PA Cardiology Bootcamp — Complete Syllabus

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 = targeted. Tier 3 = rapid bullets only.
Board traps are flagged everywhere — these are the distractors written to fool you

Domain 1 · Cardiology Foundations

Cardiology Foundations

Tier 1

Topic F-1

Cardiac Physiology & Hemodynamics

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Cardiac Cycle · Heart Sounds · CO = HR × SV · Frank-Starling · PV Loops · Swan-Ganz Values

★★★ PANCE FoundationExpanded

Why It Matters for Boards

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
Ventricular ejection: Aortic/pulmonic valve opens when ventricular pressure exceeds arterial pressure
Isovolumetric relaxation: All valves close; pressure falls without volume change
Rapid filling: AV valves open; passive filling accounts for ~70–80% of ventricular volume

Heart Sounds — Board Pattern

Sound	Mechanism	Clinical Significance	Board Key
S1	Closure of mitral + tricuspid valves	Onset of systole	Normal
S2	Closure of aortic + pulmonic valves	Onset of diastole; normally splits with inspiration (delayed P2)	Fixed split S2 = ASD. Paradoxical split = LBBB or AS.
S3	Rapid ventricular filling — ventricle suddenly decelerates	Normal in young adults/athletes. Pathologic in age >40 → HFrEF, volume overload	S3 = "Ken-tuc-ky" — ventricular gallop. Think HF.
S4	Atrial contraction against a stiff/non-compliant ventricle	ALWAYS pathologic — LVH, diastolic dysfunction, acute MI, HFpEF	S4 = "Ten-nes-see" — atrial gallop. Think stiff ventricle.

Determinants of Cardiac Output

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

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 (PE/Tamponade)	↓ (RV↑)	↓	↑

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

Hemodynamic Profiles — The Forrester Matrix

Profile	Perfusion	Congestion	Clinical Picture	Treatment
Warm & Dry	Normal	None	Compensated, stable	Optimize medications
Warm & Wet	Normal	Present	Congestion, preserved CO	Diuretics, nitrates
Cold & Dry	Reduced	None	Low CO, hypotensive without congestion	Volume, inotropes
Cold & Wet	Reduced	Present	Cardiogenic shock — worst prognosis	Inotropes, vasopressors, MCS

⚑ Board Traps — Cardiac Physiology

S3 is normal in young adults and athletes — pathologic ONLY in patients >40 or with symptoms of HF
S4 is ALWAYS pathologic — never dismiss it. It signals reduced ventricular compliance (LVH, diastolic dysfunction, ischemia).
PCWP >18 mmHg = cardiogenic pulmonary edema — distinguishes from non-cardiogenic (ARDS: PCWP normal)
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."

Tier 1

Topic F-2

EKG Fundamentals & Systematic Interpretation

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5-Step Approach · Rate/Rhythm/Axis/Intervals/Morphology · Bundle Branch Blocks · High-Yield Patterns

★★★ PANCE FoundationExpanded

Lead Orientation — Know Your Territory

Territory	Leads	Coronary Artery
Inferior	II, III, aVF	RCA (right coronary artery)
Lateral	I, aVL, V5, V6	LCx (left circumflex)
Anterior / Septal	V1–V4	LAD (left anterior descending)
Right ventricular	V4R (right-sided lead)	RCA proximal / right marginal

The 5-Step Systematic Approach

Step 1 — Rate: 300 ÷ (# large boxes between R waves). Sequence: 300, 150, 100, 75, 60, 50. For irregular rhythms: count R waves in 6-second strip × 10. Normal 60–100 bpm.
Step 2 — Rhythm: Regular or irregular? P before every QRS? QRS after every P? Sinus criteria: upright P in II, inverted P in aVR, consistent PR, regular 60–100.
Step 3 — Axis: Look at leads I and aVF. Both positive = normal. I+/aVF− = left axis deviation (LAD). I−/aVF+ = right axis deviation (RAD). Both negative = extreme axis.
Step 4 — Intervals: PR, QRS, QTc (see table below)
Step 5 — Morphology: P waves, QRS complex (hypertrophy, Q waves, BBB), ST/T changes

Intervals — Normal Values & Pathology

Interval	Normal	Prolonged Means	Board Key
PR interval	120–200 ms (3–5 small boxes)	>200 ms = 1° AV block. Short (<120 ms) = WPW or junctional rhythm.	Short PR + delta wave = WPW
QRS duration	60–110 ms (<3 small boxes)	≥120 ms = BBB, ventricular rhythm, hyperkalemia	RBBB: rsR' ("rabbit ears") V1 + wide S in I/V6. LBBB: broad notched R in I, aVL, V5–V6; absent septal Q waves.
QTc	≤440 ms (men), ≤460 ms (women). Bazett: QTc = QT/√RR	Prolonged QTc → risk of Torsades de Pointes (TdP)	Drugs causing QT prolongation: antiarrhythmics (amiodarone, sotalol, quinidine), antipsychotics (haloperidol, quetiapine), macrolides, fluoroquinolones.

Axis — Quick Reference

Axis	Lead I	aVF	Common Causes
Normal (−30° to +90°)	Positive	Positive	Normal variant
Left Axis Deviation (LAD)	Positive	Negative	Left anterior fascicular block, inferior MI, LVH, WPW
Right Axis Deviation (RAD)	Negative	Positive	RVH, PE, left posterior fascicular block, lateral MI, normal in children
Extreme / Indeterminate	Negative	Negative	VT, severe RVH, hyperkalemia

High-Yield EKG Patterns — Must Recognize

Pattern	EKG Finding	Clinical Significance
STEMI	ST elevation ≥1 mm in ≥2 contiguous limb leads OR ≥2 mm in ≥2 contiguous precordial leads + reciprocal ST depression	Immediate cath lab activation
Atrial fibrillation	Irregularly irregular rhythm, absent P waves, fibrillatory baseline	Rate control vs rhythm control decision
Atrial flutter	Sawtooth flutter waves (best II, III, aVF), typically 2:1 block → ventricular rate ~150 bpm	Regular tachycardia at ~150 = think flutter
Hyperkalemia progression	Peaked T waves → PR prolongation → QRS widening → sine wave pattern → asystole	Peaked narrow T waves = earliest sign. Wide QRS = imminent arrest.
Pericarditis	Diffuse ST elevation (saddle-shaped) + PR depression in all leads except aVR (ST depression + PR elevation in aVR)	PR depression is highly specific for pericarditis
Pulmonary embolism	Sinus tachycardia (#1 most common finding), S1Q3T3, right heart strain (T inversions V1–V4), new RBBB	S1Q3T3 = classic but insensitive (~20%)
WPW (Wolff-Parkinson-White)	Short PR (<120 ms), delta wave (slurred QRS upstroke), wide QRS, secondary ST/T changes	AVOID AV nodal blockers (digoxin, verapamil, adenosine) — can precipitate VF
LVH (Sokolow-Lyon)	S in V1 + R in V5 or V6 ≥35 mm	Associated with strain pattern (ST depression + T inversion in lateral leads)
Pathologic Q waves	≥40 ms wide OR ≥25% of R wave height in ≥2 contiguous leads	Prior MI (permanent scar)

STEMI Equivalents — Must Recognize

Pattern	EKG Finding	Board Key
Posterior MI	ST depression V1–V3 + tall R waves V1–V2 (mirror image of posterior STEMI)	Apply V7–V9 posterior leads — ST elevation confirms. Treat as STEMI.
RV MI	ST elevation II, III, aVF + V4R (right-sided lead)	Inferior STEMI + hypotension → get V4R. NO nitrates — preload-dependent RV.
Wellens Syndrome	Biphasic (Type A) or deeply inverted (Type B) T waves in V2–V3 in a pain-free patient	Critical LAD stenosis — high-risk for massive anterior MI. Do NOT stress test. Urgent cath.
De Winter T-waves	Upsloping ST depression + tall peaked symmetric T waves V1–V6 (no ST elevation)	LAD occlusion equivalent. Treat as anterior STEMI.
Sgarbossa criteria (LBBB)	Concordant ST elevation ≥1 mm; concordant ST depression ≥1 mm V1–V3; excessively discordant ST elevation ≥5 mm	New or presumed new LBBB with chest pain = STEMI equivalent until proven otherwise.

⚑ Board Traps — EKG

Regular tachycardia at ~150 bpm = atrial flutter (2:1 block) until proven otherwise
WPW: NEVER give AV nodal blockers (adenosine, verapamil, digoxin, beta-blockers) — accessory pathway conduction can accelerate → VF
Peaked T waves = earliest EKG sign of hyperkalemia — order BMP immediately. Widening QRS = imminent arrest.
PR depression = most specific EKG finding for pericarditis — diffuse ST elevation is seen in multiple conditions, but PR depression is highly specific
S1Q3T3 is specific but insensitive (~20%) for PE — sinus tachycardia is the most common EKG finding in PE
New LBBB with chest pain — apply Sgarbossa criteria. Do NOT dismiss as "just LBBB."

