Introduction
The cardiac cycle is the sequence of mechanical and electrical events that occur during a single heartbeat, enabling the heart to efficiently pump blood throughout the systemic and pulmonary circulations. Each cycle ensures unidirectional blood flow, optimal ventricular filling, and effective stroke volume. Understanding the cardiac cycle is fundamental to cardiology, physiology, and clinical practice, as abnormalities can lead to arrhythmias, heart failure, and valvular disorders.
1. Phases of the Cardiac Cycle
The cardiac cycle consists of two main phases: diastole (relaxation) and systole (contraction), further subdivided into distinct stages.
1.1 Diastole
Diastole is the period during which the heart muscle relaxes and the chambers fill with blood. It can be divided into:
- Isovolumetric relaxation:
- Begins immediately after aortic and pulmonary valve closure (dicrotic notch in aortic pressure tracing).
- All valves are closed, so no volume change occurs.
- Ventricular pressure falls rapidly.
- Rapid ventricular filling:
- Mitral and tricuspid valves open as ventricular pressure drops below atrial pressure.
- Blood flows passively from atria to ventricles.
- Accounts for ~70–80% of ventricular filling at rest.
- Diastasis (slow filling phase):
- Pressure gradients between atria and ventricles decrease.
- Slow, passive filling continues.
- Atrial systole (atrial kick):
- Atria contract to push the remaining 20–30% of blood into ventricles.
- More pronounced during high heart rates or in diastolic dysfunction.
1.2 Systole
Systole is the phase of ventricular contraction and blood ejection.
- Isovolumetric contraction:
- Initiated by ventricular depolarization (QRS complex on ECG).
- All valves are closed; no blood ejection occurs.
- Ventricular pressure rises sharply to exceed arterial pressures.
- Ventricular ejection:
- Aortic and pulmonary valves open when ventricular pressure exceeds arterial pressure.
- Blood is ejected into the aorta and pulmonary artery.
- Divided into:
- Rapid ejection: high-velocity ejection early in systole.
- Reduced ejection: slower ejection toward end of systole.
2. Electrical Events and Conduction
The cardiac cycle is tightly coordinated by the electrical conduction system, ensuring synchronized atrial and ventricular contraction.
2.1 Sinoatrial (SA) Node
- Located at the junction of the superior vena cava and right atrium.
- Acts as the primary pacemaker, initiating depolarization.
- Spontaneous depolarization rate: 60–100 bpm.
2.2 Atrial Conduction
- Impulses spread via atrial myocardium through Bachmann’s bundle to the left atrium.
- Atrial contraction corresponds to the P wave on ECG.
2.3 Atrioventricular (AV) Node
- Delays impulse transmission (~0.1 s) to allow ventricular filling.
- Located in the inferior interatrial septum near the coronary sinus.
2.4 His-Purkinje System
- Bundle of His → Right and Left bundle branches → Purkinje fibers.
- Enables rapid, coordinated ventricular contraction (QRS complex).
3. Pressure Changes During the Cardiac Cycle
3.1 Atrial Pressure
- a wave: atrial contraction
- c wave: bulging of AV valves during isovolumetric contraction
- v wave: passive atrial filling during ventricular systole
3.2 Ventricular Pressure
- Rapid rise during isovolumetric contraction
- Peak pressure during ejection (~120 mmHg in LV; ~25 mmHg in RV)
- Fall during isovolumetric relaxation
3.3 Arterial Pressure
- Systolic pressure: peak during ventricular ejection
- Diastolic pressure: lowest during ventricular relaxation
- Dicrotic notch: closure of aortic valve
4. Volume Changes and Stroke Volume
- End-Diastolic Volume (EDV): volume in ventricles at end of diastole (~120 mL)
- End-Systolic Volume (ESV): volume after systole (~50 mL)
- Stroke Volume (SV) = EDV − ESV (~70 mL)
- Ejection Fraction (EF) = SV/EDV (~55–70%)
Clinical relevance: Low EF indicates systolic heart failure; high EF can occur in hypertrophic states.
