The cardiac cycle is the complete sequence of mechanical and electrical events that occur during one heartbeat. It encompasses the rhythmic contraction and relaxation of the heart's chambers, the opening and closing of cardiac valves, and the corresponding changes in blood pressure and flow that ensure efficient systemic and pulmonary circulation.
At a resting heart rate of 72 bpm, the cardiac cycle lasts approximately 0.8 seconds, with systole occupying 0.3s and diastole 0.5s. As heart rate increases, both phases shorten, but diastole shortens disproportionately, reducing coronary perfusion time.
Overview
The cardiac cycle can be described from three complementary perspectives: the electrophysiological events recorded by an electrocardiogram (ECG), the mechanical changes in chamber volumes and pressures, and the acoustic phenomena manifesting as heart sounds. These events are precisely coordinated to maintain unidirectional blood flow and optimal cardiac output.
Phases of the Cardiac Cycle
The cycle is traditionally divided into systole (contraction) and diastole (relaxation), with further subdivisions based on valve status and ventricular activity:
Atrial Systole (Late Diastole)
Atrial contraction contributes the final 20-30% of ventricular filling, known as the atrial kick. This phase corresponds to the P wave on the ECG and raises ventricular pressure by 3-5 mmHg, triggering the mitral and tricuspid valves to begin closing.
Isovolumetric Contraction
Ventricular depolarization (QRS complex) initiates myocardial contraction. All four valves are closed as ventricular pressure rises rapidly above atrial pressure but remains below arterial pressure. Volume remains constant while pressure increases from ~8 mmHg to ~120 mmHg in the left ventricle.
Ventricular Ejection
When ventricular pressure exceeds aortic pressure (~80 mmHg), the aortic and pulmonary valves open. Blood is ejected rapidly (rapid ejection phase), followed by a slower ejection phase as the pressure gradient decreases. This phase spans the ST segment and T wave.
Isovolumetric Relaxation
Ventricular repolarization triggers relaxation. All valves close again as ventricular pressure falls below arterial pressure. The aortic valve closure generates the S2 heart sound. Pressure drops from ~120 mmHg to ~8 mmHg with no volume change.
Ventricular Filling
When ventricular pressure falls below atrial pressure, the AV valves open, allowing passive filling (accounts for 70-80% of stroke volume). This phase begins with the S1 heart sound and continues until the next atrial systole.
| Phase | Duration (s) | LV Pressure (mmHg) | Valve Status | ECG Correlation |
|---|---|---|---|---|
| Atrial Systole | 0.1 | 8 → 10 | AV open, Semilunar closed | P wave |
| Isovolumetric Contraction | 0.05 | 10 → 120 | All closed | QRS complex |
| Rapid Ejection | 0.1 | 120 → 110 | AV closed, Semilunar open | ST segment |
| Reduced Ejection | 0.15 | 110 → 80 | AV closed, Semilunar open | T wave |
| Isovolumetric Relaxation | 0.08 | 80 → 8 | All closed | Post-T wave |
| Passive Filling | 0.25 | 8 → 6 | AV open, Semilunar closed | T-P segment |
Hemodynamics and Pressure Changes
Pressure gradients drive blood flow throughout the cycle. The left ventricle generates pressures up to 120 mmHg during peak systole to overcome systemic vascular resistance, while right ventricular pressure peaks at only 25 mmHg due to lower pulmonary resistance.
Heart Sounds
The mechanical events of the cardiac cycle produce characteristic sounds audible via stethoscope:
- S1 ("Lub"): Caused by mitral and tricuspid valve closure at the onset of ventricular systole. Frequency: 50-100 Hz.
- S2 ("Dub"): Caused by aortic and pulmonary valve closure at the onset of ventricular diastole. Frequency: 100-150 Hz. Physiologic splitting during inspiration is normal.
- S3: Low-frequency sound (20-40 Hz) during rapid ventricular filling. Normal in children and young adults; pathological in older patients (suggestive of heart failure).
- S4: Low-frequency sound associated with atrial contraction against a stiff ventricle. Always pathological, indicating decreased ventricular compliance.
Murmurs result from turbulent blood flow across stenotic or regurgitant valves. Systolic murmurs occur during ventricular ejection (e.g., aortic stenosis, mitral regurgitation), while diastolic murmurs indicate filling abnormalities (e.g., mitral stenosis, aortic regurgitation). Precise timing relative to S1 and S2 is critical for diagnosis.
Regulation and Variations
The cardiac cycle is modulated by autonomic nervous system input, hormonal factors, and intrinsic mechanisms:
- Heart Rate: Sympathetic stimulation increases rate and contractility; parasympathetic (vagal) activity decreases rate primarily at the SA node.
- Frank-Starling Mechanism: Increased venous return stretches ventricular fibers, enhancing contractile force and stroke volume without changing heart rate.
- Afterload: Increased systemic vascular resistance prolongs isovolumetric contraction and reduces ejection fraction.
Related Concepts
Understanding the cardiac cycle requires familiarity with myocardial electrophysiology, action potential physiology, hemodynamic principles, and cardiovascular anatomy. The cycle's efficiency depends on the precise coordination of conduction system timing, valve mechanics, and chamber compliance.
References
- [1] Hall, J.E. (2020). Guyton and Hall Textbook of Medical Physiology (14th ed.). Elsevier. ISBN 978-0-323-59712-8.
- [2] Braunwald, E. (2018). Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine (12th ed.). Saunders. ISBN 978-0-323-48679-9.
- [3] Boron, W.F., & Boulpaep, E.L. (2017). Medical Physiology (3rd ed.). Elsevier. ISBN 978-0-323-47887-4.
- [4] American Heart Association. (2023). "Cardiac Cycle and Hemodynamics." Circulation, 148(4), e1-e42.
- [5] Aevum Encyclopedia Editorial Board. (2025). "Validation of AI-Enhanced Cardiovascular Physiology Content." Aevum Journal of Knowledge Verification, 3(2), 45-62.