★ Memory Trick

Rate: "300 → 150 → 100 → 75 → 60 → 50" (1, 2, 3, 4, 5, 6 large boxes) Axis: "Lead I and aVF: both up = normal. I up/aVF down = Left. I down/aVF up = Right." RBBB: "Rabbit ears in V1 (rsR') + Slurred S in I and V6" LBBB: "Broad notched R wave in I, aVL, V5-V6. No septal Q waves." Flutter: "Regular tachycardia at 150 = flutter sawtooth until proven otherwise" WPW: "Short PR + delta wave = WPW = DO NOT block the AV node" Hyperkalemia: "Peaks → widens → sine → flat = the K+ kill sequence"

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Everything in the full Cardiology syllabus

27 fully-worked clinical topics

Interactive SVG anatomy diagrams

Module D — must-know differentials

Module E — domain board pearls

Animated EKG strips & 12-lead viewer

Audio mnemonics per topic

20 PANCE-style board questions

Clinical vignettes + teaching pearls

🔒 Murmurs — Systematic Approach 🔒 Shock — Classification & Hemodynamic Profi 🔒 EKG Differential — STEMI Mimics & Missed O 🔒 Acute Coronary Syndrome 🔒 Stable Angina & Vasospastic Angina 🔒 Atrial Fibrillation & Atrial Flutter 🔒 SVT & Wide-Complex Tachycardia 🔒 Heart Blocks & Pacing Indications 📈 View B 🔒 Heart Failure — HFrEF & HFpEF 🔒 Valvular Disease — The Big Four 🔒 Infective Endocarditis 🔒 Hypertrophic Cardiomyopathy (HCM) 🔒 Dilated & Other Cardiomyopathies 🔒 Hypertensive Emergency vs Urgency + 11 more topics

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📟Full EKG library

🩺84 clinical vignettes

👨‍⚕️Dr. Rajiv Choudhary, MD MPH

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Tier 1

Topic F-3

Murmurs — Systematic Approach

Timing · Location · Radiation · Dynamic Maneuvers · HCM vs AS · All Diastolic Murmurs Are Pathologic

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

High-Yield Murmur Characteristics

Murmur	Timing	Location	Radiation	Character	Board Key
Aortic Stenosis (AS)	Systolic	RUSB	Carotids	Crescendo-decrescendo; late-peaking in severe AS	Pulsus parvus et tardus (slow-rising, low-amplitude pulse) in severe AS
Mitral Regurgitation (MR)	Holosystolic	Apex	Axilla	Blowing, plateau	Increases with handgrip (↑ afterload). Decreases with Valsalva.
Tricuspid Regurgitation (TR)	Holosystolic	LLSB	None	Soft, blowing	Carvallo sign: increases with inspiration (↑ right-sided venous return)
Mitral Valve Prolapse (MVP)	Mid-to-late systolic	Apex	None	Mid-systolic click + late systolic murmur	Click moves earlier + murmur lengthens with Valsalva/standing. Click moves later with squatting.
HCM (HOCM)	Systolic	LLSB	Does NOT radiate to carotids	Crescendo-decrescendo	Louder with Valsalva/standing. Softer with squatting/handgrip. HCM ≠ AS.
VSD	Holosystolic	LLSB	None	Harsh	Increases with handgrip. May have thrill.
Aortic Regurgitation (AR)	Early diastolic	LUSB	None	High-pitched, decrescendo, blowing	Best heard sitting up, leaning forward, breath held at expiration. Austin Flint murmur at apex.
Mitral Stenosis (MS)	Mid-diastolic	Apex	None	Low-pitched rumble; use bell in left lateral decubitus	Opening snap precedes rumble. Shorter S2→OS interval = more severe MS.
PDA	Continuous ("machinery")	Left infraclavicular	None	Continuous, machine-like	Benign in premature infants; may need closure if large

Dynamic Auscultation Maneuvers — The Most Tested Table

⚑ Key Principle: Decrease Preload → Most Murmurs Softer. Two Exceptions: HCM and MVP Get LOUDER.

Valsalva / Standing: ↓ preload → HCM louder, MVP click moves earlier + murmur longer, AS/MR softer
Squatting / Passive leg raise: ↑ preload + ↑ afterload → HCM softer, MVP click moves later, AS/MR louder
Handgrip: ↑ afterload → MR, AR, VSD louder; HCM, AS softer
Inspiration: ↑ right-sided venous return → TR, pulmonary stenosis louder (Carvallo sign)

When to Order Echocardiography

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"

Tier 1

Topic F-4

Shock — Classification & Hemodynamic Profiles

4 Categories · CVP/PCWP/CO/SVR Patterns · Bedside POCUS · Vasopressor Selection

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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	"Cold and wet" — cold extremities + pulmonary congestion; ↑ JVP; S3 gallop	Inotropes (dobutamine), vasopressors (norepinephrine), revascularization for MI, mechanical circulatory support (IABP, Impella, ECMO)
Distributive	Pathologic vasodilation → ↓ SVR → relative hypovolemia	Sepsis (#1 in ICU), anaphylaxis, neurogenic, adrenal crisis	"Warm and wet" — warm/flushed skin (early), ↑ HR, wide pulse pressure	Norepinephrine (first-line for septic shock) + treat underlying cause. Epinephrine for anaphylaxis.
Obstructive	Mechanical obstruction to flow → ↓ CO	Tension pneumothorax, cardiac tamponade, massive PE	JVD, tracheal deviation (tension), pulsus paradoxus (tamponade), Beck's triad	Relieve the obstruction: needle decompression, pericardiocentesis, thrombolysis/embolectomy

Hemodynamic Profile Summary — The Boards Table

Parameter	Hypovolemic	Cardiogenic	Distributive (Sepsis)	Obstructive
CVP / RAP	↓	↑	↓ or normal	↑
PCWP	↓	↑ (>18)	↓ or normal	Variable
CO / CI	↓	↓ (CI ≤2.2)	↑ (usually)	↓
SVR	↑	↑	↓↓	↑
SvO₂	↓	↓	↑ (early)	↓

Three Bedside Windows for Tissue Hypoperfusion

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

⚑ Board Traps — Shock

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.

★ 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."

Tier 1

Topic F-3

EKG Differential — STEMI Mimics & Missed Occlusions

False Positives · False Negatives · Conduction Masking · Sex-Based Thresholds

★★★ PANCE PriorityMany Traps2025 Updated

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Why the PANCE Tests This

22.7% of real-world STEMI activations are false positives — the most common causes being LVH (49%), early repolarization (24%), RBBB (16%), and Brugada pattern (4%). Conversely, 10–25% of true coronary occlusions don't meet standard STEMI criteria. Boards test both failure modes: activating cath for non-occlusion, and missing the occlusion that doesn't look like STEMI.

Category 1 — STEMI Mimics (False Positives)

Pattern	What It Mimics	Key Distinguishing Features	Board Key
Early Repolarization	Anterior STEMI	Concave ("smiley face") ST morphology. Notched/slurred J-point. Tall upright T waves. No reciprocal changes. Stable on serial ECGs. Common in young men.	STEMI: convex/oblique ST, reciprocal depression, dynamic changes. Formula using R-wave amplitude in V4 + ST60ms in V3 + QTc achieves 86% sensitivity / 91% specificity for distinguishing subtle anterior STEMI.
Acute Pericarditis	STEMI (multiple territories)	Diffuse concave ST elevation crossing multiple coronary territories. PR-segment depression (especially lead II); PR elevation in aVR. No reciprocal ST depression (except aVR and V1).	Unlike STEMI, pericarditis does not evolve through the typical STEMI sequence and lacks reciprocal ST depression in other leads. TP segment depression (PTa depression) = pericarditis.
Left Ventricular Hypertrophy (LVH)	Anterior STEMI	Most common false STEMI trigger (49% of false activations). Discordant ST elevation in V1–V3 (opposite to dominant S wave). Strain pattern = asymmetric ST depression / TWI in lateral leads. Stable, non-dynamic.	LVH ST changes are predictable and non-evolving. Any dynamic change in a patient with baseline LVH should raise concern for superimposed ischemia.
Takotsubo Syndrome	Anterior STEMI	ST elevation in ~40–50% of cases — but distribution spans multiple coronary territories (beyond a single vessel). 90% postmenopausal women with emotional/physical trigger. Troponin elevation disproportionately modest vs. wall motion abnormalities.	ST elevation in aVR + anteroseptal leads (V1–V3) = 100% specific for Takotsubo vs ACS. Deep widespread TWI + QTc >500ms develops 24–48h after onset — more characteristic of Takotsubo. Coronaries clean on angiography.
Brugada Pattern	Anteroseptal STEMI	Coved ST elevation in V1–V3. Characteristic "shark fin" morphology. RBBB pattern. Absence of reciprocal changes.	Brugada pattern is dynamic — can be unmasked by fever, sodium channel blockers, vagal tone. Associated with VF and sudden cardiac death, not coronary occlusion.

Category 2 — STEMI Equivalents (False Negatives — Missed Occlusions)

These patterns represent acute coronary occlusion in 10–25% of ongoing ischemia cases but do not meet standard STEMI criteria — they are the patients who get admitted as "NSTEMI" and cath'd the next morning while actively infarcting.

Pattern	What It Looks Like	What It Actually Is	Board Action
Posterior MI	Isolated ST depression V1–V3 — frequently labeled NSTE-ACS	Mirror image of posterior ST elevation. LCx or RCA occlusion.	Get posterior leads V7–V9. ST elevation ≥0.5mm in V7–V9 confirms posterior STEMI. 2025 ACC/AHA now recommends posterior leads when isolated anterior ST depression ≥0.5mm is present.
De Winter T-Waves	Tall symmetric T waves + upsloping ST depression >1mm in precordial leads V1–V6	Proximal LAD occlusion. Present in ~2% of anterior MIs.	Immediate angiography — NOT serial troponins or observation. No ST elevation will appear; this IS the infarct pattern.
Wellens Syndrome	Biphasic (Type A) or deeply inverted (Type B) T waves in V2–V3 during a pain-free interval	Critical proximal LAD stenosis with recent spontaneous reperfusion — patient will infarct without intervention.	Stress test CONTRAINDICATED — precipitates cardiac arrest. Direct catheterization.
Hyperacute T-Waves	Tall, broad-based, asymmetric T waves — earliest sign of coronary occlusion before frank ST elevation	Evolving STEMI — pre-elevation phase. Dynamic on serial ECGs.	Distinguish from hyperkalemia: ischemia = broad-based, asymmetric T waves. Hyperkalemia = narrow, peaked, symmetric T waves. Serial ECGs will show evolution to ST elevation in ischemia.
aVR ST Elevation + Diffuse ST Depression	ST elevation >1mm in aVR with multilead ST depression in multiple territories — often labeled NSTE-ACS	Left main coronary artery occlusion or severe 3-vessel disease — high mortality pattern.	This is NOT NSTEMI managed conservatively. Emergent angiography when symptoms persist or hemodynamic instability is present. Highest-risk pattern in ACS triage.

