > pharmacologic whenever physically possible.

Exercise ECG alone (no imaging) only works if the baseline ECG can show ischemic changes. It CANNOT be used with:

• LBBB (left bundle branch block)
• Paced rhythm
• WPW (Wolff-Parkinson-White) pattern
• ≥0.5 mm ST depression at rest
• LVH (left ventricular hypertrophy) with strain pattern
• Digoxin use

🚨 Classic Trap: Patient with LBBB needs a stress test → the answer is vasodilator stress with nuclear imaging, NOT exercise ECG and NOT dobutamine. LBBB itself can mimic ischemic ST changes during exercise, making plain exercise ECG unreliable — and dobutamine increases heart rate similarly to exercise, so it carries the same false-positive risk in LBBB. Vasodilators don't significantly raise heart rate, avoiding this problem.

• Regadenoson is the most commonly used vasodilator — a selective A2A receptor agonist, better tolerated than adenosine. Because it is selective, it is acceptable in stable mild-to-moderate asthma/COPD; adenosine and dipyridamole are not
• Dobutamine is the fallback when vasodilators are contraindicated (i.e., in a COPD patient who needs pharmacologic stress)

🚨 Classic Trap — learn it in two layers: Layer 1 (the default answer): asthma/COPD patient needs pharmacologic stress → adenosine and dipyridamole are CONTRAINDICATED (bronchospasm risk) → use dobutamine. Layer 2 (the tiebreaker): when dobutamine is also blocked — LBBB, poor echo windows, tachyarrhythmia, severe HTN — regadenoson is acceptable in stable asthma/COPD without active wheezing, because it is a selective A2A agonist. A stem that stacks LBBB + poor windows + stable asthma is asking for regadenoson, not dobutamine.

• Acute MI within 2 days
• Unstable angina not yet stabilized
• Symptomatic severe aortic stenosis
• Uncontrolled heart failure
• Acute PE or pulmonary infarction
• Acute myocarditis or pericarditis
• Acute aortic dissection

🚨 Classic Trap: Symptomatic severe AS is an ABSOLUTE contraindication to stress testing — exercise can precipitate syncope or sudden death by failing to augment cardiac output across a fixed obstruction.

• ECG: ≥1 mm horizontal or downsloping ST depression 60–80 ms after the J-point = positive. ST elevation ≥1 mm (no Q waves) = transmural ischemia/spasm
• Hemodynamics: SBP drop ≥10 mmHg from baseline during exercise = high-risk finding, suggests severe CAD or LV dysfunction — stop the test if accompanied by ischemic signs
• Imaging: Reversible defect (stress only, normal at rest) = ischemia. Fixed defect (abnormal at both stress and rest) = old infarct/scar. Partially reversible = mixed scar + ischemia

🩺 PANCE Pearl: "Reversible = alive but starving (ischemia). Fixed = dead tissue (scar)." This single sentence answers most nuclear stress test interpretation questions.

• <5 METs = poor prognosis, cannot perform many activities of daily living
• ≥10 METs = low risk of cardiac events
• Target heart rate = 85% of age-predicted max (220 − age)
• Duke Treadmill Score combines exercise time, ST deviation, and angina symptoms for overall prognosis

• Hold beta-blockers 24–48h before EXERCISE or DOBUTAMINE stress if safe — they blunt the heart rate response needed to reach target HR. They do not meaningfully affect vasodilator hyperemia, so they need not be held for a vasodilator study — and should not be stopped casually in a patient headed for vascular surgery (withdrawal ischemia)
• Hold caffeine and methylxanthines before vasodilator stress — xanthines competitively block adenosine receptors and cause false-negative results. Windows differ by source: ≥12h (2024 ACC/AHA perioperative), 24h (AHA exercise standards), 24–48h (ACR practice parameters). Know the principle; follow the guideline a question names
• Aminophylline (1–2 mg/kg) must be immediately available as the reversal agent for severe vasodilator side effects — but is not used for regadenoson-associated seizures

🚨 Classic Trap: A patient drinks coffee the morning of a scheduled regadenoson stress test → the test should be rescheduled. Caffeine directly antagonizes the adenosine receptor the test depends on.

• Can exercise + interpretable ECG → Exercise ECG alone (low-risk) or Exercise + imaging (intermediate/high-risk)
• Can exercise + LBBB/paced/WPW/baseline ST changes → Exercise + imaging required (not ECG alone)
• Cannot exercise + no bronchospasm → Vasodilator (regadenoson) + nuclear imaging or CMR
• Cannot exercise + asthma/COPD → Dobutamine + echo or nuclear imaging. But if dobutamine is also blocked (LBBB, poor acoustic windows) → regadenoson + perfusion imaging, provided the airway disease is stable
• Cannot exercise + LBBB → Vasodilator + perfusion imaging. Never exercise or dobutamine — both raise HR and create false septal defects
• Valvular disease (especially MR) → Stress echo preferred (assesses hemodynamic changes)
• Age <65, no known CAD, need anatomic answer → Coronary CTA

• AFib EKG: Irregularly irregular rhythm, absent P waves, fibrillatory baseline. Ventricular rate varies. 📟 View AFib EKG
• AFL EKG: Regular sawtooth flutter waves at ~300 bpm, typically 2:1 AV conduction → ventricular rate ~150 bpm (classic "150 bpm regular tachycardia" = flutter until proven otherwise)
• 2023 Staging: Stage 1 (at risk) → Stage 2 (pre-AF changes) → Stage 3 (paroxysmal or persistent AF) → Stage 4 (permanent AF)

• AFFIRM trial: Rate and rhythm control had comparable outcomes in stable older patients
• EAST-AFNET 4 trial: Early rhythm control (within 1 year of AF diagnosis) reduced CV death, stroke, HF hospitalization — major paradigm shift
• 2023 ACC/AHA guideline now prioritizes rhythm control especially for: age <70, recent-onset AF, AF with HFrEF, symptomatic patients
• Rate control target: HR <110 bpm at rest (lenient; RACE II trial)
• Catheter ablation: Now first-line for symptomatic paroxysmal AF and AF with HFrEF

Why 4 weeks post-CV for ALL: atrial stunning (mechanical function takes up to 1 month to recover), transient prothrombotic state, and high early AF recurrence rate — independent of CHA₂DS₂-VASc score. The <48h window carries 0.7–1.1% stroke risk in low-risk patients.

• Dronedarone: CONTRAINDICATED in permanent AF (PALLAS trial: ↑ mortality, stroke, HF) AND decompensated HF (ANDROMEDA trial: ↑ mortality)
• Amiodarone toxicity: Thyroid (hypo > hyper), pulmonary fibrosis, hepatic, corneal deposits, blue-gray skin, QT prolongation (low TdP risk). Half-life 40–55 days. Monitor TSH + LFTs every 6 months.
• Sotalol: Requires 3-day in-hospital initiation with QT monitoring. TdP risk ~2–4%. Contraindicated if QTc >450ms or CrCl <40.
• Dofetilide: Mandatory 3-day hospital initiation. Multiple drug interactions — verapamil, cimetidine, TMP, ketoconazole, HCTZ all contraindicated.

