Complete Cardiology Bootcamp Syllabus — 10 clinical domains with Foundations, Ischemic HD, Arrhythmias, Heart Failure, Valvular Disease, HTN, Pericardial Disease, Cardiomyopathies, Shock States, and Vascular Disease — now with Module D: Must-Know Differentials (7 high-yield frameworks) and Module E: Board Pearls (domain-organized clinical decision points). Each of the 6 core PANCE topics opens with 3 in-session board-style questions (recognition → management → trap) plus 2 homework questions.
10Clinical Domains
24Board Topics
4New Foundation Topics
2New Modules Added
7Must-Know Differentials
10Don't Miss Emergencies
Rajiv Choudhary, MD, MPH
Tier Key:
Tier 1 — Must Know (guaranteed PANCE)
Tier 2 — Important (frequently tested)
★ = Gap topic added from your source material
Before You Begin
How to Use This Syllabus
Teaching Philosophy
Teach the exam through real medicine — pattern recognition first, pharmacology second
Every topic follows the same 12-element structure so your brain builds predictable schema
Tier 1 topics get full depth + vignette. Tier 2 topics are targeted to the tested decision points.
Board traps are flagged everywhere — these are the distractors written to fool you
Domain 1 · Cardiology Foundations
Cardiology Foundations
Before you beginCardiology Foundations3 questions
Answer these three before you read the domain. Getting them wrong is expected and useful — attempting a question first is what makes the material below stick. Each explanation unlocks only after you submit.
Question 1 of 3 · Medium · Forrester Hemodynamic Profiles
A 68-year-old man with dilated cardiomyopathy (EF 20%) develops hypotension, cold clammy skin, and oliguria despite being volume-overloaded with bilateral crackles and 3+ pitting edema. Which Forrester hemodynamic profile best describes this presentation and which management approach is most appropriate?
Click to Reveal Answer
Correct answer: E — Wet and cold — requires inotropic support with careful diuresis
This patient is congested (crackles, edema = 'wet') and poorly perfused (hypotension, cold extremities, oliguria = 'cold'). This is the Forrester Wet+Cold quadrant — cardiogenic shock with congestion — requiring inotropic support to improve perfusion plus careful diuresis to address congestion without worsening hypotension.
Why the other choices are wrong
Wet and warm — congested but well perfused, needs diuretics alone — Incorrect. This patient is indeed 'wet,' so the congestion half is right — but he is not 'warm.' Cold clammy skin, hypotension, and oliguria all indicate inadequate perfusion, which changes management from diuretics alone to inotropic support.
Dry and warm — well compensated, no intervention needed beyond observation — Incorrect. Both halves are wrong. Bilateral crackles and 3+ edema define a congested ('wet') state, and cold extremities with oliguria define poor perfusion ('cold'). This is the sickest quadrant, not the well one.
Distributive shock — requires norepinephrine and large-volume IV fluids — Incorrect. Distributive shock produces WARM extremities from peripheral vasodilation and typically a low JVP. This patient has cold skin and volume overload, pointing to a cardiac pump failure rather than vasodilation.
Dry and cold — requires fluid resuscitation — Incorrect. The 'cold' half is correct, but giving fluid here would be harmful. Crackles and 3+ pitting edema establish that the patient is volume-overloaded, so additional fluid would worsen pulmonary congestion.
Board pearlTwo bedside questions sort every decompensated heart failure patient: wet or dry (congestion) and warm or cold (perfusion). Wet+warm is the common admission and needs diuresis alone. Wet+cold is the one that kills — diuresing a cold patient without inotropic support drops an already inadequate cardiac output further.
Covered below under Topic F-1 — Cardiac Physiology & Hemodynamics
Question 2 of 3 · Medium · Murmur Dynamic Maneuvers
A 24-year-old competitive swimmer has a grade 2/6 systolic ejection murmur at the left upper sternal border that disappears when he stands up. He has no symptoms and a normal ECG. What does the change in murmur intensity with standing indicate?
Click to Reveal Answer
Correct answer: A — This is an innocent (physiologic) murmur — standing decreases preload, which reduces flow turbulence
Standing decreases venous return (preload) to the heart, which decreases flow through the outflow tract and quiets most innocent and pathologic murmurs. An innocent flow murmur that disappears with reduced preload confirms it is not hemodynamically significant.
Why the other choices are wrong
This is hypertrophic cardiomyopathy — standing should make the murmur louder, confirming dynamic obstruction — Incorrect. The physiology stated is correct for HCM, but it is the opposite of what happened. This murmur DISAPPEARED with standing, which excludes dynamic LVOT obstruction rather than confirming it.
This is aortic stenosis and requires urgent echocardiography regardless of how the murmur changes with maneuvers — Incorrect. AS in a healthy 24-year-old would be unusual and would typically radiate to the carotids with a delayed upstroke. A soft grade 2 murmur that vanishes with reduced preload is characteristic of benign flow, not fixed obstruction.
The maneuver provides no diagnostic information in young athletes — Incorrect. Dynamic maneuvers are in fact one of the most valuable bedside tools in exactly this population, where distinguishing an athletic flow murmur from HCM has life-or-death implications for sports participation.
This is mitral regurgitation — preload changes are not relevant to its evaluation — Incorrect. Preload changes are quite relevant to MR, and MR is heard at the apex rather than the left upper sternal border. MR also tends to increase with squatting rather than disappear with standing.
Board pearlStanding and Valsalva both drop preload, and that quiets nearly every murmur. The two exceptions run the other way and are the whole reason the maneuver is tested: HOCM and mitral valve prolapse get louder with reduced preload. A murmur that vanishes on standing is reassuring; one that intensifies demands an echo.
Covered below under Topic F-3 — Murmurs, Systematic Approach
Question 3 of 3 · High Yield · Cardiomyopathy · HCM Murmur
A 22-year-old athlete has a systolic murmur at the left lower sternal border. The murmur becomes LOUDER when the patient stands up and SOFTER when squatting. Which is the MOST likely diagnosis?
Click to Reveal Answer
Correct answer: B — Hypertrophic obstructive cardiomyopathy
HOCM murmur is the only common murmur that increases with standing/Valsalva (decreased preload → smaller LV → worse LVOT obstruction → louder murmur) and decreases with squatting (increased preload → larger LV → less obstruction → softer). This is the opposite of AS, MR, and most other murmurs. Young athlete + LLSB murmur + dynamic changes = HCM until proven otherwise. Order echo immediately.
Why the other choices are wrong
Pulmonic valve stenosis — Incorrect. Pulmonic stenosis is a fixed obstruction at the pulmonic valve. Its murmur gets LOUDER with inspiration (increased right-sided venous return) and does not behave the way this murmur does with standing and squatting.
Ventricular septal defect (VSD) — Incorrect. A VSD murmur is holosystolic and harsh at the left lower sternal border, so the location fits — but it gets SOFTER with standing because reduced preload lowers the left-to-right shunt gradient. This murmur got louder.
Calcific aortic stenosis — Incorrect. AS is a fixed valvular obstruction, so its murmur softens with standing (less preload, less flow across the valve). The paradoxical LOUDENING with standing is what separates dynamic LVOT obstruction from fixed AS — the classic tested discrimination.
Mitral valve prolapse with mitral regurgitation — Incorrect — and this is now the strongest distractor here, because MVP is the other murmur that intensifies with standing. Two things separate it: MVP is heard at the apex, not the left lower sternal border, and it is introduced by a mid-systolic click. With reduced preload the click moves earlier and the murmur lengthens; in HOCM the murmur simply gets louder as the outflow gradient rises.
Board pearlBuild the murmur differential around the direction of change, not the location. Louder standing / softer squatting = HOCM. Softer standing / louder squatting = aortic stenosis, mitral regurgitation, and most others. Handgrip raises afterload: it worsens MR and AR, and quiets HOCM.
Covered below under Topic F-3 — Murmurs, Systematic Approach · full HCM workup in Domain 6, Topic CM-1
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.
The Cardiac Cycle — Sequential Events
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
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).
Core Hemodynamic Equations
Parameter
Formula
Normal Value
Cardiac Output (CO)
HR × SV
4–8 L/min
MAP
DBP + 1/3 × pulse pressure (or CO × SVR)
70–100 mmHg
SVR
(MAP − RAP) / CO × 80
800–1200 dynes·s/cm⁵
PVR
(mean PAP − PCWP) / CO × 80
≤250 dynes·s/cm⁵
Stroke Volume (SV)
CO / HR
60–100 mL/beat
Right Heart Catheterization — PANCE Essentials
PA students need to recognize what Swan-Ganz findings mean clinically — not memorize normal pressures. The key PANCE application is the hemodynamic profile:
Shock Type
PCWP
CO/CI
SVR
Cardiogenic
↑ (>18)
↓
↑
Distributive (Septic)
Normal/↓
↑
↓↓
Hypovolemic
↓
↓
↑
Obstructive — massive PE
↓ or normal (RV↑)
↓
↑
Obstructive — tamponade
↑ and equalized (RA = RV = PCWP)
↓
↑
🩺 PANCE Pearl: The boards test which profile matches the clinical scenario — not the actual mmHg values. Know the pattern, not the numbers.
CI ≤2.2 L/min/m² = cardiogenic shock — the threshold for mechanical circulatory support consideration
Frank-Starling: beyond the optimal preload, more volume = congestion not output — this is why you diurese in decompensated HF even when BP is low
★ Memory Trick
S3: "Ken-tuc-ky" (extra sound after S2) = Volume overload = HF
S4: "Ten-nes-see" (extra sound before S1) = Stiff ventricle = LVH/diastolic dysfunction
"S3 comes after S2 like a 3rd wheel. S4 comes before S1 like an announcement."
CO = HR × SV. Fix CO: rate + fill + squeeze.
PCWP: "18 is the flood zone — above 18 = cardiogenic pulmonary edema"
SVR: "Nitrates ↓ preload. ACE-I ↓ afterload. Dobutamine ↑ contractility."
🫀 Topic F-2 — EKG Interpretation lives in the EKG Syllabus. Leads, the systematic approach, intervals, axis, STEMI criteria and localization, STEMI equivalents and mimics are all taught in the PA Bootcamp EKG Syllabus, which owns this material so it stays in one place. That is why the numbering here runs F-1 → F-3. Open the EKG Syllabus ↗
🔒 Full Bootcamp Access
You've seen the preview. Unlock all 28 Cardiology topics.
These 2 topics are free — a real look at how we teach, and
Module D differentials and Module E board pearls stay open below as well.
The remaining 26 clinical topics, along with the interactive
diagrams and audio mnemonics, are included with bootcamp enrollment.
Timing · Location · Radiation · Dynamic Maneuvers · HCM vs AS · All Diastolic Murmurs Are Pathologic
★★★ PANCE Priority
🔒
Full content locked
Enter your bootcamp access code below to unlock all topic cards, clinical pearls, vignettes, and board traps.
The Cardinal Rule
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.
Systematic Auscultation — 6-Point Framework
1. Timing: Systolic (during S1→S2) vs diastolic (during S2→S1) vs continuous (throughout)
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
⚑ Board Traps — Murmurs
HCM murmur does NOT radiate to carotids — this distinguishes it from AS (which does). Both are crescendo-decrescendo at similar locations.
HCM gets LOUDER with Valsalva; AS gets SOFTER — the single most tested murmur maneuver distinction
MVP click moves EARLIER with Valsalva/standing (smaller LV → earlier prolapse). Moves LATER with squatting (↑ preload → larger LV → later prolapse).
AR is best heard with the patient sitting up, leaning forward, in full expiration
MS: shorter S2→opening snap interval = more severe stenosis (higher LA pressure → valve opens earlier)
Innocent murmurs: Soft (grade 1–2), midsystolic, no radiation, asymptomatic, normal S1/S2, no clicks. No echo required.
★ Memory Trick
All diastolic = pathologic. Systolic may be innocent.
HCM vs AS: "HCM = Harder with Valsalva. AS = Attenuated with Valsalva."
HCM: "No carotid radiation = not AS"
MVP: "Valsalva = valve prolapses sooner = click earlier + murmur longer"
Squatting: "Squatting fills the ventricle = HCM shrinks (gets softer)"
Inspiration: "Inspires right-sided murmurs to get louder (Carvallo)"
AR: "Lean forward, hold your breath, use the diaphragm — it whispers in expiration"
Domain 2 · Ischemic Heart Disease — Most Tested on PANCE
Ischemic Heart Disease
Before you beginAcute Coronary Syndromes3 in-session · 2 homework
Core Topic 2 — Acute Coronary Syndromes. Attempt the three in-session questions before the domain is taught — they run in the room, in this order: recognition, then management, then the trap. The two homework questions are for tonight, after the teaching. Getting them wrong first is expected and useful; each explanation unlocks only after you submit.
Enter your bootcamp access code above to unlock these questions along with the rest of this domain.
In-sessionQ1 of 3 · NSTEMI · Diagnosis & Timing
A 48-year-old man presents with chest pain at rest. ECG shows ST depressions in V3–V6. Troponin is elevated. What is the diagnosis and best next step?
Click to Reveal Answer
Correct answer: C — NSTEMI — invasive coronary angiography within 24 hours
Ischemic symptoms plus ST depression plus a rise in troponin define NSTEMI. He goes on antithrombotic therapy now and to an early invasive strategy. Timing follows risk: a positive troponin with dynamic ST depression is a high-risk feature, so this patient earns angiography within 24 hours. Intermediate-risk NSTEMI without those features can wait 24–72 hours. Anyone with refractory ischemia, hemodynamic or electrical instability, or acute heart failure goes immediately instead.
Why the other choices are wrong
Unstable angina — discharge with outpatient follow-up — Incorrect. Unstable angina is ischemia without troponin elevation. His troponin is up, so this is an infarct, and discharge would be dangerous.
STEMI — activate the cath lab for emergent reperfusion — Incorrect. STEMI requires ST elevation (or a STEMI equivalent). He has depressions.
Pericarditis — start NSAIDs and colchicine — Incorrect. Pericarditis gives diffuse ST elevation with PR depression and pleuritic, positional pain — not territorial ST depression with a rising troponin.
Vasospastic angina — start a calcium channel blocker and nitrates — Incorrect. Vasospastic (Prinzmetal) angina produces transient ST elevation during pain with angiographically normal coronaries, and troponin is usually normal or only minimally raised. Territorial ST depression with a definite troponin rise is thrombotic disease, not vasospasm.
Board pearlSort chest pain in two steps: ST elevation or not, then troponin up or not. Elevation = cath lab now. Depression or T-wave inversion with a positive troponin = NSTEMI, treat and take to angiography early. Same picture with a negative troponin = unstable angina.
Covered below under Topic C-1 — Acute Coronary Syndrome
In-sessionQ2 of 3 · STEMI · Reperfusion Strategy
A 60-year-old woman presents with 2 hours of chest pain. ECG shows 3 mm ST elevation in leads II, III, and aVF. What is the best next step?
Click to Reveal Answer
Correct answer: D — Emergent PCI within 120 minutes
ST elevation in II, III, and aVF is an inferior STEMI. Primary PCI is the preferred reperfusion strategy: within 90 minutes of first medical contact at a PCI-capable hospital, and within 120 minutes when transfer is required. Fibrinolytics are the fallback only when that 120-minute window cannot be met.
Why the other choices are wrong
Obtain CT angiography of the chest — Incorrect. The diagnosis is already made on the ECG; imaging only delays reperfusion. (The exception to think about, not to order reflexively, is a genuine suspicion of aortic dissection.)
Start a heparin drip and observe — Incorrect. Anticoagulation is adjunctive. Observing a STEMI without reperfusion means watching myocardium die.
Administer fibrinolytics immediately — Incorrect. Second-line. Lytics are for the STEMI who cannot reach a cath lab within 120 minutes, and they carry intracranial hemorrhage risk that primary PCI does not.
Arrange coronary angiography the following morning — Incorrect. This is the delay trap in a different costume. Reperfusion benefit in STEMI is measured in minutes, not hours — deferring to the next day abandons myocardium that is infarcting right now.
Board pearlInferior STEMI carries two traps: check a right-sided ECG for RV involvement, and be very cautious with nitrates — an RV infarct is preload-dependent, and nitroglycerin can drop the pressure to the floor. Bradycardia plus hypotension in an inferior MI is RV infarct until proven otherwise.
Covered below under Topic C-1 — Acute Coronary Syndrome
In-sessionQ3 of 3 · STEMI · Pharmacoinvasive Strategy
A patient with STEMI arrives at a non-PCI-capable hospital. Transfer to a PCI center will take 3 hours. The patient is 50 years old with no contraindications. What is the best next step?
Click to Reveal Answer
Correct answer: A — Give full-dose fibrinolytics, then transfer for PCI within 24 hours
PCI cannot be delivered within 120 minutes, so give a fibrinolytic (full dose in a patient under 75 with no contraindications) as soon as possible — ideally within 30 minutes of arrival — and transfer for angiography within 24 hours. That is the pharmacoinvasive strategy. If reperfusion fails, transfer immediately for rescue PCI rather than waiting.
Why the other choices are wrong
Perform thrombolysis only if his symptoms worsen en route — Incorrect. Backwards. Lytic benefit is greatest earliest and falls off sharply with delay.
Start heparin and aspirin and await transfer — Incorrect. Antithrombotics do not reopen an occluded artery. Withholding reperfusion here is the error the question is testing.
Wait for transfer and perform PCI at the receiving hospital — Incorrect. Three hours of ongoing occlusion means substantially more infarcted myocardium. Time is muscle.
Give half-dose fibrinolytics, then transfer for rescue PCI — Incorrect. Half-dose lytic followed by immediate PCI — the facilitated PCI strategy — was formally tested and abandoned: it increased bleeding and reinfarction without improving outcomes. Give the full lytic dose, then transfer.
Board pearlThe number that governs the whole decision is 120 minutes from first medical contact to wire crossing. Beatable, go to PCI. Not beatable, give lytics fast and transfer anyway. Screen for absolute contraindications before lysing: prior intracranial hemorrhage, known structural cerebrovascular lesion, ischemic stroke within 3 months, suspected aortic dissection, active bleeding.
Covered below under Topic C-1 — Acute Coronary Syndrome
Homework — after the session
HomeworkQ1 of 2 · ACS · First Test
A 55-year-old man presents with crushing substernal chest pain radiating to the left arm for 45 minutes. He is diaphoretic and nauseated. What is the best initial diagnostic test?
Click to Reveal Answer
Correct answer: D — 12-lead ECG
A 12-lead ECG must be obtained and interpreted within 10 minutes of arrival in any patient with suspected ACS. It is the single test that separates STEMI from NSTE-ACS, and that distinction determines whether the patient goes to the cath lab now or is managed medically with risk stratification. Troponin follows; it does not come first.
Why the other choices are wrong
High-sensitivity troponin — Incorrect. Essential for diagnosing NSTEMI, and the ECG and troponin are usually drawn nearly together — but troponin takes time to turn positive and a normal early value does not exclude infarction. The ECG comes first.
Chest X-ray — Incorrect. Useful for alternative diagnoses such as pneumothorax or a widened mediastinum, but it never diagnoses ACS and must not delay the ECG.
CT coronary angiography — Incorrect. Has a role in low-to-intermediate risk chest pain workup, not in the acute evaluation of a patient who looks like this.
Bedside transthoracic echocardiogram — Incorrect. Echocardiography is valuable for wall-motion assessment and for excluding alternatives such as tamponade or dissection, but it is neither the first nor the fastest test in a patient who needs an ECG within 10 minutes.
Board pearlECG within 10 minutes — that number is worth memorizing verbatim. And a single normal ECG never rules out ACS: repeat it every 15–30 minutes if pain persists, because occlusion evolves.
Covered below under Topic C-1 — Acute Coronary Syndrome
HomeworkQ2 of 2 · ACS · Antithrombotic Therapy
Which medication combination should be initiated in ALL patients presenting with ACS without contraindications?
The immediate pharmacologic backbone of ACS is antithrombotic: aspirin 162–325 mg chewed, a P2Y12 inhibitor (ticagrelor or prasugrel preferred over clopidogrel in most ACS), and a parenteral anticoagulant such as unfractionated heparin or enoxaparin. This attacks both platelet aggregation and thrombin generation at the culprit plaque.
Why the other choices are wrong
Clopidogrel + warfarin + beta-blocker — Incorrect. Warfarin has no role in acute ACS management, and this regimen omits aspirin entirely.
Aspirin + statin + ACE inhibitor — Incorrect. High-intensity statin and an ACE inhibitor are genuinely important and are started during the admission, but they are secondary prevention — they do not treat the thrombus that is occluding the artery right now.
Aspirin + calcium channel blocker + nitrate — Incorrect. Nitrates relieve pain and calcium channel blockers have niche uses (vasospasm, rate control when beta-blockers are contraindicated), but neither is part of the universal ACS regimen.
Aspirin + P2Y12 inhibitor + high-intensity statin — Incorrect — and it is close. All three belong in ACS care, but this regimen omits the parenteral anticoagulant. Dual antiplatelet therapy plus heparin (or a low-molecular-weight heparin, or bivalirudin) is what treats the active thrombus; the statin is prevention.