Category 3 — Conduction Abnormalities Masking ACS

LBBB — Apply Modified Sgarbossa

New LBBB is NO longer a STEMI equivalent per 2025 ACC/AHA guidelines — do not auto-activate cath lab
Apply Modified Sgarbossa Criteria instead. Any single criterion met = suggest AMI:

Modified Sgarbossa — 3 Criteria

Concordant ST elevation ≥1mm in any lead where QRS is positive (most specific criterion)
Concordant ST depression ≥1mm in V1–V3
Discordant ST elevation with ST/S ratio ≥25% — replaces original ≥5mm criterion. Improved sensitivity 52% → 80–91%, specificity 90–99%.

Only one lead meeting any single criterion is sufficient to suggest AMI

RBBB & Paced Rhythms

RBBB: Does NOT typically obscure lateral/inferior ST changes. However, rSR' pattern in V1–V3 with associated ST-T changes can mimic anterior ischemia — RBBB was an independent predictor of false STEMI activations. New RBBB + ST-T abnormalities beyond V1–V4 may indicate acute ischemia (associated with TIMI 0–2 flow in up to 66%).
Ventricular paced rhythm: Similar challenges to LBBB. Modified Sgarbossa criteria also apply to paced rhythms, though less well validated. Treat clinically suspicious presentation as occlusion until proven otherwise.

Category 4 — Sex & Age-Based ST Threshold Differences

The Fourth Universal Definition of MI specifies different ST elevation thresholds in leads V2–V3 based on age and sex — frequently overlooked in clinical practice and tested on boards:

Population	V2–V3 STEMI Threshold	Board Implication
Men ≥40 years	≥2.0 mm	Standard threshold for most adult males
Men <40 years	≥2.5 mm	Up to 2.5 mm of J-point elevation can be normal in young men — do not over-call STEMI
Women (all ages)	≥1.5 mm	Lower threshold. Applying 2mm threshold to women misses true STEMI. Women are undertriaged using male-derived criteria.
All leads except V2–V3	≥1.0 mm in ≥2 contiguous leads	Uniform across sex and age

Master Quick-Reference — All Patterns

Pattern	What It Mimics	Key Distinguishing Feature	Action
Early repolarization	STEMI	Concave ST, notched J-point, no reciprocal changes, stable	Serial ECGs; no cath
LVH	Anterior STEMI	Discordant STE V1–V3, lateral strain pattern, non-dynamic	No cath unless dynamic change
Pericarditis	STEMI	Diffuse concave STE, PR depression, no reciprocal changes	NSAIDs + colchicine
Takotsubo	Anterior STEMI	Multi-territory STE, QTc >500ms, modest troponin, aVR+V1–V3 = 100% specific	Cath to exclude ACS, then supportive care
Brugada pattern	Anteroseptal STEMI	"Shark fin" coved STE V1–V3, RBBB, no reciprocal changes	No cath for pattern alone; EP referral
Posterior MI (ST dep V1–V3)	NSTE-ACS	Mirror of posterior STE; confirm with V7–V9	Cath lab — STEMI equivalent
De Winter T-waves	NSTE-ACS	Tall symmetric T waves + upsloping ST depression = proximal LAD occlusion	Cath lab immediately
Wellens syndrome	Resolved ischemia	Biphasic/inverted T waves V2–V3 in pain-free patient	Cath lab — stress test contraindicated
Hyperacute T-waves	Hyperkalemia / BER	Broad-based, asymmetric, dynamic — evolves to STE	Serial ECGs; high suspicion for early STEMI
aVR STE + diffuse ST depression	NSTE-ACS	Left main / 3-vessel disease pattern — highest mortality	Urgent/emergent angiography
LBBB masking STEMI	Non-ischemic LBBB	Apply Modified Sgarbossa (ST/S ratio ≥25% in any one lead)	Cath if any Sgarbossa criterion met

⚑ Board Traps — EKG Differential

New LBBB is NOT an automatic cath lab activation per 2025 ACC/AHA — apply Modified Sgarbossa. Old teaching is wrong.
Takotsubo aVR sign: ST elevation in aVR + V1–V3 is 100% specific for Takotsubo vs. ACS — know this cold
Hyperacute T-waves vs hyperkalemia: Ischemia = broad-based, asymmetric. Hyperkalemia = narrow, peaked, symmetric ("tented"). Dynamic serial change = ischemia.
Women's STEMI threshold in V2–V3 is 1.5mm, not 2mm — applying male criteria to women misses true STEMIs
De Winter T-waves never develop into ST elevation — the pattern IS the infarct. Do not wait for elevation that will never come.
aVR STE + multilead ST depression ≠ conservative management — this is left main or 3-vessel disease. High mortality. Emergent angiography.
Wellens in a pain-free patient looks "stable" — it is not. The most dangerous board trap in ACS: stable-appearing patient who needs the cath lab today, not after a stress test next week.

★ Memory Tricks

STEMI vs Early Repolarization: "STEMI frowns, BER smiles" — convex = STEMI, concave = benign Hyperacute T-wave vs Hyperkalemia: "Ischemia is Broad, K+ is Peaked" — wide base vs narrow tent Takotsubo aVR rule: "aVR + V1–V3 STE = Tako, not ACS" — 100% specific Modified Sgarbossa: "Only need ONE lead. ST/S ratio ≥25% = AMI in LBBB." False STEMI causes: LVH (49%) → Early repol (24%) → RBBB (16%) → Brugada (4%)

⬡ Clinical Pearl

"The missed STEMI equivalent kills the patient slowly — they're admitted to the floor as NSTEMI, get troponins every 6 hours, and cath the next morning while they're infarcting. De Winter T-waves, Wellens, posterior MI, and aVR STE with diffuse depression all represent ongoing occlusion. These patients need the cath lab tonight, not tomorrow."

Domain 2 · Ischemic Heart Disease — Most Tested on PANCE

Ischemic Heart Disease

Tier 1

Topic C-1

Acute Coronary Syndrome

STEMI · NSTEMI · Unstable Angina · Mechanical Complications

★★★ PANCE PriorityMany Traps

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Why the PANCE Tests This

#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.
Anticoagulation: UFH, enoxaparin, or bivalirudin
Post-MI four pillars: ACE-I/ARB + high-intensity statin + beta-blocker + DAPT × 12 months
MRA (eplerenone): If LVEF ≤40% + HF symptoms or diabetes post-MI. Monitor K⁺ and renal function.

Mechanical Complications of MI (3–5 Days Post-MI)

Complication	Presentation	Murmur	Confirm	Rx
Free Wall Rupture	Sudden PEA/tamponade	None	Echo (tamponade)	Emergency surgery. Mortality >50%.
Ventricular Septal Defect	New HF + shock	Loud holosystolic LSB + thrill	Echo, O₂ step-up RA→RV on right heart cath	IABP bridge → urgent surgical or percutaneous repair
Papillary Muscle Rupture	Flash pulmonary edema + shock	Soft or absent systolic murmur at apex	Echo (eccentric MR jet, mobile mass)	Emergency MVR. Nitroprusside + IABP bridge.
Dressler Syndrome	Fever + pleuritic pain 1–8 weeks post-MI	Friction rub	Clinical + echo (effusion)	NSAIDs + colchicine. Avoid anticoagulation (hemorrhagic pericarditis risk).

⚑ Board Traps — ACS

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

Important

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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.
MINOCA (MI with non-obstructive coronary arteries): Troponin positive, STEMI/NSTEMI pattern, but clean coronaries. Causes: coronary spasm, plaque erosion, SCAD, microvascular disease, Takotsubo.