• Step 1: No RS complex in any precordial lead? → VT
• Step 2: RS interval >100ms in any precordial lead? → VT
• Step 3: AV dissociation? → VT (most reliable if present)
• Step 4: Morphologic VT criteria in V1–V2 and V6? → VT
• If none of above → SVT with aberrancy (diagnosis of exclusion)

Concordance (all precordial QRS all-positive or all-negative) → VT. Fusion and capture beats = pathognomonic for VT.

• Antiarrhythmics: Sotalol, dofetilide, procainamide (high risk). Amiodarone (low risk despite prolonging QT).
• Antibiotics: Macrolides (azithromycin, erythromycin), fluoroquinolones (levofloxacin, moxifloxacin)
• Antipsychotics: Haloperidol, ziprasidone, thioridazine
• Antiemetics: Ondansetron (high-dose), metoclopramide
• Antidepressants: TCAs, citalopram, escitalopram
• Other: Methadone, hydroxychloroquine

This is sinus node disease and ectopy — distinct from the AV conduction blocks covered next in Topic A-4 — Heart Blocks & Pacing Indications. The two highest-yield decisions here are the pacemaker-before-antiarrhythmic rule in brady-tachy syndrome, and knowing when frequent PVCs stop being benign.

• Spectrum of findings: inappropriate sinus bradycardia, sinus pauses or arrest, sinoatrial exit block, failure of rate to rise with exertion (chronotropic incompetence), and alternating bradycardia with atrial tachyarrhythmia.
• Presentation: fatigue, exercise intolerance, lightheadedness, presyncope or syncope in an older adult. Symptoms must be correlated with the rhythm — an asymptomatic pause is not an indication to pace.
• Causes: age-related fibrosis of the sinus node is the most common. Also drugs (beta-blockers, non-dihydropyridine CCBs, digoxin, amiodarone, clonidine, lithium), ischemia of the RCA territory, hypothyroidism, obstructive sleep apnea, infiltrative disease, and increased vagal tone.
• Workup: ECG plus ambulatory monitoring to link symptoms to rhythm. Always review the medication list and check TSH before diagnosing intrinsic disease — reversible causes come first.
• Treatment: remove the offending drug if possible. Permanent pacemaker for symptomatic sinus node dysfunction once reversible causes are excluded.

• Pattern: episodic atrial tachyarrhythmia (usually atrial fibrillation) alternating with symptomatic bradycardia or long pauses on termination.
• The trap: the tachycardia begs for rate control or an antiarrhythmic — but any drug that suppresses the tachycardia will further suppress an already diseased sinus node, producing dangerous pauses or asystole.
• A pacemaker must be in place before, or at the same time as, rate-controlling or antiarrhythmic therapy. Pace first, then treat the tachycardia.
• Anticoagulation decisions still follow CHA₂DS₂-VASc, independent of the pacing decision.

🩺 PANCE Pearl: A junctional rhythm plus nausea, visual color changes or confusion in a patient on digoxin is digoxin toxicity — not a primary conduction problem.

• Terminology: bigeminy = every other beat is a PVC. Trigeminy = every third. Couplet = two in a row. Three or more consecutive at >100 bpm = ventricular tachycardia (non-sustained if under 30 seconds).
• Uniform (monomorphic) PVCs arise from one focus; multiform PVCs suggest more diffuse disease or a metabolic trigger.

• In a structurally normal heart, PVCs are benign and require reassurance rather than suppression. Reduce caffeine, alcohol and stimulants; correct electrolytes and hypomagnesemia; screen for hyperthyroidism.
• A PVC burden above roughly 10–15% of total beats can cause PVC-induced cardiomyopathy — a genuinely reversible cause of reduced ejection fraction. Quantify the burden on ambulatory monitoring and obtain an echocardiogram.
• Treatment when symptomatic or high burden: beta-blocker first line; non-dihydropyridine CCB as an alternative in preserved EF; catheter ablation of the PVC focus for refractory cases or established PVC-induced cardiomyopathy, which can normalize the EF.
• Red flags demanding structural workup: exertional PVCs or PVCs that worsen with exercise, syncope, family history of sudden death, PVCs in the setting of known cardiomyopathy or prior MI.

• Hydralazine/Isosorbide dinitrate: Self-identified Black patients with persistent symptoms on GDMT, or if ACEi/ARB/ARNI not tolerated
• Ivabradine: Sinus rhythm + HR ≥70 on maximally tolerated BB (Class IIa)
• Diuretics: Symptom relief (loop diuretics). No mortality benefit.
• BNP interpretation: >400 likely HF. <100 HF unlikely. Falsely low in obesity. NT-proBNP preferred in patients on sacubitril/valsartan (ARNI inhibits BNP degradation → BNP rises with treatment — use NT-proBNP for monitoring)

• Inotropes (dobutamine/milrinone): ONLY for cardiogenic shock / low cardiac output states (Cold & Wet). Increase mortality with prolonged use.

• Etiology: Calcific/degenerative (age >65 — most common); Bicuspid AV (age <65 — most common in younger); Rheumatic (rare in developed countries)
• Severe AS echo criteria: Valve area ≤1.0 cm², mean gradient ≥40 mmHg, aortic velocity ≥4.0 m/s
• Survival post-symptom onset: Angina = 5 years; Syncope = 3 years; Dyspnea/HF = 2 years
• Asymptomatic severe AS: Echo surveillance q6–12 months. Exercise stress testing may unmask symptoms.
• Symptomatic severe AS = AVR (Class I). SAVR for low surgical risk; TAVR now approved all risk categories.
• No effective medical therapy for severe AS — only AVR is definitive

• Classic triad: Fever + new/changing murmur + positive blood cultures
• Peripheral signs: Janeway lesions (painLESS, palmar/plantar, embolic), Osler nodes (painFUL, finger/toe, immune complex), Roth spots (retinal), splinter hemorrhages

• Valve dysfunction causing HF — most common surgical indication
• Heart block, annular abscess, or fistula formation
• Fungal IE or highly resistant organisms
• Persistent bacteremia/fever >5–7 days despite appropriate antibiotics
• Large mobile vegetations >10mm + embolic events
• Prosthetic valve IE with relapsing infection or dehiscence

• Who needs it: Prosthetic valves (including TAVR), prior IE, unrepaired cyanotic CHD, cardiac transplant with valvulopathy
• What procedure: Dental procedures involving gingival manipulation or oral mucosa perforation ONLY. NOT GI or GU procedures.
• Drug: Amoxicillin 2g PO 30–60 min before procedure. If penicillin-allergic: cephalexin 2g, azithromycin or clarithromycin 500mg, or doxycycline 100mg. Clindamycin is no longer recommended (2021 AHA update — C. difficile risk).
• MVP without MR = no prophylaxis required

Aortic stenosis is the most tested valvular lesion on the PANCE. The exam almost never asks you to pick a drug — it asks you to recognize severity from the exam, choose the confirmatory study, and decide whether this patient needs a valve. Symptom onset is the hinge: before symptoms the disease is followed, after symptoms it is operated on.

