Memory tricks for cardiac physiology

Cardiac output (CO) is the volume of blood pumped per minute. Normal resting CO = ~5 L/min. HR normal = 60–100 bpm. SV normal = ~70 mL/beat. CO = 70 × 70 ≈ 5 L/min. During exercise CO can increase to 20–25 L/min in trained athletes. Three factors determine stroke volume: Preload (end-diastolic volume — filling), Afterload (resistance to ejection), Contractility (force of contraction). Ejection fraction (EF) = SV/EDV × 100%. Normal EF ≥ 55%. EF <40% = heart failure with reduced ejection fraction (HFrEF).

The Frank-Starling law states that the force of cardiac contraction increases as the end-diastolic volume (preload) increases — up to a physiological limit. More blood returning to the heart → ventricles fill more → sarcomeres stretch → more optimal overlap of actin and myosin → stronger contraction → more blood ejected. This is why the heart automatically adjusts its output to match venous return without needing neural input. Clinical relevance: in heart failure, the Frank-Starling curve is depressed — the heart cannot generate adequate force even at high filling volumes.

Phase 0: Rapid depolarization — voltage-gated Na+ channels open, Na+ rushes in (+30 mV). Phase 1: Brief repolarization — K+ channels (Ito) open briefly. Phase 2: Plateau (unique to cardiac muscle) — slow Ca2+ channels open, Ca2+ enters AND K+ exits — they balance → flat plateau. Ca2+ triggers Ca2+-induced Ca2+ release from SR → contraction. Phase 3: Repolarization — Ca2+ channels close, K+ channels stay open → repolarization. Phase 4: Resting potential (-90 mV). The long plateau = long refractory period → prevents tetany (cardiac muscle cannot be tetanized).

The SA node has no stable resting potential — it spontaneously depolarizes due to If ("funny") channels that allow Na+ to leak in during diastole. This slow depolarization (pacemaker potential) reaches threshold → Ca2+ channels open (not Na+ like in ventricles) → action potential → spreads through atria → AV node → bundle of His → Purkinje fibers. SA node fires at 60–100 bpm. AV node at 40–60 bpm (escape rhythm). Ventricles at 20–40 bpm. Higher centers always suppress lower ones — SA node dominates because it fires fastest.

Ventricular diastole (filling): mitral and tricuspid valves OPEN, aortic and pulmonary CLOSED. Passive filling (70%), then atrial systole (30% — the "atrial kick"). Isovolumetric contraction: ALL valves CLOSED — pressure builds with no volume change. Systole (ejection): aortic and pulmonary valves OPEN when ventricular pressure exceeds aortic — blood ejected. Isovolumetric relaxation: ALL valves CLOSED again — pressure falls. Heart sounds: S1 = mitral/tricuspid closing (start of systole). S2 = aortic/pulmonary closing (start of diastole).

Chronotropy = heart rate. Positive chronotropy: sympathetic (NE), epinephrine, thyroid hormone. Negative chronotropy: parasympathetic (ACh), beta-blockers, digoxin. Inotropy = force of contraction. Positive inotropy: sympathetic, Ca2+, digoxin. Negative inotropy: beta-blockers, heart failure, acidosis. Dromotropy = conduction velocity through AV node. Beta-blockers slow dromotropy (used for arrhythmias). Bainbridge reflex: increased venous return → stretch right atrium → increases HR reflexively — ensures heart pumps what it receives.

The PV loop plots LV pressure (y-axis) against LV volume (x-axis) through one cardiac cycle. Point A: mitral valve opens, filling begins. A→B: ventricular filling (diastole) — volume increases, pressure low. Point B: mitral valve closes (end-diastolic volume, ~130 mL). B→C: isovolumetric contraction — pressure rises, no volume change. Point C: aortic valve opens. C→D: ejection — volume decreases to ~60 mL (end-systolic volume). Width of loop = stroke volume. Area inside loop = work done by ventricle per beat.

Unlike every other organ, the heart muscle is perfused mainly during diastole — not systole. During systole, intramyocardial pressure compresses the coronary vessels (especially subendocardial). During diastole, myocardium relaxes → coronary vessels open → blood flows. This is critical: very fast heart rates (tachycardia) shorten diastole more than systole → less time for coronary filling → myocardial ischemia even with normal coronary arteries. Aortic diastolic pressure is the driving pressure for coronary perfusion. Low diastolic BP = poor coronary perfusion.

Venous return must equal cardiac output in the steady state. Sympathetic venoconstriction: reduces venous capacitance → increases venous pressure → more return. Pressure gradient: right atrial pressure ~0 mmHg creates gradient from venous system (8 mmHg). Abdominal/thoracic pump: inspiration lowers thoracic pressure → expands heart and great veins → sucks blood in. Skeletal muscle pump: leg muscles compress veins during walking → one-way valves prevent backflow → blood moves toward heart. Failure: prolonged standing → venous pooling → reduced venous return → syncope.

Preload = end-diastolic volume (EDV) — the stretch before contraction. Afterload = aortic pressure — the load the ventricle must overcome. High afterload (hypertension) → increased myocardial workload → hypertrophy.

Stretch-sensitive receptors in carotid sinus and aortic arch detect BP rise → inhibit sympathetic, activate parasympathetic → bradycardia + vasodilation → BP drops back to normal. Opposite response for hypotension.

EF = Stroke Volume ÷ End-Diastolic Volume × 100. Normal EF ≥ 55%. EF < 40% = heart failure with reduced EF (HFrEF). Key clinical marker for systolic function assessment via echocardiogram.

S1 = AV valve closure at START of systole (lub). S2 = semilunar valve closure at START of diastole (dub). S3 = ventricular filling sound (normal in kids, pathologic in adults = HF). S4 = atrial kick against stiff ventricle (hypertension, HCM).