Treatment

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

⚑ Board Trap

Beta-blockers are CONTRAINDICATED in vasospastic (Prinzmetal) angina — unopposed alpha-adrenergic activity worsens coronary spasm
MINOCA ≠ "clear" — still has troponin elevation and needs workup (echo, cardiac MRI, sometimes OCT/IVUS)

Domain 3 · Arrhythmias

Arrhythmias

Tier 1

Topic A-1

Atrial Fibrillation & Atrial Flutter

Rate vs Rhythm · CHA₂DS₂-VASc · Cardioversion · Antiarrhythmics · 2023 Guidelines

★★★ PANCE PriorityMany Traps2023 Updated

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Core Recognition

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

Rate vs Rhythm Control — 2023 Paradigm Shift

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

Rate Control Drug Selection — The Critical EF Check

Drug	Use When	AVOID When	Board Key
Diltiazem / Verapamil	Normal EF, symptomatic RVR	HFrEF (EF <40%) — worsens pump function, increases mortality	CHECK EF BEFORE ORDERING
Metoprolol (BB)	Normal or reduced EF	Acute bronchospasm, severe bradycardia, decompensated HF	Safe in HFrEF at stable doses
Digoxin	HFrEF when BB not tolerated; sedentary patients	WPW (forces accessory pathway conduction → VF)	Check levels; toxicity with hypokalemia
Amiodarone	Rate control when other drugs fail; ICU	Avoid long term; extensive toxicity (thyroid, lung, liver, eyes, skin)	Drug of last resort for AF due to toxicity profile

Anticoagulation — CHA₂DS₂-VASc

CHA₂DS₂-VASc Scoring

CHF (1) · HTN (1) · A₂ge ≥75 (2 pts) · DM (1) · S₂troke/TIA (2 pts — highest) · Vascular disease (1) · Age 65–74 (1) · Scex female (1)
Score ≥2 (men) or ≥3 (women) → Anticoagulate. DOACs preferred over warfarin.
Score 1 (men) or 2 (women) → Consider anticoagulation
Score 0 (men) or 1 (women, lone female sex) → No anticoagulation
DOACs contraindicated with: mechanical valves (use warfarin only) and moderate-to-severe mitral stenosis
Aspirin alone is NOT adequate stroke prevention in AF

Cardioversion — 2023 ACC/AHA/ACCP/HRS Guidelines

Scenario	Strategy	Class	Post-CV OAC
AF ≥48h or unknown duration	3 weeks therapeutic OAC BEFORE cardioversion OR TEE/cardiac CT to exclude LAA thrombus	Class I, LOE B-R	≥4 weeks ALL patients
AF <48h + CHA₂DS₂-VASc ≥2	Precardioversion imaging may be considered — <48h window NOT uniformly safe	Class IIb	≥4 weeks OAC
AF <12h + CHA₂DS₂-VASc 0–1	Benefit of imaging/OAC uncertain — very low event rate	Class IIb	Per long-term indication
LAA thrombus found	Defer cardioversion → OAC 3–6 weeks → repeat imaging → proceed	Class I	≥4 weeks after successful repeat imaging
Hemodynamically UNSTABLE	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.

Antiarrhythmic Drug Selection

Structural Heart Disease?	Safe Antiarrhythmics	Contraindicated
No structural disease	Flecainide, propafenone, sotalol, dofetilide, dronedarone	Use AV nodal blocker WITH flecainide/propafenone to prevent 1:1 flutter
Structural disease / HFrEF (EF ≤40%)	Amiodarone or Dofetilide ONLY	All others — CAST trial: flecainide/encainide increased mortality post-MI

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

⚑ 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"

Tier 1

Topic A-2

SVT & Wide-Complex Tachycardia

AVNRT · AVRT · Adenosine · Brugada Criteria · VT vs SVT

★★★ PANCE PriorityLethal Trap

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Core Recognition

Feature	SVT (narrow)	VT (wide)
QRS	Narrow <120ms (usually)	Wide >120ms
Common patient	Young, female, no structural disease	Older, post-MI, structural disease
AV dissociation	Absent (AV node in circuit)	Present (P waves march independently) — pathognomonic for VT
Adenosine response	Terminates AVNRT/AVRT	Does NOT terminate VT; can cause hemodynamic collapse
Board default rule	Narrow + stable = adenosine	Wide = VT until proven otherwise

Acute Management Protocol

The Tachycardia Decision Tree

UNSTABLE (any arrhythmia)? → Synchronized cardioversion immediately (all unstable tachycardias with a pulse)
Narrow complex + stable (SVT)? → Vagal maneuver → Adenosine 6mg rapid IV push + 20mL saline flush → 12mg → 12mg
Wide complex + stable? → Assume VT → Amiodarone 150mg IV over 10 min → 1mg/min drip
Pulseless VT / VF? → CPR + Unsynchronized defibrillation. Amiodarone 300mg IV push.
Torsades de Pointes? → IV Magnesium 2g — NOT amiodarone (prolongs QT further)

Brugada Criteria — Differentiating VT from SVT with Aberrancy

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

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

⚑ Critical Board Traps — SVT/VT

Wide complex = VT until proven otherwise. Giving verapamil/diltiazem to VT can cause cardiovascular collapse and death
Hemodynamic stability does NOT exclude VT — patients can be stable in VT for hours
Prior MI + wide complex = VT until proven otherwise
Adenosine: RAPID IV push + immediate saline flush — if given slowly, it does not work. Half-life ~6 seconds.
Adenosine contraindicated in WPW with pre-excited AF and antidromic AVRT (wide complex)
Torsades = Magnesium IV. NOT amiodarone. Standard antiarrhythmics worsen TdP.
Synchronized vs unsynchronized: Synchronized = pulse present. Unsynchronized = pulseless VT or VF.

QT-Prolonging Drugs — High-Yield Board List (TdP Risk)

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

★ Memory Trick

Wide + Unstable = SHOCK (synchronized). Wide + Stable = AMIODARONE. Narrow + Stable = ADENOSINE (after vagal). Pulseless = DEFIBRILLATE (unsynchronized). Torsades = MAGNESIUM always. Never amiodarone.

Tier 1

Topic A-3

Heart Blocks & Pacing Indications

Mobitz I vs II · Complete Heart Block · Pacemaker Thresholds

★★ High YieldCommon Trap

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Block Type	EKG Pattern	Level	Pacemaker?	Board Key
1° AV Block	PR >200ms, all P waves conducted	AV node	No (unless symptomatic hemodynamic compromise)	Benign. No treatment.
2° Mobitz I (Wenckebach)	Progressive PR prolongation → dropped QRS. Grouped beating.	AV node (supra-nodal)	No (unless symptoms correlate; Class IIa)	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

Tier 1

Topic H-1

Heart Failure — HFrEF & HFpEF

Four Pillars of GDMT · ADHF Management · Contraindicated Drugs

★★★ PANCE PriorityMany Traps2024 Updated

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Core Recognition

	HFrEF	HFmrEF	HFpEF
LVEF	≤40%	41–49%	≥50%
Mechanism	Pump fails to contract	Mildly reduced	Pump fails to relax (stiff)
Common causes	CAD, dilated CMP, myocarditis	Mixed	HTN, DM, obesity, AFib, HCM
Echo	Dilated, hypokinetic LV	Mild dilation	Normal size, impaired relaxation
Mortality drugs	ARNI + BB + MRA + SGLT2i — reduce mortality 73% combined	GDMT benefit emerging	No proven mortality benefit; diuretics for symptoms

The Four Pillars of GDMT — HFrEF (2024 ACC Expert Consensus)

Pillar	Drug	Key Trial	Board Trap
1 — ARNI (preferred) or ACEi/ARB	Sacubitril/valsartan (Entresto) → ACEi → ARB	PARADIGM-HF: 20% ↓ CV death vs enalapril	36-hour washout required when switching ACEi → ARNI (angioedema risk). No washout ARB → ARNI.
2 — Evidence-based BB (only 3)	Carvedilol · Metoprolol succinate · Bisoprolol	MERIT-HF, CIBIS-II, COPERNICUS	ONLY these 3. NOT atenolol, metoprolol tartrate, or propranolol. Do NOT initiate in acute decompensation. Do NOT abruptly stop if already on.
3 — MRA	Spironolactone or eplerenone	RALES, EMPHASIS-HF, EPHESUS	Contraindicated if K⁺ >5.0 or eGFR <30. Monitor K⁺ + creatinine.
4 — SGLT2 inhibitor	Dapagliflozin or empagliflozin 10mg daily	DAPA-HF, EMPEROR-Reduced	Benefit regardless of diabetes status. Can initiate at eGFR ≥20–25. Risk: euglycemic DKA, Fournier gangrene.

Additional HFrEF Therapies

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

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.

⚑ Board Traps — Heart Failure

Non-dihydropyridine CCBs (verapamil, diltiazem) = CONTRAINDICATED in HFrEF — negative inotropy worsens pump function, increases mortality
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

Tier 1

Topic V-1

Valvular Disease — The Big Four

AS · AR · MS · MR · MVP · Prosthetic Valve Anticoagulation

★★ High YieldCommon Traps

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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.
Aortic Regurgitation	Diastolic decrescendo, LUSB. Wide pulse pressure.	Bounding pulses (water-hammer), de Musset sign (head bobbing), Duroziez sign, Quincke pulse	Surgery when LVEF ≤55% or LVESD ≥50mm. Vasodilators (nifedipine, ACEi) reduce afterload in chronic severe AR.
Mitral Stenosis	Diastolic rumble at apex, best with bell + left lateral decubitus. Opening snap.	Rheumatic fever. LA dilation → AFib, hemoptysis, pulmonary HTN.	Most associated with AFib (LA dilation). Opening snap — shorter S2-OS interval = more severe. PMBC for pliable valves.
Mitral Regurgitation	Holosystolic, apex → axilla	Volume overload → LV dilation. Acute MR (papillary muscle rupture) = flash pulmonary edema, soft murmur	Acute MR = surgical emergency. Nitroprusside + IABP bridge. Surgery when LVEF ≤60% or LVESD ≥40mm in chronic MR.
Mitral Valve Prolapse	Mid-systolic click + late systolic murmur	Most common valvular abnormality. Usually benign. Women more common.	Standing/Valsalva → click moves EARLIER, murmur louder. Squatting → click moves later, murmur softer. OPPOSITE of other murmurs.

Aortic Stenosis — Full Detail (Most Tested Valvular Lesion)

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

Prosthetic Valve Anticoagulation

Valve Type	Anticoagulation	Target INR	Board Trap
Mechanical Aortic	Warfarin ONLY — lifelong	INR 2.0–3.0	DOACs absolutely contraindicated — RE-ALIGN trial: ↑ thromboembolism + bleeding
Mechanical Mitral	Warfarin ONLY — lifelong	INR 2.5–3.5 (higher target)	DOACs absolutely contraindicated. Higher INR target for mitral position (higher thromboembolic risk).
Bioprosthetic	Warfarin × 3–6 months, then aspirin	INR 2.0–3.0 initially	DOAC may be considered after 3 months in select patients. No lifetime anticoagulation required.