Fixed obstruction → LV pressure overload → concentric hypertrophy → diastolic dysfunction and subendocardial ischemia → eventual systolic failure.

• The hypertrophied, non-compliant ventricle is critically preload-dependent — this single fact explains every medication warning in this topic.
• It is also rate- and rhythm-dependent: loss of the atrial kick with new AF can precipitate abrupt decompensation.
• Angina occurs without epicardial coronary disease — supply–demand mismatch from a thick ventricle with a high pressure load.

• Classic triad: angina, exertional syncope, dyspnea/heart failure. All three signify severe, late disease.
• Approximate untreated survival after symptom onset: angina ≈ 5 years, syncope ≈ 3 years, heart failure ≈ 2 years. Learn them in that order — dyspnea/heart failure carries the worst prognosis.
• Exertional syncope is a mechanical failure to augment cardiac output against a fixed obstruction — not a vasovagal event.

🩺 PANCE Pearl: Asymptomatic severe AS and symptomatic severe AS are different diseases for exam purposes. The severity numbers do not change management — symptoms do.

• ECG: LVH ± left atrial enlargement. CXR: valve calcification, post-stenotic aortic dilation.
• TTE is the diagnostic test of choice. Severe AS — any one of: Vmax ≥4.0 m/s, mean gradient ≥40 mmHg, AVA ≤1.0 cm² (or ≤0.6 cm²/m² indexed).
• Uncontrolled hypertension underestimates severity — repeat the study after blood pressure control.
• Low-flow / low-gradient AS: when LVEF is reduced, a low gradient does not exclude severe AS. Use dobutamine stress echo to separate true-severe from pseudo-severe, and CT aortic valve calcium score (>1300 AU women, >2000 AU men) as a flow-independent confirmation.
• BNP >3× upper limit of normal in severe AS suggests decompensation.
• Exercise testing: contraindicated once symptomatic (risk of syncope and arrest). It is useful only to unmask symptoms in the apparently asymptomatic patient, or to detect an abnormal BP response.

• No medical therapy alters the natural history. Statins do not slow progression. Treat hypertension and comorbidities on their own merits.
• Preload and afterload are precious. Use nitrates, other vasodilators, and diuretics with real caution in severe AS — dropping preload against a fixed obstruction causes catastrophic hypotension.
• Maintain sinus rhythm where possible; treat new AF promptly.

🩺 PANCE Pearl: SAVR vs TAVI is shared decision-making weighing age, surgical risk, lifetime valve strategy, and anatomy — not a memorized cutoff. TAVI indications continue to expand across risk categories. European guidelines differ from U.S. guidelines on LVEF thresholds and use age ≥65 as the bioprosthesis cutoff.

Mitral stenosis is rheumatic until proven otherwise. The PANCE stem almost always plants a clue — immigration from a region with endemic rheumatic disease, untreated childhood strep pharyngitis, or a young pregnant patient who suddenly cannot breathe. The physiology is entirely about diastolic filling time, and every management decision follows from that.

• Rheumatic heart disease — overwhelmingly dominant. Commissural fusion, leaflet thickening, chordal shortening.
• Mitral annular calcification (elderly, usually mild).
• Congenital mitral stenosis (rare).

Obstructed LA emptying → ↑ LA pressure → LA dilation → pulmonary venous congestion → pulmonary hypertension → right heart failure.

• LA dilation is the source of most complications: atrial fibrillation, LA thrombus, and systemic embolism including stroke.
• Tachycardia shortens diastole and worsens the gradient. This is why decompensation is triggered by exercise, pregnancy, fever, anemia, or new-onset AF — the valve did not change, the filling time did.
• Note what is preserved: the LV is normal. Heart failure symptoms here are from the left atrium and lungs, not from LV systolic dysfunction.

• Exertional dyspnea and orthopnea, fatigue, palpitations or AF, hemoptysis, embolic stroke.
• Ortner syndrome — hoarseness from a dilated left atrium compressing the recurrent laryngeal nerve.
• Dysphagia from esophageal compression by the enlarged left atrium.
• Progression is slow — over decades. A patient can be asymptomatic for 20–40 years after the initial rheumatic insult.

• ECG: left atrial enlargement (P mitrale — notched P in lead II), atrial fibrillation, RVH.
• CXR: straightened left heart border, double density at the right heart border, elevated left mainstem bronchus, Kerley B lines.
• TTE: valve morphology, mitral valve area, mean gradient, PA pressure. Severe MS: MVA ≤1.5 cm².
• TEE is mandatory before percutaneous mitral balloon commissurotomy (PMBC) — to exclude LA thrombus and quantify MR.

• Rate control — beta-blockers or non-dihydropyridine calcium channel blockers — to lengthen diastolic filling time. This is the therapeutic lever.
• Diuretics for pulmonary congestion.
• Anticoagulation with warfarin for atrial fibrillation, prior embolism, or LA thrombus. DOACs are not established in rheumatic mitral stenosis — use warfarin.
• Secondary rheumatic fever prophylaxis where indicated.
• No medical therapy alters valve anatomy — relief requires a mechanical intervention.

🩺 PANCE Pearl: Because progression is slow, surgery is generally deferred until NYHA III–IV symptoms, particularly when repair is being contemplated. Contrast this with AS and MR, where earlier intervention is favored.

Aortic regurgitation is tested in two completely different forms. Chronic AR is a slow, eponym-rich disease with a long compensated phase. Acute AR is a surgical emergency in which none of the famous peripheral signs appear — and expecting them is how a dissection gets missed.

🩺 PANCE Pearl: Always ask whether the problem is the valve or the aorta. Root pathology changes the operation (valve-sparing root replacement) and mandates aortic imaging and family screening.

• Early, high-pitched, blowing decrescendo diastolic murmur at the left sternal border (3rd–4th ICS) — best heard sitting, leaning forward, in held expiration; louder with handgrip (increased afterload).
• Austin Flint murmur — low-pitched apical mid-to-late diastolic rumble from the regurgitant jet striking the mitral leaflet. Do not mistake it for mitral stenosis: there is no opening snap and S1 is not loud.
• Displaced, hyperdynamic apical impulse.

🩺 PANCE Pearl: All seven eponyms are one finding — a wide pulse pressure. Learn the mechanism and you own the list.