Board pearlDistinguish what stops the clot from what prevents the next event. Antiplatelet plus anticoagulant is the acute answer; statin, ACE inhibitor, beta-blocker, and cardiac rehabilitation are the discharge answer. Watch prasugrel's contraindication: prior stroke or TIA.
Covered below under Topic C-1 — Acute Coronary Syndrome
#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.
Core Recognition Pattern
Type
EKG
Troponin
Key Action
STEMI
ST elevation ≥1mm in ≥2 contiguous leads (V2–V3: ≥2mm men, ≥1.5mm women)
Elevated
PCI ≤90 min. Lytics if PCI >120 min from FMC.
NSTEMI
ST depression, TWI, or normal
Elevated
Invasive strategy 24–48h. No immediate lytics.
Unstable Angina
ST changes or normal
Normal
Antiplatelet + anticoagulation. Conservative or invasive per risk.
Type 2 MI
Variable
Elevated
Treat the CAUSE (sepsis, tachycardia, anemia) — NOT PCI unless true occlusion
Classic Board Presentation
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)
Diagnostic Workup
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)
Treatment Algorithm
MONA-B — Updated Protocol
M — Morphine: Only for refractory pain. Caution in NSTEMI — delays P2Y12 absorption, possible ↑ mortality
O — Oxygen: ONLY if SpO₂ <90%. Hyperoxia causes coronary vasoconstriction — do NOT give routinely
N — Nitroglycerin: SL × 3, then IV. CONTRAINDICATED: RV MI, hypotension, PDE-5 inhibitor use (sildenafil 24h, tadalafil 48h)
A — Aspirin: 162–325 mg chewed immediately. Continued at 81 mg indefinitely.
B — Beta-blocker: Oral within 24 hours if no acute HF, shock, heart block, or bronchospasm
DAPT: Aspirin + P2Y12 inhibitor. Ticagrelor (preferred) or prasugrel. Clopidogrel if high bleeding risk.
Type 2 MI: Higher mortality than Type 1. Treat the precipitant (sepsis, anemia, tachycardia), NOT with PCI unless true occlusion
Inferior STEMI + hypotension: Get right-sided EKG. RV MI. Give IV fluids. NO nitrates — drops preload, causes cardiovascular collapse.
O₂ in normoxic ACS: Do NOT give. Worsens outcomes per DETO2X-AMI trial.
Papillary muscle rupture murmur may be SOFT or ABSENT despite severe MR — do not rely on murmur intensity
Troponin ≠ ACS: Elevated troponin in PE, myocarditis, sepsis, CKD. Dynamic rise/fall + ischemic features = MI.
New LBBB: Apply Sgarbossa criteria — not automatic cath lab activation
Wellens + stress test = contraindicated → go straight to cath
Fibrinolytics: NEVER for isolated ST depression (even if posterior MI suspected — confirm first with posterior leads)
★ Memory Trick
STEMI Timing: "90 for PCI, 30 for Lytics" (door-to-balloon and door-to-needle goals)
Post-MI drugs: ACE + STATIN + BETA + DAPT = "A Stab at the Beta"
Inferior MI + Hypotension = RV MI → Fluids YES, Nitro NO
Clinical Vignette
A 64-year-old woman with diabetes presents with 3 hours of jaw pain, nausea, and fatigue. No chest pain. BP 88/60, HR 52. EKG shows 2mm ST elevation in II, III, aVF. She received sublingual nitroglycerin in the ambulance and her BP dropped to 68/40.
Answer: Inferior STEMI with RV involvement. The nitro caused preload reduction → cardiovascular collapse. Get V4R (likely shows ST elevation). Give 1L IV NS bolus. Activate cath lab. Her inferior MI pattern + bradycardia + hypotension = RV MI until proven otherwise. Never give nitrates in inferior MI with hemodynamic compromise.
Rapid Review Bullets
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
Tier 2
Topic C-2
Stable Angina & Vasospastic Angina
Prinzmetal · MINOCA · Diagnosis · Medical Management
★★ PANCE Blueprint
🔒
Full content locked
Enter your bootcamp access code below to unlock all topic cards, clinical pearls, vignettes, and board traps.
Core Recognition
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.
Enter your bootcamp access code below to unlock all topic cards, clinical pearls, vignettes, and board traps.
Why It Matters for Boards
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
Step 1 — Can the Patient Exercise?
Scenario
Choose
Why
Can exercise to ≥5 METs
Exercise stress test
Always preferred — gives functional capacity + prognostic data that pharmacologic tests cannot
Cannot exercise (deconditioned, amputee, severe arthritis, PAD)
Pharmacologic stress
Vasodilator or dobutamine substitutes for the workload
🩺 PANCE Pearl: "Can the patient walk on a treadmill?" is the first branch point in every stress test question. Exercise > pharmacologic whenever physically possible.
Step 2 — Is the Baseline ECG Interpretable?
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.
Pharmacologic Agents — Vasodilator vs Dobutamine
Agent
Mechanism
Used With
Contraindications
Adenosine / Dipyridamole / Regadenoson
Coronary vasodilation → flow heterogeneity
SPECT, PET, cardiac MRI
Bronchospastic disease (asthma/COPD), high-degree AV block, hypotension
Dobutamine
↑ HR, contractility, O₂ demand (sympathomimetic)
Echocardiography or nuclear imaging
Severe HTN, significant arrhythmias, HOCM, aortic dissection
Regadenoson is the most commonly used vasodilator — selective A2A receptor agonist, better tolerated than adenosine
Dobutamine is the fallback when vasodilators are contraindicated (i.e., in a COPD patient who needs pharmacologic stress)
🚨 Classic Trap: Asthma/COPD patient needs pharmacologic stress → vasodilators are CONTRAINDICATED (bronchospasm risk) → use dobutamine instead.
Imaging Modality Selection
Modality
Key Feature
Best Use / Limitation
Exercise ECG alone
No imaging, no radiation, lowest cost
Low-risk patients with interpretable baseline ECG only
Stress Echocardiography
Assesses wall motion, no radiation
High specificity; limited by obesity/poor windows
SPECT (nuclear)
Tc-99m sestamibi/tetrofosmin or Thallium-201
Widely available; radiation exposure; attenuation artifacts in obesity
PET (nuclear)
Higher accuracy than SPECT, lower radiation
Preferred over SPECT when available; limited access/cost
Stress Cardiac MRI
Assesses function, ischemia, scar/viability — no radiation
Avoid gadolinium in renal dysfunction; limited by cost/availability
Coronary CTA
Anatomic (not stress-based) — high NPV
Preferred <65y without known CAD; avoid with renal dysfunction/contrast allergy
Absolute Contraindications
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.
Positive (Ischemic) Test Criteria
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.
Exercise Capacity & Prognosis
<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
Pre-Test Prep — High-Yield Details
Hold beta-blockers 24–48h before if safe — they blunt the heart rate response needed to reach target HR
Hold caffeine ≥12h before vasodilator stress — caffeine blocks adenosine receptors and can cause a false-negative result
🚨 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.
Quick Decision Algorithm
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
Age <65, no known CAD, need anatomic answer → Coronary CTA
Domain 3 · Arrhythmias
Arrhythmias
Before you beginAtrial Fibrillation / Flutter3 in-session · 2 homework
Core Topic 3 — Atrial Fibrillation & Flutter. Attempt the three in-session questions before the domain is taught — they run in the room, in this order: recognition, then management, then the trap. The two homework questions are for tonight, after the teaching. Getting them wrong first is expected and useful; each explanation unlocks only after you submit.
Enter your bootcamp access code above to unlock these questions along with the rest of this domain.
In-sessionQ1 of 3 · AFib · Acute Rate Control
A 65-year-old man with atrial fibrillation and a ventricular rate of 148 bpm is hemodynamically stable, with no known heart failure. What is the best initial treatment for rate control?
Click to Reveal Answer
Correct answer: D — IV metoprolol
In hemodynamically stable atrial fibrillation with rapid ventricular response, the first-line agents are an IV beta-blocker (metoprolol) or a non-dihydropyridine calcium channel blocker (diltiazem). Both slow AV nodal conduction within minutes.
Why the other choices are wrong
Synchronized cardioversion — Incorrect. Reserved for hemodynamic instability — hypotension, ischemia, pulmonary edema, altered mentation. He is stable.
Digoxin alone — Incorrect. Onset is hours, and it controls resting rate poorly with exertion. Useful as an add-on, or as a first choice in decompensated HFrEF or hypotension where beta-blockers and calcium channel blockers are unsafe.
Amiodarone — Incorrect. Primarily a rhythm-control agent here. It does slow the AV node and has a role when first-line agents fail or are contraindicated, but it is not the initial choice, and it carries thyroid, pulmonary, hepatic, and ocular toxicity.
IV adenosine 6 mg rapid push — Incorrect. Adenosine terminates arrhythmias that depend on the AV node for reentry, such as AVNRT. Atrial fibrillation is driven by chaotic atrial activity that does not require the AV node, so adenosine produces a brief block and no lasting rate control.
Board pearlThe branch point is ejection fraction. Preserved EF: beta-blocker or diltiazem, either is fine. Reduced EF: beta-blocker if compensated, and digoxin or amiodarone if decompensated — never verapamil or diltiazem in decompensated HFrEF.
Covered below under Topic A-1 — Atrial Fibrillation & Atrial Flutter · see also Topic H-1
In-sessionQ2 of 3 · AFib · Stroke Prevention
A 72-year-old woman with newly diagnosed atrial fibrillation has hypertension, diabetes, and a prior stroke. Her CHA₂DS₂-VASc score is 6. What is the best next step for stroke prevention?
Click to Reveal Answer
Correct answer: B — Direct oral anticoagulant (e.g., apixaban)
A CHA₂DS₂-VASc score of 2 or more in men, or 3 or more in women, warrants oral anticoagulation. Hers is 6, and she has already had a stroke. DOACs (apixaban, rivaroxaban, edoxaban, dabigatran) are preferred over warfarin in nonvalvular atrial fibrillation: equal or better stroke prevention, less intracranial hemorrhage, no INR monitoring.
Why the other choices are wrong
Aspirin 81 mg daily — Incorrect. Aspirin is clearly inferior to anticoagulation for cardioembolic stroke prevention in atrial fibrillation and is no longer recommended as a substitute.
Aspirin plus clopidogrel — Incorrect. Dual antiplatelet therapy is less effective than anticoagulation and carries a comparable bleeding burden — the worst of both.
No anticoagulation needed — Incorrect. A score of 6 with a prior stroke is among the highest-risk presentations you will see.
Left atrial appendage occlusion device — Incorrect. Percutaneous appendage occlusion is reserved for patients with a genuine long-term contraindication to anticoagulation, such as recurrent life-threatening bleeding. It is an alternative for those who cannot take a DOAC, not a first choice for someone who can.
Board pearlTwo situations still require warfarin, not a DOAC: a mechanical heart valve and moderate-to-severe rheumatic mitral stenosis. Everything else nonvalvular gets a DOAC. Also note that the stroke risk is the same for paroxysmal and persistent atrial fibrillation — the pattern does not lower the score.
A patient with new-onset atrial fibrillation is being considered for elective cardioversion. The duration of atrial fibrillation is unknown. What must be done before cardioversion?
Click to Reveal Answer
Correct answer: D — Anticoagulate 3 weeks or perform TEE to exclude left atrial thrombus
When atrial fibrillation has lasted more than 48 hours or the duration is unknown, an organized atrial thrombus may already have formed. Either anticoagulate therapeutically for at least 3 weeks before cardioversion, or perform a TEE to exclude left atrial appendage thrombus and cardiovert under anticoagulation. Either way, anticoagulation continues for at least 4 weeks afterward, because atrial mechanical function lags behind electrical recovery.
Why the other choices are wrong
No preparation needed — proceed directly — Incorrect. Cardioverting an unprepared patient with a possible atrial thrombus can dislodge it and cause a stroke. The exception is hemodynamic instability, where you cardiovert immediately regardless.
Start aspirin for 4 weeks — Incorrect. Aspirin does not prevent cardioembolic stroke in this setting.
Obtain a stress test — Incorrect. Not part of the pre-cardioversion pathway.
Obtain a transthoracic echocardiogram instead — Incorrect — wrong window. A TTE cannot reliably visualize the left atrial appendage, which is where the thrombus forms. Excluding appendage thrombus requires a transesophageal study; a reassuring TTE does not make cardioversion safe.
Board pearlThe 48-hour mark governs everything. Under 48 hours with low risk, you may cardiovert with anticoagulation started at the time of the procedure. Over 48 hours or unknown: 3 weeks of anticoagulation or a TEE first, then 4 weeks of anticoagulation after — regardless of CHA₂DS₂-VASc score.
A 68-year-old man presents with palpitations and an irregularly irregular pulse at 142 bpm. What is the best initial diagnostic test?
Click to Reveal Answer
Correct answer: E — 12-lead ECG
The 12-lead ECG confirms atrial fibrillation — absent organized P waves, an irregularly irregular rhythm — and simultaneously tells you the ventricular rate, whether there is pre-excitation or bundle branch block, and whether ischemic changes are present. It is fast, universally available, and drives the next decision.
Why the other choices are wrong
Cardiac catheterization — Incorrect. No role in diagnosing an arrhythmia.
Holter monitor — Incorrect. Ambulatory monitoring is for intermittent or paroxysmal symptoms when the arrhythmia is not present in front of you. This patient is in it now.
Transesophageal echocardiogram — Incorrect. TEE is used to exclude left atrial appendage thrombus before cardioversion, not to make the diagnosis.
Serum TSH and electrolyte panel — Incorrect — as the initial test. Thyroid and electrolyte studies are part of the standard first-visit workup once atrial fibrillation is established, and thyrotoxicosis is a genuine precipitant. But they identify a cause; they do not make the diagnosis.
Board pearl“Irregularly irregular” in a stem is atrial fibrillation until proven otherwise, and the confirmatory test is always the 12-lead ECG. Then work the standard first-visit panel: TSH, electrolytes, CBC, and a TTE for structural disease.
HomeworkQ2 of 2 · AFib + HFrEF · Refractory Rhythm
A 70-year-old woman with persistent atrial fibrillation and HFrEF (LVEF 30%) has failed rate control with beta-blockers. What is the best next step?
Click to Reveal Answer
Correct answer: A — Refer for catheter ablation
Catheter ablation is recommended for symptomatic atrial fibrillation in HFrEF when medical rate or rhythm control has failed or is not tolerated. In this population, restoring sinus rhythm by ablation improves ejection fraction, quality of life, and heart failure hospitalization compared with continued drug therapy — the atrial fibrillation is contributing to the cardiomyopathy, not just coexisting with it.
Why the other choices are wrong
Add digoxin for additional rate control — Incorrect. A reasonable adjunct for rate in HFrEF, but it leaves her in atrial fibrillation and does not address the rhythm driving her decline.
Start flecainide — Incorrect. Class IC antiarrhythmics are contraindicated in structural heart disease and reduced ejection fraction because of proarrhythmic mortality risk. This is the dangerous distractor.
Increase metoprolol to the maximum tolerated dose — Incorrect. She has already failed beta-blockade, and pushing the dose in HFrEF risks symptomatic bradycardia and fatigue without controlling the rhythm.
Start sotalol for rhythm control — Incorrect. Sotalol has both class III and beta-blocking activity, and in HFrEF it carries real risk: QT prolongation with torsades, plus negative inotropy in a ventricle that cannot afford it. If a drug is used for rhythm here, amiodarone is the safer choice.
Board pearlTwo rhythm drugs are the tested landmines: flecainide and propafenone are out in structural heart disease, and sotalol and dofetilide prolong the QT. In HFrEF the safe antiarrhythmic choices are amiodarone or dofetilide with monitoring — and increasingly, ablation.
Covered below under Topic A-1 — Atrial Fibrillation & Atrial Flutter · see also Topic H-1
Immediate cardioversion regardless of duration or OAC status
Class I
OAC ASAP + ≥4 weeks
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.
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.
⚑ Critical Board Traps — AFib
EF check before rate control drug — diltiazem/verapamil in HFrEF is the #1 tested lethal drug error
WPW + AFib = AV nodal blockers CONTRAINDICATED (adenosine, digoxin, diltiazem, verapamil, beta-blockers) — forces conduction down accessory pathway → VF → cardiac arrest. Use procainamide or cardioversion.
Amiodarone is CYP450 inhibitor — increases warfarin levels (reduce warfarin by 30–50%), digoxin levels
Aspirin alone ≠ stroke prevention in AF
Post-CV OAC 4 weeks is mandatory for ALL patients regardless of CHA₂DS₂-VASc or AF duration — atrial stunning
DOAC with mechanical valve = ABSOLUTELY CONTRAINDICATED (RE-ALIGN trial: ↑ thromboembolism and bleeding)
★ Memory Trick
AFib Rate Control: "DELAY"
Diltiazem if EF normal · metoprolol if EF Low · digoxin if Elderly/sedentary · Amiodarone if all fail Yet urgent
Antiarrhythmics: "Structural disease? FLUNK everyone except Amiodarone and Dofetilide"
1st Degree · Mobitz I vs Mobitz II · Complete Heart Block · Pacemaker Indications
★★★ PANCE Priority
🔒
Full content locked
Enter your bootcamp access code below to unlock all topic cards, clinical pearls, vignettes, and board traps.
📈 Ladder diagram — the conduction-slope view of PR lengthening versus fixed PR now lives in the PA Bootcamp EKG Syllabus, Rhythm Recognition. Open the EKG Syllabus ↗
Common in athletes, sleep. Usually benign. Pacing rarely needed.
2° Mobitz II
Constant PR → sudden dropped QRS. No progressive lengthening.
Infranodal (His-Purkinje)
YES — regardless of symptoms (Class I)
High risk of sudden complete heart block. Wide QRS = more dangerous.
3° (Complete) AV Block
Complete AV dissociation. Atrial rate > ventricular rate. Escape rhythm.
Infranodal
YES — regardless of symptoms (Class I)
Wide QRS escape = most dangerous. Unreliable with risk of asystole.
⚑ Board Trap
Mobitz I = usually benign, no pacing. Mobitz II and 3rd degree = pacemaker regardless of symptoms.
Mobitz II with wide QRS = most dangerous pattern — diffuse conduction system disease, can deteriorate to asystole without warning
Wenckebach that worsens with exercise suggests infranodal block (not typical AV node Wenckebach) — may need pacing
Domain 4 · Heart Failure
Heart Failure
Before you beginHeart Failure3 in-session · 2 homework
Core Topic 1 — Heart Failure. Attempt the three in-session questions before the domain is taught — they run in the room, in this order: recognition, then management, then the trap. The two homework questions are for tonight, after the teaching. Getting them wrong first is expected and useful; each explanation unlocks only after you submit.
Enter your bootcamp access code above to unlock these questions along with the rest of this domain.
In-sessionQ1 of 3 · HFrEF · Four-Pillar GDMT
A 58-year-old woman is diagnosed with HFrEF (LVEF 30%). She is hemodynamically stable with no contraindications. Which of the following is the best initial pharmacologic regimen?
Click to Reveal Answer
Correct answer: C — ACEi/ARB (or ARNI), beta-blocker, MRA, and SGLT2 inhibitor
ACC/AHA guidelines recommend “quadruple therapy” — ARNI (or ACEi/ARB) + an evidence-based beta-blocker (carvedilol, metoprolol succinate, or bisoprolol) + an MRA + an SGLT2 inhibitor — as foundational guideline-directed medical therapy for HFrEF. All four classes reduce mortality, and current practice is to start them early at low dose and uptitrate rather than maximize one pillar before adding the next.
Why the other choices are wrong
Hydralazine plus isosorbide dinitrate as the initial regimen — Incorrect. This combination is an alternative for patients who cannot tolerate an ACEi/ARB/ARNI, and an add-on for persistently symptomatic self-identified Black patients — not first-line monotherapy.
Digoxin and furosemide — Incorrect. Digoxin reduces hospitalizations but not mortality, and loop diuretics treat congestion only. Neither is disease-modifying.
Calcium channel blocker plus a thiazide diuretic for afterload reduction — Incorrect. Non-dihydropyridine calcium channel blockers (diltiazem, verapamil) are contraindicated in HFrEF because of their negative inotropic effect.
Beta-blocker and loop diuretic alone, adding other agents only if symptoms persist — Incorrect — and this is the sequencing trap. The four pillars are started together (or in rapid succession) at low doses and then titrated, because each cuts mortality independently. Waiting for symptoms before adding the rest leaves proven benefit on the table.
Board pearlFour pillars, all mortality-reducing: ARNI or ACEi/ARB + beta-blocker + MRA + SGLT2 inhibitor. Two gates before an MRA: K⁺ below 5.0 and eGFR at or above 30. SGLT2 inhibitors need only eGFR at or above 20 and work regardless of diabetes status.
In-sessionQ2 of 3 · HFpEF · Evidence-Based Therapy
A 65-year-old woman with HFpEF (LVEF 60%) presents with worsening dyspnea and peripheral edema. Which medication has the strongest evidence for reducing heart failure hospitalization in HFpEF?