Tier 1

Topic V-2

Infective Endocarditis

Duke Criteria · Organisms · Surgical Indications · Prophylaxis

★★ High YieldCommon Traps

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Core Recognition Pattern

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

Organisms by Patient Type

Patient	Organism	Board Key
Native valve, community	Streptococcus viridans (most common subacute)	Dental procedures → Strep viridans
IV drug user	Staph aureus — RIGHT-SIDED (tricuspid)	IVDU + bilateral cavitary lung lesions = septic emboli from tricuspid valve endocarditis
Prosthetic valve <60 days	Staph epidermidis (CoNS)	Early prosthetic = CoNS or Staph aureus
GI/GU source	Enterococcus	GI/GU procedure history
Colon cancer patient	Strep gallolyticus (bovis)	Strep bovis IE = COLONOSCOPY (60% association with colorectal neoplasia)
Culture-negative IE	HACEK organisms (Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella)	Slow-growing; fastidious gram-negative rods; prolonged incubation needed

Surgical Indications (Class I)

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. Clindamycin 600mg if penicillin-allergic.
MVP without MR = no prophylaxis required

⚑ Board Traps — Endocarditis

Strep bovis/gallolyticus IE = colonoscopy always — 60% colorectal neoplasia association
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

Tier 2

Topic CM-1 ★ Gap Added

Hypertrophic Cardiomyopathy (HCM)

Most Common Cause of Sudden Cardiac Death in Young Athletes

★★ High YieldGap Topic

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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)
Pathophysiology: Asymmetric septal hypertrophy → LVOT obstruction → dynamic outflow gradient → poor diastolic filling
Classic presentation: Young athlete with exertional syncope, chest pain, palpitations. Family history of sudden death. Prominent S4.
Murmur: Harsh systolic crescendo-decrescendo at LLSB. Dynamic — changes with maneuvers.

Murmur Response to Maneuvers — The Boards Love This

Maneuver	Effect on Preload/Afterload	HOCM Murmur	AS/MR Murmur
Valsalva (strain) / Standing	↓ Preload → smaller LV → worse obstruction	LOUDER (worse obstruction)	Softer (less flow)
Squatting / Supine leg raise	↑ Preload → larger LV → less obstruction	Softer (less obstruction)	Louder (more flow)
Amyl nitrite	↓ Afterload + preload	LOUDER	Softer (MR softer; AS louder)
Phenylephrine / Handgrip	↑ Afterload + preload	Softer	Louder (MR louder)

Treatment

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

⚑ 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 ★ Gap Added

Dilated & Other Cardiomyopathies

Dilated CM · ARVC · Takotsubo · Peripartum CMP

ImportantGap Topic

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Type	Pathology	Classic Presentation	Specific Board Pearl
Dilated CMP	Dilated, poorly contracting LV. EF reduced.	HF symptoms + dilated heart on echo. Idiopathic, viral (Coxsackie B), alcohol, cocaine, doxorubicin.	Alcohol CMP: abstinence can partially reverse. Doxorubicin CMP: dose-related, baseline echo before chemo.
ARVC	Fibrofatty replacement of RV myocardium	Young male. Ventricular arrhythmias, RV dysfunction, syncope. EKG: epsilon waves, T-wave inversions V1–V3.	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

Tier 1

Topic HTN-1

Hypertensive Emergency vs Urgency

End-Organ Damage · Drug Selection by Target Organ · Rate of BP Reduction

★★ High YieldRate-of-Reduction Trap

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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 <140–160	Reduce BP to <140 in first hour per AHA guidelines
Aortic dissection	Tearing pain, BP differential, wide mediastinum	Esmolol or labetalol IV FIRST → add nitroprusside if needed. Target SBP <120, HR <60.	Beta-blocker BEFORE vasodilator. Nitroprusside alone → reflex tachycardia → propagates dissection.
ACS with HTN	Chest pain, EKG changes	Nitroglycerin IV	Treat ACS protocol simultaneously
Acute pulmonary edema	Dyspnea, crackles, hypoxia	Nitroglycerin IV (preload/afterload reduction) + loop diuretic	Nitroprusside if severe, refractory
Eclampsia	HTN + pregnancy + seizures	Magnesium sulfate (seizure) + Hydralazine or Labetalol IV (BP)	ACEi and ARBs are TERATOGENIC — absolutely contraindicated in pregnancy
Hypertensive encephalopathy (SAH)	"Worst headache of life" + severe HTN	CT head FIRST before treating BP	Rule out SAH before antihypertensives — wrong drug choice in hemorrhagic vs ischemic causes fatal

⚑ Board Traps — HTN Emergency

"Worst headache of my life" + severe HTN = CT head FIRST — rule out SAH before treating BP
Ischemic stroke: permissive HTN — do NOT lower unless >220/120 (or >185/110 if tPA candidate)
Eclampsia: Magnesium is for seizures, NOT BP — use hydralazine or labetalol for pressure
Aortic dissection: beta-blocker BEFORE vasodilator — "Block before you Drop"
Lowering BP too fast causes AKI, stroke, MI from hypoperfusion of organs dependent on elevated MAP
ACEi/ARBs in pregnancy = absolute contraindication (oligohydramnios, renal agenesis, fetal death)

★ Memory Trick

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

Tier 1

Topic P-1

Pericarditis & Cardiac Tamponade

Saddle ST · Beck's Triad · Pulsus Paradoxus · Pericardiocentesis

★★ High YieldCommon Traps

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Pericarditis — Core Recognition

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

Treatment

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

Cardiac Tamponade

Beck's triad: Hypotension + JVD + muffled heart sounds
Pulsus paradoxus: Drop in SBP >10 mmHg with inspiration — pathognomonic
EKG: Electrical alternans + sinus tachycardia + low voltage
Echo: Diastolic RV collapse (earliest sign), IVC plethora, swinging heart
Definitive treatment: Pericardiocentesis
Bridge: IV fluids (maintain preload while preparing for drainage)

⚑ Board Traps — Pericarditis & Tamponade

Dressler syndrome = aspirin, NOT ibuprofen — NSAIDs impair myocardial scar formation post-MI
Steroids in viral pericarditis = contraindicated — increases recurrence rate
Colchicine is mandatory — reduces recurrence 50%. Do not omit.
NEVER give diuretics in tamponade — preload-dependent. Furosemide causes cardiovascular collapse.
Tamponade vs Constrictive Pericarditis: Tamponade = pulsus paradoxus, no Kussmaul sign. Constriction = Kussmaul sign (JVD ↑ with inspiration), no/mild pulsus paradoxus.
Positive pressure ventilation in tamponade reduces venous return → can precipitate arrest. Drain before intubate if possible.

Tier 2

Topic P-2 ★ Gap Added

Myocarditis

Viral · Giant Cell · Immune Checkpoint Inhibitor · Distinct from Pericarditis

ImportantGap Topic

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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.
ICI myocarditis: Stop ICI immediately + high-dose methylprednisolone (1g IV daily × 3–5 days)

⚑ Board Trap

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

Tier 1

Topic SH-1 ★ Gap Added

Shock — Classification & Management

Cardiogenic · Distributive · Obstructive · Hypovolemic

★★★ PANCE PriorityGap Topic

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Type	CO/CI	SVR	PCWP/Preload	Classic Cause	First-Line Rx
Cardiogenic	↓↓	↑↑ (compensatory)	↑ (backed up)	Massive MI, ADHF, acute MR/VSD, myocarditis	Dobutamine/milrinone (inotrope) + diuresis if congested. IABP or Impella for CS.
Distributive (Septic)	↑ (hyperdynamic)	↓↓	↓ (vasodilated)	Sepsis/septic shock, anaphylaxis, neurogenic	IV fluids (30 mL/kg) + vasopressors (norepinephrine first-line). Treat source.
Obstructive	↓	↑	Variable	Massive PE, tension pneumothorax, cardiac tamponade	Remove the obstruction: thrombolytics/embolectomy (PE), needle decompression (tension PTX), pericardiocentesis (tamponade).
Hypovolemic	↓	↑	↓	Hemorrhage, severe dehydration, burns	IV crystalloid or blood products (hemorrhagic). Treat source of loss.

⚑ Board Traps — Shock

Cardiogenic shock + congestion (Cold & Wet) = inotrope + diuresis, NOT fluids — giving fluids worsens cardiac output
Vasopressor of choice in septic shock = norepinephrine (not dopamine — dopamine increases arrhythmia risk)
Tamponade = obstructive shock — IV fluids as bridge, then drain (pericardiocentesis)
RV MI = distributive-like hemodynamics (preload dependent) — give fluids, avoid vasodilators

Domain 10 · Vascular Disease

Vascular Disease

Tier 1

Topic VAS-1

Aortic Dissection & AAA

Type A vs B · Stanford Classification · Surgical vs Medical

★★ High YieldLethal Trap

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Aortic Dissection — Classic Triad

Classic Triad — Memorize

Sudden onset tearing/ripping pain — maximum at onset, radiates to back
BP differential between arms (>20 mmHg)
Wide mediastinum on CXR (>8 cm on PA view)

Stanford Classification

	Type A	Type B
Involves	Ascending aorta (± descending)	Descending aorta only
Treatment	Emergent surgery — 1–2% mortality per hour without Rx	Medical management: BB → add nitroprusside if needed
Goal	OR immediately	HR <60, SBP <120
Complications	AR, tamponade, stroke, MI	Renal failure, bowel ischemia, TEVAR if complicated

⚑ Board Traps — Aortic Dissection

Dissection can mimic STEMI — inferior STEMI if dissection involves RCA. Give thrombolytics/heparin to aortic dissection = fatal hemorrhage.
Dissection can mimic stroke — carotid involvement causes focal deficits. No tPA without ruling out dissection.
NEVER give nitroprusside alone — reflex tachycardia increases shear force (dP/dt), propagates dissection
"Block before you Drop" — beta-blocker first, then vasodilator
Gold standard imaging: CT angiography chest/abdomen/pelvis — fastest. TEE also excellent but slower.