• TTE is first-line — severity, LV dimensions, LVEF, and root/ascending aortic dimensions.
• Cardiac MR quantifies regurgitant volume and fraction and detects fibrosis when echo is equivocal. CT for aortic anatomy and procedural planning.
• The serial numbers that drive surgery: LVEF, LVESD, LVESD index, LVEDD. These are followed over time — a single value matters less than the trajectory.

• Vasodilators — ACE inhibitors/ARBs, dihydropyridine CCBs — for hypertension in AR. Medical therapy is not a substitute for surgery once an indication exists.
• Bradycardia is poorly tolerated — a longer diastole means more regurgitation. Avoid non-vasodilating beta-blockers where possible. Exception: beta-blockade remains appropriate in Marfan syndrome and other aortopathy.
• Acute severe AR: emergency surgery. Temporize with vasodilators and inotropes. Intra-aortic balloon pump is CONTRAINDICATED (diastolic augmentation worsens the regurgitation), as is heavy beta-blockade (the tachycardia is compensatory).

• Ascending aortic surgery for Marfan with root disease ≥50 mm — Class I.
• Consider at ≥55 mm in all patients; ≥45 mm with Marfan plus additional risk factors; ≥50 mm with a bicuspid valve plus risk factors or coarctation.
• Valve-sparing root replacement (David procedure) is preferred in younger patients with normal cusps and root dilation, at experienced centers.

The single most important step in any MR question is classifying it as primary or secondary. Primary MR is a broken valve that needs a mechanical repair. Secondary MR is a sick ventricle with a structurally normal valve, and it needs the ventricle treated first. Give the "primary MR" answer to a secondary MR stem and you will get it wrong every time.

• Chronic: LV volume overload → eccentric hypertrophy, LA dilation, atrial fibrillation, pulmonary hypertension.
• LVEF reads deceptively "supranormal" because the ventricle ejects into the low-impedance left atrium. An LVEF of 50–60% in severe MR already signals meaningful dysfunction — this is why the surgical threshold is set unusually high.
• Acute: papillary muscle rupture 2–7 days post-MI, chordal rupture, or endocarditis → abrupt pulmonary edema and shock with a normal-sized LA and LV. No time has passed for compensatory dilation.

• Holosystolic blowing apical murmur radiating to the axilla — louder with handgrip and squatting (increased afterload), softer with Valsalva.
• Soft S1, S3, laterally displaced apex with chronic severe MR.
• Mitral valve prolapse: mid-systolic click ± late systolic murmur. Valsalva or standing moves the click EARLIER and lengthens the murmur; squatting moves it later. This is the opposite direction from most murmurs.
• Acute severe MR may produce only a soft, short, early systolic murmur despite profound hemodynamic compromise — the LA pressure rises so fast that the gradient disappears in late systole.

• TTE: mechanism, severity, LVEF, LVESD, PA pressure. TEE for repair feasibility and intraoperative guidance.
• Severe primary MR: effective regurgitant orifice area ≥0.40 cm², regurgitant volume ≥60 mL, regurgitant fraction ≥50%, vena contracta ≥0.7 cm.

• Primary MR: no medical therapy delays the need for surgery. Treat hypertension if present; do NOT give vasodilators to the normotensive asymptomatic patient.
• Secondary MR: full guideline-directed medical therapy for HFrEF first — ACEi/ARB/ARNI, beta-blocker, MRA, SGLT2 inhibitor — plus CRT when indicated. Reassess severity after optimization.
• Acute severe MR: afterload reduction with nitroprusside, IABP as a bridge, urgent surgery.

🩺 PANCE Pearl: Repair is strongly preferred over replacement whenever anatomically feasible. Timely successful repair yields survival equivalent to an age-matched population — which is why the exam pushes early referral.

Most common cause of sudden cardiac death in young athletes (age <35). The PANCE tests recognition, drug contraindications, and the key physical exam maneuvers that change the murmur intensity.

• Genetics: Autosomal dominant; sarcomere protein mutations (myosin heavy chain, troponin)
• Pathophysiology: Asymmetric septal hypertrophy → LVOT obstruction → dynamic outflow gradient → poor diastolic filling
• Classic presentation: Young athlete with exertional syncope, chest pain, palpitations. Family history of sudden death. Prominent S4.
• Murmur: Harsh systolic crescendo-decrescendo at LLSB. Dynamic — changes with maneuvers.

• Mainstay: Beta-blockers (first-line) or non-dihydropyridine CCBs (verapamil) — decrease HR → longer diastolic filling, reduce LVOT gradient
• ICD: For high-risk patients (prior SCA, family history of sudden death, severe hypertrophy, NSVT, hypotensive BP response to exercise)
• Septal reduction therapy: Surgical myectomy (first-line for eligible patients) or alcohol septal ablation for drug-refractory LVOT obstruction
• Mavacamten (myosin inhibitor): FDA approved 2022 for symptomatic obstructive HCM — reduces LVOT gradient

• Hypertension affects ~116 million US adults — the single most common chronic condition tested on PANCE
• Only ~44% of US adults with HTN have BP controlled to goal — management questions are heavily tested
• Primary (essential) HTN accounts for 85–95% of all hypertension and is a diagnosis of exclusion

🩺 PANCE Pearl: Memorize these thresholds exactly — boards test the boundary numbers (e.g., 129/79 = Elevated, not Stage 1).

• Office technique: seated ≥5 min, back supported, feet flat, arm at heart level, no caffeine/exercise/smoking within 30 min. Average ≥2 readings, 1 min apart, on ≥2 occasions
• HBPM (home): ≥2 readings AM (before meds) and PM, averaged over ≥2 days
• ABPM (24-hr ambulatory): best predictor of long-term CVD outcomes; identifies nocturnal dipping
• White coat HTN: elevated office BP, normal out-of-office BP
• Masked HTN: normal office BP, elevated out-of-office BP — carries HIGHER CVD risk than white coat

🚨 Classic Trap: Masked hypertension is more dangerous than white coat hypertension because it goes undiagnosed and undertreated despite normal-appearing office readings.

🩺 PANCE Pearl: The 2025 guideline replaced the Pooled Cohort Equations (10% threshold) with the PREVENT calculator (7.5% threshold) — boards may test this shift.

🩺 PANCE Pearl: Lifestyle modification alone achieves goal BP in only ~27% of patients — most patients eventually need pharmacotherapy too.

• Thiazide/thiazide-like diuretics: chlorthalidone preferred over HCTZ (longer half-life, proven CVD reduction)
• ACE inhibitors: lisinopril, enalapril, ramipril
• ARBs: losartan, valsartan, candesartan — better tolerated than ACEi (less cough/angioedema)
• Dihydropyridine CCBs: amlodipine, nifedipine LA

🚨 Classic Trap: Beta-blockers are NOT first-line for primary HTN unless there's a compelling indication (heart failure, ischemic heart disease, rate control). Don't pick metoprolol as initial monotherapy for uncomplicated HTN.