5. Pressure-Volume Loops
Pressure-volume (PV) loops visually represent ventricular mechanics:
- Isovolumetric contraction: vertical rise in pressure at constant volume.
- Ventricular ejection: volume decreases; pressure rises then falls.
- Isovolumetric relaxation: pressure falls at constant volume.
- Ventricular filling: volume rises with minimal pressure change.
PV loops illustrate stroke work, preload, afterload, and contractility.
6. Heart Sounds and the Cardiac Cycle
- S1 (“lub”): closure of mitral and tricuspid valves at start of systole
- S2 (“dub”): closure of aortic and pulmonary valves at end of systole
- S3: rapid ventricular filling; may indicate heart failure in adults
- S4: atrial contraction against stiff ventricle (hypertrophy, ischemia)
Timing:
- S1: coincides with QRS
- S2: coincides with end of T wave
7. Cardiac Cycle Phases in Detail
| Phase | Events | Valves | Pressure Changes | Volume Changes |
|---|---|---|---|---|
| Atrial systole | Atria contract | AV valves open | Atrial pressure ↑ | Ventricular volume ↑ |
| Isovolumetric contraction | Ventricles contract | All valves closed | Ventricular pressure ↑ sharply | Volume constant |
| Rapid ejection | Ventricles continue contraction | Semilunar valves open | Ventricular pressure > arterial pressure | Volume decreases |
| Reduced ejection | Ventricular pressure declines | Semilunar valves open | Pressure ↓ | Volume ↓ slowly |
| Isovolumetric relaxation | Ventricles relax | All valves closed | Pressure ↓ | Volume constant |
| Rapid filling | AV valves open | Ventricular pressure < atrial pressure | Ventricular pressure low | Volume ↑ rapidly |
| Diastasis | Passive filling | AV valves open | Small pressure gradient | Volume ↑ slowly |
8. Factors Influencing the Cardiac Cycle
- Heart Rate (HR): Higher HR shortens diastole more than systole, affecting filling and stroke volume.
- Preload: Ventricular end-diastolic volume; influenced by venous return.
- Afterload: Pressure ventricles must overcome to eject blood.
- Contractility: Intrinsic myocardial strength; affected by sympathetic stimulation, inotropes.
- Compliance: Ventricular stiffness alters diastolic filling.
9. Coronary Blood Flow and Cardiac Cycle
- Coronary perfusion occurs mainly during diastole because systolic contraction compresses intramyocardial vessels.
- Right coronary artery perfusion is less impeded by systole than left coronary artery perfusion due to lower RV pressures.
10. Autonomic Regulation
- Sympathetic stimulation: increases HR, contractility, and conduction velocity → shorter diastole, higher cardiac output
- Parasympathetic stimulation: decreases HR, prolongs diastole → allows more filling
- Baroreceptor reflexes help maintain stable blood pressure during changes in cycle length
11. Pathophysiological Considerations
11.1 Heart Failure
- Systolic HF: reduced contractility → low stroke volume, elevated EDV
- Diastolic HF: stiff ventricle → impaired filling, elevated atrial pressures
11.2 Arrhythmias
- Atrial fibrillation → loss of atrial systole → decreased ventricular filling
- AV block → delayed ventricular contraction → altered cycle timing
11.3 Valvular Disease
- Mitral stenosis: impaired rapid filling → pressure gradient from LA to LV
- Aortic stenosis: prolonged isovolumetric contraction, increased afterload
- Regurgitant valves: abnormal backflow → altered pressure-volume relations
12. Clinical Measurement of Cardiac Cycle Events
- Electrocardiography (ECG): electrical events corresponding to phases
- Phonocardiography: heart sounds timing
- Cardiac catheterization: pressure tracings, volume measurements
- Echocardiography: real-time visualization of valve movement, filling, ejection fraction
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