Cardiac Cycle

Why the cardiac cycle matters

• 3 billion beats per lifetime. An average human heart beats about 100,000 times per day, 35 million times per year, and roughly 2.5–3 billion times across an 80-year lifespan — every cycle moving 70 mL of blood. The total volume pumped over a lifetime is around 175 million liters.
• Anchors all clinical cardiology. Blood pressure (120/80 mmHg) is literally the systolic and diastolic pressures. Heart sounds, ECG intervals (PR, QRS, QT), echocardiographic ejection fraction, stress tests, catheterization pressures — every cardiology measurement is a variant on tracking the cycle's mechanical or electrical events.
• Frank-Starling law explains exercise physiology. Greater venous return → greater end-diastolic volume → greater sarcomere stretch → stronger contraction → greater stroke volume. This is why endurance training increases stroke volume from ~70 mL to ~130 mL and resting heart rate from 70 to 50 bpm — the same cardiac output achieved with fewer, stronger beats.
• Diastole shortens disproportionately at high rates. Going from 75 to 180 bpm, total cycle drops from 0.8 to 0.33 s. Systole stays around 0.2 s but diastole compresses from 0.5 to 0.13 s, leaving little time for filling. This is why tachycardia eventually compromises output and why beta-blockers help failing hearts by slowing rate.
• Cardiac output reflects total energy demand. Resting CO is ~5 L/min (oxygen consumption ~250 mL/min). At maximal exercise an untrained adult reaches ~20 L/min; an elite endurance athlete can hit 35–40 L/min, supporting VO2 max of 80+ mL/kg/min. The cycle's ability to scale via both rate and stroke volume is what defines aerobic capacity.
• Valve disease is mechanical failure of the cycle. Aortic stenosis raises the systolic pressure ramp; mitral regurgitation lets blood backflow during systole; mitral stenosis impedes filling during diastole. Each shows up as a characteristic distortion of the pressure-volume loop or murmur on auscultation.
• The cycle is autonomous. An isolated, perfused mammalian heart will continue beating for hours without any external nerve input — the SA node sets the pace intrinsically at about 100 bpm; vagal tone normally damps this to ~70 bpm. Heart transplants illustrate this: the recipient's nerves are severed but the donor heart still beats.

Common misconceptions

• The heart pumps faster, not harder, during exercise. Both increase. Stroke volume rises from 70 to 130 mL during heavy exertion — a 1.5–2x effect — while heart rate rises 2–3x. The two factors multiply in cardiac output, so the heart works substantially harder per beat as well as more often.
• Atria do most of the filling work. Most ventricular filling is passive, driven by the pressure gradient during early diastole as the ventricle relaxes. Atrial contraction adds only the final ~20 mL ('atrial kick') of the ~70 mL end-diastolic volume — about 20–30 percent of filling at rest, and even less at high heart rates. This is why atrial fibrillation is well-tolerated by many patients despite losing the atrial kick.
• Blood pressure is just the pressure in the heart. The 120/80 cuff measurement is brachial artery pressure, not ventricular pressure. Peak left ventricular systolic pressure is also ~120 mmHg, but diastolic ventricular pressure drops to near zero between beats — the diastolic '80' refers to the residual arterial pressure, not the ventricle.
• Ejection fraction means ejected percentage of total blood volume. Ejection fraction = stroke volume / end-diastolic volume = ~70/120 = ~58 percent. That is the fraction of the ventricle's contents ejected per beat, not the fraction of body blood volume. Normal range is 50–70 percent; below 40 percent indicates systolic heart failure.
• The lub-dub is the heart muscle contracting. S1 and S2 are valve closure sounds, not muscle sounds. The heart muscle's contraction itself is essentially silent. The lub-dub depends on the snap of the AV and semilunar valves and the resulting blood deceleration.
• The right and left sides cycle independently. They cycle in synchrony but at different pressures. Right ventricle peaks at ~25 mmHg (low-pressure pulmonary circuit), left at ~120 mmHg (high-pressure systemic circuit). Both eject the same stroke volume per beat — otherwise blood would pool somewhere — and the synchronization is enforced by the same conduction system.

How the cardiac cycle works

Each cycle begins electrically. The sinoatrial (SA) node, a cluster of pacemaker cells in the right atrial wall, depolarizes spontaneously about 60–100 times per minute. The wave spreads through the atria, triggering atrial contraction (the P wave on the ECG), then reaches the atrioventricular (AV) node, which inserts a deliberate ~100 ms delay. The signal travels down the bundle of His, into the left and right bundle branches, and out through the Purkinje fibers, depolarizing the entire ventricular wall in roughly 80 ms (the QRS complex). Ventricular contraction begins immediately afterward.