🚨 Classic Trap: NEVER combine ACEi + ARB (or + direct renin inhibitor) — this combination is potentially harmful (hyperkalemia, AKI) and is a frequently tested "wrong answer" pairing.

• Stage 2 HTN: 2025 guideline → initiate with 2 first-line agents, preferably as a single-pill fixed-dose combination
• Black patients: thiazides or CCBs preferred initial monotherapy — ACEi is LESS effective for BP lowering and stroke prevention in this population
• Complementary combos: ACEi/ARB + CCB, ACEi/ARB + thiazide, CCB + thiazide

• SPRINT trial (2015): intensive SBP <120 vs standard <140 in non-diabetics — 25% reduction in CVD events and all-cause mortality. Excluded diabetics and prior stroke patients.
• ACCORD trial: intensive BP in diabetics — no significant primary benefit, but did reduce stroke
• An SBP reduction of 10 mmHg decreases CVD events by ~20–30%

🚨 Classic Trap: SPRINT results do NOT directly apply to diabetics — the trial specifically excluded them. Don't cite SPRINT to justify aggressive targets in a diabetic patient.

• Onset <30 years or >55 years without typical risk factors
• Resistant or refractory HTN
• Abrupt onset or acute worsening of previously controlled HTN
• Severe/accelerated HTN with target organ damage
• Unprovoked hypokalemia
• Adrenal incidentaloma

• Far more common than previously thought — accounts for 8–20% of secondary HTN
• Screen: plasma aldosterone-to-renin ratio (ARR) under standardized conditions — must correct hypokalemia and withdraw MRAs 4–6 weeks before testing
• Confirm: oral sodium loading test or IV saline infusion test
• Subtype: adrenal CT + adrenal vein sampling
• Treat: unilateral adenoma → adrenalectomy. Bilateral hyperplasia → MRA (spironolactone/eplerenone)

🩺 PANCE Pearl: Resistant HTN + unprovoked hypokalemia = think primary aldosteronism first.

• Classic triad: episodic headache, sweating, palpitations (with pallor)
• Associated with neurofibromatosis (café-au-lait spots), MEN2, VHL
• Screen: plasma free metanephrines (most sensitive) or 24-hr urine fractionated metanephrines
• Localize: CT or MRI abdomen/pelvis
• Preop: alpha-blockade FIRST (phenoxybenzamine or doxazosin), THEN beta-blockade

🚨 Classic Trap: NEVER give a beta-blocker before alpha-blockade in pheochromocytoma — unopposed alpha stimulation can precipitate a hypertensive crisis. This exact sequence trap appears repeatedly on boards.

• Screen: renal duplex Doppler, CTA, or MRA
• Medical therapy preferred for atherosclerotic RAS (CORAL trial — no benefit from stenting)
• Angioplasty (without stenting) may benefit FMD

• Young woman + early-onset HTN + renal bruit → fibromuscular dysplasia
• Resistant HTN + hypokalemia → primary aldosteronism
• Episodic headache + sweating + palpitations + pallor → pheochromocytoma
• Snoring + obesity + resistant HTN → obstructive sleep apnea (most prevalent secondary cause in resistant HTN)
• Upper extremity HTN + absent femoral pulses + rib notching → coarctation of aorta
• Moon face + striae + central obesity + hyperglycemia → Cushing syndrome
• Flash pulmonary edema + renal bruit → atherosclerotic renal artery stenosis
• Café-au-lait spots + HTN → pheochromocytoma (NF1 association)

🩺 PANCE Pearl: These buzzword pairings are exam gold — memorize them as a set. Secondary HTN questions are usually pattern-recognition, not calculation.

• Definition: BP above goal despite ≥3 optimally dosed antihypertensives of different classes (including a diuretic), OR controlled BP requiring ≥4 agents
• Affects ~10–15% of treated hypertensives
• Workup: confirm adherence, exclude white coat effect, rule out secondary causes, assess interfering substances (NSAIDs, OCPs, stimulants)

🚨 Classic Trap: Always rule out pseudoresistance (nonadherence, white coat effect, improper cuff technique) BEFORE diagnosing true resistant HTN and ordering an extensive secondary workup.

• MRAs (spironolactone, eplerenone): preferred 4th agent for resistant HTN — best studied (PATHWAY-2 trial)
• Beta-blockers: metoprolol succinate, carvedilol, nebivolol
• Alpha-1 antagonists: doxazosin
• Central alpha-2 agonists: clonidine — last line, CNS effects, rebound HTN on abrupt withdrawal
• Direct vasodilators: hydralazine (pair with diuretic + BB), minoxidil (pair with loop diuretic + BB)
• Loop diuretics: preferred when GFR <30 or symptomatic HF (thiazides lose efficacy)

🚨 Classic Trap: Clonidine withdrawal can precipitate a hypertensive crisis — never stop abruptly. This is a frequently tested pharmacology trap.

• Target: reduce SBP ~25% in first hour, then <160/100 over 2–6 hrs, then gradual normalization over 24–48 hrs
• Exception — aortic dissection: SBP <120 within the FIRST hour (most aggressive target)
• Avoid rapid correction to normal range — risk of watershed ischemia from loss of cerebral autoregulation

🚨 Classic Trap: The distinction between emergency and severe-without-organ-damage is organ damage, NOT the absolute BP number. A BP of 220/130 with no symptoms and no organ damage still gets oral meds as an outpatient — do not reflexively admit and start IV drips based on the number alone. Avoid sublingual nifedipine — unpredictable, precipitous drops.

• Preferred: labetalol, extended-release nifedipine
• Contraindicated: ACEi, ARBs, direct renin inhibitors, atenolol, nitroprusside, MRAs
• Chronic HTN in pregnancy: treat to <140/90. Severe HTN (≥160/110): lower within 30–60 minutes
• Low-dose aspirin (81 mg/day) recommended for preeclampsia prevention

🚨 Classic Trap: ACEi/ARBs are absolutely contraindicated in pregnancy (fetotoxic) — this is one of the most frequently tested drug-contraindication pairs on PANCE.

• CKD: target <130/80. ACEi/ARB preferred (renoprotective, slows proteinuria). Switch thiazide → loop diuretic when GFR <30. Monitor K+ and creatinine after starting ACEi/ARB
• Elderly (≥65): SPRINT showed benefit of intensive treatment even ≥75 years. Start low, go slow — watch for orthostatic hypotension, falls, AKI. Avoid alpha-blockers as monotherapy
• Black patients: higher prevalence, earlier onset, more severe HTN. Thiazides/CCBs preferred initial agents — ACEi less effective for BP lowering and stroke prevention in this population

• Labs: BMP, CBC, lipid panel, TSH, urinalysis, urine albumin-to-creatinine ratio
• ECG: assess for LVH (Sokolow-Lyon or Cornell criteria — independent CVD risk factor), arrhythmia
• Organ systems affected: Heart (LVH, HF, CAD) · Brain (stroke, TIA, vascular dementia) · Kidney (CKD, albuminuria) · Eyes (retinopathy — AV nicking, hemorrhages, papilledema) · Vasculature (PAD, aneurysm)

🩺 PANCE Pearl: Microalbuminuria is the earliest marker of hypertensive nephropathy — order urine albumin-to-creatinine ratio at baseline for every new HTN diagnosis.

