The Heart & Cardiac Cycle

The heart is best understood not as one pump but as two pumps arranged in series, sharing a common wall (the septum) and beating in synchrony. The right heart (right atrium + right ventricle) receives deoxygenated blood from the body and pumps it through the pulmonary circuit to the lungs at low pressure. The left heart (left atrium + left ventricle) receives oxygenated blood from the lungs and pumps it through the systemic circuit to the entire body at much higher pressure. Because the two ventricles are in series, in the steady state they must eject the same stroke volume per beat — otherwise blood would pool in one circuit. Each side has two valves. Atrioventricular (AV) valves — the tricuspid valve on the right, the mitral (bicuspid) valve on the left — sit between atrium and ventricle and prevent backflow into the atria during ventricular contraction. Semilunar valves — the pulmonary valve on the right, the aortic valve on the left — sit between ventricle and great artery and prevent backflow into the ventricles during relaxation. Crucially, none of these valves has its own muscle to open or shut it deliberately; each is a flap of tissue that opens when pressure upstream exceeds pressure downstream and slams shut when the gradient reverses. This single fact — valves are passive, pressure-gated check valves — explains essentially every heart sound, murmur, and pressure waveform you will ever interpret. The cardiac cycle is the repeating sequence of mechanical events — chamber pressure changes, volume changes, and valve opening/closing — that occurs during one heartbeat, divided into diastole (the ventricles relax and fill) and systole (the ventricles contract and eject). Understanding the cycle means tracking, moment to moment, which chamber has the highest pressure and therefore which valves are open, closed, or in the act of slamming shut. This framework connects directly to Cardiac Action Potential & Conduction (the electrical trigger for each contraction), Cardiac Output & Its Regulation (how stroke volume and heart rate combine to set flow), and Blood Pressure & Its Regulation (how ejected volume and arterial properties set systemic pressure).

Chamber and valve anatomy. Blood flows: systemic veins → right atrium → tricuspid valve → right ventricle → pulmonary valve → pulmonary artery → lungs → pulmonary veins → left atrium → mitral valve → left ventricle → aortic valve → aorta → systemic circulation. The left ventricle wall is roughly 2–3 times thicker than the right ventricle wall because it must generate systemic arterial pressures (~120/80 mmHg) versus pulmonary pressures (~25/8 mmHg) — a direct structure-function match to the resistance each pump faces. The AV valves are tethered by chordae tendineae to papillary muscles, which contract with the ventricular wall to prevent the valve leaflets from prolapsing backward into the atria under high ventricular pressure.

The seven phases of one cardiac cycle, tracked through the left heart (the right heart does the same thing at lower pressures, simultaneously): 1. Atrial systole. The atrium contracts, topping off the ventricle with the final ~20–30% of end-diastolic volume ("atrial kick"). Atrial pressure briefly exceeds ventricular pressure. AV valve open, semilunar valve closed. 2. Isovolumetric contraction. Ventricular systole begins (triggered by the QRS complex of the ECG). Ventricular pressure rises steeply. As soon as it exceeds atrial pressure, the AV valve snaps shut — producing heart sound S1. Because both valves are now closed, ventricular volume cannot change even though pressure is rising rapidly — hence "isovolumetric." 3. Ventricular ejection (rapid, then reduced). Once ventricular pressure exceeds aortic pressure (~80 mmHg), the aortic valve opens and blood is ejected. Ejection is fastest early (rapid ejection) then slows (reduced ejection) as ventricular pressure peaks (~120 mmHg) and begins to fall. 4. Isovolumetric relaxation. The ventricle begins diastole; pressure falls quickly. When ventricular pressure drops below aortic pressure, the aortic valve snaps shut — producing heart sound S2. Both valves closed again; volume constant while pressure plummets. 5. Rapid ventricular filling. Once ventricular pressure falls below atrial pressure, the AV valve opens and blood that has been accumulating in the atrium rushes into the ventricle. 6. Diastasis. Filling slows to a trickle as atrial and ventricular pressures nearly equalize; this is the longest but least dramatic phase, shortened markedly at high heart rates. 7. Return to atrial systole, closing the loop.

