Cardiac Physiology & Pathology

Stage 01 — Click-to-learn anatomy

Hover the heart — every region is clickable

A coronal cross-section of the heart with interactive hotspots on every major structure. Move your cursor over a chamber, wall, valve, or vessel and the right panel updates with normal physiology and the pathology patterns you need to recognize. Click to pin.

Interactive cardiac anatomy

Myocardium Venous (RA/RV) Arterial (LA/LV) Valve leaflet Coronary Conduction Pericardium

Hover any region → 📌 PINNED

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Hover any chamber, wall, valve, or vessel to see normal anatomy, common pathology patterns, and their ECG / imaging correlates.

Click to pin the detail panel until you pick another.

The 17-segment model — a quick reference

Regional wall motion abnormalities map to coronary territories. This is the language every echo/MRI report uses.

Segments	Territory	Supplied by	Typical pattern
1, 7, 13, 17 (anterior + apex)	LAD	Left anterior descending	Anterior/apical MI — classic Q waves V1–V4, anterior wall akinesia; largest territory.
2, 3, 8, 9, 14 (septum)	LAD (proximal)	Septal perforators of LAD	Septal MI; may block bundle of His → BBB/AV block.
5, 6, 11, 12, 16 (lateral)	LCx	Left circumflex	Lateral MI — often ECG-silent ("posterior" MI on V1–V2 as R wave).
4, 10, 15 (inferior)	RCA (dominant)	Right coronary	Inferior MI — bradycardia, AV block, RV involvement (V4R).

Stage 02 — Shape tells the story

Every cardiomyopathy has a signature shape

Pick any remodeling pattern below — normal, concentric/eccentric hypertrophy, apical HCM, ballooning, amyloid, dilated, restrictive — and the panel updates with the mechanism, who gets it, how it looks on imaging, and what the ECG shows.

Shape gallery — click or hover

Pick a pattern → 📌 PINNED

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Hover a shape above for its mechanism, imaging signature, and ECG correlate.

Stage 03 — Tracings that tell on the patient

An ECG gallery of the classic patterns

Every ECG below is hand-drawn in SVG — rhythm-strip accurate, not just a photo. Hover or click any card to see the diagnostic criteria, underlying mechanism, and what to do about it.

Interactive ECG gallery

Single-lead schematic — not to scale. Most patterns span multiple leads; criteria below describe the full 12-lead picture.

Hover a tracing → 📌 PINNED

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Hover any of the tracings above to see criteria, mechanism, and clinical significance.

How to read a 12-lead in 30 seconds

Rate → Rhythm → Axis → Intervals → Hypertrophy → Ischemia. Rate: 300/large boxes between QRS. Rhythm: is there a P before every QRS? Axis: leads I and aVF — both up = normal; I up, aVF down = LAD; I down, aVF up = RAD. Intervals: PR 120–200 ms, QRS <120 ms, QTc <440 (M)/460 (F). Hypertrophy: Sokolow-Lyon (S V1 + R V5/V6 ≥35 mm). Ischemia: any ST elevation/depression, T-wave inversion, Q waves.

Amyloid pearl: when the ECG shows low voltage but the echo shows thick walls, that discordance is the most specific clue for cardiac amyloidosis. Normal hypertensive LVH should have high voltage to match the thickness.

Stage 04 — The single best cardiac diagram

Pressure-volume loops — layer them up

Toggle any disease state on the right to overlay its PV loop on the normal. Filling slope (EDPVR) rises in HFpEF/amyloid/restriction. Contractility slope (ESPVR) falls in HFrEF. Stroke volume, afterload, and preload are all readable directly off the loop.

Overlay PV loops

Loop anatomy: the bottom line is diastolic filling along the EDPVR; right side is isovolumic contraction (volume fixed, pressure rises); top is ejection ending at the ESPVR; left side is isovolumic relaxation. Area inside = stroke work.

What each loop teaches

Loop	Signature shape	Clinical correlate
HFrEF	Shifted right (↑EDV), short and wide; ESPVR slope flattened	Dilated, weak ventricle. Stroke volume preserved partly by dilation. Target: ARNI/BB/MRA/SGLT2i to restore contractility + reverse remodeling.
HFpEF / restrictive	Steep EDPVR (tall bottom curve); loop narrow and tall-pressured	Stiff ventricle. Small volume change → big pressure jump. LAP rises → pulmonary congestion. Target: SGLT2i, diuresis, finerenone, treat HTN.
Aortic stenosis	Tall (very high peak pressure), normal-width	Pressure overload. Concentric hypertrophy. LV generates huge pressure to cross the valve. Target: TAVR/SAVR — medical therapy doesn't fix it.
Aortic regurgitation	Very wide (large EDV + low-ish afterload), rounded	Combined volume + pressure overload. Large stroke volume, low diastolic pressure (wide pulse pressure). Target: surgical AVR when LV dilates or symptoms appear.
Mitral regurgitation	Wide, no true IVC phase (ejects back into LA immediately)	Volume overload with reduced effective afterload. EF often overestimates true function. Target: repair > replace; transcatheter options (MitraClip) for functional MR.
HCM (obstructive)	Normal-looking but dynamic — gradient worsens with ↓preload/↑contractility	Dynamic LVOT obstruction. Treat with BB / non-DHP CCB / disopyramide / mavacamten. Avoid vasodilators + inotropes.