• Classic triad: Pleuritic chest pain (better sitting forward, worse lying flat) + pericardial friction rub + diffuse saddle-shaped ST elevation with PR depression on EKG
• Most common cause: Viral (~85%) — post-URI, young patient
• EKG stages: 1) Diffuse ST elevation + PR depression → 2) ST normalizes, T flattens → 3) T-wave inversions → 4) EKG normalizes
• Pericarditis vs STEMI: Pericarditis = diffuse (all leads), saddle-shaped, PR depression. STEMI = focal (contiguous), convex "tombstone," reciprocal changes.

• Viral pericarditis: NSAIDs + Colchicine 0.5mg BID × 3 months (reduces recurrence by 50%) + exercise restriction until asymptomatic + CRP normalized
• Dressler syndrome (post-MI): Use ASPIRIN — NOT ibuprofen or indomethacin (impair myocardial scar formation)
• Uremic pericarditis: DIALYSIS is the treatment — not NSAIDs
• Steroids: AVOID in viral (increases recurrence). Use only if NSAIDs truly contraindicated.

• Beck's triad: Hypotension + JVD + muffled heart sounds 📟 View Electrical Alternans EKG
• Pulsus paradoxus: Drop in SBP >10 mmHg with inspiration — characteristic, though not unique to tamponade (also severe asthma/COPD, massive PE, hypovolemia)
• EKG: Electrical alternans + sinus tachycardia + low voltage
• Echo: Diastolic RV collapse (earliest sign), IVC plethora, swinging heart
• Definitive treatment: Pericardiocentesis
• Bridge: IV fluids (maintain preload while preparing for drainage)

• Definition: Inflammation of the myocardium (heart muscle itself — distinct from pericarditis which involves the pericardial sac)
• Most common cause: Viral (Coxsackievirus B, adenovirus, COVID-19, influenza, HIV)
• Classic presentation: Young patient, recent viral illness, chest pain + dyspnea + fatigue. May present as new HFrEF. Elevated troponin.
• New entity: Immune checkpoint inhibitor (ICI) myocarditis: Life-threatening; occurs in patients on pembrolizumab, nivolumab, ipilimumab. High mortality (~25%). Early high-dose steroids critical.
• Giant cell myocarditis: Rare, aggressive, associated with autoimmune conditions. Often requires heart transplant.

• Gold standard: Endomyocardial biopsy (rarely needed; reserve for rapidly progressive or unclear etiology)
• Cardiac MRI: Non-invasive gold standard in practice — shows myocardial edema and late gadolinium enhancement
• Treatment: Supportive (standard HFrEF GDMT if reduced EF develops). Avoid NSAIDs (worsen myocarditis). Rest. No competitive sports until resolved.
• ICI myocarditis: Stop ICI immediately + high-dose methylprednisolone (1g IV daily × 3–5 days)

Shock = circulatory failure with inadequate tissue oxygen delivery and utilization → cellular hypoxia and organ dysfunction. Hypotension is common but NOT required — shock can occur with a "normal" blood pressure, especially in patients with baseline hypertension.

• Neurologic: Altered mental status, confusion, agitation
• Cutaneous: Mottling, cool/clammy extremities, prolonged capillary refill (>2 seconds)
• Renal: Oliguria (urine output <0.5 mL/kg/hr)

• DVT classic: Unilateral leg swelling, pain, warmth, erythema. Homans sign unreliable. Wells DVT score for pretest probability.
• PE classic: Dyspnea, pleuritic chest pain, tachycardia, hypoxia. Massive PE: hypotension + hypoxia + RV strain.
• EKG findings in PE: Sinus tachycardia (most common). S1Q3T3 pattern (classic but insensitive). New RBBB. T-wave inversions V1–V4 (RV strain).
• Diagnostic approach: Wells score + D-dimer (low probability + negative D-dimer = rule out PE without imaging). If moderate/high probability → CT pulmonary angiography (gold standard).

• Classic: Claudication (exertional calf pain, relieved by rest), cool extremity, diminished pulses
• ABI (Ankle-Brachial Index): Normal ≥0.9. Borderline 0.7–0.9. Mild PAD 0.5–0.69. Severe <0.5. >1.4 = non-compressible (calcified vessels, seen in DM).
• Critical limb ischemia: Rest pain, non-healing ulcers, gangrene — vascular surgery emergency
• Treatment: Supervised exercise (first-line for claudication), antiplatelet (aspirin or clopidogrel), statin + BP control. Cilostazol for claudication (PDE3 inhibitor — CONTRAINDICATED in HF).

• USPSTF Screening: One-time abdominal ultrasound in men aged 65–75 who have ever smoked (≥100 cigarettes lifetime)
• Normal aorta: <3 cm. AAA defined as ≥3 cm dilation.
• Elective repair threshold: ≥5.5 cm in men, ≥5.0–5.5 cm in women (or >0.5 cm/6 months growth)
• Ruptured AAA presentation: Triad of abrupt severe abdominal/back pain + pulsatile abdominal mass + hypotension. Immediate surgical emergency — do not wait for CT.

Lipid questions are almost never "what is the LDL." They test which intensity of statin this specific patient needs, and what you add when a statin alone is not enough. Learn the four benefit groups and the intensity table and most lipid vignettes answer themselves.

• Screening: Fasting or non-fasting lipid panel. USPSTF supports assessment in adults 40–75. Repeat every 4–6 years if normal and low risk.
• 10-year ASCVD risk (Pooled Cohort Equations, ages 40–79): <5% low · 5–7.4% borderline · 7.5–19.9% intermediate · ≥20% high
• Risk enhancers that push a borderline/intermediate patient toward treatment: family history of premature ASCVD, LDL ≥160, metabolic syndrome, CKD, chronic inflammatory disease, preeclampsia or early menopause, South Asian ancestry, Lp(a) elevation.
• Coronary artery calcium (CAC) score — the tiebreaker for intermediate risk when the decision is genuinely uncertain. CAC 0 → may defer statin. CAC 1–99 → favor statin, especially age ≥55. CAC ≥100 or ≥75th percentile → start a statin.

🩺 PANCE Pearl: Groups 1 and 2 need no calculator at all. If the stem says prior MI or LDL ≥190, the answer is high-intensity statin — stop calculating.

• Secondary prevention threshold: in patients with clinical ASCVD on maximally tolerated statin, an LDL that remains ≥70 mg/dL is the trigger to add ezetimibe, then a PCSK9 inhibitor. For very high-risk ASCVD the same logic applies more aggressively.
• Bile acid sequestrants (cholestyramine, colesevelam) still exist but raise triglycerides and are rarely the board answer.