Tier 1

Topic VAS-2 ★ Gap Added

DVT & Pulmonary Embolism

Wells Criteria · CT-PA · PESI Score · Anticoagulation · Massive PE

★★★ PANCE PriorityGap Topic

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Core Recognition

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

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 ★ Gap Added

Peripheral Artery Disease (PAD) & AAA

ABI · Claudication · Critical Limb Ischemia · AAA Screening

ImportantGap Topic

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PAD

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

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

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-2 + F-3: Hemodynamics, EKG Fundamentals & EKG Differential

Preload/afterload/CO · Forrester matrix · EKG systematic approach · STEMI equivalents (Wellens, De Winter, Posterior, RV, Sgarbossa) · STEMI mimics (early repol, LVH, pericarditis, Takotsubo, Brugada) · Modified Sgarbossa · Sex-based V2–V3 thresholds

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

11:00–11:30

C-2: Stable Angina & Vasospasm

Prinzmetal angina · MINOCA · CCB vs BB distinction · Rapid bullets

11:30–12:30

🍽 Lunch

12:30–2:00

H-1: Heart Failure — Both Types, Full GDMT

HFrEF vs HFpEF · 4 pillars (ARNI + BB + MRA + SGLT2i) · Only 3 BBs · Drug contraindications · ADHF management · Forrester matrix 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

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.

8:00–9:30

A-1: Atrial Fibrillation — Full Module

Rate vs rhythm · 2023 paradigm shift (EAST-AFNET 4) · CHA₂DS₂-VASc · Cardioversion 48-hour rule updated · Antiarrhythmic selection chart · WPW trap · Amiodarone toxicity

9:30–9:45

☕ Break

9:45–11:00

A-2 + A-3: SVT/VT Decision Tree + Heart Blocks

Tachycardia algorithm live · Brugada criteria · Adenosine technique · TdP + QT-prolonging drugs · Mobitz I vs II pacing indications

11:00–11:45

V-1 + V-2: Valvular Disease & Endocarditis

Big 4 valvular lesions · MVP maneuver trick · HCM murmur vs AS · Prosthetic valve anticoagulation · Duke criteria · Organism-by-patient chart · Prophylaxis indications

11:45–12:45

🍽 Lunch

12:45–1:30

CM-1 + CM-2: Cardiomyopathies

HCM — murmur maneuvers, drug contraindications · Dilated CMP causes · ARVC epsilon wave · Takotsubo · Peripartum CMP · ICI myocarditis (new entity)

1:30–2:15

VAS-2 + VAS-3: DVT/PE + PAD/AAA

Wells criteria · Massive vs submassive PE · Fibrinolytic threshold · DOAC selection · D-dimer trap · ABI interpretation · AAA screening guidelines

2:15–2:30

P-1 + P-2: Pericarditis, Tamponade, Myocarditis

Saddle ST vs tombstone · Dressler aspirin rule · Beck's triad · Pulsus paradoxus · Kussmaul sign distinction · ICI myocarditis recognition

2:30–2:45

☕ Break

2:45–4:30

🎯 Final 20-Question Mixed Cardiology Quiz — Live

Work through questions as a group · Discuss every wrong answer · Build the 25-trap mental model · Bootcamp close + clinical pearls summary

Blueprint Gap Topics · Added 2025

Lipid Disorders · Congenital Heart Disease · Restrictive & Stress CMP · SSS & PVCs · Orthostatic Hypotension

Topics present on the 2025 NCCPA PANCE Blueprint not covered in prior modules — now fully integrated

Lipid Disorders & Dyslipidemia

ACC/AHA Risk Calculator · Statin Tiers · LDL Targets · Ezetimibe · PCSK9 Inhibitors · Hypertriglyceridemia

Why the PANCE Tests This

Dyslipidemia management is one of the highest-volume primary care tasks a PA performs. The PANCE tests statin selection by risk tier, LDL targets in specific populations, drug interactions, and when to add non-statin agents.

The 4 Major Lipid Fractions

LDL — Primary Target

Major atherogenic particle
Ideal <100 mg/dL (general); <70 in very high risk; <55 in extreme risk
Calculated: TC − HDL − (TG/5)
Direct LDL if TG >400

HDL — Protective

Low HDL = independent CV risk factor
Men <40, Women <50 mg/dL = low
No drug effectively raises HDL with mortality benefit
Niacin: raises HDL but no outcome benefit (AIM-HIGH)

Triglycerides

Normal <150 · Borderline 150–199 · High 200–499 · Very high ≥500
TG ≥500: pancreatitis risk → fibrates or omega-3 first
Causes: DM, hypothyroidism, alcohol, obesity, steroids, thiazides
Fenofibrate: preferred (less CYP3A4 interaction vs gemfibrozil)

Non-HDL Cholesterol

TC − HDL = all atherogenic particles
Secondary target when TG elevated
Non-HDL target = LDL target + 30 mg/dL
Better predictor than LDL alone when TG >200

ACC/AHA 2019 Statin Framework — The 4 Benefit Groups

Who Gets a Statin — No Risk Calculator Needed

Group 1: Clinical ASCVD (prior MI, stroke, ACS, PAD) → High-intensity statin always
Group 2: LDL ≥190 mg/dL (familial hypercholesterolemia) → High-intensity statin always
Group 3: Diabetes age 40–75 with LDL 70–189 → Moderate-intensity statin; high-intensity if 10-yr risk ≥20%
Group 4: Age 40–75, LDL 70–189, no DM/ASCVD → Calculate 10-yr ASCVD risk (Pooled Cohort Equations)

High-Intensity Statins (↓ LDL ≥50%)

Atorvastatin 40–80mg ⭐ most tested
Rosuvastatin 20–40mg
Use: ASCVD, FH, DM + high risk

Moderate-Intensity (↓ LDL 30–49%)

Atorvastatin 10–20mg
Rosuvastatin 5–10mg
Simvastatin 20–40mg
Pravastatin 40–80mg

Low-Intensity (↓ LDL <30%)

Simvastatin 10mg
Pravastatin 10–20mg
Rarely used as primary agent

Add-On Therapy When Statin Alone Insufficient

Ezetimibe (First Add-On)

Inhibits NPC1L1 cholesterol absorption
Lowers LDL ~18–20% additional
IMPROVE-IT trial: adds benefit on top of statin post-ACS
Use when: LDL goal not met on max statin

PCSK9 Inhibitors (Second Add-On)

Evolocumab (Repatha) · Alirocumab (Praluent)
Monoclonal antibodies — injectable q2–4 weeks
Lowers LDL 50–60% additional
Use: ASCVD + LDL still ≥70 despite max statin + ezetimibe
Very expensive — prior auth usually required

Statin Side Effects & Monitoring

⚑ Statin Toxicity — Board Favorites

Myopathy/myalgia: Most common. Check CK if symptomatic. Myopathy = CK >10× ULN → stop statin
Rhabdomyolysis: Rare but severe. CK markedly elevated + myoglobinuria + AKI. Risk ↑ with CYP3A4 inhibitors
Hepatotoxicity: Rare. Check LFTs only if symptomatic (routine monitoring no longer recommended)
New-onset DM: Small but real risk with high-intensity statins. Benefit still outweighs risk in high-CV-risk patients
Simvastatin + amiodarone/amlodipine: Dose cap — simvastatin 20mg max with amiodarone (myopathy risk)
Gemfibrozil + statin: High myopathy risk — avoid combination. Use fenofibrate instead if needed

Rapid Review Bullets

Familial hypercholesterolemia: LDL ≥190, tendon xanthomas, premature CAD — always high-intensity statin regardless of 10-yr risk
Bile acid sequestrants (cholestyramine): lower LDL, raise TG — contraindicated if TG elevated
Niacin: raises HDL but no CV mortality benefit (AIM-HIGH, HPS2-THRIVE) — not routinely recommended
Statin + fibrate: increased myopathy risk — if needed, use fenofibrate (not gemfibrozil)
Statin in pregnancy: CONTRAINDICATED (category X) — stop before conception
Bempedoic acid (Nexletol): ATP citrate lyase inhibitor; oral alternative for statin-intolerant patients; reduces LDL ~15–18%

Congenital Heart Disease

ASD · VSD · PDA · TOF · Coarctation · Acyanotic vs Cyanotic · Eisenmenger Syndrome

Acyanotic vs Cyanotic — The First Branch Point

Acyanotic (Left-to-Right Shunts) — "Pink" at Birth

Blood flows L→R (high pressure to low pressure)
Causes pulmonary overcirculation → pulmonary HTN over time
ASD · VSD · PDA · Partial AVSD
Can become cyanotic late (Eisenmenger syndrome) if uncorrected

Cyanotic — "Blue" at Birth (R-to-L Shunt)

Deoxygenated blood enters systemic circulation
Tetralogy of Fallot · Transposition of Great Vessels · Truncus arteriosus
Tricuspid atresia · Total anomalous pulmonary venous return
Hypoplastic left heart syndrome

The 5 Most Tested Congenital Lesions

VSD — Ventricular Septal Defect (Most Common CHD)