Stage 05 — One cardiac cycle, all channels

Wiggers diagram — pressure, volume, ECG, sounds

The single most important physiology diagram in medicine. Pressures in the aorta, LV, and LA plotted against time, stacked with LV volume, the ECG, and heart sounds. Hover a phase below to highlight it on all channels.

One cardiac cycle — all channels synchronized

Stage 06 — Preload meets output

Frank-Starling — all the variables that move the curve

Stroke volume rises with preload — but the curve's position depends on contractility, afterload, heart rate, and neurohormonal state. Toggle each variable below to see how therapies, disease states, and hemodynamic changes shift the operating point.

Interactive Frank-Starling family of curves

Toggle curves & variables

Corollaries to carry into rounds

Observation	Why
Giving IV fluids rarely helps decompensated HFrEF	The patient is on the flat part of the curve — more preload just raises LAP, not CO.
Diuresis often preserves output	Moving left on the flat portion drops filling pressure with minimal SV loss.
RV dysfunction is preload-dependent	RV lives on a steeper, less forgiving curve — too little preload = cardiogenic shock.
HFpEF = steep EDPVR, not a flat SV curve	The problem is that preload can't be raised without huge pressure jumps → pulmonary congestion before SV increases.
Afterload matters too	Classical Starling uses preload only — in real life, afterload (SVR) modifies SV for the same preload. Vasodilators shift the curve up in MR/AR.
Exercise shifts normal curve up	Sympathetic activation ↑ contractility + ↑ HR + venous return. Failing heart can't augment output → exercise intolerance.
Sepsis = warm shock	Vasodilation drops SVR → curve shifts down + right. Need fluids + vasopressors + possibly inotropes.

Stage 07 — Electricity at the cellular level

Action potentials — myocytes vs nodes, and how drugs change them

The ventricular myocyte AP has 5 phases driven by distinct ion channels. Nodal cells (SA/AV) have a different shape — no true phase 1, slower upstroke, and funny current (I_f) driving automaticity. Toggle drugs below to see exactly which phases they alter and why.

Ventricular myocyte action potential

Phases: 0 = rapid Na⁺ depolarization; 1 = transient K⁺ repolarization (notch); 2 = plateau (Ca²⁺ in, K⁺ out balanced); 3 = rapid repolarization (K⁺ out dominates); 4 = resting (Na⁺/K⁺ ATPase restores). Phase 2 is what makes the QT interval long — and why drugs that prolong it risk TdP.

SA / AV nodal action potential

Key differences from myocyte: Phase 4 is NOT flat — funny current (I_f) causes slow diastolic depolarization → automaticity. Phase 0 is Ca²⁺-dependent (L-type), not Na⁺ — hence the slower upstroke. No phase 1 notch. This is why nodal cells set the heart rate and why calcium channel blockers slow the heart.

Vaughan-Williams classification at a glance

Class	Mechanism	Drugs	AP effect	Clinical use
Ia	Na⁺ block (moderate)	Procainamide, quinidine, disopyramide	↓ Phase 0 slope, prolongs APD/QT	AF, VT; disopyramide for obstructive HCM
Ib	Na⁺ block (weak, fast off)	Lidocaine, mexiletine	↓ Phase 0 minimally, shortens APD	VT/VF (acute), ischemic VT; mexiletine to shorten QT in LQT3
Ic	Na⁺ block (strong, slow off)	Flecainide, propafenone	Markedly ↓ Phase 0 slope, widens QRS	AF/SVT in structurally normal hearts. AVOID in CAD/HF (CAST trial).
II	β-blocker	Metoprolol, carvedilol, atenolol, propranolol	↓ Phase 4 slope (nodal), ↓ Ca²⁺ current	Rate control, VT suppression, post-MI, HFrEF (mortality benefit)
III	K⁺ channel block	Amiodarone, sotalol, dofetilide, ibutilide	Prolongs Phase 3 → ↑ APD/ERP/QT	AF/VT; amiodarone safest in structural heart disease
IV	Ca²⁺ channel block (non-DHP)	Diltiazem, verapamil	↓ Phase 0 slope (nodal), ↓ Phase 2 plateau	Rate control in AF, AVNRT/AVRT. AVOID in HFrEF.
Other	I_f block	Ivabradine	↓ Phase 4 slope (SA node only)	HR reduction in HFrEF (SHIFT trial); inappropriate sinus tachy
Other	Adenosine receptor	Adenosine	Opens K_ACh → hyperpolarizes AV node	Acute SVT termination (6→12mg rapid IV push)
Other	Cardiac glycoside	Digoxin	Inhibits Na⁺/K⁺ ATPase → ↑ intracellular Ca²⁺; vagotonic on AV node	Rate control in AF + HFrEF; ↓ hospitalization (DIG trial, no mortality benefit)