Click to Reveal Answer
Correct answer: B — Empagliflozin
SGLT2 inhibitors (empagliflozin, dapagliflozin) are the first-line disease-modifying therapy in HFpEF and carry the strongest guideline recommendation. EMPEROR-Preserved showed a 21% relative reduction in the composite of cardiovascular death or heart failure hospitalization with empagliflozin in patients with LVEF above 40%, driven mainly by fewer hospitalizations. The benefit is independent of diabetes status. Diuretics still treat her congestion, but they are symptomatic therapy.
Why the other choices are wrong
Lisinopril — Incorrect. ACE inhibitors and ARBs have repeatedly failed to show definitive hospitalization or mortality benefit in HFpEF trials, even though treating her hypertension remains important.
Metoprolol succinate — Incorrect. Beta-blockers have not reduced mortality or hospitalization in HFpEF, and by blunting the heart rate response they can worsen exercise tolerance. Keep them if she needs one for another indication.
Amlodipine — Incorrect. Lowers blood pressure with no heart failure outcome benefit, and it commonly causes peripheral edema that gets mistaken for worsening congestion.
Spironolactone — Incorrect — though it is the best of the wrong answers. TOPCAT suggested benefit in HFpEF but missed its primary endpoint, leaving MRAs with a weaker (2b) recommendation. The question asks for the strongest evidence, and only the SGLT2 inhibitors have a clearly positive dedicated trial program.
Board pearlHFpEF has exactly one pillar with hard outcome data: an SGLT2 inhibitor. Everything else is treating comorbidity — diuretics for congestion, blood pressure control for the hypertensive substrate, rate control for atrial fibrillation. An MRA and an ARNI carry weaker (2b) recommendations in selected patients.
A 55-year-old man with newly diagnosed HFrEF has an LVEF of 28% and NYHA class II symptoms. BNP is 850 pg/mL. Which of the following is the most appropriate next step after initiating GDMT?
Click to Reveal Answer
Correct answer: D — Repeat echocardiogram in 3–6 months to reassess LVEF
Reassess the ejection fraction after 3 months or more of optimized guideline-directed medical therapy, before committing to device therapy. A meaningful proportion of patients recover ejection fraction on four-pillar therapy, which changes ICD and CRT eligibility entirely — so the echo is what determines whether a device conversation is even needed.
Why the other choices are wrong
Immediate ICD placement — Incorrect. Primary-prevention ICD requires at least 3 months of optimized GDMT with a persistent LVEF at or below 35% and a reasonable expectation of survival beyond one year. Implanting now may commit him to a device he no longer qualifies for.
Referral for advanced heart failure and transplant evaluation — Incorrect. Premature. Transplant evaluation is for advanced, refractory disease after GDMT has been optimized, not NYHA class II at diagnosis.
Start IV milrinone — Incorrect. Inotropes are for refractory end-stage disease or as a bridge to advanced therapies, not for a stable outpatient.
Refer for cardiac resynchronization therapy evaluation now — Incorrect. CRT requires a wide QRS — generally 150 ms or more with a left bundle branch pattern — and, like the ICD, a persistently low EF after GDMT has been optimized. No QRS duration is given, and therapy has only just started.
Board pearlThe sequence is fixed and heavily tested: GDMT first, echo at 3–6 months, device only if the EF stays at or below 35%. Do not let a low initial EF pull you into ordering the ICD on day one.
A 62-year-old man presents with progressive dyspnea on exertion, orthopnea, and bilateral lower extremity edema. Exam reveals bibasilar crackles and an S3 gallop. What is the best initial diagnostic test?
Click to Reveal Answer
Correct answer: C — Transthoracic echocardiogram
Transthoracic echocardiography (TTE) is the first-line diagnostic test for suspected heart failure. It gives you left ventricular ejection fraction, chamber size, wall motion, valvular function, and diastolic parameters in one study — everything needed to separate HFrEF from HFpEF and to direct therapy. Natriuretic peptides (BNP/NT-proBNP) support the diagnosis but do not replace imaging.
Why the other choices are wrong
Cardiac catheterization — Incorrect. Invasive and reserved for cases needing hemodynamic assessment or coronary evaluation, not the initial workup of new heart failure.
Coronary CT angiography — Incorrect. Defines coronary anatomy but tells you nothing about ejection fraction, filling pressures, or valve function.
Cardiac MRI — Incorrect. Superb structural and tissue characterization (and the test of choice for suspected infiltrative disease), but it is a second-line study used when echocardiography is inconclusive.
Right heart catheterization with pressure measurement — Incorrect. Invasive hemodynamics are reserved for cases where volume status or filling pressures remain genuinely unclear, or where pulmonary hypertension needs characterizing. Echocardiography answers the initial question non-invasively.
Board pearlNew heart failure = echo first. The single question the echo answers is the one that drives every subsequent decision: is the EF reduced or preserved? Order an ECG and BNP alongside it, but the echo is the answer to “best initial diagnostic test.”
A 70-year-old man with HFrEF (LVEF 25%) on optimal GDMT presents with acute decompensation: severe dyspnea at rest, JVD, and bilateral crackles. BP is 145/90 mmHg. What is the best next step?
Click to Reveal Answer
Correct answer: E — Administer IV furosemide
This is acute decompensated heart failure that is wet and warm — congested but adequately perfused, with a blood pressure of 145/90. IV loop diuretics are the correct first move to relieve congestion. Oral bioavailability is unreliable in a congested gut, so give the loop diuretic intravenously.
Why the other choices are wrong
Start a dobutamine infusion — Incorrect. Inotropes are for the wet and cold patient — hypotension with inadequate cardiac output. Giving an inotrope to a patient at 145/90 adds arrhythmia and mortality risk for no benefit.
Perform emergent cardiac catheterization — Incorrect. Emergent catheterization is for ACS. Nothing here points to an acute ischemic event.
Add digoxin — Incorrect. Onset is far too slow for acute decongestion, and digoxin does not treat volume overload.
Start IV nitroglycerin as monotherapy — Incorrect — as monotherapy. A nitroglycerin infusion is a reasonable adjunct for a hypertensive, congested patient and unloads the ventricle quickly. It does not remove volume, and this patient's problem is the volume.
Board pearlDecongestion has its own set of tested details. Give the loop diuretic IV, not oral — gut wall edema makes absorption unreliable — at roughly 1 to 2.5 times the home daily oral dose. And do not stop the GDMT: withdrawing the beta-blocker or ACEi/ARNI in a patient who is congested but well perfused is a classic wrong answer, reserved for hypotension or true shock. Track daily weights and strict intake/output, and expect a modest early creatinine rise during effective diuresis — that alone is not a reason to stop. If urine output stalls, escalate the loop dose or add a thiazide.
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)
Acute Decompensated Heart Failure (ADHF)
LMNOP Protocol
L — Lasix (IV furosemide): Mainstay. Give IV even if on oral (gut absorption impaired in ADHF). Continuous infusion may be superior to bolus in severe congestion.
N — Nitroglycerin IV: Excellent for preload/afterload reduction if SBP >90. Works in 2 minutes.
O — Oxygen: Titrate to SpO₂ ≥94%. CPAP/BiPAP reduces intubation in flash pulmonary edema.
P — Position: Sit upright, legs dependent — immediate preload reduction.
Inotropes (dobutamine/milrinone): ONLY for cardiogenic shock / low cardiac output states (Cold & Wet). Increase mortality with prolonged use.
Nesiritide = no longer recommended — no mortality benefit, causes hypotension
Do NOT initiate BB in acute decompensated HF ("wet" patient). Start only when euvolemic.
Metoprolol tartrate ≠ metoprolol succinate — tartrate has NO mortality benefit in HFrEF. Only succinate is evidence-based.
ARNI + ACEi = absolutely contraindicated together (angioedema risk). 36h washout from ACEi before starting ARNI.
S3 gallop = systolic dysfunction (HFrEF). S4 gallop = diastolic dysfunction (HFpEF, LVH). Boards test this distinction.
★ Memory Trick
HFrEF GDMT — "A BEAST": ARNI · BB (carvedilol/metosucc/bisoprolol) · SGLT2i · MRA (spironolactone/eplerenone) — quadruple therapy
Only 3 BBs work: "Can My Boss care?" = Carvedilol · Metoprolol succinate · Bisoprolol
Domain 5 · Valvular Disease
Valvular Disease & Endocarditis
Before you beginValvular Heart Disease3 in-session · 2 homework
Core Topic 4 — Valvular Heart Disease. Attempt the three in-session questions before the domain is taught — they run in the room, in this order: recognition, then management, then the trap. The two homework questions are for tonight, after the teaching. Getting them wrong first is expected and useful; each explanation unlocks only after you submit.
Enter your bootcamp access code above to unlock these questions along with the rest of this domain.
In-sessionQ1 of 3 · Murmur Recognition
A 45-year-old woman has a holosystolic murmur best heard at the apex, radiating to the axilla. What is the most likely diagnosis?
Click to Reveal Answer
Correct answer: C — Mitral regurgitation
A holosystolic (pansystolic) murmur loudest at the apex and radiating to the axilla is the textbook finding of mitral regurgitation. Location and radiation are what separate the systolic murmurs from one another.
Why the other choices are wrong
Tricuspid regurgitation — Incorrect. Also holosystolic, but at the left lower sternal border, and it gets louder with inspiration (Carvallo sign). Look for JVD, a pulsatile liver, and peripheral edema.
Aortic stenosis — Incorrect. Crescendo-decrescendo systolic murmur at the right upper sternal border radiating to the carotids, not the axilla.
Mitral stenosis — Incorrect. A diastolic low-pitched rumble at the apex with an opening snap.
Ventricular septal defect — Incorrect. A VSD also produces a holosystolic murmur, but it is harsh and loudest at the left lower sternal border, often with a palpable thrill, and it does not radiate to the axilla.
Board pearlUse the maneuvers to break ties: inspiration amplifies right-sided murmurs, expiration amplifies left-sided ones. Handgrip (increased afterload) makes MR and AR louder while making the HOCM murmur softer; standing or Valsalva does the reverse for HOCM.
Covered below under Topic V-1 — Valvular Disease, The Big Four · see also Topic F-3
In-sessionQ2 of 3 · Aortic Stenosis · Intervention
A 78-year-old woman has severe symptomatic aortic stenosis (valve area 0.8 cm², mean gradient 48 mmHg) with exertional dyspnea. What is the best next step?
Click to Reveal Answer
Correct answer: B — Aortic valve replacement (surgical or transcatheter)
Symptomatic severe aortic stenosis carries a grim prognosis without intervention — roughly 50% mortality within 2 years of symptom onset. Valve replacement, surgical (SAVR) or transcatheter (TAVR), is the only treatment that changes that. The choice between SAVR and TAVR turns on surgical risk, age, anatomy, and patient preference, decided by a heart team; at 78 with severe AS, TAVR is often favored.
Why the other choices are wrong
Medical management with diuretics and vasodilator therapy — Incorrect. No medical therapy alters the natural history of severe AS, and vasodilators are dangerous here: with a fixed obstruction the ventricle cannot raise output to compensate for dropping systemic resistance, so blood pressure can collapse.
Serial echocardiographic monitoring every 6 months — Incorrect. Watchful waiting is for asymptomatic severe AS. She is symptomatic, which is precisely the trigger for intervention.
Start a beta-blocker — Incorrect. Does nothing for mechanical outflow obstruction, and excessive rate slowing can reduce cardiac output.
Balloon aortic valvuloplasty as the definitive treatment — Incorrect. Valvuloplasty gives only transient relief in calcific adult aortic stenosis and carries a high restenosis rate. Its role is a bridge in the unstable patient or palliation — not definitive therapy. (Contrast mitral stenosis, where balloon valvuloplasty is definitive for suitable anatomy.)
Board pearlSymptomatic severe AS = replace the valve, no matter how mild the symptoms sound. Also intervene in asymptomatic severe AS when the LVEF drops below 50% or the patient is already having other cardiac surgery.
Covered below under Topic V-1 — Valvular Disease, The Big Four
In-sessionQ3 of 3 · Mitral Regurgitation · Surgical Triggers
A patient with severe chronic primary mitral regurgitation has an LVEF of 55% and an LV end-systolic dimension of 42 mm. He is asymptomatic. What is the best next step?
Click to Reveal Answer
Correct answer: D — Refer for mitral valve repair rather than replacement
He is asymptomatic, but he has already crossed both surgical thresholds. In severe chronic primary MR, intervention is indicated (Class I) once the LVEF falls to 60% or below or the LVESD reaches 40 mm or more — either one is sufficient, and he meets both at 55% and 42 mm. These numbers look deceptively normal, which is the whole point: in a volume-overloaded ventricle unloading into a low-pressure left atrium, an “EF of 55%” already signals contractile impairment. Repair is preferred over replacement when the anatomy allows a durable result.
Why the other choices are wrong
Start an ACE inhibitor and a diuretic — Incorrect. Vasodilators do not alter the natural history of primary (degenerative) MR and are not a substitute for fixing the valve. Medical therapy has a real role in secondary MR, where the problem is the ventricle rather than the leaflets.
Serial echocardiographic monitoring every 6–12 months — Incorrect, and this is the trap. Surveillance is correct only while the LVEF stays above 60% and the LVESD stays under 40 mm. Continuing to watch him allows irreversible LV dysfunction, and post-operative outcomes are measurably worse once surgery is delayed past these thresholds.
Cardiac catheterization to measure the regurgitant fraction — Incorrect. Not the next diagnostic step when the echo data are adequate, though coronary assessment is routine as part of pre-operative planning once the decision to operate is made.
Refer for transcatheter edge-to-edge repair rather than surgery — Incorrect. Transcatheter edge-to-edge repair is for patients at prohibitive surgical risk, or for secondary MR that persists on optimal medical therapy. This patient has primary degenerative MR and no stated surgical risk, so open repair remains the durable answer.
Board pearlTwo numbers decide surgery in asymptomatic severe primary MR: LVEF 60% or below, or LVESD 40 mm or above. Either one, on its own, is a Class I indication. Symptoms are also a Class I indication regardless of the numbers — so “asymptomatic with normal-looking EF” is never by itself a reason to keep waiting.
Covered below under Topic V-1 — Valvular Disease, The Big Four
Homework — after the session
HomeworkQ1 of 2 · Valvular Disease · Initial Workup
A 75-year-old man presents with exertional syncope, angina, and dyspnea. Exam reveals a harsh crescendo-decrescendo systolic murmur at the right upper sternal border radiating to the carotids. What is the best initial diagnostic test?
Click to Reveal Answer
Correct answer: C — Transthoracic echocardiogram
This is the classic triad of severe aortic stenosis — syncope, angina, dyspnea — with the matching murmur. TTE is the initial test for every suspected valve lesion: it establishes valve morphology, quantifies severity (mean gradient, peak velocity, calculated valve area), and assesses ventricular function and chamber size.
Why the other choices are wrong
Chest X-ray — Incorrect. May show cardiomegaly or valve calcification, but it cannot grade severity.
Exercise stress test — Incorrect. Actively contraindicated in symptomatic severe aortic stenosis — the fixed obstruction cannot meet exercise demand, risking syncope, arrhythmia, or death.
Cardiac catheterization — Incorrect. Reserved for discordant clinical and echo findings, or for coronary assessment before intervention.
Transesophageal echocardiogram — Incorrect. TEE gives superb valve images but is invasive and unnecessary as a first study. TTE is what grades severity here; TEE is reserved for inadequate transthoracic windows or for pre-procedural planning.
Board pearlIn aortic stenosis, the appearance of any symptom is the turning point in the natural history. Memorize the severe-AS numbers: peak velocity 4 m/s or more, mean gradient 40 mmHg or more, valve area 1.0 cm² or less.
Covered below under Topic V-1 — Valvular Disease, The Big Four
HomeworkQ2 of 2 · Mitral Stenosis · Recognition
A 30-year-old woman with a history of rheumatic fever presents with dyspnea and a low-pitched diastolic rumble at the apex with an opening snap. What is the most likely diagnosis?
Click to Reveal Answer
Correct answer: E — Mitral stenosis
A low-pitched diastolic rumble at the apex following an opening snap is essentially diagnostic of mitral stenosis, and rheumatic heart disease remains its most common cause worldwide. Expect a loud S1 early on, and watch for the complications that actually harm these patients: atrial fibrillation, pulmonary hypertension, and hemoptysis.
Why the other choices are wrong
Aortic regurgitation — Incorrect. A blowing early decrescendo diastolic murmur at the left sternal border, classically with a wide pulse pressure and bounding peripheral pulses.
Atrial septal defect — Incorrect. A fixed split S2 with a systolic pulmonary flow murmur — the split is the giveaway.
Mitral regurgitation — Incorrect. Holosystolic at the apex radiating to the axilla, not diastolic.
Tricuspid stenosis — Incorrect. Tricuspid stenosis is rare, and its diastolic rumble is loudest at the left lower sternal border and increases with inspiration. It presents with right-sided congestion — JVD, ascites, hepatomegaly — not the pulmonary findings described.
Board pearlRheumatic mitral stenosis is one of the two settings that still demands warfarin rather than a DOAC when atrial fibrillation develops (the other is a mechanical valve). Definitive treatment for suitable anatomy is percutaneous balloon mitral valvuloplasty.
Covered below under Topic V-1 — Valvular Disease, The Big Four
Tier 1
Topic V-1
Valvular Disease — The Big Four
AS · AR · MS · MR · MVP · Prosthetic Valve Anticoagulation
★★★ PANCE Priority
🔒
Full content locked
Enter your bootcamp access code below to unlock all topic cards, clinical pearls, vignettes, and board traps.
Valve Lesion
Murmur
Classic Findings
Key Traps
Aortic Stenosis
Systolic crescendo-decrescendo, RUSB → carotids. Parvus et tardus.
SAD triad: Syncope → Angina → Dyspnea (in order of worsening prognosis). Single/absent S2.
NO vasodilators or nitrates (fixed obstruction → catastrophic hypotension). Murmur becomes SOFT as CO falls — severe AS can have a quiet murmur.
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
Endocarditis Prophylaxis — Only Highest-Risk
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).
Blood cultures × 3 BEFORE antibiotics — once antibiotics started, cultures become negative
Staph aureus is now the most common cause of IE overall (surpassed Strep viridans due to IVDU and healthcare-associated exposure)
Prophylaxis NOT indicated for GI or GU procedures — only dental with gingival manipulation
Domain 6 · Cardiomyopathies
Cardiomyopathies
Before you beginCardiomyopathies3 questions
Answer these three before you read the domain. Getting them wrong is expected and useful — attempting a question first is what makes the material below stick. Each explanation unlocks only after you submit.
Enter your bootcamp access code above to unlock these questions along with the rest of this domain.
Question 1 of 3 · Medium · Reversible Dilated Cardiomyopathy
A 42-year-old man with a 15-year history of daily heavy alcohol use presents with progressive dyspnea and bilateral leg edema. Echocardiogram shows EF of 18%, four-chamber dilation, and moderate mitral regurgitation. What is the single most important intervention to improve his prognosis?
Click to Reveal Answer
Correct answer: D — Complete alcohol cessation
This is alcoholic (toxic) dilated cardiomyopathy — one of the few potentially reversible causes of dilated CMP. Complete cessation of alcohol use can lead to significant, sometimes dramatic, recovery of ejection fraction, and is the single most important prognostic factor, more important than any pharmacologic intervention alone.
Why the other choices are wrong
Urgent referral for heart transplant evaluation — Incorrect — as an initial step. Because alcoholic cardiomyopathy is potentially reversible with cessation, transplant evaluation would be premature before giving the patient the opportunity to recover EF through abstinence and GDMT — this is reserved for refractory cases that don't improve.
Diuretic therapy alone, since this addresses his most prominent symptom of edema — Incorrect. Diuretics manage symptomatic volume overload but do not address the reversible underlying cause or change long-term prognosis the way alcohol cessation does.
Starting maximal-dose GDMT (ACEi, beta-blocker, MRA, SGLT2i) without addressing alcohol use — Incorrect — as the primary answer. While GDMT is appropriate and should be initiated, it does not address the underlying reversible cause. Without cessation of alcohol use, the cardiomyopathy will likely persist or progress despite optimal medical therapy.
Implantable cardioverter-defibrillator placement immediately — Incorrect — as the most important first step. ICD placement for primary prevention is typically deferred for at least 3-6 months while EF is reassessed after cessation and GDMT optimization, since EF may improve significantly and obviate the need for a device.
Board pearlAlways ask whether a dilated cardiomyopathy is one of the reversible ones before settling into chronic management: alcohol, tachycardia-mediated, thyroid disease, peripartum, myocarditis, cocaine, and chemotherapy (anthracyclines, trastuzumab). Removing the cause can restore EF outright. This is also why primary-prevention ICD placement waits 3–6 months of therapy before EF is reassessed.