Mechanically, the cycle proceeds in four phases. Filling (diastole, ~400 ms): mitral and tricuspid valves are open, ventricles fill passively from the atria, volume rises from end-systolic ~50 mL to end-diastolic ~120 mL; atrial systole adds the final ~20 mL kick. Isovolumetric contraction (~50 ms): ventricles contract with all four valves closed, pressure rises rapidly, volume fixed at ~120 mL; produces the S1 'lub'. Ejection (~250 ms): once ventricular pressure exceeds aortic (~80 mmHg) the aortic valve opens and stroke volume of ~70 mL is ejected; left ventricular pressure peaks at ~120 mmHg. Isovolumetric relaxation (~80 ms): aortic valve snaps shut at the dicrotic notch (S2 'dub'), all valves are again closed while the ventricle relaxes and pressure plummets. When pressure drops below atrial, the mitral valve reopens and filling begins again. The whole cycle takes about 0.8 s at 75 bpm and is summarized geometrically by the pressure-volume loop, whose enclosed area equals the mechanical work delivered per beat.

Systole vs diastole

Property	Systole	Diastole
Phase of cycle	Contraction, ejection	Relaxation, filling
Duration at 75 bpm	~0.3 s	~0.5 s
LV pressure	Rises to ~120 mmHg	Drops to near 0 mmHg
Aortic valve	Open during ejection	Closed
Mitral valve	Closed	Open during filling
Ventricular volume	Falls 120 → 50 mL	Rises 50 → 120 mL
Coronary perfusion	Mostly stops in LV (high wall pressure)	Most coronary flow occurs here
BP component	Systolic ~120 mmHg	Diastolic ~80 mmHg
ECG correlate	QRS through T wave	T-end through next P wave

Four phases of the pressure-volume loop

Phase	Valves	Volume	Pressure	Duration	Direction on PV loop
Filling	Mitral open, aortic closed	50 → 120 mL	Low (0–10 mmHg LV)	~400 ms	Bottom edge, left-to-right
Isovolumetric contraction	All four closed	120 mL (fixed)	10 → 80 mmHg LV	~50 ms	Right vertical, upward
Ejection	Aortic open	120 → 50 mL	80 → 120 → 80 mmHg	~250 ms	Top edge, right-to-left
Isovolumetric relaxation	All four closed	50 mL (fixed)	80 → ~10 mmHg	~80 ms	Left vertical, downward
Atrial kick	Mitral open	+20 mL final boost	Brief atrial pressure rise	~100 ms	Final tail of filling
Stroke volume	Ejected during ejection	~70 mL/beat	Bridges 80–120 mmHg ramp	—	Width of loop

Famous experiments and case studies

• William Harvey 1628 — De Motu Cordis. By tying off arteries and veins on live animals and quantifying how much blood the heart ejects per hour, Harvey proved blood circulates in a closed loop rather than being continuously made by the liver. The book is the foundation of modern physiology and was published in Frankfurt rather than England to avoid the medical establishment that had endorsed Galen's view for 1500 years.
• Marcello Malpighi 1661 — capillary discovery. Harvey could not directly observe the connection between arteries and veins. Marcello Malpighi, working at the University of Bologna with the new microscope, observed capillaries in frog lungs and mesentery — closing the circulation loop and confirming Harvey's hypothesis 33 years after publication.
• Otto Frank 1898, Ernest Starling 1914 — Frank-Starling law. Frank in Munich and Starling in London independently showed that within physiologic limits, the heart pumps whatever volume it receives — increased venous return stretches the ventricle, increasing contraction force and stroke volume. The basis for understanding how cardiac output adjusts to demand without conscious control.
• Werner Forssmann 1929 — first cardiac catheterization. Forssmann, a 25-year-old surgical resident in Eberswalde, Germany, threaded a urinary catheter from his own forearm vein into his right atrium and walked to the radiology department to take an X-ray confirming placement. He was fired but his work eventually led to modern cardiac catheterization. Nobel Prize 1956 (shared with Cournand and Richards).
• Heart transplantation, Christiaan Barnard 1967. The first successful human-to-human heart transplant in Cape Town. The recipient lived 18 days. Modern transplant survival exceeds 50 percent at 15 years. The transplanted heart retains its intrinsic cycle but lacks neural input — illustrating that the cycle's pacing is autonomous, governed by the SA node alone.