• Icosapent ethyl (purified EPA, 4 g/day) reduced cardiovascular events in patients with ASCVD or diabetes and triglycerides 135–499 on a statin (REDUCE-IT). Note this is not ordinary fish oil.
• Gemfibrozil + statin = highest rhabdomyolysis risk. If a fibrate must be combined with a statin, use fenofibrate.

• Recognition: LDL ≥190 in an adult (or ≥160 in a child), tendon xanthomas, xanthelasma, corneal arcus before age 45, and a family history of premature coronary disease.
• Genetics: Most commonly autosomal dominant LDL-receptor mutation. Heterozygous ≈1 in 250; homozygous is rare and causes coronary disease in childhood.
• Management: High-intensity statin plus ezetimibe, usually plus a PCSK9 inhibitor. Cascade screening of first-degree relatives is required.

• Follow-up lipid panel 4–12 weeks after starting or changing therapy, then every 3–12 months. The goal is confirming the expected percent reduction and adherence.
• Do NOT check LFTs or CK routinely. Obtain a baseline ALT; check CK only if the patient develops muscle symptoms and LFTs only if hepatotoxicity is suspected.
• Statin-associated muscle symptoms: myalgia is common and usually tolerable; true myopathy with CK elevation is uncommon; rhabdomyolysis is rare. Management is to stop, allow washout, then rechallenge with a lower dose or a different statin.
• Interactions: simvastatin and lovastatin are the most CYP3A4-dependent — hazardous with azoles, macrolides, protease inhibitors, and grapefruit. Pravastatin, rosuvastatin and pitavastatin are the safest choices in polypharmacy.
• Statins modestly increase new-onset diabetes; the cardiovascular benefit still outweighs it and is not a reason to stop.

Congenital questions are pattern recognition on the murmur plus one physical finding. The exam rarely asks you to manage these lesions — it asks you to name them. Sort every stem first into acyanotic (left-to-right) versus cyanotic (right-to-left), then match the murmur.

• Acyanotic — left-to-right shunt: ASD, VSD, PDA. Blood recirculates through the lungs, so the child is pink but volume-overloaded. Presents with a murmur, failure to thrive, or heart failure symptoms — not cyanosis.
• Cyanotic — right-to-left shunt: Tetralogy of Fallot, transposition, tricuspid atresia, truncus arteriosus, total anomalous pulmonary venous return. Deoxygenated blood bypasses the lungs, so the child is blue and does not improve with oxygen.
• Obstructive without shunt: coarctation of the aorta, congenital aortic or pulmonic stenosis.

🩺 PANCE Pearl: Cyanosis that does not improve with supplemental oxygen means a fixed right-to-left shunt. Cyanosis that does improve points to a pulmonary cause instead.

• Sequence: long-standing uncorrected left-to-right shunt → chronic pulmonary overcirculation → irreversible pulmonary vascular remodeling → pulmonary pressure exceeds systemic → the shunt reverses to right-to-left → cyanosis, clubbing, polycythemia.
• Once established it is irreversible, and shunt closure becomes contraindicated — closing the defect removes the pressure release valve and precipitates right heart failure.
• Definitive treatment is lung or combined heart-lung transplantation. This is why timely repair of a large shunt matters.

• Prostaglandin E1 keeps the ductus open and is life-saving in any lesion where systemic or pulmonary flow depends on it — transposition, critical coarctation, pulmonary atresia, hypoplastic left heart. Indomethacin closes it.
• Down syndrome → endocardial cushion defects: ASD, VSD, and complete atrioventricular canal defect.
• Turner syndrome → coarctation of the aorta and bicuspid aortic valve.
• DiGeorge (22q11) → conotruncal defects: truncus arteriosus, tetralogy, interrupted aortic arch.
• Marfan → aortic root dilation, aortic regurgitation, mitral valve prolapse.
• Congenital rubella → PDA. Maternal diabetes → transposition and septal hypertrophy. Maternal lithium → Ebstein anomaly.

• Epidemiology: the most common congenital heart defect in childhood; in adults second only to bicuspid aortic valve. Incidence roughly 5–50 per 1,000 live births.
• Anatomic types: perimembranous (~75%), muscular, inlet/AV-canal type, outlet/conal. Clinically grouped as muscular vs nonmuscular, because natural history diverges sharply between the two.
• Acquired VSD: post-MI septal rupture (typically 3–5 days after infarct) and chest trauma. A new harsh holosystolic murmur with shock several days after an MI is septal rupture, not a congenital defect.

• Small defect: asymptomatic with a loud murmur. Smaller defect = louder murmur — intensity tracks the pressure gradient, not the shunt volume.
• Moderate or large defect: pulmonary overcirculation — tachypnea, tachycardia, diaphoresis with feeds, poor feeding, hepatomegaly, failure to thrive. Onset typically at 4–8 weeks as pulmonary vascular resistance falls.
• Murmur: harsh holosystolic at the left lower sternal border ± palpable thrill; increases with handgrip (raised afterload increases the left-to-right shunt).
• Large shunts: apical mid-diastolic mitral flow rumble, loud P2, hyperdynamic precordium.

• TTE with color Doppler defines location, size, shunt direction and magnitude, chamber sizes, and estimated PA pressure.
• ECG/CXR: LA and LV enlargement with large shunts. RVH suggests pulmonary hypertension — a warning sign, not a normal finding.
• Cardiac catheterization to measure pulmonary vascular resistance before closure in selected patients, particularly with late presentation.
• Small muscular VSD: reassurance; follow every 3–5 years until the murmur resolves, then discharge. Repeat TTE adds no value absent clinical change. Counsel on the rare endocarditis risk.
• All nonmuscular VSDs need ongoing cardiology follow-up unless spontaneous closure occurs; small defects without left heart dilation followed every 1–2 years with TTE.
• Moderate/large VSD in infancy: infants <3 months seen every 2–4 weeks. Medical therapy for pulmonary overcirculation — diuretics, afterload reduction, calorie-dense or NG feeds. Pulmonary artery banding as palliation when complete repair is not feasible in a young infant.

• Symptoms or left heart dilation that fail to improve with medical therapy.
• Large defects should be closed in infancy regardless of symptoms — to prevent irreversible pulmonary vascular disease.
• Children >6 months with persistent or progressive LV dilation or symptoms.
• Outlet/perimembranous defects with aortic valve prolapse or progressive aortic regurgitation — consider closure even if the shunt is small.
• Modality: surgical patch closure is standard; transcatheter device closure is an option for selected muscular and perimembranous defects.
• Eisenmenger physiology is a contraindication to closure.