Covered below under Topic CM-2 — Dilated & Other Cardiomyopathies
Question 2 of 3 · High Yield · Cardiomyopathy · HCM Drug Trap
A 34-year-old with hypertrophic obstructive cardiomyopathy develops exertional dyspnea. Which of the following is CONTRAINDICATED?
Click to Reveal Answer
Correct answer: A — Sublingual nitroglycerin
In HOCM, vasodilators are contraindicated — nitroglycerin, ACEi, ARBs, hydralazine, and diuretics all reduce preload or afterload, worsening LVOT obstruction → syncope or sudden death. Beta-blockers (metoprolol, propranolol) and verapamil are first-line treatments — they reduce heart rate and improve diastolic filling. Disopyramide (Class IA antiarrhythmic with negative inotropic effect) is used for refractory obstructive symptoms.
Why the other choices are wrong
Disopyramide for refractory obstruction — Incorrect. Disopyramide is actually a therapeutic option in HOCM. Its negative inotropic effect reduces the force of septal contraction and therefore relieves LVOT obstruction — it is used as second-line therapy when beta-blockers fail.
Propranolol — Incorrect. Beta-blockers are FIRST-LINE in HOCM. They reduce contractility and slow heart rate, which lengthens diastolic filling time, enlarges the LV cavity, and reduces outflow obstruction.
Metoprolol succinate — Incorrect. Like propranolol, metoprolol is a beta-blocker and therefore beneficial in HOCM. Both nonselective and cardioselective agents work through the same mechanism of reduced contractility and improved diastolic filling.
Verapamil — Incorrect. Verapamil is a recognized alternative to beta-blockers in HOCM because it is negatively inotropic and improves diastolic relaxation. It requires caution in severe obstruction, but it is not the contraindicated answer here.
Board pearlHOCM is preload- and afterload-dependent, so anything that shrinks the ventricle worsens the obstruction: nitrates, ACEi/ARBs, hydralazine, dihydropyridine CCBs, and aggressive diuresis. Treat with beta-blockers or verapamil; disopyramide is added for refractory obstruction. And volume plus a beta-blocker — not nitroglycerin — is the answer when a HOCM patient becomes hypotensive.
Covered below under Topic CM-1 — Hypertrophic Cardiomyopathy (HCM)
Question 3 of 3 · High Yield · HCM and Sudden Cardiac Death
A 17-year-old basketball player collapses during practice and is resuscitated from ventricular fibrillation. His uncle died suddenly at age 28 during a football game. Echocardiogram shows LV wall thickness of 22mm with systolic anterior motion of the mitral valve. Which medication is absolutely contraindicated in his ongoing management?
Click to Reveal Answer
Correct answer: B — Digoxin — it is a positive inotrope that worsens left ventricular outflow tract obstruction
This presentation (young athlete, sudden cardiac arrest from VF, family history of sudden death, massive LV hypertrophy with systolic anterior motion of the mitral valve) is classic hypertrophic cardiomyopathy (HCM) with sudden cardiac death risk. Digoxin, along with nitrates and pure vasodilators, decreases preload and/or increases contractility — both of which worsen dynamic LVOT obstruction in HCM and can precipitate hemodynamic collapse. He requires ICD placement for secondary prevention.
Why the other choices are wrong
Aspirin — antiplatelet agents worsen outflow tract obstruction — Incorrect. Aspirin has no mechanistic relationship to LVOT obstruction and is not contraindicated in HCM based on this mechanism.
Lisinopril — ACE inhibitors are absolutely contraindicated in HCM — Incorrect. While ACE inhibitors are used cautiously in obstructive HCM (since afterload reduction can theoretically worsen obstruction), they are not in the same category of absolute, classic contraindication as digoxin and nitrates, which directly worsen the core pathophysiology through preload/inotropy effects.
Verapamil — calcium channel blockers are absolutely contraindicated in all cardiomyopathies — Incorrect. Non-dihydropyridine calcium channel blockers like verapamil are actually used as second-line therapy in HCM (when beta-blockers are insufficient or not tolerated) because they also reduce contractility, similar to beta-blockers — they are not contraindicated.
Metoprolol — beta-blockers should never be used in cardiomyopathy of any type — Incorrect. Beta-blockers are actually first-line therapy in HCM — they reduce contractility and heart rate, which decreases LVOT obstruction. This is the opposite of digoxin's effect and is appropriate, not contraindicated.
Board pearlYoung athlete + exertional collapse + family history of sudden death = HCM until an echo says otherwise. Wall thickness at or above 30 mm, unexplained syncope, a family history of sudden death, massive LVH, and non-sustained VT are the risk markers driving ICD placement. Here the arrest already happened, so the ICD is secondary prevention — and first-degree relatives need screening.
Covered below under Topic CM-1 — Hypertrophic Cardiomyopathy (HCM)
Tier 2
Topic CM-1
Hypertrophic Cardiomyopathy (HCM)
Most Common Cause of Sudden Cardiac Death in Young Athletes
★★ PANCE Blueprint★ Gap Added
🔒
Full content locked
Enter your bootcamp access code below to unlock all topic cards, clinical pearls, vignettes, and board traps.
Why It Matters
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.
Core Recognition
Genetics: Autosomal dominant; sarcomere protein mutations (myosin heavy chain, troponin)
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
⚑ Board Traps — HCM
Digoxin, diuretics, and vasodilators (including nitrates, ACEi) are CONTRAINDICATED — reduce preload/afterload → worsen LVOT obstruction → syncope or sudden death
HCM murmur INCREASES with Valsalva/standing — opposite of AS, MR, and most other murmurs
Athletes with HCM must be restricted from competitive sports
HCM is NOT dilated CM — heart is stiff and hypertrophied, not dilated and weak
★ Memory Trick
HCM murmur: "Lower the Load = Louder" — anything that ↓ preload or afterload (standing, Valsalva, dehydration) makes HCM murmur worse/louder
"Fill it up = softer" — squatting, lying down, volume loading makes HCM softer
Tier 2
Topic CM-2
Dilated & Other Cardiomyopathies
Dilated CM · ARVC · Takotsubo · Peripartum CMP
★★ PANCE Blueprint★ Gap Added
🔒
Full content locked
Enter your bootcamp access code below to unlock all topic cards, clinical pearls, vignettes, and board traps.
Epsilon wave = pathognomonic for ARVC. Exercise restriction mandatory. ICD for VT/VF.
Takotsubo (Stress CMP)
Transient apical ballooning of LV. Catecholamine surge.
Post-emotional or physical stress (usually postmenopausal women). STEMI-like presentation. Apical ballooning on echo. Coronaries clean.
MINOCA cause. Usually reversible in 4–8 weeks. Treat supportively. Avoid catecholamines (worsen spasm).
Peripartum CMP
New HFrEF in last month of pregnancy or within 5 months postpartum
Dyspnea, edema, reduced EF. Diagnosis of exclusion.
Use BB (safe in pregnancy: labetalol, metoprolol) and hydralazine/nitrates. ACEi/ARBs teratogenic — CONTRAINDICATED in pregnancy.
Domain 7 · Hypertension
Hypertension
Before you beginHypertension3 in-session · 2 homework
Core Topic 5 — Hypertension. Attempt the three in-session questions before the domain is taught — they run in the room, in this order: recognition, then management, then the trap. The two homework questions are for tonight, after the teaching. Getting them wrong first is expected and useful; each explanation unlocks only after you submit.
Enter your bootcamp access code above to unlock these questions along with the rest of this domain.
In-sessionQ1 of 3 · Stage 1 HTN · Risk-Based Decision
A 45-year-old woman has a blood pressure of 134/86 mmHg. Her 10-year ASCVD risk is 6%. What is the best initial management?
Click to Reveal Answer
Correct answer: E — Lifestyle modifications alone
This is stage 1 hypertension (130–139 systolic or 80–89 diastolic) with a 10-year ASCVD risk under 10%, so start with nonpharmacologic therapy: DASH-style diet, sodium reduction, weight loss, aerobic exercise, moderated alcohol. Reassess in 3–6 months and add medication if she has not reached goal.
Why the other choices are wrong
No intervention needed — Incorrect. 134/86 is hypertension by current thresholds. Doing nothing misses a real opportunity.
Start amlodipine and hydrochlorothiazide — Incorrect. Two agents is a stage 2 strategy, and this is over-treatment at low risk.
Start lisinopril — Incorrect. Drug therapy in stage 1 is indicated when the 10-year ASCVD risk is 10% or higher, or when there is established cardiovascular disease, diabetes, or CKD. Hers is 6% with none of those.
Start chlorthalidone at a low dose — Incorrect. Chlorthalidone is an excellent first-line thiazide-type agent — the objection is not the drug but the decision to treat. At stage 1 with a 10-year risk of 6% and no compelling comorbidity, drug therapy is not yet indicated.
Board pearlFor stage 1, the 10% ASCVD risk threshold is the whole question. Under 10% with no compelling comorbidity: lifestyle, then reassess. At 10% or above, or with diabetes, CKD, or clinical ASCVD: lifestyle plus a first-line drug.
Covered below under Topic HTN-0a — Primary Hypertension
In-sessionQ2 of 3 · Hypertensive Emergency
A 60-year-old man presents to the ED with a blood pressure of 220/130 mmHg, headache, blurred vision, and a creatinine that has risen from 1.2 to 2.8 mg/dL. What is the best next step?
Click to Reveal Answer
Correct answer: A — IV nicardipine, lowering MAP no more than 25% in the first hour
Severe hypertension with acute end-organ injury — here acute kidney injury plus neurologic and visual symptoms — is a hypertensive emergency. Admit for a titratable IV agent and lower the mean arterial pressure by no more than about 25% in the first hour, then toward 160/100 over the next 2–6 hours. Chronic hypertension shifts the cerebral autoregulation curve rightward, so dropping the pressure too fast causes cerebral, coronary, and renal ischemia.
🚨 Agent selection matters here. This patient's creatinine is rising, and nitroprusside should be avoided in renal impairment — it is metabolized to cyanide and cleared as thiocyanate, both of which accumulate when the kidneys fail. Nicardipine or clevidipine is the appropriate choice. Reserve nitroprusside for settings with preserved renal function and short expected duration.
Why the other choices are wrong
IV furosemide bolus — Incorrect. Does not reliably control blood pressure, and volume depletion may worsen his acute kidney injury.
Discharge with oral medications and 48-hour follow-up — Incorrect. Active end-organ damage requires admission.
Oral amlodipine and recheck in 1 hour — Incorrect. Oral agents have unpredictable onset and cannot be titrated or stopped quickly. Oral therapy is for hypertensive urgency, where there is no end-organ damage.
IV labetalol, normalizing the pressure within the hour — Incorrect — and the drug is not the problem. Labetalol is a perfectly acceptable agent in hypertensive emergency; the target is what makes this wrong. Normalizing the pressure acutely, in a patient whose autoregulation curve is shifted right, precipitates cerebral, coronary, and renal ischemia.
Board pearlThe single distinction that matters is end-organ damage: present = emergency, IV therapy, admit; absent = urgency, oral therapy, close follow-up. Three exceptions to the gradual-lowering rule need faster, lower targets: aortic dissection (systolic below 120 within 20 minutes with a beta-blocker first), severe preeclampsia or eclampsia, and pheochromocytoma crisis (alpha-blockade before beta-blockade).
Covered below under Topic HTN-1 — Hypertensive Emergency vs Urgency
In-sessionQ3 of 3 · Secondary HTN · Resistant Pattern
A 35-year-old woman has resistant hypertension despite three medications including a diuretic. She has hypokalemia (K⁺ 2.9 mEq/L) and metabolic alkalosis. What is the most likely secondary cause?
Click to Reveal Answer
Correct answer: C — Primary hyperaldosteronism
Resistant hypertension with spontaneous or easily provoked hypokalemia and metabolic alkalosis is the classic signature of primary hyperaldosteronism (Conn syndrome). Excess aldosterone drives sodium retention with potassium and hydrogen ion wasting. Screen with a morning plasma aldosterone-to-renin ratio: aldosterone high, renin suppressed.
Why the other choices are wrong
Coarctation of the aorta — Incorrect. Upper extremity hypertension with diminished femoral pulses, an arm-to-leg gradient, and rib notching — usually identified much younger.
Pheochromocytoma — Incorrect. Episodic hypertension with the triad of headache, palpitations, and diaphoresis, often with tremor and pallor. It does not produce this electrolyte pattern; screen with plasma free metanephrines.
Renal artery stenosis — Incorrect. Suggested by an abdominal bruit, a creatinine rise after starting an ACEi or ARB, or recurrent flash pulmonary edema. Fibromuscular dysplasia is the form seen in young women. Renin is high here, and marked hypokalemia is less typical.
Cushing syndrome from an adrenal adenoma — Incorrect — and it is the closest competitor, because very high cortisol does spill over onto the mineralocorticoid receptor and can produce hypertension with hypokalemic alkalosis. What is missing is the rest of the phenotype: central obesity, purple striae, proximal muscle weakness, easy bruising, and hyperglycemia.
Board pearlScreen for secondary hypertension when the presentation does not fit: onset under 30 or over 55, resistance to three drugs including a diuretic, spontaneous hypokalemia, or abrupt loss of control in a previously stable patient. Primary hyperaldosteronism is the most common identifiable cause of resistant hypertension — and the most commonly missed.
Covered below under Topic HTN-0b — Secondary Hypertension · see also Topic HTN-0c
Homework — after the session
HomeworkQ1 of 2 · Hypertension · First-Line Agents
A 52-year-old man is found to have a blood pressure of 152/94 mmHg on three separate visits. He has no other comorbidities. What is the first-line pharmacologic treatment?
Click to Reveal Answer
Correct answer: B — Thiazide, ACE inhibitor, ARB, or calcium channel blocker
There are four first-line classes for primary hypertension: thiazide-type diuretics, ACE inhibitors, ARBs, and calcium channel blockers. He is stage 2 (systolic 140 or above, or diastolic 90 or above), so start medication together with lifestyle change — and note that guidelines favor beginning with two first-line agents from different classes in stage 2, since single-agent therapy rarely reaches goal from this starting point. Target is below 130/80.
Why the other choices are wrong
Clonidine or another central alpha-2 agonist — Incorrect. A central alpha-2 agonist, second- or third-line, limited by sedation, dry mouth, and dangerous rebound hypertension on abrupt withdrawal.
Loop diuretic such as furosemide or torsemide — Incorrect. Not a first-line antihypertensive. Loops are for volume overload states — heart failure, advanced CKD (eGFR under roughly 30, where thiazides lose potency).
Alpha-1 blocker such as doxazosin or terazosin — Incorrect. Not first-line for blood pressure; associated with orthostatic hypotension. Useful when a man also has symptomatic BPH, but as an add-on.
Beta-blocker such as metoprolol, atenolol, or carvedilol — Incorrect. Beta-blockers are no longer first-line for uncomplicated hypertension — head-to-head trials showed less stroke protection than the other classes. They move to first-line only when a second indication exists: post-MI, HFrEF, rate control, or certain arrhythmias.
Board pearlKnow when a first-line class becomes the class: ACEi or ARB with diabetic nephropathy, albuminuria, CKD, or HFrEF; thiazide or dihydropyridine CCB as reasonable first choices in Black patients without those indications; ACEi and ARB are contraindicated in pregnancy.
Covered below under Topic HTN-0a — Primary Hypertension
HomeworkQ2 of 2 · HTN + Diabetic Nephropathy
A 50-year-old man with hypertension and type 2 diabetes has a blood pressure of 148/92 mmHg. His urine albumin-to-creatinine ratio is 350 mg/g. What is the best first-line antihypertensive?
Click to Reveal Answer
Correct answer: A — ACE inhibitor or ARB
Albuminuria at 300 mg/g or higher plus diabetes and hypertension makes an ACE inhibitor or ARB the required first agent. Beyond lowering blood pressure, RAAS blockade reduces intraglomerular pressure and slows the progression of both albuminuria and CKD. Use one or the other — never both together. Check creatinine and potassium within 1–2 weeks of starting, and accept a creatinine rise up to about 30%.
Why the other choices are wrong
Hydrochlorothiazide — Incorrect. A fine first-line agent in uncomplicated hypertension, but it provides no targeted renal protection and may worsen glycemic control and uric acid.
Amlodipine — Incorrect. Effective for blood pressure but without the specific renoprotective effect of RAAS blockade. Reasonable as a second agent, which he will likely need at 148/92.
Metoprolol — Incorrect. Not first-line for hypertension without another indication such as HFrEF, post-MI, or rate control, and it can mask the adrenergic warning signs of hypoglycemia.
Combined ACE inhibitor and ARB — Incorrect — and actively harmful. Dual RAAS blockade was tested in ONTARGET and ALTITUDE and produced more hyperkalemia, hypotension, and acute kidney injury with no added benefit. Use one agent, titrated to the maximum tolerated dose.
Board pearlAlbuminuria is the trigger word: diabetes plus albuminuria means an ACEi or ARB, whatever else you add. Then remember the modern add-ons that protect the kidney in diabetic CKD: an SGLT2 inhibitor, and finerenone for persistent albuminuria on a maximally tolerated RAAS blocker.
Covered below under Topic HTN-0a — Primary Hypertension · see also Topic C-4
2025 ACC/AHA BP Categories · PREVENT Risk Calculator · First-Line Drug Selection · BP Targets
★★★ PANCE Priority
🔒
Full content locked
Enter your bootcamp access code below to unlock all topic cards, clinical pearls, vignettes, and board traps.
Why It Matters for Boards
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
BP Classification (2017 ACC/AHA, reaffirmed 2025)
Category
Systolic
Diastolic
Normal
<120
<80
Elevated
120–129
<80
Stage 1 HTN
130–139
or 80–89
Stage 2 HTN
≥140
or ≥90
🩺 PANCE Pearl: Memorize these thresholds exactly — boards test the boundary numbers (e.g., 129/79 = Elevated, not Stage 1).
Accurate BP Measurement
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.
Risk-Based Treatment Initiation (2025 AHA/ACC)
Patient Profile
Start Meds At
All adults
Average BP ≥140/90
CVD, prior stroke, diabetes, CKD, or 10-yr risk ≥7.5% (PREVENT)
BP ≥130/80
No risk factors + 10-yr risk <7.5%
BP ≥130/80 after 3–6 months of failed lifestyle changes
🩺 PANCE Pearl: The 2025 guideline replaced the Pooled Cohort Equations (10% threshold) with the PREVENT calculator (7.5% threshold) — boards may test this shift.
🚨 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.
Combination Therapy & Special Populations
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
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.
Tier 2
Topic HTN-0b
Secondary Hypertension
When to Suspect · Primary Aldosteronism · Pheochromocytoma · Renal Artery Stenosis · Buzzword Pairings
★★ PANCE Blueprint
🔒
Full content locked
Enter your bootcamp access code below to unlock all topic cards, clinical pearls, vignettes, and board traps.
When to Suspect Secondary HTN
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
Primary Aldosteronism — Most Common Endocrine Cause
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
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.
Renovascular Hypertension
Type
Population
Key Finding
Atherosclerotic RAS
Older patients, diffuse atherosclerosis
Flash pulmonary edema, renal bruit
Fibromuscular dysplasia (FMD)
Young women
"String of beads" on angiography
Screen: renal duplex Doppler, CTA, or MRA
Medical therapy preferred for atherosclerotic RAS (CORAL trial — no benefit from stenting)
🩺 PANCE Pearl: These buzzword pairings are exam gold — memorize them as a set. Secondary HTN questions are usually pattern-recognition, not calculation.
Enter your bootcamp access code below to unlock all topic cards, clinical pearls, vignettes, and board traps.
Resistant Hypertension — Definition & Workup
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.
Second-Line Agents
MRAs (spironolactone, eplerenone): preferred 4th agent for resistant HTN — best studied (PATHWAY-2 trial)
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.
Hypertensive Emergency vs Severe HTN Without Organ Damage
Definition
Management
Hypertensive Emergency
>180/120 WITH acute organ damage (HF, encephalopathy, ICH, AKI, dissection, ACS)
ICU + IV agents (nicardipine, labetalol, clevidipine)
Severe HTN, no organ damage
>180/120 WITHOUT acute organ damage
Oral meds, outpatient — NO IV agents needed
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.
Pregnancy
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, Elderly & Black Patients
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
Target Organ Damage — Baseline Workup for New HTN
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.
Tier 1
Topic HTN-1
Hypertensive Emergency vs Urgency
End-Organ Damage · Drug Selection by Target Organ · Rate of BP Reduction
★★★ PANCE Priority
🔒
Full content locked
Enter your bootcamp access code below to unlock all topic cards, clinical pearls, vignettes, and board traps.
Core Distinction
Hypertensive Emergency
Hypertensive Urgency
Defining feature
End-organ damage PRESENT
NO end-organ damage
BP reduction rate
Max 20–25% in first hour. Never normalize acutely.
Gradual over 24–48 hours. Oral meds.