Key volumes. End-diastolic volume (EDV, ~120–130 mL) is the volume just before contraction begins; end-systolic volume (ESV, ~50–60 mL) is what remains after ejection. Stroke volume (SV = EDV − ESV) is therefore ~70 mL, and ejection fraction (EF = SV/EDV) is normally 55–70%. Note the ventricle never empties completely — a physiological reserve that matters enormously when contractility falls in heart failure.

Heart sounds and their mechanistic origin. S1 ("lub") is caused by the abrupt closure of the AV valves and the vibration of blood and ventricular walls when this happens, marking the start of isovolumetric contraction. S2 ("dub") is caused by the closure of the semilunar valves at the start of isovolumetric relaxation. A third sound (S3), sometimes normal in children and young adults but pathological in older adults, corresponds to turbulent rapid filling; a fourth sound (S4) corresponds to atrial contraction against a stiff ventricle. Murmurs are turbulence noises caused by valves that don't open fully (stenosis) or don't close fully (regurgitation/insufficiency) — their timing within the cycle (systolic vs. diastolic) pinpoints which valve is diseased.

The modern picture of the cardiac cycle was assembled from two complementary lines of evidence separated by decades: direct pressure measurement inside living hearts, and the graphical synthesis that turned those measurements into a teachable model.

Carl Wiggers and simultaneous multi-channel recording (1910s–1920s). Working at Western Reserve University, physiologist Carl J. Wiggers built instrumentation to record, simultaneously and in real time, aortic pressure, left ventricular pressure, left atrial pressure, ventricular volume, the ECG, and phonocardiogram (heart sound) tracings from experimental animals (primarily dogs), using pressure transducers connected via fluid-filled catheters and optical recording systems. Before this, physiologists had measured these variables in isolation, making it hard to establish exact temporal relationships — for instance, precisely when in the pressure cycle a valve closure sound occurred. Wiggers' innovation was temporal alignment: by recording all signals on the same moving photographic paper against a common time base, he could show, for the first time with rigor, that the first heart sound coincides exactly with the crossover of atrial and ventricular pressure (AV valve closure) and the second heart sound coincides with the crossover of ventricular and aortic pressure (semilunar valve closure). This composite chart — pressure curves for aorta, ventricle, and atrium, plotted against ventricular volume, the ECG, and phonocardiogram, all on one time axis — is now called the Wiggers diagram and remains the canonical figure used to teach the cardiac cycle in every physiology course.

Direct cardiac catheterization confirms the model in humans. Wiggers' data came from animal models with externally implanted transducers, leaving open the question of whether human hearts behaved identically. This was settled by Werner Forssmann, who in 1929 performed cardiac catheterization on himself — threading a urinary catheter through his own antecubital vein into his right atrium and confirming its position by X-ray — demonstrating that direct access to human heart chambers was possible without lethal consequence, a claim his supervisors had considered too dangerous to test. This opened the door for André Cournand and Dickinson Richards in the 1940s to refine catheterization into a quantitative diagnostic tool, directly measuring right heart and pulmonary artery pressures in human patients and validating that the pressure sequences Wiggers described in dogs held true in humans. Forssmann, Cournand, and Richards jointly received the Nobel Prize in Physiology or Medicine in 1956 for this work. Later refinements — most notably the balloon-tipped, flow-directed Swan-Ganz catheter developed by Jeremy Swan and William Ganz in 1970 — allowed pulmonary capillary wedge pressure (a proxy for left atrial pressure) to be measured at the bedside, extending Wiggers-diagram physiology directly into clinical cardiology and critical care. Together, these experiments established, with quantitative pressure-tracing evidence rather than inference, that (1) valve opening and closing are governed strictly by the sign of the pressure gradient across them, (2) heart sounds correspond precisely to specific valve closure events, and (3) the same qualitative pressure sequence holds across species including humans, differing mainly in absolute pressures and cycle duration.

