Cardiovascular

Cardiac Cycle

Systole and diastole — valves, pressures, and heart sounds

The cardiac cycle is one heartbeat: roughly 0.8 seconds at rest. Diastole (filling, ~0.5 s) is followed by systole (ejection, ~0.3 s). Four valves enforce one-way flow: tricuspid and mitral (AV valves) close at start of systole producing S1; aortic and pulmonic (semilunar) close at start of diastole producing S2. Stroke volume is 60-100 mL; cardiac output ≈ 5 L/min at rest, 25 L/min in exercise. Ejection fraction (SV/EDV) is normally 55-70%.

  • Cycle duration at rest~0.8 sec (75 bpm)
  • Stroke volume60-100 mL
  • Cardiac output rest4-8 L/min
  • Ejection fraction55-70% normal
  • S1 soundAV valves closing (mitral, tricuspid)
  • S2 soundSemilunar valves closing (aortic, pulmonic)

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Why the cardiac cycle matters

  • Heart failure diagnosis. Echo measures EF, wall motion, valve function.
  • Murmur evaluation. Timing and quality identify the affected valve.
  • Hemodynamic monitoring. ICU pulmonary artery and arterial waveforms reflect cycle phases.
  • Drug effects. Beta-blockers slow HR, lengthen diastole, improve ischemia.
  • Pacemaker timing. AV delay programmed to optimize filling and output.
  • Exercise physiology. Stroke volume rises ~30% with training; HR rises with exertion.
  • Cardiogenic shock. Low CO + high filling pressures define mechanical pump failure.

Common misconceptions

  • "Lub-dub" is one beat — but two events. S1 marks systole start; S2 marks systole end.
  • Heart "rests" during diastole. Coronary perfusion and active relaxation happen — both energy-dependent.
  • Ejection fraction tells the whole story. Half of heart failure has preserved EF (HFpEF).
  • Atrial contribution is negligible. Loss of atrial kick in AFib drops CO ~20%, more in stiff hearts.
  • Higher HR always means more output. Above ~150 bpm, filling time is too short — CO falls.
  • Murmur means disease. Innocent flow murmurs are common in fever, pregnancy, athletes.

Frequently asked questions

What are the phases?

Atrial systole (P wave) tops off ventricles with ~20% of EDV. Isovolumic contraction (QRS): all valves closed; pressure rises rapidly. Ventricular ejection: aortic/pulmonic open when ventricular > arterial pressure. Isovolumic relaxation: all valves closed; pressure falls. Rapid filling: AV valves open when atrial > ventricular pressure. Diastasis: slow passive filling.

Why does systole shorten with tachycardia?

Both phases shorten, but diastole shortens disproportionately. At HR 60: diastole 0.6 s, systole 0.4 s. At HR 180: diastole 0.15 s, systole 0.18 s. Coronary perfusion happens in diastole — fast hearts get less coronary blood, worsening ischemia. Beta-blockers help angina partly by lengthening diastole.

What is Frank-Starling law?

Greater end-diastolic volume → greater stroke volume, up to a point. Mechanism: stretched sarcomeres develop more force (optimal sarcomere length ~2.2 μm). Allows beat-to-beat matching of right and left output. In heart failure, the curve flattens — ventricles fill but can't translate volume into output, leading to congestion.

What determines stroke volume?

Three factors. Preload (EDV/wall tension at end-diastole), increased by venous return. Afterload (resistance ventricle ejects against), increased by hypertension and aortic stenosis. Contractility (intrinsic strength), increased by sympathetic stimulation, calcium, digoxin; decreased by ischemia, beta-blockers, acidosis. SV = EDV − ESV.

What does ejection fraction tell you?

Fraction of EDV ejected. HFrEF: EF ≤40%, classic systolic failure (ischemic, dilated cardiomyopathy). HFpEF: EF ≥50% with symptoms — diastolic dysfunction from hypertension, aging, diabetes. HFmrEF: 41-49%. Treatments differ: HFrEF responds to GDMT (ARNI, beta-blocker, MRA, SGLT2i); HFpEF mainly SGLT2i and diuretics.

What causes heart murmurs?

Turbulent flow from valvular disease or shunts. Aortic stenosis: systolic ejection murmur, radiates to carotids, slow-rising pulse. Mitral regurgitation: holosystolic at apex, radiates to axilla. Aortic regurgitation: early diastolic, decrescendo, leaning forward. Mitral stenosis: opening snap then diastolic rumble. Echocardiography quantifies severity.

How does the ECG match the cycle?

P wave: atrial depolarization → atrial systole. PR interval: AV node delay (0.12-0.20 s). QRS: ventricular depolarization → systole begins. ST segment: ventricles depolarized, ejection ongoing. T wave: ventricular repolarization → relaxation. QT prolongation predisposes to torsades. The mechanical events lag electrical by ~50-100 ms.