Setting
Hospital admission, IV medications
Outpatient or ED, oral agents, close follow-up
Drug Selection by Emergency Type
Emergency
Presentation
Preferred Agent
Special Consideration
Hypertensive encephalopathy / PRES
AMS, headache, seizure, cortical blindness
Nicardipine or Labetalol IV
Gradual 20–25% reduction in first hour
Ischemic stroke
Focal deficits, within tPA window
Permissive HTN — do NOT aggressively lower BP
Do NOT lower unless >220/120 (or >185/110 if giving tPA). Penumbra depends on MAP.
Hemorrhagic stroke / ICH
Focal deficits, severe headache
Nicardipine → target SBP 130–150
For presenting SBP 150–220, lower to 130–150. Avoid acute reduction below 130 (AHA/ASA 2022).
Aortic dissection
Tearing pain, BP differential, wide mediastinum
Esmolol or labetalol IV FIRST → add nitroprusside if needed. Target SBP <120, HR <60.
Aortic Dissection: "Block before you Drop" — BB first, then vasodilator
Eclampsia: Mag for the brain, Labetalol/Hydralazine for the BP
Ischemic stroke: HANDS OFF unless >220/120. The penumbra needs that pressure.
SAH: "Worst headache → CT first, treat second"
Domain 8 · Pericardial Disease
Pericardial Disease
Before you beginPericardial Disease3 questions
Answer these three before you read the domain. Getting them wrong is expected and useful — attempting a question first is what makes the material below stick. Each explanation unlocks only after you submit.
Enter your bootcamp access code above to unlock these questions along with the rest of this domain.
Question 1 of 3 · Medium · Pericarditis · Dressler Syndrome
A 56-year-old man presents 3 weeks after an anterior MI with new pleuritic chest pain, low-grade fever, and a pericardial friction rub. ECG shows diffuse ST elevation. Which is the MOST appropriate anti-inflammatory treatment?
Click to Reveal Answer
Correct answer: E — Aspirin 650mg TID + colchicine
This is Dressler syndrome (post-cardiac injury pericarditis, 1–8 weeks post-MI). Use aspirin as the NSAID of choice — NOT ibuprofen or indomethacin, which impair myocardial scar formation after infarction. Colchicine is mandatory to reduce recurrence by 50%. Steroids increase recurrence rate and should be avoided unless NSAIDs/colchicine are truly contraindicated.
Why the other choices are wrong
Colchicine monotherapy for 3 months — Incorrect. Colchicine is mandatory in this setting and reduces recurrence, so it is a necessary component — but it is not sufficient monotherapy for acute symptom control. It is always paired with an anti-inflammatory.
Indomethacin 50mg TID — Incorrect. Indomethacin is effective for ordinary pericarditis but should be avoided after myocardial infarction. NSAIDs other than aspirin impair myocardial healing and scar formation in the post-MI ventricle.
Ibuprofen 600mg TID — Incorrect. Ibuprofen is standard for idiopathic pericarditis, which makes this the most tempting distractor. In POST-MI pericarditis it is avoided because it interferes with infarct healing and may increase the risk of wall thinning.
Prednisone 40mg daily with a slow taper — Incorrect. Corticosteroids relieve symptoms quickly but are associated with higher recurrence rates and, post-MI, with impaired scar formation. They are reserved for refractory cases or when NSAIDs are contraindicated.
Board pearlPost-MI pericarditis has two forms: peri-infarction pericarditis in the first few days, and Dressler syndrome at 1–8 weeks, which is immune-mediated. In either case use aspirin, not ibuprofen or indomethacin — other NSAIDs impair myocardial scar formation. Colchicine is added to nearly every pericarditis regimen because it roughly halves recurrence; steroids increase it.
Covered below under Topic P-1 — Pericarditis & Cardiac Tamponade
Question 2 of 3 · High Yield · Cardiac Tamponade
A 45-year-old with newly diagnosed lung adenocarcinoma develops progressive dyspnea over 3 days. BP 84/60, HR 128, JVD present, lungs clear. Heart sounds are muffled. Pulsus paradoxus is 18 mmHg. Bedside echo shows a large pericardial effusion with RV diastolic collapse. What is the immediate life-saving intervention?
Click to Reveal Answer
Correct answer: A — Emergent pericardiocentesis
This presentation is classic cardiac tamponade: Beck's triad (hypotension, JVD, muffled heart sounds), pulsus paradoxus >10 mmHg, and echocardiographic RV diastolic collapse. Tamponade causes exaggerated ventricular interdependence — during inspiration, increased RV filling compresses the underfilled LV within the fixed pericardial space, causing the abnormal drop in systolic BP. Emergent pericardiocentesis to relieve the pericardial pressure is immediately life-saving.
Why the other choices are wrong
IV diuretics to reduce fluid overload — Incorrect — and dangerous. Diuretics would further reduce preload in a patient who is already preload-dependent due to tamponade physiology, worsening hypotension and potentially precipitating cardiovascular collapse.
Aggressive IV fluid bolus alone, without pericardiocentesis — Incorrect — as definitive management. While IV fluids can provide temporary hemodynamic support by increasing preload while preparing for pericardiocentesis, fluids alone do not address the underlying mechanical problem and are not a substitute for drainage.
Urgent cardiac catheterization to assess coronary anatomy — Incorrect. This patient's presentation is not consistent with acute coronary syndrome — it is tamponade physiology from a malignant pericardial effusion, which requires drainage, not coronary catheterization.
High-dose IV corticosteroids to reduce pericardial inflammation — Incorrect. While steroids may have a role in some inflammatory pericardial conditions, they do nothing to relieve the immediate mechanical compression causing hemodynamic compromise — only physical drainage of the effusion addresses the emergency.
Board pearlTamponade is a clinical diagnosis — Beck's triad plus pulsus paradoxus over 10 mmHg — and echo confirms it; it is never the reason to wait. Give volume and drain the pericardium. Avoid diuretics and vasodilators, which drop the filling pressure the patient is depending on. Distinguish from constrictive pericarditis, where Kussmaul sign and a pericardial knock appear instead of pulsus paradoxus.
Covered below under Topic P-1 — Pericarditis & Cardiac Tamponade
Question 3 of 3 · Medium · Myopericarditis vs STEMI
A 19-year-old college student presents with 5 days of chest pain that worsens when lying flat and improves leaning forward. He had an upper respiratory infection 2 weeks ago. Troponin is 3.2 ng/mL. ECG shows diffuse ST elevation with PR depression. How does this presentation differentiate from STEMI?
Click to Reveal Answer
Correct answer: E — Diffuse ST elevation with PR depression, positional pain, and a viral prodrome
This is myopericarditis. Key distinguishing features from STEMI: ST elevation is DIFFUSE across multiple non-contiguous leads (rather than localized to a single coronary territory), PR depression is present (pathognomonic for pericardial involvement and not seen in STEMI), the pain is positional (worse lying flat, better sitting forward — a pericardial pain pattern), and there is a recent viral prodrome in a young patient without typical cardiac risk factors. The troponin elevation reflects myocardial inflammation, not ischemic infarction.
Why the other choices are wrong
The presence of any troponin elevation always confirms STEMI and mandates emergent catheterization — Incorrect. Troponin elevation occurs in both myopericarditis (from myocardial inflammation) and STEMI (from ischemic necrosis) — troponin elevation alone cannot distinguish between them. The ECG pattern and clinical context are what differentiate the two.
Age alone rules out cardiac causes, so no further cardiac workup is needed in a 19-year-old — Incorrect. While young age makes STEMI less likely, troponin elevation and ECG changes still require careful cardiac evaluation — age alone should never be used to dismiss a cardiac workup, only to help weigh probability alongside other features.
Localized ST elevation in a single coronary distribution is the hallmark of myopericarditis — Incorrect. — this describes STEMI, not myopericarditis. Myopericarditis classically causes diffuse ST elevation across multiple lead groups that don't correspond to a single coronary artery territory, which is the opposite of this answer.
Reciprocal ST depression in aVR is expected and supports the diagnosis of myopericarditis — Incorrect. Myopericarditis characteristically lacks the reciprocal ST changes seen in STEMI — the absence of reciprocal depression (rather than its presence) supports myopericarditis over STEMI.
Board pearlPR-segment depression is the single most specific ECG finding for pericarditis and is essentially never seen in STEMI — the one rare exception is atrial infarction, which can shift the PR segment but is accompanied by a localized ST pattern rather than a diffuse one. Add diffuse ST elevation crossing coronary territories, positional pleuritic pain, and a viral prodrome, and the picture separates cleanly. Troponin elevation means myocardial involvement — myopericarditis — which warrants activity restriction and follow-up echo, but it does not make it an infarct.
Covered below under Topic P-2 — Myocarditis · see also Topic P-1 and Differential D-1
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
Enter your bootcamp access code below to unlock all topic cards, clinical pearls, vignettes, and board traps.
Core Recognition
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.
Diagnosis & Treatment
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.
Myocarditis ≠ pericarditis: Myocarditis = myocardium involved → troponin elevation + HF + arrhythmias. Pericarditis = pericardial sac → friction rub + saddle ST elevation, usually NO significant troponin elevation.
Cancer patient on immunotherapy + new chest pain + troponin elevation + new reduced EF = ICI myocarditis until proven otherwise. Stop the drug, start steroids.
Domain 9 · Shock States
Shock States
Before you beginShock States3 questions
Answer these three before you read the domain. Getting them wrong is expected and useful — attempting a question first is what makes the material below stick. Each explanation unlocks only after you submit.
Enter your bootcamp access code above to unlock these questions along with the rest of this domain.
Question 1 of 3 · Medium · Anaphylactic Shock Management
A 33-year-old woman with known anaphylaxis to bee stings is stung at a picnic. Within minutes she develops BP 62/40, HR 142, diffuse urticaria, and stridor. She has no epinephrine auto-injector available. What is the first drug, dose, and route of administration?
Click to Reveal Answer
Correct answer: C — Epinephrine 1:1000, 0.3mg intramuscularly in the lateral thigh
This is anaphylactic (distributive) shock from massive histamine/IgE-mediated vasodilation. Epinephrine is the only drug that reverses all the pathophysiologic pathways of anaphylaxis simultaneously (vasoconstriction, bronchodilation, reduced mediator release) and must be given FIRST — intramuscularly in the lateral thigh (vastus lateralis), which achieves faster absorption than subcutaneous injection.
Why the other choices are wrong
IV methylprednisolone as the first-line agent to prevent biphasic reaction — Incorrect. Corticosteroids have delayed onset (hours) and are given primarily to help prevent biphasic anaphylactic reactions — they have no role as first-line therapy for the acute, immediately life-threatening presentation.
Epinephrine 1:1000, 0.3mg given subcutaneously — Incorrect — route. While the dose and concentration are correct, subcutaneous injection has slower and less reliable absorption than intramuscular injection in the setting of anaphylactic shock with poor peripheral perfusion — IM is the correct route, specifically into the lateral thigh.
IV diphenhydramine 50mg as the first-line agent — Incorrect. Antihistamines like diphenhydramine are adjunctive therapy only — they address urticaria/itching but do not reverse the life-threatening hypotension and bronchospasm of anaphylaxis. Giving antihistamines before epinephrine is a common and dangerous error.
Normal saline bolus alone, reserving epinephrine for refractory cases only — Incorrect. While IV fluids are an important adjunct for anaphylactic shock, epinephrine must be given immediately as first-line therapy — it should never be reserved or delayed for refractory cases, since early administration is what prevents progression to refractory shock in the first place.
Board pearlEpinephrine IM in the lateral thigh is first and immediate in anaphylaxis — 0.3 mg of 1:1000 in an adult, repeatable every 5–15 minutes. It is the only agent that addresses every arm of the reaction at once. Antihistamines and steroids treat the rash and may blunt the late phase; neither is a substitute, and waiting on them is the classic fatal error. Watch for biphasic recurrence for 4–6 hours.
Question 2 of 3 · High Yield · Sepsis · Vasopressor Selection
A 65-year-old with septic shock is started on dopamine peripherally. Which is the MOST appropriate correction?
Click to Reveal Answer
Correct answer: B — Switch to norepinephrine — first-line vasopressor for septic shock
SSC 2021: norepinephrine is first-line vasopressor for septic shock — NOT dopamine. SOAP II trial showed dopamine has higher arrhythmia risk and worse outcomes. Peripheral initiation is acceptable — do not delay for central access. Vasopressin is second-line (add when NE ≥0.25 mcg/kg/min).
Why the other choices are wrong
Move to central line first before any vasopressor — Incorrect. Central access is preferable for prolonged infusion, but delaying vasopressor initiation to place a line is harmful in shock. Norepinephrine can be started peripherally through a well-sited large-bore cannula with monitoring for extravasation.
Continue dopamine — appropriate first-line vasopressor — Incorrect. Dopamine was once first-line, which is why this persists as a distractor. The SOAP II trial demonstrated significantly more arrhythmias with dopamine and a mortality signal favouring norepinephrine.
Add hydrocortisone before vasopressors — Incorrect. Corticosteroids are considered for shock that remains refractory DESPITE adequate fluids and vasopressors. Giving steroids before optimising the vasopressor does not address the immediate hemodynamic problem.
Switch to vasopressin — preferred over norepinephrine — Incorrect. Vasopressin is a valid SECOND agent, typically added when norepinephrine requirements climb, and it is norepinephrine-sparing. It is not the preferred first-line agent.
Board pearlNorepinephrine is first-line in septic shock; vasopressin is added as the second agent, and dopamine is out because of arrhythmia risk. Do not delay pressors waiting on central access — peripheral initiation is acceptable while access is obtained. Target a MAP of 65 mmHg. Contrast with cardiogenic shock, where the problem is contractility and an inotrope is needed alongside any vasopressor.
Question 3 of 3 · High Yield · Emergency · Massive PE
A 48-year-old woman presents with massive pulmonary embolism (BP 78/50, HR 128, SpO₂ 84% on 4L NC). She has no recent surgery, active bleeding, or intracranial history. Which is the MOST appropriate treatment?
Click to Reveal Answer
Correct answer: D — Systemic fibrinolytics (alteplase 100mg IV over 2 hours)
Massive PE = hemodynamic instability (SBP <90 or vasopressor requirement) with confirmed PE and no absolute contraindications to fibrinolytics. This is the threshold for systemic alteplase 100mg IV over 2 hours — the hemodynamic compromise means anticoagulation alone is insufficient. IVC filter does not treat the acute hemodynamic crisis. Surgical embolectomy is the alternative if fibrinolytics are contraindicated.
Why the other choices are wrong
Rivaroxaban PO and monitor — Incorrect. Oral anticoagulation is appropriate for hemodynamically STABLE PE, but this patient is in shock at 78/50. Anticoagulation prevents clot propagation without dissolving existing thrombus, so it cannot reverse the acute RV failure.
IV unfractionated heparin infusion alone without thrombolysis — Incorrect. Heparin is given, but alone it is insufficient for massive PE with hemodynamic instability. It halts clot growth while relying on endogenous fibrinolysis, which is far too slow when the patient is already hypotensive.
Immediate inferior vena cava filter placement without lysis — Incorrect. An IVC filter prevents FUTURE emboli from reaching the lungs but does nothing about the clot already obstructing the pulmonary circulation. Filters are reserved for patients who cannot be anticoagulated.
Enoxaparin subcutaneously with admission to a monitored floor bed — Incorrect. Both the therapy and the disposition are wrong. Subcutaneous LMWH is inadequate for massive PE, and a patient at 78/50 on 84% saturation needs ICU-level care, not a medical floor.
Board pearlMassive (high-risk) PE is defined hemodynamically — SBP under 90 or a pressor requirement — and that is the threshold for systemic thrombolysis, not anticoagulation alone. Submassive PE (normotensive with RV strain or troponin elevation) is anticoagulated and watched closely. An IVC filter prevents new emboli and treats nothing acutely; embolectomy is for when lytics are contraindicated or fail.
Covered below under Topic SH-1 — Shock, Classification & Management · obstructive shock; see also Topic VAS-2
Enter your bootcamp access code below to unlock all topic cards, clinical pearls, vignettes, and board traps.
Definition
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.
The Four Categories of Shock
Type
Mechanism
Classic Causes
Clinical Picture
First-Line Treatment
Hypovolemic
↓ intravascular volume → ↓ preload → ↓ CO
Hemorrhage, dehydration, burns, third-spacing
Cool, clammy skin; flat neck veins; tachycardia
Volume resuscitation (crystalloid; blood products for hemorrhage); source control
Cardiogenic
Primary pump failure → ↓ CO despite adequate preload
Acute MI (most common), decompensated HF, myocarditis, valvular catastrophe, arrhythmia
Cardiogenic shock: PCWP >18 + CI ≤2.2 + high SVR — "cold and wet." This hemodynamic profile distinguishes it from distributive shock (which has low SVR and high CO).
Septic shock can have LOW CO with low SVR ("mixed shock") — sepsis causes myocardial depression. High CO early, low CO late or in severe sepsis.
Normal BP does NOT rule out shock — oliguria + altered mental status + elevated lactate = shock despite BP 110/70 in a patient with baseline SBP 160.
Norepinephrine is first-line vasopressor for septic shock — NOT dopamine (higher arrhythmia risk per SOAP II trial)
Cardiogenic shock: avoid aggressive fluids — PCWP is already elevated. Inotropes + vasopressors + mechanical support, NOT volume loading.
Tamponade = obstructive shock — IV fluids as a bridge, then drain (pericardiocentesis)
RV MI = preload-dependent cardiogenic shock (SVR is high, not low) — give fluids, avoid nitrates, diuretics and morphine
★ Memory Trick
Shock types: "Hypo = empty tank. Cardio = broken pump. Distributive = open valves. Obstructive = blocked pipe."
Cardiogenic: "Cold and Wet — low CO + high PCWP. CI ≤2.2 = the threshold."
Distributive (sepsis): "High CO, low SVR — vasodilation = warm early, cold late"
Hemodynamic profiles: "↓ CVP + ↓ PCWP = empty (hypovolemic). ↑ CVP + ↑ PCWP = backed up (cardiogenic)."
"Normal BP ≠ no shock — check lactate, urine output, mental status."
Domain 10 · Vascular Disease
Vascular Disease
Before you beginVascular Disease3 questions
Answer these three before you read the domain. Getting them wrong is expected and useful — attempting a question first is what makes the material below stick. Each explanation unlocks only after you submit.
Enter your bootcamp access code above to unlock these questions along with the rest of this domain.
Question 1 of 3 · Medium · Pulmonary Embolism Risk Stratification
A 38-year-old woman on oral contraceptives presents with 3 days of pleuritic chest pain and dyspnea. HR 112, SpO₂ 92%, BP 118/74. Wells score is 6. ECG shows sinus tachycardia. What should guide the decision to begin anticoagulation before confirmatory CT imaging is obtained?
Click to Reveal Answer
Correct answer: B — A Wells score >4 (high probability) supports starting anticoagulation empirically while awaiting CT pulmonary angiography
The Wells score is a validated pretest probability tool, and a score >4 indicates high clinical probability of PE. In high-probability patients without an absolute contraindication to anticoagulation, empiric treatment should begin immediately rather than waiting for imaging confirmation, since the risk of clinical deterioration from delayed treatment outweighs the small risk of unnecessary anticoagulation if imaging is ultimately negative.
Why the other choices are wrong
Anticoagulation should never be started until CT pulmonary angiography confirms the diagnosis — Incorrect. This approach unnecessarily delays treatment in high-probability patients and increases risk of clinical deterioration or embolic progression — current guidelines support empiric treatment in high pretest probability scenarios pending confirmatory imaging.
A D-dimer test should be obtained first regardless of Wells score, since it is more accurate than clinical scoring — Incorrect. D-dimer testing is most useful in LOW probability patients to help rule out PE (high negative predictive value) — in high-probability patients (Wells >4), D-dimer adds little value since a negative result would not reliably exclude PE, and pursuing it would only delay appropriate treatment.
Unfractionated heparin with a loading bolus must always be used as a parenteral bridge before starting a DOAC — Incorrect. Direct oral anticoagulants (e.g., rivaroxaban, apixaban) are first-line for most hemodynamically stable PE patients and do NOT require a parenteral bridge — heparin bridging is reserved for specific situations, not as a default requirement.
Thrombolytics should be given immediately given her elevated heart rate — Incorrect. Thrombolytics are reserved for massive PE with hemodynamic instability (hypotension) — this patient is hemodynamically stable (BP 118/74), so standard anticoagulation, not thrombolysis, is appropriate.
Board pearlA high pretest probability justifies empiric anticoagulation before imaging — the risk of a few hours of untreated PE exceeds the risk of a dose of heparin later shown unnecessary. D-dimer belongs only to low-probability patients, where a negative result rules PE out; ordering it in a high-probability patient cannot exclude anything and only delays care. Estrogen-containing contraceptives are a standing provoking factor.
Covered below under Topic VAS-2 — DVT & Pulmonary Embolism
Question 2 of 3 · High Yield · Aortic Dissection Management
A 62-year-old hypertensive man has sudden tearing chest pain radiating to his back. BP right arm 178/96, left arm 142/84. CXR shows widened mediastinum. What should be done in the first 5 minutes regarding blood pressure and heart rate management?