Example 1 — Stroke volume and ejection fraction from echocardiographic volumes. A patient's echocardiogram reports an end-diastolic volume of 142 mL and an end-systolic volume of 58 mL. Heart rate is 68 beats/min. Step 1 — stroke volume: SV = EDV − ESV = 142 − 58 = 84 mL Step 2 — ejection fraction: EF = SV / EDV = 84 / 142 = 0.592 ≈ 59% This falls within the normal range (55–70%), so despite an EDV that is somewhat above the textbook average (~120–130 mL, perhaps reflecting a larger body size or elevated preload), the ventricle's pumping efficiency is normal — a useful distinction, since EDV alone doesn't diagnose dysfunction. Step 3 — cardiac output: CO = SV × HR = 84 mL × 68 /min = 5712 mL/min ≈ 5.7 L/min, within the normal resting range of 4–8 L/min, foreshadowing the calculations central to Cardiac Output & Its Regulation. If this patient's EF had instead been 30% (say, EDV 180 mL, ESV 126 mL, SV 54 mL), the diagnosis would shift toward systolic heart failure: the ventricle fills to a larger-than-normal volume (elevated preload, often from fluid retention) yet ejects a smaller fraction of it, because impaired contractility prevents ventricular pressure from rising fast or high enough to eject blood efficiently.

Example 2 — Aortic stenosis and its pressure-volume consequences. A patient has calcific aortic stenosis: the aortic valve leaflets are thickened and the valve orifice is narrowed from a normal ~3–4 cm² to 0.7 cm² (severe stenosis). Reasoning through the cycle: during isovolumetric contraction, left ventricular pressure must rise as usual until it exceeds aortic pressure to force the valve open — but because the orifice is narrow, ejecting the same stroke volume through it requires a much larger pressure gradient (analogous to needing higher pressure to push the same flow through a narrower pipe, following principles related to the Hagen–Poiseuille relationship, where resistance rises sharply as radius decreases). Consequently:

• Peak LV systolic pressure rises dramatically (commonly to 180–200+ mmHg) while aortic pressure downstream stays only modestly elevated or even low-normal — creating a large trans-valvular pressure gradient (often >40 mmHg at peak, versus a normal near-zero gradient across an open valve).
• The ejection phase becomes prolonged and turbulent, generating a harsh systolic murmur (crescendo-decrescendo, heard between S1 and S2, the exact timing predicted by the mechanism above) as blood jets through the narrow orifice.
• Chronic pressure overload causes the LV wall to thicken (concentric hypertrophy) as a compensatory response, increasing contractile force to overcome the fixed outflow obstruction — but this thickened wall also becomes stiffer, impairing diastolic filling and elevating end-diastolic pressure, which can back up into the pulmonary circuit and cause breathlessness.
• Ejection fraction can remain deceptively normal for years, because the hypertrophied muscle compensates — masking the severity of obstruction until the ventricle eventually decompensates.

This example shows how a single anatomical lesion (a narrowed valve orifice) predictably deranges every phase of the pressure-volume cycle discussed above, and why murmur timing is a direct clinical readout of the underlying mechanism.

Understanding the cardiac cycle underlies nearly all of modern cardiology and much of critical care medicine. Echocardiography measures EDV, ESV, ejection fraction, and valve gradients non-invasively, using exactly the pressure-volume logic described above to diagnose heart failure, valve stenosis, and regurgitation. Cardiac catheterization and coronary angiography, direct descendants of Forssmann's self-experiment, remain routine procedures for measuring intracardiac pressures and diagnosing valvular and coronary disease. Prosthetic and bioprosthetic heart valves, implanted in patients with severe stenosis or regurgitation, are engineered specifically to replicate passive, pressure-gated opening and closing behavior with minimal turbulence and no mechanical actuator. Auscultation — listening for S1, S2, murmurs, and gallops — remains a frontline, low-cost diagnostic skill taught to every medical student precisely because sound timing maps directly onto the mechanistic sequence of the cardiac cycle. Intra-aortic balloon pumps and ventricular assist devices, used in cardiogenic shock and as bridges to heart transplantation, are timed to inflate and deflate in coordination with the natural cardiac cycle to augment coronary perfusion during diastole and reduce afterload during systole. Finally, understanding how heart rate compresses diastole disproportionately explains why very rapid arrhythmias (e.g., supraventricular tachycardia) can cause inadequate ventricular filling and a collapse in cardiac output even when the heart muscle itself is structurally normal — a direct clinical consequence of the timing principles established by Wiggers nearly a century ago.

Ask the tutor: Can you walk me through how the pressure-volume loop changes shape in mitral regurgitation compared to a normal heart?