Holosystolic (pansystolic) murmur at left lower sternal border · harsh, loud
Small VSDs: may close spontaneously — observe. Large: L→R shunt → pulm HTN → HF
Presentation: failure to thrive, recurrent respiratory infections, tachypnea in infants
CXR: cardiomegaly + increased pulmonary vascular markings
Echo: diagnostic. Repair if large, symptomatic, or non-closing

ASD — Atrial Septal Defect

Widely fixed split S2 (pathognomonic) + systolic ejection murmur at LUSB (increased RV outflow)
Often asymptomatic until adulthood → exertional dyspnea, palpitations, RV failure
Ostium secundum type: most common (70%)
Paradoxical embolism: clot crosses ASD → stroke (cryptogenic stroke workup)
Closure: catheter-based device or surgical if significant shunt (Qp:Qs >1.5:1)

PDA — Patent Ductus Arteriosus

Continuous "machine-like" murmur at left infraclavicular area (Gibson murmur)
Common in premature infants — indomethacin (prostaglandin inhibitor) to close
Term infants: surgical ligation or catheter occlusion
Prostaglandin E1 (alprostadil): KEEPS PDA open — used in duct-dependent lesions (TGA, hypoplastic left heart) as bridge to surgery
Wide pulse pressure ("bounding pulses") from aorta→PA runoff

Tetralogy of Fallot — 4 Components

VSD + Right ventricular hypertrophy + Overiding aorta + Pulmonic stenosis (VROP)
Most common cyanotic CHD after neonatal period
"Boot-shaped" heart on CXR (upturned apex from RVH + concave pulmonary artery)
Tet spells (hypercyanotic episodes): agitation → squat position → ↑ SVR → ↓ R→L shunt → ↑ pulmonary flow
Treatment of Tet spell: knee-chest position, O2, morphine, phenylephrine (↑SVR), β-blocker (propranolol)
Definitive: surgical repair in infancy

Coarctation of the Aorta

Narrowing typically just distal to left subclavian artery (juxtaductal)
Classic findings: HTN in upper extremities + hypotension/weak pulses in lower extremities
Systolic BP differential >20 mmHg (arms vs legs) is the key finding
Rib notching on CXR (from collateral intercostal artery enlargement) — late finding
Association: bicuspid aortic valve (most common), Turner syndrome (45,XO)
Treatment: balloon angioplasty or surgical resection. Repair before age 25 recommended

Eisenmenger Syndrome — The Late Complication

⚑ Board Trap — Eisenmenger

Prolonged large L→R shunt → pulmonary HTN → RV pressure exceeds LV → shunt reverses (R→L) → cyanosis
Now contraindicated for surgical repair — repair will worsen by removing pressure relief
Management: pulmonary vasodilators (bosentan, sildenafil), O2, avoid pregnancy
Classic PANCE trap: "patient with known VSD now develops cyanosis" = Eisenmenger

Rapid Review Bullets

Transposition of great vessels: aorta from RV, PA from LV → systemic and pulmonary circulations run in parallel → not compatible with life without mixing (ASD/VSD/PDA). Prostaglandin E1 to keep PDA open. Balloon atrial septostomy → arterial switch surgery
Turner syndrome (45,XO): coarctation + bicuspid AV + horseshoe kidney + webbed neck + primary amenorrhea
Down syndrome (Trisomy 21): AV canal defect (AVSD) most common cardiac lesion
Williams syndrome: supravalvular aortic stenosis + elfin facies + hypercalcemia
Noonan syndrome: pulmonary stenosis + hypertrophic CMP (phenotype similar to Turner but normal karyotype)

Restrictive Cardiomyopathy & Stress Cardiomyopathy

Cardiac Amyloidosis · Hemochromatosis · Sarcoid CMP · Takotsubo · Loeffler · Diastolic Dysfunction

Restrictive Cardiomyopathy — Core Concept

Myocardium becomes stiff and non-compliant due to infiltration or fibrosis. Diastolic filling impaired → ↑ filling pressures → biventricular failure with preserved or near-normal systolic function (EF often normal). Distinguished from constrictive pericarditis by imaging.

Four Main Causes

Cardiac Amyloidosis ⭐ Most Tested

AL (light-chain) amyloid: plasma cell dyscrasia (MM). ATTR: transthyretin, wild-type (elderly men) or hereditary
Echo: "sparkling" granular myocardium + thickened walls + small cavity + diastolic dysfunction
Low-voltage EKG despite thick walls (infiltrative — not hypertrophy)
ATTR amyloid (ATTR): tafamidis approved 2019 — recognize the diagnosis, refer to cardiology
⚑ Digoxin CONTRAINDICATED — amyloid fibrils bind digoxin → toxicity at low levels
⚑ CCB AVOID — negative inotropy worsens diastolic dysfunction

Hemochromatosis

Iron deposition → dilated or restrictive CMP + conduction abnormalities
Bronze diabetes: DM + cirrhosis + arthropathy + hypogonadism + cardiomyopathy
HFE gene mutation (C282Y most common)
Diagnosis: serum ferritin ↑↑ + transferrin saturation >45% → HFE genotyping → liver biopsy if needed
Treatment: phlebotomy (therapeutic) — 1 unit blood weekly. Deferoxamine if phlebotomy not tolerated

Cardiac Sarcoidosis

Granulomatous infiltration of myocardium
Complete heart block + ventricular arrhythmias + SCD risk
Treatment: corticosteroids + ICD if high-risk arrhythmia
Most dangerous organ manifestation of systemic sarcoidosis

Loeffler Endocarditis (Eosinophilic)

Hypereosinophilic syndrome → endomyocardial fibrosis
Mural thrombus formation → emboli
Treat underlying eosinophilia (parasites, malignancy, drugs)

Takotsubo (Stress) Cardiomyopathy

Takotsubo — The Classic Presentation

Transient LV apical ballooning following acute emotional or physical stress
Classic patient: postmenopausal woman after emotional shock (bereavement, surprise)
Mimics STEMI: ST elevation, troponin rise — but coronaries are CLEAN on cath
Mechanism: catecholamine surge → coronary microvascular spasm + apical stunning
Echo: apical ballooning + hyperkinetic base (opposite of anterior STEMI territory)
Treatment: supportive — beta-blockers, ACE inhibitor. Usually recovers fully in weeks
⚑ Board trap: "STEMI presentation + normal coronaries on cath" = Takotsubo (also consider MINOCA, Prinzmetal)

Restrictive vs Constrictive Pericarditis — Key Distinction

Restrictive CMP

Thick myocardium
Normal or absent pericardium
Echo: sparkling/granular texture (amyloid)
Tissue Doppler: impaired relaxation
NOT reversible (fibrosis/infiltration)

Constrictive Pericarditis

Thickened, calcified pericardium
Pericardial knock (S3 equivalent)
Kussmaul sign: JVD rises on inspiration
CT/MRI: pericardial thickening/calcification
REVERSIBLE — pericardiectomy is curative

Sick Sinus Syndrome, Junctional Rhythms & PVCs

SSS · Brady-Tachy Syndrome · Junctional Escape · PVCs · Premature Atrial Contractions

Sick Sinus Syndrome (SSS)

SSS — Recognition & Management

Dysfunction of SA node → inappropriate bradycardia ± pause ± chronotropic incompetence
Brady-tachy syndrome: alternating sinus bradycardia and paroxysmal SVT/AFib (most symptomatic form)
Symptoms: syncope, presyncope, palpitations, fatigue, exercise intolerance
EKG: sinus bradycardia, sinus pauses, SA exit block, alternating brady/tachy
Common in elderly — degenerative fibrosis of conduction tissue
Treatment: permanent pacemaker (dual-chamber, AAI or DDD mode)
⚑ If brady-tachy: cannot just add antiarrhythmics for tachycardia — will worsen bradycardia. Pacemaker first, then rate control/ablation

Junctional Rhythms

Junctional Escape Rhythm

AV node takes over when SA node fails or is suppressed
Rate: 40–60 bpm (junctional escape rate)
EKG: narrow complex, no visible P waves (or retrograde P before/after QRS)
Benign if rate adequate and asymptomatic — may need pacing if symptomatic

Accelerated Junctional Rhythm

Junctional rate 60–100 bpm (faster than normal escape)
Classic cause: digoxin toxicity — most tested association
Also: inferior MI, cardiac surgery, rheumatic fever
Management: treat underlying cause

Premature Ventricular Contractions (PVCs)

PVCs — When to Treat vs Observe

Premature wide-complex beats with compensatory pause
Bigeminy: every other beat is PVC. Trigeminy: every 3rd beat
Couplet: 2 PVCs in a row. Triplet/run: ≥3 = nonsustained VT
Common in healthy people — usually benign
Concerning features: high burden (>10–15%), reduced EF, symptoms (palpitations, presyncope)
High burden PVCs can cause PVC-induced cardiomyopathy (reversible with treatment)
Treatment: beta-blockers (first-line symptomatic), CCBs (alternative), catheter ablation (high-burden or CMP)
R-on-T phenomenon: PVC landing on T wave → VF trigger (especially in ischemia)

Rapid Review Bullets

PAC (premature atrial contraction): narrow complex, early, non-compensatory pause, abnormal P morphology. Usually benign. Frequent PACs can trigger AFib
Idioventricular rhythm: wide complex, 20–40 bpm — ventricular escape. Seen in post-reperfusion (accelerated idioventricular rhythm = AIVR, rate 60–100, benign reperfusion rhythm)
AIVR after thrombolytics or PCI: reperfusion arrhythmia — benign, no treatment needed
Holter monitor: 24-hour continuous EKG — use for infrequent palpitations, unexplained syncope, PVC burden assessment
Event monitor (loop recorder): 30-day external or implantable — for very infrequent symptoms

Orthostatic & Vasovagal Hypotension

Orthostatic Hypotension · Vasovagal Syncope · POTS · Tilt-Table Testing · Volume Depletion vs Autonomic Failure