Click to Reveal Answer
Correct answer: E — Give IV esmolol first to control heart rate (<60), then add IV nicardipine to achieve SBP <120
This presentation (tearing pain, blood pressure differential between arms, widened mediastinum) is classic for aortic dissection. The critical anti-impulse therapy sequence is heart rate FIRST, then blood pressure — beta-blockade (esmolol) must be started before or with vasodilators because lowering blood pressure alone (e.g., with nicardipine first) triggers reflex tachycardia, which increases aortic wall shear stress (dP/dt) and can propagate the dissection. Target is SBP <120 AND HR <60.
Why the other choices are wrong
Target a more permissive blood pressure of SBP <160 to avoid hypoperfusion of distal organs and the spinal cord — Incorrect. The target in acute aortic dissection is a tighter SBP <120 AND HR <60 — this aggressive target is specifically chosen to minimize aortic wall shear stress and reduce the risk of dissection propagation or rupture, not the more permissive target used in other hypertensive conditions.
Administer thrombolytics to address the suspected vascular occlusion — Incorrect — and potentially catastrophic. Thrombolytics are absolutely contraindicated in aortic dissection — they would dramatically worsen bleeding into the dissected aortic wall and could be fatal.
Give IV nicardipine alone first to rapidly lower blood pressure to target — Incorrect — and potentially dangerous. Vasodilators given without prior or simultaneous beta-blockade cause reflex tachycardia, which increases the rate of pressure rise in the aorta (dP/dt) and can worsen or propagate the dissection — heart rate control must come first or concurrently.
Obtain an exercise stress test to evaluate for concurrent coronary disease before treating — Incorrect — and dangerous. Exercise stress testing is entirely inappropriate and dangerous in suspected acute aortic dissection — this is a surgical/medical emergency requiring immediate confirmatory imaging (CT angiography) and BP/HR control, not provocative testing.
Board pearlAnti-impulse therapy goes rate first, then pressure. A vasodilator given alone triggers reflex tachycardia, raising dP/dt and extending the dissection — so esmolol precedes nicardipine. Targets are HR under 60 and SBP under 120. Type A (ascending) is surgical; type B (descending) is medical unless it is complicated. Arm-to-arm BP differential and a widened mediastinum are the bedside clues.
Covered below under Topic VAS-1 — Aortic Dissection
Question 3 of 3 · High Yield · Peripheral Artery Disease and ABI
A 68-year-old smoker complains of bilateral calf cramping after walking 2 blocks that resolves with rest. His ABI is 0.62 in the right leg and 0.71 in the left. What is the most appropriate first-line medical intervention?
Click to Reveal Answer
Correct answer: C — Supervised exercise (walking) program, plus antiplatelet therapy and a statin
This is peripheral artery disease presenting as intermittent claudication, with ABI values of 0.41–0.90 confirming mild-moderate PAD severity (normal ABI is 1.00–1.40; critical limb ischemia is ≤0.40). First-line management for claudication is a supervised exercise program, which has strong evidence for improving walking distance and symptoms, combined with antiplatelet therapy (aspirin or clopidogrel) and statin therapy for cardiovascular risk reduction. This conservative approach should be tried before considering revascularization.
Why the other choices are wrong
Immediate referral for surgical revascularization given bilateral symptoms — Incorrect — as the first step. Revascularization is reserved for patients who fail conservative therapy (supervised exercise + medical management) or who have critical limb ischemia (rest pain, tissue loss) — it is not the first-line approach for stable intermittent claudication.
Anticoagulation with warfarin to prevent thrombotic progression — Incorrect. PAD management centers on antiplatelet therapy (not anticoagulation) along with risk factor modification — warfarin is not standard first-line therapy for atherosclerotic PAD.
Compression stockings to improve venous and arterial blood flow — Incorrect. Compression stockings are used for venous insufficiency, not arterial disease — in fact, compression can be harmful in significant PAD by further compromising arterial perfusion to already ischemic tissue.
Cilostazol alone, without exercise therapy or antiplatelet agents — Incorrect. While cilostazol can be added for symptomatic relief in claudication, it is not used in isolation — the foundation of first-line therapy remains supervised exercise plus antiplatelet and statin therapy, with cilostazol as an adjunct in selected patients.
Board pearlRead the ABI numerically: 1.00–1.40 normal, 0.91–0.99 borderline, 0.41–0.90 claudication, at or below 0.40 critical limb ischemia. An ABI above 1.40 is non-compressible calcified vessels — common in diabetes and CKD — and is uninterpretable, so use toe-brachial index instead. Claudication is treated with supervised exercise, an antiplatelet, and a statin first; cilostazol is added for refractory symptoms, and revascularization is reserved for lifestyle-limiting disease or rest pain.
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).
Treatment by Severity
Severity
Definition
Treatment
Low-risk PE
PESI Class I–II, hemodynamically stable, no RV strain
DOACs (rivaroxaban or apixaban — no parenteral bridge needed). Consider outpatient treatment if PESI low risk.
Submassive PE
Hemodynamically stable + RV dysfunction or biomarker elevation (troponin, BNP)
Systemic anticoagulation. Consider catheter-directed thrombolysis or systemic fibrinolytics based on bleeding risk.
Massive PE
Hemodynamic instability (SBP <90 or vasopressor requirement)
Systemic fibrinolytics (alteplase 100mg IV over 2h) if no absolute contraindications. Surgical embolectomy or catheter intervention if lytics contraindicated.
⚑ Board Traps — DVT/PE
Massive PE = obstructive shock — give IV fluids cautiously (RV is already stressed). Vasopressors (norepinephrine) for hypotension.
DOACs for first-line PE anticoagulation — rivaroxaban and apixaban do NOT require initial parenteral anticoagulation. Dabigatran and edoxaban require 5–10 days of LMWH first.
D-dimer is a rule-OUT test, not a rule-IN test — elevated D-dimer in many conditions (cancer, surgery, pregnancy, infection). Only useful in low pre-test probability.
Cancer-associated VTE: LMWH or rivaroxaban/apixaban preferred over warfarin
Provoked vs unprovoked PE matters for duration: Provoked (reversible risk factor) = 3 months anticoagulation. Unprovoked = indefinite (with regular reassessment).
Tier 2
Topic VAS-3
Peripheral Artery Disease (PAD) & AAA
ABI · Claudication · Critical Limb Ischemia · AAA Screening
★★ PANCE Blueprint★ Gap Added
🔒
Full content locked
Enter your bootcamp access code below to unlock all topic cards, clinical pearls, vignettes, and board traps.
Treatment: Supervised exercise (first-line for claudication), antiplatelet (aspirin or clopidogrel), statin + BP control. Cilostazol for claudication (PDE3 inhibitor — CONTRAINDICATED in HF).
AAA — Abdominal Aortic Aneurysm
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.
⚑ Board Trap
Cilostazol CONTRAINDICATED in heart failure (any degree) — PDE3 inhibitor, increases cAMP → proarrhythmic, positive inotrope effects in failing heart
Ruptured AAA = do not delay surgery for CT if patient is hemodynamically unstable
Teaching Structure
2-Day Bootcamp Teaching Sequence
1
Day One — Foundation to Core Clinical
Start with frameworks. Build to highest-yield clinical topics. Every session anchors on pattern recognition.
8:00–8:30
Opening: Why Cardiology Rules the PANCE
PANCE blueprint breakdown · Tier 1–3 prioritization · How to use this module · The 3 cognitive moves that answer 80% of cardiology questions
8:30–9:15
F-1 + F-3: Hemodynamics & Murmurs
Preload/afterload/CO · Stevenson profiles · heart sounds · dynamic murmur maneuvers. EKG interpretation is covered in the EKG Syllabus — complete it before Day 1.
9:15–9:30
☕ Break
9:30–11:00
C-1: Acute Coronary Syndrome — Deep Dive
STEMI vs NSTEMI vs UA · MONA-B updated protocol · Reperfusion strategy · Mechanical complications · Post-MI medications · 3 vignettes live
HFrEF vs HFpEF · 4 pillars (ARNI + BB + MRA + SGLT2i) · Only 3 BBs · Drug contraindications · ADHF management · Stevenson profiles in practice
2:00–2:30
HTN-1: Hypertensive Emergency
Emergency vs urgency · Drug selection by organ · Rate-of-reduction rule · Dissection trap · Eclampsia trap · Ischemic stroke permissive HTN
2:30–2:45
☕ Break
2:45–4:00
SH-1 + VAS-1: Shock States & Aortic Dissection
Cardiogenic vs distributive vs obstructive vs hypovolemic · Hemodynamic profiles · Vasopressor selection · Dissection Stanford A vs B · "Block before you Drop"
4:00–4:30
⚡ Day 1 Rapid Fire — The 15 Rules You Cannot Forget
Live flashcard run-through · Top traps from Day 1 · Audience Q&A
2
Day Two — Arrhythmias, Valvular, Vascular, Mixed Qs
The hard stuff. Arrhythmia decision trees live. Valvular murmur maneuvers at the board. Final 20-Q mixed quiz.
Topics present on the 2025 NCCPA PANCE Blueprint not covered in prior modules — now fully integrated
Before you beginDyslipidemia & Atherosclerotic Risk3 in-session · 2 homework
Core Topic 6 — Dyslipidemia & Atherosclerotic Risk. Attempt the three in-session questions before the domain is taught — they run in the room, in this order: recognition, then management, then the trap. The two homework questions are for tonight, after the teaching. Getting them wrong first is expected and useful; each explanation unlocks only after you submit.
Enter your bootcamp access code above to unlock these questions along with the rest of this domain.
In-sessionQ1 of 3 · Primary Prevention · Intermediate Risk
A 55-year-old man with no history of cardiovascular disease has an LDL of 145 mg/dL and a 10-year ASCVD risk of 12%. What is the best next step?
Click to Reveal Answer
Correct answer: A — Initiate moderate-intensity statin therapy
For adults aged 40–75 with an LDL of 70 mg/dL or higher and an intermediate 10-year ASCVD risk (7.5% to under 20%), start a moderate-intensity statin after a clinician-patient risk discussion, aiming for a 30–49% LDL reduction. If the decision feels genuinely uncertain, a coronary artery calcium score can break the tie.
Why the other choices are wrong
Initiate high-intensity statin therapy from the outset — Incorrect. High-intensity is for high risk (20% or above), clinical ASCVD, or LDL of 190 mg/dL or higher. It becomes reasonable at intermediate risk when risk enhancers are present, but it is not the baseline answer.
Start ezetimibe — Incorrect. Add-on therapy for patients who do not reach goal on a maximally tolerated statin, or who cannot tolerate statins — not initial monotherapy.
Lifestyle modifications only, with reassessment in 6 months — Incorrect. Lifestyle change is mandatory for everyone, but it is not sufficient by itself at intermediate risk with this LDL.
Initiate moderate-intensity statin plus ezetimibe — Incorrect. Combination therapy is for patients who miss their percent-reduction target on a maximally tolerated statin, not for initiation. Start the statin, then reassess the lipid panel in 4–12 weeks.
Board pearlLearn the risk bands cold: under 5% low, 5–7.4% borderline, 7.5–19.9% intermediate, 20% or above high. Risk enhancers that push toward treatment: family history of premature ASCVD, LDL 160 or above, metabolic syndrome, CKD, chronic inflammatory disease, preeclampsia or early menopause, and South Asian ancestry.
Covered below under Topic C-4 — Lipid Disorders & Dyslipidemia
In-sessionQ2 of 3 · Severe Hypercholesterolemia
A 45-year-old man has an LDL of 210 mg/dL. He has no history of ASCVD. What is the best initial treatment?
Click to Reveal Answer
Correct answer: C — Start high-intensity statin therapy
An LDL of 190 mg/dL or higher is severe primary hypercholesterolemia and is a statin indication in its own right — start a high-intensity statin without calculating a 10-year risk score, because lifetime exposure to an LDL this high makes the risk high regardless of what a 10-year equation returns. Aim for a 50% or greater reduction, and add ezetimibe if LDL stays at or above 100.
Why the other choices are wrong
Lifestyle modifications for 6 months first — Incorrect. Lifestyle change is part of treatment but delaying pharmacotherapy at this LDL is not defensible.
Calculate the 10-year ASCVD risk before deciding — Incorrect. Risk calculation is for the intermediate zone, where the decision is genuinely uncertain. At an LDL of 190 or above the decision is already made, and a reassuring 10-year number would be misleading.
Start fibrate therapy — Incorrect. Fibrates target triglycerides, not LDL, and are not first-line here. Their role is severe hypertriglyceridemia (500 mg/dL or above) for pancreatitis prevention.
Start a PCSK9 inhibitor — Incorrect. PCSK9 inhibitors sit at the top of the escalation ladder, after a maximally tolerated statin and ezetimibe have failed to reach target. They are not initial therapy, even at this LDL.
Board pearlThree groups get a statin with no risk calculator needed: clinical ASCVD, LDL 190 or above, and diabetes at ages 40–75. An LDL of 190 or more should also prompt you to think familial hypercholesterolemia — screen first-degree relatives, and look for tendon xanthomas and premature family events.
Covered below under Topic C-4 — Lipid Disorders & Dyslipidemia
In-sessionQ3 of 3 · Secondary Prevention · Statin Intensity
A 50-year-old woman had an MI 6 months ago. Her current LDL is 85 mg/dL on a moderate-intensity statin. What is the best next step?
Click to Reveal Answer
Correct answer: D — Increase to a high-intensity statin
Established clinical ASCVD calls for high-intensity statin therapy (atorvastatin 40–80 mg or rosuvastatin 20–40 mg) targeting an LDL reduction of 50% or more. A moderate-intensity statin is undertreatment in secondary prevention, and an LDL of 85 does not exempt her — escalate the statin first, before adding anything on.
Why the other choices are wrong
Continue the current regimen since her LDL is already below 100 — Incorrect. The metric in ASCVD is percent reduction on a maximally tolerated statin, not a single comfortable-looking number. An LDL threshold of 70 is the trigger for adding therapy, not permission to stay on a submaximal dose.
Switch to ezetimibe monotherapy — Incorrect. Ezetimibe lowers LDL by roughly 15–20% and is clearly inferior to a high-intensity statin for secondary prevention.
Add a PCSK9 inhibitor — Incorrect. Reserved for very high-risk ASCVD whose LDL remains at 70 mg/dL or above on a maximally tolerated statin plus ezetimibe. She has not yet had a maximal statin.
Add ezetimibe without changing the statin dose — Incorrect — wrong rung, wrong order. Ezetimibe is added once the statin is already maximally tolerated and the LDL still sits at or above 70. She is on a moderate dose, so the statin is escalated first.
Board pearlThe escalation ladder in ASCVD is strictly ordered: maximally tolerated statin → add ezetimibe if LDL stays at or above 70 → then a PCSK9 inhibitor. Do not skip a rung, and note that muscle aches alone are not a reason to abandon statins — check a CK, rechallenge, or try a different statin.
Covered below under Topic C-4 — Lipid Disorders & Dyslipidemia
Homework — after the session
HomeworkQ1 of 2 · Diabetes · Statin Intensity
A 52-year-old woman with diabetes and an LDL of 95 mg/dL has no history of ASCVD. What statin intensity is recommended?
Click to Reveal Answer
Correct answer: E — Moderate-intensity statin
Adults aged 40–75 with diabetes and an LDL of 70 mg/dL or higher should receive at least a moderate-intensity statin, regardless of the calculated 10-year risk. Diabetes is a standalone indication. High-intensity becomes reasonable when there are multiple ASCVD risk factors or diabetes-specific enhancers — long duration, albuminuria, retinopathy, neuropathy, or reduced eGFR.
Why the other choices are wrong
No statin needed — LDL is below 100 — Incorrect. The trigger in diabetes is the diagnosis plus an LDL of 70 or higher, not crossing 100.
Low-intensity statin — Incorrect. Low-intensity dosing (under 30% LDL reduction) is inadequate for diabetes-associated risk and is reserved for patients who cannot tolerate more.
High-intensity statin — Incorrect as the baseline answer. Reasonable with additional risk factors, but moderate-intensity is the minimum standard for uncomplicated diabetes in this age range.
Moderate-intensity statin plus ezetimibe — Incorrect. Combination therapy is not the starting point in primary prevention. Begin the moderate-intensity statin, then check the percent LDL reduction in 4–12 weeks and escalate if she falls short.
Board pearlDo not run the risk calculator for a 40–75-year-old with diabetes — the statin is already indicated. Then ask the follow-up question the exam likes: do diabetes-specific enhancers push this patient to high-intensity?
Covered below under Topic C-4 — Lipid Disorders & Dyslipidemia
HomeworkQ2 of 2 · Monitoring · Lipid Panel Timing
After initiating statin therapy, when should a follow-up lipid panel be obtained to assess response?
Click to Reveal Answer
Correct answer: B — 4–12 weeks
Recheck a lipid panel 4 to 12 weeks after starting a statin or changing the dose. That window is long enough for the full LDL-lowering effect to appear and short enough to catch nonadherence or inadequate response early. Once the patient is stable and at goal, repeat every 3–12 months.
Why the other choices are wrong
1 week — Incorrect. Too early — the maximal LDL reduction has not yet developed, so the value will understate the response.
6 months — Incorrect. Too long for the first assessment. Half a year of undertreatment or unrecognized nonadherence is avoidable.
1 year — Incorrect. Delays identification of nonresponders and nonadherent patients well past the point of usefulness.
3 to 6 months — Incorrect — that is the maintenance interval, not the first check. Once a patient is stable and at target, every 3 to 12 months is appropriate. The initial response assessment happens earlier.
Board pearl4–12 weeks after starting or adjusting, then every 3–12 months when stable. Judge the result as percent LDL reduction: high-intensity should deliver 50% or more, moderate-intensity 30–49%. Routine liver enzyme and CK monitoring is not recommended in asymptomatic patients — check them when symptoms appear.
Covered below under Topic C-4 — Lipid Disorders & Dyslipidemia
Enter your bootcamp access code below to unlock all topic cards, clinical pearls, vignettes, and board traps.
Why It Matters for Boards
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 & Risk Assessment
Screening: Fasting or non-fasting lipid panel. USPSTF supports assessment in adults 40–75. Repeat every 4–6 years if normal and low risk.
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.
The Four Statin Benefit Groups — Memorize These
Group
Who
Statin Intensity
1 — Clinical ASCVD
Prior MI, ACS, stable angina, revascularization, stroke/TIA, PAD
HIGH intensity (age ≤75)
2 — Severe hypercholesterolemia
LDL ≥190 mg/dL at any age — no risk calculator needed
HIGH intensity
3 — Diabetes, age 40–75
Any diabetic in this age band regardless of LDL
MODERATE minimum; high if multiple risk factors or 10-yr risk ≥20%
4 — Primary prevention, age 40–75
LDL 70–189 with 10-year ASCVD risk ≥7.5% after risk discussion
MODERATE (high if risk ≥20%)
🩺 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.
Fibrate (fenofibrate preferred) or icosapent ethyl. Address secondary causes.
≥1000 mg/dL
Pancreatitis risk
Urgent triglyceride lowering — fibrate, very low fat diet, insulin infusion if diabetic. Plasmapheresis in severe cases.
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.
Familial Hypercholesterolemia
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.
Monitoring & Statin Adverse Effects
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.
⚑ Board Traps — Lipids
Statins are contraindicated in pregnancy — stop before conception. Bile acid sequestrants are the traditional option if treatment is essential.
LDL ≥190 needs no risk calculator — that alone is high-intensity statin territory (benefit group 2).
Do not order routine surveillance LFTs or CK on asymptomatic statin patients — a classic distractor.
Niacin is no longer recommended for cardiovascular risk reduction (AIM-HIGH, HPS2-THRIVE showed no benefit and added harm).
Gemfibrozil plus a statin carries the highest rhabdomyolysis risk — fenofibrate is the safer fibrate.
Ezetimibe before PCSK9 — the sequence matters. PCSK9 inhibitors come after statin plus ezetimibe has failed.
Triglycerides ≥1000 = pancreatitis risk, and that becomes the priority over LDL.
An intermediate-risk patient who is truly undecided is the one who benefits from a coronary calcium score — not the high-risk or ASCVD patient, who should simply be treated.
★ Memory Trick
The four benefit groups: "ASCVD · 190 · Diabetes · 7.5%"
High intensity = "Atorva 40–80, Rosuva 20–40" — the only two that drop LDL ≥50%
Add-on order: "Statin → Ezetimibe → PCSK9" (cheap to expensive, oral to injectable)
Secondary prevention: "70 is the trigger" — ASCVD with LDL still ≥70 means add on
Triglycerides: "500 treat the number, 1000 fear the pancreas"
Fibrate safety: "Gemfibrozil grabs muscle — Fenofibrate is the Friendly one"
Monitoring: "Check lipids, not livers" — no routine LFT/CK
Enter your bootcamp access code below to unlock all topic cards, clinical pearls, vignettes, and board traps.
Why It Matters for Boards
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.
The Fundamental Split
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.