Restrictive cardiomyopathy is the heart failure patient whose ventricle is neither dilated nor obviously hypertrophied but cannot fill. The exam tests two discriminations: identifying the infiltrating disease from one signature clue, and separating restriction from constrictive pericarditis — because constriction is surgically curable and restriction is not.

Takotsubo (stress cardiomyopathy) is covered in Topic CM-2 — Dilated & Other Cardiomyopathies alongside the other non-ischemic cardiomyopathies; it is not repeated here.

• Stiff, non-compliant ventricle with normal or reduced cavity size and a preserved ejection fraction. The problem is filling, not squeezing.
• Echo shows marked biatrial enlargement with normal-sized ventricles — the atria dilate because they are pushing against a wall.
• Elevated filling pressures on both sides produce the mixed picture: right-sided congestion dominates — elevated JVP, hepatomegaly, ascites, peripheral edema — often out of proportion to pulmonary findings.
• These patients are preload-dependent. Aggressive diuresis or vasodilation drops cardiac output sharply.
• Prominent S4, and diastolic dysfunction with a restrictive filling pattern on Doppler.

🩺 PANCE Pearl: Low voltage with thick walls is the single most reliable amyloid clue. In LVH from hypertension the voltage is high — amyloid does the opposite of what the wall thickness predicts.

The exam asks you to separate benign reflex syncope from dangerous cardiac syncope, and to identify the mechanism behind orthostatic symptoms using the heart rate response alone. For the broader syncope differential see Differential D-2 — Syncope; this card covers the orthostatic and reflex mechanisms in depth.

• Orthostatic hypotension: a fall in systolic BP of ≥20 mmHg or in diastolic BP of ≥10 mmHg within 3 minutes of standing (or head-up tilt).
• Technique matters: measure supine after 5 minutes of rest, then at 1 and 3 minutes of standing. Record the heart rate with every reading — the HR response is the diagnostic information.
• Delayed orthostatic hypotension occurs beyond 3 minutes and is an early marker of autonomic failure.
• Supine hypertension with orthostatic hypotension in the same patient is characteristic of autonomic failure and makes treatment genuinely difficult.

🩺 PANCE Pearl: The presence or absence of compensatory tachycardia is the single most useful piece of data. A large BP drop with no heart rate response means the autonomic reflex itself has failed.

• Mechanism: a triggered reflex producing vasodilation and/or bradycardia — the opposite of the appropriate response to standing.
• Triggers: prolonged standing, heat, crowded rooms, pain, venipuncture or the sight of blood, emotional distress, coughing, micturition, defecation, swallowing.
• Prodrome is the diagnostic feature: nausea, warmth, diaphoresis, pallor, tunnel or greying vision, and lightheadedness building over seconds to minutes.
• Recovery is rapid and complete once supine. Brief myoclonic jerks can occur and are frequently mistaken for a seizure, but there is no true post-ictal confusion, no tongue biting and no prolonged disorientation.
• Carotid sinus hypersensitivity is a related reflex syncope in older adults, triggered by head turning, shaving or a tight collar.

• Syncope during exertion — think aortic stenosis, hypertrophic cardiomyopathy, anomalous coronary, or exercise-induced arrhythmia. Exertional syncope is never assumed vasovagal.
• No prodrome — abrupt collapse without warning suggests an arrhythmia.
• Syncope while supine, or preceded by palpitations or chest pain.
• Family history of sudden cardiac death, or known structural heart disease or prior MI.
• An abnormal ECG — any conduction abnormality, pre-excitation, prolonged QT, Brugada pattern, or evidence of prior infarction.
• Any of these warrants a cardiac evaluation — echocardiography, ambulatory or prolonged rhythm monitoring, and ischemic assessment as indicated.

• Education and trigger avoidance, plus recognizing the prodrome early enough to lie down.
• Counter-pressure maneuvers at the first symptom: leg crossing with tensing, handgrip, arm tensing. Simple, effective, and a favourite exam answer.
• Liberalize salt and fluid (roughly 2–3 L daily and increased sodium unless heart failure, CKD or hypertension prohibits it). A rapid bolus of water can abort symptoms.
• Waist-high compression stockings and abdominal binders; rise slowly and in stages; elevate the head of the bed for supine hypertension.
• Deprescribe the offending antihypertensive, alpha-blocker or diuretic before adding a new drug.
• Pharmacologic options: midodrine (alpha-1 agonist — avoid within 4–5 hours of bedtime because of supine hypertension), fludrocortisone (volume expansion — monitor potassium and edema), droxidopa for neurogenic orthostatic hypotension, and pyridostigmine as an alternative.
• Tilt-table testing is not first line. Reserve it for cases that remain unclear after history, physical examination, orthostatic vitals and an ECG. Pacing has only a narrow role in recurrent syncope with documented profound cardioinhibitory bradycardia.

• Tearing quality + BP differential + widened mediastinum → dissection until proven otherwise. Stop all antithrombotic therapy.
• Pleuritic quality + positional relief + diffuse EKG changes → pericarditis. Not a focal STEMI.
• JVD + hypotension + clear lungs + muffled sounds → obstructive shock. Tamponade vs tension PTX vs massive PE.
• Forceful vomiting + chest pain → rule out Boerhaave before attributing to Mallory-Weiss or GERD.
• Normal EKG + normal troponin + pleuritic pain + risk factors → get CT-PA for PE before discharge.

BNP <100 pg/mL effectively rules out acute HF as the primary cause of dyspnea (NPV ~96%). BNP >400 pg/mL strongly suggests HF. BNP 100–400 is a gray zone — clinical context determines interpretation. Importantly, BNP is elevated in PE, renal failure, and sepsis — it is not specific to HF.

• HCM is an outflow obstruction — a smaller LV cavity worsens the obstruction → louder murmur. Anything that decreases preload shrinks the LV → murmur gets louder.
• AS is a fixed obstruction — the murmur loudness reflects flow across the valve. More flow (more preload) = louder murmur.
• MVP: The click occurs when the valve prolapses. A smaller LV (less preload) causes prolapse earlier in systole → click moves earlier and murmur lengthens toward holosystolic.
• Inspiration increases right-sided murmurs only (TR, PS) — Carvallo sign. Does NOT significantly affect left-sided murmurs.

• Step 1 — Check the neck veins (JVD):
  • JVD absent → Hypovolemic or Distributive (empty or vasodilated)
  • JVD present → Cardiogenic or Obstructive (backed up or blocked)
• Step 2 — Check the lungs:
  • JVD + pulmonary edema (crackles, Kerley B) → Cardiogenic shock (backed up LV)
  • JVD + clear lungs → Obstructive shock (tamponade, tension PTX, massive PE — obstruction before the LV)

• Bilateral edema → systemic cause: HF, cirrhosis, nephrotic syndrome, hypothyroidism, drugs, bilateral venous insufficiency
• Unilateral edema → local cause: DVT, lymphatic obstruction, cellulitis, Baker's cyst rupture, compartment syndrome