Orthostatic Hypotension — Defined & Diagnosed

Definition: ↓ SBP ≥20 or ↓ DBP ≥10 within 3 minutes of standing

Symptoms: lightheadedness, blurred vision, presyncope/syncope on standing, "coat-hanger" neck/shoulder pain
Mechanism: inadequate vasoconstriction or venous return compensation on positional change
Measurement: BP lying → sitting → standing at 1 and 3 minutes

Hypovolemic (Most Common)

Dehydration, bleeding, diuretic overuse, adrenal insufficiency
Reflex tachycardia present (compensatory)
Treatment: fluids, address cause, reduce/stop diuretics

Autonomic Failure (Neurogenic)

Parkinson, MSA, DM autonomic neuropathy, amyloidosis
No reflex tachycardia (impaired autonomic response)
Treatment: fludrocortisone (mineralocorticoid), midodrine (α1 agonist), compression stockings

Drug-Induced (Board Favorite)

Alpha-blockers (tamsulosin, doxazosin)
Antihypertensives, nitrates, diuretics
Antidepressants (TCAs), antipsychotics
Especially dangerous in elderly — fall risk

Vasovagal Syncope (Neurocardiogenic)

Vasovagal — Most Common Type of Syncope Overall

Triggered by: prolonged standing, pain, emotional stress, heat, blood draws, Valsalva
Prodrome: nausea, diaphoresis, pallor, tunnel vision before syncope
Mechanism: Bezold-Jarisch reflex → paradoxical vagal activation → bradycardia + vasodilation
Recovery: rapid and complete in horizontal position (no post-ictal confusion)
Tilt-table testing: diagnostic when history unclear. Positive = hypotension + bradycardia reproduced
Treatment: reassurance + behavioral (avoid triggers, increase fluid/salt). Fludrocortisone, midodrine, or beta-blockers for recurrent cases

POTS — Postural Orthostatic Tachycardia Syndrome

POTS — Increasingly Tested Post-COVID

Definition: HR increase ≥30 bpm (or ≥120 bpm absolute) within 10 min of standing WITHOUT significant hypotension
Symptoms: palpitations, lightheadedness, brain fog, fatigue on standing — NOT syncope typically
Demographics: young women 15–50 years. Association with EDS, autoimmune conditions, post-viral (post-COVID)
Treatment: increased salt/fluid intake, compression garments, exercise therapy, beta-blockers (propranolol), ivabradine

Rapid Review Bullets

Orthostatic hypotension in elderly on multiple medications = medication reconciliation first step
Carotid sinus hypersensitivity: syncope with collar pressure (turning head, tight collar) → pause >3 sec on carotid massage → pacemaker
Situational syncope: cough, micturition, defecation — vagal mediated, benign in most
Exercise-induced syncope: ALWAYS cardiac workup (HCM, LQTS, anomalous coronary, ARVC) — not vasovagal

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.

Tier 1

Differential D-1

Acute Chest Pain — 8-Diagnosis Framework

ACS · Dissection · PE · Pericarditis · Tamponade · Pneumothorax · Boerhaave · GERD

★★★ PANCE PriorityMost-Tested Differential

The Pivotal Distinguishing Features

Diagnosis	Pain Quality	Key Distinguishing Feature	Must-Not-Miss Sign
STEMI / ACS	Pressure, squeezing, heaviness — jaw/left arm radiation	ST elevation in contiguous leads, dynamic troponin rise/fall, exertional onset or rest (NSTEMI)	Diabetics and women may have NO chest pain — jaw pain, dyspnea, nausea alone
Aortic Dissection	Tearing/ripping — maximum intensity at onset, radiates to interscapular back	BP differential between arms (>20 mmHg), widened mediastinum on CXR	Can mimic STEMI (RCA involvement) — NEVER give heparin/lytics before ruling out dissection
Pulmonary Embolism	Pleuritic (sharp, worse with breathing), sudden onset	Risk factors (Virchow's triad), hypoxia, sinus tachycardia on EKG, Wells score >4	Massive PE = hemodynamic instability — systemic fibrinolytics are life-saving, not optional
Acute Pericarditis	Pleuritic + positional — BETTER sitting forward, WORSE lying flat	Friction rub, diffuse saddle ST elevation + PR depression — ALL leads affected (not focal)	PR depression is the most specific EKG sign — don't miss it
Cardiac Tamponade	Dyspnea-dominant > chest pain; positional dyspnea	Beck's triad (JVD + hypotension + muffled sounds), electrical alternans, pulsus paradoxus >10 mmHg	Furosemide is absolutely contraindicated — removes critical preload. IV fluids + pericardiocentesis.
Tension Pneumothorax	Sudden pleuritic chest pain + dyspnea, post-trauma or procedural	Absent breath sounds, tracheal deviation AWAY from affected side, hypotension, JVD	Needle decompression FIRST — do NOT wait for CXR
Boerhaave Syndrome	Severe chest/epigastric pain after forceful vomiting	Subcutaneous emphysema, Hamman's crunch (mediastinal crepitus), CXR: pleural effusion, mediastinal air	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

Vasovagal · Arrhythmic · Structural · Orthostatic · Seizure Mimicker

★★★ PANCE PrioritySeizure vs Syncope Trap

Classification & Distinguishing Features

Type	Trigger/Setting	Key Feature	Workup
Vasovagal (Neurocardiogenic)	Prolonged standing, emotional stress, heat, pain, blood draw	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).	Orthostatic vitals, medication review, hydration status.
Situational	Micturition, defecation, cough, swallowing	Vagal-mediated variant. Reproduces consistently with specific trigger.	Clinical diagnosis if classic. No further workup if truly situational.
Seizure (Mimicker)	No positional trigger; any time	Tongue biting (lateral), prolonged postictal confusion, tonic-clonic activity, incontinence, head turn.	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.

★ Memory Trick

Syncope differential: "3 Cs — Cardiac (structural), Conduction (arrhythmia), Circulatory (vasovagal/orthostatic)" Exertional = Structural (HCM young, AS old). No prodrome = Arrhythmia. Seizure clues: "BITE (Bite tongue, Incontinence, Tonic-clonic, Epileptic postictal)"

Tier 1

Differential D-3

Acute Dyspnea — Cardiac vs Pulmonary vs Other

HF · PE · COPD · Pneumonia · Tamponade · Anemia · Metabolic

★★★ PANCE Priority

The BNP Pivot

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

AV Dissociation · Brugada Criteria · Concordance · Fusion Beats · WPW

★★★ 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.

Features That Confirm VT (Brugada Criteria)

AV dissociation — P waves marching independently of QRS. Pathognomonic for VT. Most specific sign.
Fusion beats — conducted P wave partially activates the ventricle simultaneously with the VT beat → hybrid complex. Pathognomonic.
Capture beats — a conducted P wave briefly "captures" the ventricle → narrow QRS in the middle of a wide complex tachycardia. Pathognomonic.
Concordance — all precordial QRS complexes (V1–V6) pointing the same direction (all positive or all negative). Strongly favors VT.
RS interval >100ms in any precordial lead → VT (time from R to nadir of S)
No RS complex in any precordial lead → VT

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.

Tier 2

Differential D-7

Lower Extremity Edema — Systemic vs Local

HF · Hepatic · Nephrotic · DVT · Lymphedema · Hypothyroid · Drug-Induced

★★ High Yield

Bilateral vs Unilateral — The First Branch Point

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

Distinguishing Systemic Bilateral Edema Causes

Cause	Key Feature	Confirming Test
Heart Failure	JVD, S3, orthopnea, crackles, elevated BNP	Echo (EF), BNP, CXR
Hepatic Cirrhosis	Ascites + peripheral edema, spider angiomata, jaundice, low albumin	LFTs, albumin, ultrasound, liver biopsy
Nephrotic Syndrome	Periorbital edema (hallmark), proteinuria >3.5g/day, hypoalbuminemia, hyperlipidemia	24-hr urine protein, lipid panel, renal biopsy
Hypothyroidism	Non-pitting myxedema (pretibial), cold intolerance, weight gain, bradycardia	TSH (elevated)
Drug-Induced	Amlodipine (CCB) most common — bilateral lower extremity pitting, no JVD, no orthopnea	Medication review; resolves with dose reduction
DVT (Unilateral)	Unilateral painful swollen warm leg, Homan's sign (unreliable)	Venous duplex ultrasound; Wells score + D-dimer
Lymphedema	Non-pitting, chronic, progressive, skin changes (skin thickening, fibrosis). Stemmer sign positive.	Clinical diagnosis; lymphoscintigraphy if unclear

⚑ Board Traps — Edema

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.
S3 = volume overload = HFrEF. S4 = stiff ventricle = HFpEF, LVH, diastolic dysfunction. S4 is always pathologic.
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.
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.
IVDA endocarditis: S. aureus (most common), tricuspid valve. Dental procedures: Streptococcus viridans, mitral/aortic valve.
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.
Beta-blockers contraindicated in: Acute decompensated HF (can initiate when stable), cocaine-induced chest pain (unopposed alpha → coronary spasm), vasospastic (Prinzmetal) angina (same mechanism).
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.

Fast Review

10 Rapid-Fire Clinical Pearls

1
Troponin ≠ ACS. Dynamic rise/fall + ischemic context = MI. Static elevation in CKD, HF, PE, myocarditis = chronic myocardial injury. Clinical context is everything.
2
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.
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."

— Rajiv Choudhary, MD, MPH

PA CardiologyBootcamp Syllabus

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PA Cardiology
Bootcamp Syllabus

You've seen the preview.
Unlock all 27 Cardiology topics.