Acyanotic Lesions — Murmur First
Lesion
Murmur
Signature Finding
Board Key
Atrial Septal Defect (ASD)
Soft systolic flow murmur at the pulmonic area
Fixed, wide split S2 — does not vary with respiration
Fixed split S2 = ASD. Ostium secundum is the most common type. Risk of paradoxical embolism and later atrial arrhythmia.
Ventricular Septal Defect (VSD)
Harsh holosystolic murmur at the left lower sternal border, often with a thrill
Most common congenital heart defect overall
A LOUDER murmur means a SMALLER defect (more turbulence). Small VSDs often close spontaneously; large ones cause heart failure at 4–8 weeks as pulmonary resistance falls.
Patent Ductus Arteriosus (PDA)
Continuous "machine-like" murmur, best at the left infraclavicular area
Bounding pulses, wide pulse pressure
Indomethacin closes it, prostaglandin E1 keeps it open. Associated with prematurity and congenital rubella.
Coarctation of the Aorta
Systolic murmur, often interscapular
Upper extremity hypertension with weak femoral pulses and radiofemoral delay
Rib notching and the "3 sign" on chest x-ray. Associated with bicuspid aortic valve and Turner syndrome.
Cyanotic Lesions
Lesion
Anatomy
Imaging / Exam
Board Key
Tetralogy of Fallot
Pulmonic stenosis · RVH · Overriding aorta · VSD
Boot-shaped heart on chest x-ray
Most common cyanotic lesion beyond infancy. Tet spells — sudden cyanosis relieved by squatting or the knee-chest position, which raises systemic resistance and reduces the right-to-left shunt.
Transposition of the Great Arteries
Aorta arises from the RV, pulmonary artery from the LV — parallel circulations
"Egg on a string" cardiac silhouette
Most common cyanotic lesion presenting in the first days of life. Survival depends on mixing — prostaglandin E1 to keep the ductus open, then arterial switch.
Tricuspid Atresia
Absent tricuspid valve; requires ASD and VSD to survive
Left axis deviation with small RV
Cyanosis from birth; needs surgical palliation.
Truncus Arteriosus
Single arterial trunk from both ventricles
Single loud S2
Cyanosis plus early heart failure from pulmonary overcirculation.
Total Anomalous Pulmonary Venous Return
Pulmonary veins drain to the right side
"Snowman" silhouette
Obstructed form is a neonatal emergency with severe cyanosis.
🩺 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.
Eisenmenger Syndrome — The Endpoint You Must Recognize
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.
Ductal-Dependent Lesions & Syndrome Associations
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.
Fixed split S2 = ASD. A split that widens normally with inspiration is physiologic, not an ASD.
A louder VSD murmur means a smaller defect — counterintuitive, and tested for exactly that reason. A large VSD may be nearly silent.
Continuous machine-like murmur = PDA. Continuous means through systole and diastole, which almost no other lesion produces.
Upper extremity hypertension with weak femoral pulses = coarctation — check all four extremities before calling it essential hypertension in a young patient.
Squatting relieves a tet spell by increasing systemic vascular resistance. Standing or crying makes it worse.
Once Eisenmenger physiology is established, do NOT close the shunt — this is the trap in the older unrepaired patient.
Indomethacin closes, prostaglandin opens. Reversing these two is the single most common medication error on this topic.
Cyanosis that fails to correct with oxygen is cardiac, not pulmonary.
★ Memory Trick
Tetralogy — "PROVe": Pulmonary stenosis · RVH · Overriding aorta · VSD
"Fixed and split, think ASD" — the split that never moves
"Machine in the chest = PDA" — continuous, not systolic
"IN-domethacin IN-closes the duct; ProstaglandIN Props it open"
Coarctation: "High up top, low down below" — arm hypertension, weak femorals
Tet spell: "Squat to stop the spell"
Eisenmenger: "Once it reverses, don't repair"
Turner → coarctation · Down → cushion defects · DiGeorge → conotruncal
Enter your bootcamp access code below to unlock all topic cards, clinical pearls, vignettes, and board traps.
Why It Matters for Boards
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.
Restrictive Physiology — What Defines It
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.
The Infiltrative Causes — One Clue Each
Cause
Signature Clue
Diagnosis
Management
Cardiac Amyloidosis
LOW-voltage EKG despite THICK walls on echo — the voltage/wall-thickness mismatch. Also apical sparing on strain imaging.
Serum/urine light chains and immunofixation for AL type; technetium pyrophosphate (PYP) scan for transthyretin type; biopsy if needed
AL type: treat the plasma cell disorder. ATTR: tafamidis. Avoid digoxin — it binds amyloid fibrils and causes toxicity at normal levels.
Hereditary Hemochromatosis
"Bronze diabetes" — skin pigmentation, diabetes, cirrhosis, arthropathy, with restrictive or later dilated cardiomyopathy
Elevated transferrin saturation and ferritin; HFE gene testing (C282Y)
Phlebotomy — cardiac dysfunction is reversible if treated early. Chelation if anemic.
Cardiac Sarcoidosis
Young or middle-aged adult with unexplained AV block or ventricular arrhythmia — conduction disease out of proportion to age
Cardiac MRI with patchy late gadolinium enhancement; FDG-PET; extracardiac sarcoid supports it
Corticosteroids plus immunosuppression. ICD for high-grade block or ventricular arrhythmia. Pacing for AV block.
Loeffler Endocarditis
Hypereosinophilia with endomyocardial fibrosis and apical thrombus
🩺 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.
Restrictive Cardiomyopathy vs Constrictive Pericarditis
Feature
Restrictive Cardiomyopathy
Constrictive Pericarditis
Problem lies in
The myocardium itself
The pericardium surrounding it
Kussmaul sign
Usually absent
Present — JVP rises with inspiration
Pericardial calcification
Absent
Often present on CXR or CT
Wall thickness
Increased (infiltrated myocardium)
Normal myocardium, thickened pericardium
Atrial size
Marked biatrial enlargement
Less prominent
Septal bounce / respirophasic shift
Absent
Present on echo
BNP
Markedly elevated
Lower than expected for the degree of congestion
Treatment
Treat the underlying infiltrative disease; poor prognosis
Low-voltage EKG with thick ventricular walls = amyloidosis, not hypertensive LVH. This mismatch is the whole question.
Avoid digoxin in cardiac amyloidosis — it binds amyloid fibrils and produces toxicity at apparently therapeutic levels.
Unexplained high-grade AV block in a young adult should raise cardiac sarcoidosis — do not simply implant a pacemaker without investigating why.
Restriction is preload-dependent. Aggressive diuresis, nitrates or other vasodilators can precipitate hypotension and low output.
Constriction is curable, restriction is not — distinguishing them changes the entire management pathway, so look for Kussmaul sign, pericardial calcification and a septal bounce.
Hemochromatosis cardiomyopathy can reverse with phlebotomy if caught early — one of the few reversible cardiomyopathies, alongside alcohol and Takotsubo.
Preserved ejection fraction does not mean a normal heart — restrictive disease presents with an EF that looks reassuring.
★ Memory Trick
Amyloid: "Thick walls, thin voltage" — the mismatch is the diagnosis
Amyloid drug rule: "Amyloid Absorbs digoxin" — avoid it
Hemochromatosis: "Bronze skin, sweet blood, stiff heart" — and phlebotomy reverses it
Sarcoid: "Young heart, old conduction" — block or VT before its time
Restriction vs constriction: "Kussmaul and Calcium mean the Casing" (pericardium)
"Constriction you can Cut out. Restriction you cannot."
Restrictive physiology: "Small stiff room, huge waiting hall" — normal ventricles, giant atria
Enter your bootcamp access code below to unlock all topic cards, clinical pearls, vignettes, and board traps.
Why It Matters for Boards
This is sinus node disease and ectopy — distinct from the AV conduction blocks covered in Topic A-3 — 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.
Sick Sinus Syndrome (Sinus Node Dysfunction)
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.
Brady-Tachy Syndrome — The Tested Trap
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.
Junctional Rhythms
Rhythm
Rate
EKG
Significance
Junctional escape
40–60 bpm
Narrow QRS with absent, inverted or retrograde P waves
A protective backup when the sinus node fails. Do not suppress it — find and fix the reason the sinus node stopped.
Accelerated junctional
60–100 bpm
Same morphology, faster than escape
Classic in digoxin toxicity; also ischemia, myocarditis, post-cardiac surgery.
Junctional tachycardia
>100 bpm
Narrow QRS, no preceding upright P in lead II
Strongly suggests digoxin toxicity — check the level and the potassium.
🩺 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.
Premature Complexes — PACs vs PVCs
Feature
PAC (atrial)
PVC (ventricular)
QRS width
Narrow (normal conduction)
Wide (>120 ms), bizarre morphology
Preceding P wave
Present but early and abnormally shaped
Absent
Following pause
Non-compensatory — resets the sinus node
Compensatory — sinus node keeps its own timing
Other clues
May be non-conducted (a "dropped" beat)
Fusion and capture beats; T wave opposite the QRS direction
Significance
Usually benign; frequent PACs predict future atrial fibrillation
Benign in a structurally normal heart; burden and context determine risk
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.
PVC Burden — When Ectopy Becomes Disease
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.
⚑ Board Traps — SSS, Junctional Rhythms & Ectopy
Brady-tachy syndrome: pace BEFORE you give the antiarrhythmic or rate-control drug. Treating the tachycardia first can produce asystole.
Review medications and check TSH before diagnosing intrinsic sinus node disease — beta-blockers, diltiazem, digoxin, amiodarone and hypothyroidism all mimic it, and all are reversible.
Do not suppress a junctional escape rhythm — it is the backup keeping the patient alive. Treat the cause of sinus failure.
Junctional tachycardia in a digoxin patient = digoxin toxicity, not a primary arrhythmia.
Do not treat asymptomatic PVCs with antiarrhythmics. The CAST trial showed that suppressing post-MI PVCs with Class IC agents increased mortality.
A high PVC burden is a reversible cause of cardiomyopathy — quantify it and get an echo rather than dismissing frequent PVCs as benign.
An asymptomatic pause is not a pacemaker indication. Sinus node dysfunction requires symptom-rhythm correlation.
Sinus bradycardia in a trained athlete or during sleep is normal physiology, not sick sinus syndrome.
★ Memory Trick
Brady-tachy: "Pace first, then place the drug" — never the reverse
Reversible mimics of SSS: "Drugs, Thyroid, Vagus" — check all three before pacing
PAC vs PVC: "Early and narrow = Atrial. Wide and rude = Ventricular."
Pauses: "PAC resets the clock (non-compensatory). PVC does not (compensatory)."
Junctional tachycardia: "Junctional + digoxin = toxic until proven otherwise"
PVC burden: "Over 10%, order the echo"
CAST rule: "Silencing PVCs after MI silences the patient" — no Class IC
Escape rhythms are friends: "Don't shoot the lifeboat"
Enter your bootcamp access code below to unlock all topic cards, clinical pearls, vignettes, and board traps.
Why It Matters for Boards
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.
Definitions & How to Measure
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.
Parkinson disease, multiple system atrophy, pure autonomic failure, diabetic or amyloid autonomic neuropathy. Often anhidrosis, constipation, erectile dysfunction, urinary retention.
Non-pharmacologic measures first, then midodrine, fludrocortisone or droxidopa.
Medication-induced
Variable
Alpha-1 blockers (tamsulosin, doxazosin), diuretics, nitrates, TCAs, antipsychotics, dopamine agonists, alcohol. Highest risk soon after initiation or dose increase.
Review and deprescribe first — this is the most common reversible cause in older adults.
POTS
HR rise ≥30 bpm (≥40 in adolescents) or to >120 bpm within 10 minutes — WITHOUT orthostatic hypotension
Young patients, often female; palpitations, lightheadedness, fatigue, exercise intolerance. Frequently post-viral.
Increase salt and fluid, compression garments, graded recumbent-to-upright exercise; beta-blocker or ivabradine if needed.
🩺 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.
Vasovagal (Neurally Mediated) Syncope
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.
Red Flags That Make Syncope Cardiac, Not Reflex
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.
Management — Non-Pharmacologic First
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.
⚑ Board Traps — Orthostatic & Reflex Syncope
Absence of compensatory tachycardia = neurogenic autonomic failure, not simple dehydration. Fluids alone will not fix it.
POTS is tachycardia WITHOUT hypotension. If the blood pressure drops it is orthostatic hypotension, not POTS.
Review the medication list before ordering any test — alpha-1 blockers such as tamsulosin are a classic culprit in an older man who falls after a dose increase.
Tilt-table testing is not the first step and is a common distractor. History, orthostatic vitals and an ECG come first.
Exertional syncope is never vasovagal — it demands evaluation for aortic stenosis, hypertrophic cardiomyopathy and arrhythmia.
Myoclonic jerks during syncope do not make it a seizure. The discriminators are prodrome, rapid full recovery, and the absence of post-ictal confusion or tongue biting.
Midodrine at bedtime causes supine hypertension — dose it during waking hours only.
Do not diagnose orthostatic hypotension without recording the heart rate alongside each blood pressure — without it the mechanism is unknowable.
★ Memory Trick
"20 over 10 in 3" — SBP ≥20 or DBP ≥10 within 3 minutes
The mechanism is in the pulse: "Fast = dry. Flat = failed nerves."
POTS: "Pulse Only, Tension Stays" — HR climbs, BP holds
Vasovagal: "Warm, woozy, wet, then wake up fast" — prodrome then quick recovery
Cardiac red flags: "Exertion, no warning, family history" — none of these are vasovagal
Treatment order: "Salt, socks, squeeze — then midodrine"
Midodrine: "Mid-day, not midnight" — supine hypertension at bedtime
Tilt table is the last resort, not the first test
Module D · Must-Know Differentials
High-Yield Differentials & Distinguishing Features
The following differentials represent the highest-frequency diagnostic challenges on the PANCE/PANRE. For each, the exam tests your ability to identify the single distinguishing feature that separates one diagnosis from another — not just whether you know the diagnoses exist.
Surgical emergency — if missed, mediastinitis has >50% mortality
GERD / Esophageal Spasm
Burning, epigastric, postprandial; spasm can mimic ACS perfectly
Relieves with antacids or nitrates (spasm); normal troponin, normal EKG, no diaphoresis
EKG and troponin are negative — NEVER diagnose GERD without ruling out ACS first in correct clinical context
Diagnostic Pivot Points — The 60-Second Assessment
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.
⚑ Board Traps — Chest Pain Differential
Aortic dissection + inferior ST elevation = RCA involvement from dissection flap — NOT a primary STEMI. Heparin or cath lab activation here is fatal.
Esophageal spasm relieves with nitrates — do NOT use this as proof it's cardiac. NTG also relieves esophageal spasm.
The "typical" ACS presentation is atypical in diabetics, women, and elderly. Jaw pain + diaphoresis without chest pressure = NSTEMI until troponin confirms otherwise.
Pericarditis EKG is diffuse — if you see focal ST elevation with reciprocal changes, that's STEMI not pericarditis.
PE can present with pleuritic chest pain AND hemoptysis — do not anchor on pneumonia without ruling out PE in high-risk patients.
Tier 1
Differential D-2
Syncope — Cardiac vs Neurally Mediated vs Orthostatic
Prodrome: nausea, diaphoresis, lightheadedness before LOC. Rapid full recovery.
Tilt-table test if recurrent. No workup needed for classic first episode.
Arrhythmic (Cardiac)
Without warning — no prodrome. Exertion or rest.
Sudden LOC without prodrome. Palpitations may precede. EKG: QT prolongation, Brugada, heart block, WPW.
EKG immediately. Holter/event monitor. Echo. Electrophysiology study if unexplained.
Structural Cardiac
Exertional syncope — hallmark of outflow obstruction
HCM: young athlete, exertional, LLSB murmur louder with Valsalva. AS: elderly, exertional, classic triad (SAD).
Exertional syncope = emergent echo. Do NOT stress test before echo in HCM.
Orthostatic Hypotension
Standing up from seated/lying position
SBP drop ≥20 or DBP drop ≥10 mmHg within 3 min of standing. Dehydration, medications (alpha-blockers, diuretics), autonomic neuropathy (DM, Parkinson's).
EEG, neurology consult. EKG to rule out arrhythmic cause.
The Board Rule on Exertional Syncope
⚑ Cannot Miss
Exertional syncope = structural cardiac cause until proven otherwise. HCM (young), AS (elderly), anomalous coronary artery, arrhythmia (CPVT, LQTS, Brugada). Always echo first.
ABCD2 score does NOT apply to syncope — that score is for TIA. Syncope and TIA are distinct. True syncope has no focal neurologic deficit.
Vasovagal: prodrome is key. No prodrome in a high-risk patient (structural disease, arrhythmia substrate) = cardiac workup regardless of clinical appearance.
Lateral tongue biting = seizure (not syncope). Anterior tongue biting can occur in either.
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.
Distinguishing Cardiac from Pulmonary Dyspnea
Feature
Cardiac HF
COPD/Asthma
PE
Pneumonia
Orthopnea/PND
Present — highly specific for HF
Absent (may have nocturnal symptoms)
Absent
Absent
JVD
Present (volume overload)
May be present if cor pulmonale
Present (RV strain)
Absent
S3 gallop
Present in HFrEF (volume overload)
Absent
Absent
Absent
Wheeze
May have "cardiac asthma"
Classic feature
Usually absent
May have focal
Fever
Absent (unless ADHF from infection)
May be present (infectious exacerbation)
Low-grade if infarction
Present
BNP
Elevated (>400)
Normal (unless cor pulmonale)
Moderately elevated
Normal
CXR
Cardiomegaly, Kerley B lines, vascular congestion, bilateral effusions
Hyperinflation, flat diaphragm
May be normal; Hampton's hump, Westermark sign
Focal consolidation
⚑ Board Traps — Dyspnea
Orthopnea and PND are highly specific for HF — ask about these in every patient with dyspnea. "How many pillows do you sleep on?" is not small talk.
Cardiac asthma: HF can cause wheezing from bronchospasm due to pulmonary edema. Treat the HF, not just the wheeze. BNP distinguishes.
PE can have a normal CXR — normal CXR + dyspnea + hypoxia + tachycardia = PE until ruled out.
Pulsus paradoxus >10 mmHg in a dyspneic patient = tamponade or severe asthma. Get echo immediately.
Tier 1
Differential D-4
Systolic Murmur Differential — Dynamic Maneuvers
HCM vs AS vs MR vs MVP · Valsalva · Squatting · Handgrip · Inspiration
★★★ Most Tested Maneuver TableHCM vs AS Trap
The One Table You Must Know Cold
Maneuver
Effect on Preload/Afterload
HCM
AS
MR
MVP (click timing)
Valsalva (strain phase)
↓ preload
LOUDER
Softer
Softer
Click moves EARLIER, murmur lengthens
Standing
↓ preload
LOUDER
Softer
Softer
Click moves EARLIER, murmur lengthens
Squatting
↑ preload + ↑ afterload
SOFTER
Louder
Louder
Click moves LATER, murmur shortens
Passive leg raise
↑ preload
SOFTER
Louder
Louder
Click moves LATER
Handgrip isometric
↑ afterload
Softer
Softer
LOUDER (↑ regurgitant fraction)
Variable
Inspiration
↑ right-sided venous return
Minimal change
Minimal change
Minimal change
Minimal change
The Core Principle Behind the Table
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.
⚑ The Single Most-Tested Murmur Distinction
HCM vs AS distinction: Both are crescendo-decrescendo systolic murmurs. HCM is at LLSB and does NOT radiate to carotids. AS is at RUSB and radiates to carotids. HCM louder with Valsalva; AS softer. Young athlete + LLSB + Valsalva louder = HCM. Elderly + RUSB + carotid radiation + Valsalva softer = AS.
All diastolic murmurs are pathologic — never dismiss. Order echo.
MVP click/murmur moves EARLIER with Valsalva — the single most confusing MVP concept. Think "smaller ventricle = earlier prolapse = earlier click."
Tier 1
Differential D-5
Wide Complex Tachycardia — VT vs SVT with Aberrancy
VT Until Proven Otherwise · Causes & Distinguishing Clues · Drug Contraindications · WPW · Hyperkalemia
★★★ PANCE PriorityLethal Misclassification Trap
The Non-Negotiable Board Rule
⚑ Start Here — Before Any Other Analysis
Wide complex tachycardia = VT until proven otherwise. Full stop. Hemodynamic stability does NOT exclude VT. Patients can sustain VT for hours while appearing stable.
Prior MI + wide complex = VT. Structural heart disease makes aberrant conduction unlikely and VT overwhelmingly likely.
Never give verapamil or diltiazem to wide complex tachycardia — if it's VT, cardiovascular collapse will occur.
🫀 Morphologic VT criteria — AV dissociation, fusion and capture beats, precordial concordance, RS >100 ms, QRS >160 ms and the Vereckei aVR rule are taught in the PA Bootcamp EKG Syllabus, which owns this material so it stays in one place. Open the EKG Syllabus ↗
Causes of Wide Complex Tachycardia — Full Differential
Cause
Mechanism
Distinguishing Clue
Ventricular Tachycardia
Ventricular origin — depolarization does not use His-Purkinje system
AV dissociation, fusion/capture beats, structural heart disease, post-MI
SVT with aberrant conduction (BBB)
SVT conducted with pre-existing or rate-dependent BBB
Prior EKG shows same BBB morphology. Concordance absent. Brugada criteria not met.
WPW with pre-excited AFib
AF conducted rapidly down accessory pathway
Irregularly irregular + wide complex = WPW+AFib. Do NOT give AV nodal blockers → VF.
Antidromic AVRT (WPW)
Antegrade conduction down accessory pathway — retrograde up AV node
Regular wide complex. Delta wave morphology. WPW known or suspected.
Hyperkalemia
Depolarization slowing from high extracellular K⁺
Context: renal failure, peaked T waves preceding widening, sinusoidal pattern
Sodium channel blocker toxicity
TCA overdose, flecainide, propafenone toxicity
History of ingestion, prolonged QRS >160ms, sodium bicarbonate reverses
★ Memory Trick
Wide complex = VT default. Override only with strong evidence of SVT aberrancy.
"VT fingerprints: AV Dissociation, Fusion beats, Capture beats, Concordance"
Age >35 + MI history + wide complex = VT. Period.
WPW+AFib: irregular + wide + delta = DO NOT block the AV node
Tier 1
Differential D-6
Undifferentiated Shock — Bedside Differentiation
Cardiogenic vs Distributive vs Obstructive vs Hypovolemic · JVD as the First Divider
★★★ PANCE PriorityFluid Choice Trap
The Two-Step Bedside Framework
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)
The Critical Fluid vs Vasopressor Decision
Shock Type
Skin
JVD
Lungs
Fluids?
Vasopressor?
Hypovolemic
Cool, clammy
Absent
Clear
Yes — aggressive
Only if refractory to fluids
Distributive (Septic)
Warm, flushed (early)
Absent or low
Clear (early)
Yes — 30 mL/kg initial
Norepinephrine first-line
Cardiogenic
Cool, clammy
PRESENT
Wet (edema)
NO — worsens congestion
Norepinephrine + inotrope (dobutamine)
Obstructive (Tamponade)
Cool
PRESENT
Clear
IV fluids as bridge
Limited benefit — drain the obstruction
Obstructive (Tension PTX)
Cool
PRESENT
Absent sounds ipsilateral
Minimize
Needle decompression immediately
⚑ Board Traps — Shock Differentiation
JVD + clear lungs + hypotension = obstructive shock — not cardiogenic. Tamponade, tension PTX, and massive PE all present this way.
Giving fluids to cardiogenic shock = worsening pulmonary edema — PCWP already elevated. Inotrope + diuresis is the correct approach.
RV MI mimics distributive shock — clear lungs, JVD, hypotension. Treat with fluids (preload-dependent). Do NOT give nitrates or diuretics.
Dopamine is NOT first-line in septic shock (SOAP II trial: higher arrhythmia risk). Norepinephrine is standard of care.
Normal BP does not rule out shock — tissue hypoperfusion can occur with BP 110/70 in a previously hypertensive patient. Check lactate, urine output, mental status.
Periorbital edema in the morning = nephrotic syndrome (low oncotic pressure). Not HF, which causes dependent edema.
Amlodipine edema has no JVD, no orthopnea, no elevated BNP — it's a side effect, not decompensated HF. Do not diurese aggressively.
Lymphedema is non-pitting — pitting edema is from fluid; non-pitting is from protein and fibrosis in the interstitium.
Homan's sign is unreliable — neither sensitive nor specific for DVT. Do not use it as the primary diagnostic criterion.
Module E · Comprehensive Board Pearls
Board Pearls — Organized by Domain
These pearls represent the precise clinical decision points most frequently tested on the PANCE and PANRE. They are not random facts — they are the exact places where real patients die and where boards separate passing from failing candidates.
Tier 1
Board Pearls — Coronary Artery Disease
ACS, STEMI Equivalents & Post-MI Management
★★★ Highest Yield
New LBBB + chest pain = STEMI equivalent. Apply Sgarbossa criteria. Activate the cath lab. Do not dismiss it as "just LBBB."
Posterior MI: ST depression + tall R wave in V1–V2 = reciprocal mirror image of posterior STEMI. Apply posterior leads V7–V9. Treat as STEMI.
RV MI = Inferior STEMI + hypotension + clear lungs. Get V4R. Give IV fluids. NO nitrates, NO diuretics, NO morphine — all reduce preload and cause cardiovascular collapse.
Wellens syndrome: Biphasic/deeply inverted T waves in V2–V3 in a pain-FREE patient = critical proximal LAD stenosis. Stress test is absolutely contraindicated. Send to cath immediately.
De Winter T-waves: Upsloping ST depression + tall peaked T waves V1–V6 (no ST elevation) = LAD occlusion equivalent. Treat as anterior STEMI.
Door-to-balloon <90 minutes for primary PCI. Thrombolytics if PCI unavailable within 120 minutes of first medical contact.
Supplemental O₂ in ACS: only if SpO₂ <90%. Hyperoxia worsens infarct size (DETO2X-AMI trial). Do NOT give oxygen to every ACS patient.
Post-MI medication cascade: Aspirin + P2Y12 inhibitor + statin + beta-blocker + ACEi (if EF <40%) + aldosterone antagonist (if EF <40% + HF or DM, if eGFR adequate).
Post-MI complications timeline: Free wall rupture = Day 1–3 → VSD = Day 3–5 → Papillary muscle rupture = Day 2–7. Soft murmur despite severe MR in papillary rupture = false reassurance. Echo urgently.
DAPT duration: 12 months post-ACS. 6 months post-elective PCI (stable CAD). Can shorten with high bleeding risk on guidance.
Aortic dissection can mimic STEMI. Tearing pain + BP differential + widened mediastinum = dissection first. Heparin in this scenario = fatal pericardial hemorrhage.
Tier 1
Board Pearls — Heart Failure
HFrEF GDMT · Drug Selection · Contraindications
★★★ Highest Yield
Only 3 beta-blockers proven in HFrEF: Carvedilol, Metoprolol succinate, Bisoprolol. Not atenolol, not metoprolol tartrate, not propranolol. Evidence is drug-specific.
4 pillars of HFrEF GDMT with mortality benefit: ARNI (sacubitril/valsartan) or ACEi/ARB + beta-blocker (one of the 3) + MRA (spironolactone/eplerenone) + SGLT2 inhibitor (dapagliflozin/empagliflozin).
SGLT2 inhibitors reduce HF hospitalization and CV death in HFrEF — regardless of diabetes status. This is a new class effect, not just a diabetes medication.
ACEi → ARNI transition: 36-hour washout required to prevent angioedema. No washout needed when switching from ARB to ARNI.
BNP cutoffs: <100 effectively rules out acute HF. >400 strongly supports HF. BNP is elevated in PE, renal failure, and sepsis — not specific to HF.
Non-dihydropyridine CCBs (diltiazem, verapamil) are contraindicated in HFrEF — negative inotropy worsens pump failure and increases mortality. CHECK EF before ordering rate control for AFib.
Hydralazine + nitrate combination: Alternative if ACEi/ARB intolerant. Also has specific mortality benefit in self-identified Black patients with HFrEF (A-HeFT trial).
BiPAP before intubation in acute decompensated HF — reduces need for mechanical ventilation and improves outcomes.
Ivabradine: For HFrEF patients on maximally tolerated beta-blocker with resting HR >70 — reduces HF hospitalization. Not a first-line agent.
Tier 1
Board Pearls — Arrhythmias
AFib · Heart Blocks · VT/VF · WPW · TdP
★★★ Highest YieldLethal Drug Errors
WPW + AFib = NEVER give AV nodal blockers (adenosine, digoxin, diltiazem, verapamil, beta-blockers). Forces accessory pathway conduction → uncontrolled rate → VF → cardiac arrest. Procainamide or synchronized cardioversion only.
EF check before rate control drug for AFib is the single most tested clinical decision in cardiology. Diltiazem/verapamil in HFrEF = negatively inotropic = decompensation. Use metoprolol in compensated HFrEF; in acutely decompensated HFrEF use digoxin or IV amiodarone.
Post-cardioversion OAC 4 weeks is mandatory for ALL patients regardless of CHA₂DS₂-VASc score or AFib duration. Atrial stunning takes up to 1 month to resolve.
Antiarrhythmic in structural heart disease / HFrEF: Amiodarone or dofetilide ONLY. Flecainide/propafenone/sotalol/dronedarone are contraindicated (CAST trial mortality increase).
Dronedarone contraindicated in permanent AFib (PALLAS: increased mortality/stroke) and decompensated HF (ANDROMEDA: increased mortality).
Torsades de Pointes = IV magnesium sulfate 2g. NOT amiodarone (prolongs QT further). NOT procainamide. NOT lidocaine. Magnesium regardless of serum Mg level.
Mobitz II and 3rd degree heart block always require permanent pacing — regardless of symptoms. Mobitz II has sudden unpredictable progression to complete heart block.
Mobitz I (Wenckebach): Progressive PR prolongation before dropped QRS. Usually inferior/nodal. May be observed unless symptomatic. Atropine can help transiently.
Atropine works above the His bundle (nodal blocks). It is unreliable/ineffective for infranodal (Mobitz II, complete heart block) — proceed to pacing.
Amiodarone is a CYP450 inhibitor: Increases warfarin levels (reduce warfarin 30–50%), digoxin levels, statin levels. Monitor closely on initiation.
Adenosine half-life ~6 seconds — must be given as rapid IV push with immediate saline flush. Central line preferred. Monitor with crash cart at bedside.
Regular tachycardia at ~150 bpm = atrial flutter with 2:1 block until proven otherwise. Look for sawtooth waves in II, III, aVF.
Tier 1
Board Pearls — Valvular Disease & Cardiomyopathy
AS · MR · Endocarditis · HCM · Peripartum CMP
★★★ Highest Yield
All diastolic murmurs are pathologic. Never dismiss a diastolic murmur as innocent. Always order echocardiography.
Aortic stenosis triad: angina → syncope → heart failure. Mean survival without AVR: 5 years (angina), 3 years (syncope), 1–2 years (HF). Symptomatic severe AS = refer for AVR/TAVR.
Vasodilators are contraindicated in severe AS — ACEi, nitrates, aggressive diuresis. Fixed obstruction cannot compensate for dropped SVR → catastrophic hypotension.
DOACs are absolutely contraindicated with mechanical heart valves. RE-ALIGN trial: increased thromboembolism AND bleeding. Warfarin only. Target INR 2.5–3.5 for mitral position.
HCM is the most common cause of sudden cardiac death in young athletes. Restriction from competitive sports is mandatory. ICD for high-risk features (prior VT/VF, massive LVH, family history of SCD, LVOT gradient >30mmHg).
HCM drug contraindications: Vasodilators (nitrates, ACEi, hydralazine) and diuretics worsen LVOT obstruction → syncope or sudden death. Use beta-blockers or verapamil.
Duke criteria for endocarditis: 2 major, 1 major + 3 minor, or 5 minor = diagnosis. Do NOT rely on signs alone — positive blood cultures + echo vegetation is sufficient (2 major criteria).
S. gallolyticus (bovis) endocarditis = colonoscopy mandatory. 60% association with colorectal neoplasia. This is a non-negotiable board fact.
ARVC: Epsilon wave (pathognomonic) + T-wave inversions V1–V3 + young male with ventricular arrhythmias + fibrofatty RV replacement. Exercise restriction and ICD.
Peripartum CMP: New HFrEF last month of pregnancy to 5 months postpartum. ACEi/ARBs teratogenic — use hydralazine + nitrates in pregnancy. Beta-blockers safe (labetalol, metoprolol).
Tier 1
Board Pearls — HTN, Pericardial & Vascular
Hypertensive Emergency · Dissection · Tamponade · PAD · PE
★★★ Highest Yield
Hypertensive emergency: reduce MAP by no more than 25% in the first hour. Faster reduction causes ischemic injury to organs dependent on elevated MAP (brain, heart, kidney).
Aortic dissection: "Block before you Drop." Beta-blocker FIRST (esmolol, labetalol) to reduce HR <60, THEN add nitroprusside if needed. Nitroprusside alone causes reflex tachycardia → increased dP/dt → dissection propagates.
Type A dissection (ascending) = surgical emergency — 1–2% mortality per hour. Simultaneous cardiac surgery call and imaging. Do not wait.
Ischemic stroke: permissive hypertension — do NOT lower BP unless >220/120 (or >185/110 if tPA candidate). The ischemic penumbra depends on that pressure gradient.
Eclampsia: magnesium sulfate is for seizure prophylaxis/treatment — NOT for BP control. Use labetalol or hydralazine IV for BP. ACEi/ARBs absolutely contraindicated in pregnancy.
AAA screening: One-time abdominal ultrasound in men aged 65–75 who have ever smoked (USPSTF Grade B). Repair threshold: ≥5.5 cm or growth >0.5 cm in 6 months.
Cardiac tamponade: NEVER give diuretics or nitrates. Furosemide removes the critical preload needed by the compressed ventricle → cardiovascular collapse. IV fluids bridge; pericardiocentesis is definitive.
Dressler syndrome (post-MI pericarditis): Use ASPIRIN as the NSAID of choice — NOT ibuprofen or indomethacin, which impair myocardial scar formation.
Colchicine is mandatory for pericarditis (viral or recurrent) — reduces recurrence by 50% (COPE and ICAP trials). Do not omit.
Tamponade vs constrictive pericarditis distinction: Tamponade = pulsus paradoxus (JVD falls or stays same with inspiration). Constriction = Kussmaul sign (JVD RISES with inspiration).
Massive PE (SBP <90 + hemodynamic instability): Systemic fibrinolytics if no contraindications. Anticoagulation alone is insufficient. Surgical embolectomy if lytics contraindicated.
ABI interpretation: Normal ≥0.9. Borderline 0.7–0.89. PAD <0.7. Critical limb ischemia <0.4. ABI >1.4 = non-compressible vessels (calcified, DM/renal failure) — false normal.
Cilostazol (PDE3 inhibitor) for claudication is CONTRAINDICATED in any degree of heart failure — proarrhythmic and positive inotrope effects in the failing heart.
Tier 1
Board Pearls — Cardiovascular Pharmacology
Contraindications · Drug Interactions · Pregnancy · Monitoring
★★★ Highest YieldDrug Contraindication Traps
Nitrates + PDE-5 inhibitors (sildenafil, tadalafil) = severe hypotension. Absolute contraindication. Time window: 24 hours for sildenafil, 48 hours for tadalafil.
ACEi/ARBs in pregnancy = absolute contraindication — oligohydramnios, renal agenesis, fetal death (Category D/X). Switch to labetalol, methyldopa, or hydralazine.
Digoxin toxicity can cause any arrhythmia. Classic = PAT with block. Exacerbated by hypokalemia, hypomagnesemia, and hypothyroidism. Treat with digoxin-specific antibody fragments (Digibind).
Statins contraindicated in pregnancy — Category X. Myopathy risk increases significantly with concurrent cyclosporine, fibrates (gemfibrozil), and certain antibiotics (clarithromycin).
Spironolactone causes gynecomastia (anti-androgen effect) — use eplerenone as a more selective MRA alternative when this is problematic.
Amiodarone half-life 40–55 days — toxicity monitoring required: TSH + LFTs every 6 months, annual CXR (pulmonary fibrosis), ophthalmology exam (corneal deposits, optic neuropathy). Most common side effect: hypothyroidism.
Thiazide diuretics cause: Hypokalemia, hyponatremia, hyperuricemia (precipitate gout), hyperglycemia, hypercalcemia, hyperlipidemia (minor). First-line for uncomplicated HTN in most patients and in Black patients without DM.
Loop diuretics (furosemide) ototoxicity is dose-dependent and markedly increased with concurrent aminoglycosides — avoid combination if possible.
Metformin contraindicated if eGFR <30 (hold if <45 for iodinated contrast procedures) — risk of lactic acidosis. Most important drug adjustment in CKD patients.
Warfarin interactions: Amiodarone (↑ INR), fluconazole (↑ INR), rifampin (↓ INR), carbamazepine (↓ INR). The boards love the amiodarone-warfarin interaction specifically.
The EF check before rate control in AFib is the single most tested concept in cardiology arrhythmias. Diltiazem in HFrEF (EF <40%) = negatively inotropic → acute decompensation. Use metoprolol if compensated; digoxin or IV amiodarone if acutely decompensated.
3
Inferior STEMI + hypotension = RV MI until proven otherwise. Get right-sided leads. Give IV fluids. NO nitrates, NO diuretics, NO morphine — all reduce preload and can be fatal.
4
Wide complex tachycardia = VT until proven otherwise. Hemodynamic stability does NOT exclude VT. Prior MI + wide complex = VT. Treat with amiodarone if stable. Cardiovert if unstable. Never adenosine for wide complex.
5
Three beta-blockers for HFrEF — only three. Carvedilol · Metoprolol succinate · Bisoprolol. Not atenolol, not metoprolol tartrate, not propranolol. Evidence base is drug-specific, not class-wide.
6
Post-cardioversion OAC for 4 weeks is mandatory for ALL patients regardless of AFib duration or CHA₂DS₂-VASc score. Atrial stunning takes up to 1 month to resolve. The boards test this — it is not optional.
7
Aortic stenosis + vasodilators = catastrophic hypotension. Fixed obstruction cannot compensate for dropped SVR. No ACEi, no nitrates, no aggressive diuresis. Refer for AVR when symptomatic.
8
Strep bovis/gallolyticus endocarditis = colonoscopy. 60% association with colorectal neoplasia. Always. No exceptions. This is a non-negotiable board fact that appears repeatedly.
9
Wellens syndrome + stress test = contraindicated. Biphasic or deeply inverted T waves V2–V3 during a pain-free interval = critical proximal LAD stenosis. Stress testing can precipitate cardiac arrest. Go straight to cath.
10
Torsades de Pointes = IV magnesium sulfate. Not amiodarone (prolongs QT further — contraindicated). Not lidocaine. Not procainamide. Magnesium is the answer regardless of serum Mg level.
Clinical Emergency List
10 "Don't Miss" Cardiology Emergencies
1. STEMI — Right Ventricular MI
Inferior STEMI + hypotension + JVD + clear lungs. Nitrates, diuretics, morphine = fatal. Get V4R. Give IV fluids. Cath lab immediately. Miss this = patient dies from iatrogenic preload reduction.
2. WPW + Atrial Fibrillation → VF
Pre-excited AF + AV nodal blocker = VF → cardiac arrest. Never give adenosine, digoxin, diltiazem, or verapamil. Procainamide or cardioversion. Most commonly tested lethal drug error on boards.
3. Aortic Dissection Masquerading as STEMI
Tearing pain + BP differential + widened mediastinum + inferior ST elevation (RCA involvement). Heparin or lytics = fatal hemorrhage. CT angiography first. NEVER activate cath lab without ruling out dissection.
4. Cardiac Tamponade — Diuretic Trap
Beck's triad + pulsus paradoxus + electrical alternans. Furosemide removes the preload the compressed heart needs = cardiovascular collapse. IV fluids as bridge, then pericardiocentesis.
5. Papillary Muscle Rupture (Post-MI)
Day 3–5 post-inferior MI + sudden flash pulmonary edema + cardiogenic shock. Soft or absent systolic murmur despite severe MR — do not be falsely reassured by quiet exam. Echo urgently. Emergency surgery.
6. Massive PE — Fibrinolytic Decision
Hemodynamic instability (SBP <90) + confirmed massive PE + no absolute contraindications. Anticoagulation alone is insufficient. Systemic alteplase 100mg IV over 2h. Surgical embolectomy if lytics contraindicated.
7. Wellens Syndrome — The Silent Bomb
Pain-free patient + biphasic/inverted T waves V2–V3 + about-to-have a massive anterior MI. Stress test is absolutely contraindicated — inducing ischemia precipitates arrest. Directly to cath lab. This patient looks fine but is not.
8. Type A Aortic Dissection
Ascending aorta involvement = 1–2% mortality per hour without surgery. IV labetalol/esmolol first (HR <60), THEN nitroprusside if needed. Call cardiothoracic surgery simultaneously. Do not wait for "more imaging."
9. Complete Heart Block — Ventricular Escape
Wide QRS escape rhythm at 20–40 bpm + AV dissociation. Ventricular escape rhythm is unreliable — risk of asystole without warning. Emergency pacing. Atropine is a temporizing measure only (often ineffective below His bundle). Permanent pacemaker regardless of symptoms.
10. ICI Myocarditis — Cancer Therapy Emergency
Patient on pembrolizumab/nivolumab/ipilimumab + new chest pain + elevated troponin + new reduced EF. Mortality ~25% if not recognized. Stop immunotherapy immediately. High-dose methylprednisolone 1g IV daily × 3–5 days. Do not delay treatment for biopsy confirmation.
⬡ Closing Statement
"This syllabus covers every testable cardiology concept on the PANCE from hemodynamics to HCM. Know the traps — they are not random. They are the exact decision points where real patients die. Master the pattern, trust the framework, and the exam follows."