describe the cardiac cycle, with reference to the relationship between blood pressure changes during systole and diastole and the opening and closing of valves

The Heart – Cardiac Cycle

Learning Objective

Describe the cardiac cycle, explaining how the changes in ventricular and arterial blood pressure during systole and diastole cause the atrioventricular (AV) and semilunar valves to open and close.

1. Anatomical Overview (AO1)

  • Layers of the heart wall – epicardium (outer), myocardium (contractile middle), endocardium (inner lining).

  • Pericardium – double‑walled sac (fibrous + serous) that protects and limits cardiac motion.

  • Chambers and septa – right atrium (RA) and left atrium (LA) separated from the right ventricle (RV) and left ventricle (LV) by the atrioventricular (tricuspid & mitral) valves; the two ventricles are divided by the interventricular septum.

  • Wall‑thickness differences – LV myocardium ≈ 10–12 mm (generates high systemic pressure); RV myocardium ≈ 3–4 mm; atrial walls ≈ 2 mm. The thicker LV wall explains why aortic systolic pressure (~120 mm Hg) is far greater than pulmonary‑artery systolic pressure (~25 mm Hg).

  • Major vessels & circulatory circuits

    • Pulmonary circuit: RA → RV → pulmonary artery → lungs → pulmonary veins → LA.

    • Systemic circuit: LA → LV → aorta → body tissues → venae cavae → RA.

    • The aorta and pulmonary artery are the great arteries; the pulmonary veins and vena cava are the great veins.

  • Coronary circulation – coronary arteries (right & left) arise from the aortic sinuses and supply the myocardium; cardiac veins drain into the coronary sinus and then the right atrium.

  • Valves – AV valves (tricuspid on the right, mitral on the left) sit between atria and ventricles; semilunar valves (pulmonary and aortic) sit between ventricles and their respective great arteries.

2. Electrical Control (AO2 – brief)

  • SA node (sino‑atrial) in the right atrial wall initiates each impulse – the natural pacemaker.

  • Impulse spread across both atria → atrial contraction (atrial systole).

  • AV node (atrioventricular) introduces a delay of ≈ 0.04 s, allowing the ventricles to finish filling.

  • His‑Purkinje system (bundle of His → right & left bundle branches → Purkinje fibres) conducts the impulse rapidly through the ventricular myocardium, producing coordinated ventricular contraction.

  • The electrical sequence directly triggers the mechanical phases: SA‑node → atrial systole, AV‑node delay → ventricular filling, His‑Purkinje → ventricular systole.

3. Mechanical Phases of the Cardiac Cycle (AO2)

The cycle is divided into six mechanical phases that correspond to characteristic pressure changes and valve motions.

Phase (systole/diastole)Ventricular pressure (mm Hg)Arterial pressure (mm Hg)AV‑valve stateSemilunar‑valve state
Left‑ventricle values are shown; right‑ventricle values are lower (≈ 1/5) but follow the same pattern.
Isovolumetric contraction5 → 80 → 120≈ 80 (aorta)Closed (ventricular > atrial pressure)Closed (ventricular < arterial pressure)
Rapid ejection120 → 100 mm Hg (falling)120 → 80 mm Hg (rising then falling)ClosedOpen (ventricular > arterial pressure)
Reduced ejection (twitch)100 → 80 mm Hg100 → 80 mm HgClosedOpen, then begins to close as pressures equalise
Isovolumetric relaxation80 → 5 mm Hg≈ 80 mm Hg (still high)Closed (ventricular > atrial pressure)Closed (ventricular < arterial pressure)
Rapid ventricular filling5 → 12 mm Hg≈ 80 mm Hg (unchanged)Open (atrial > ventricular pressure)Closed
Diastasis (slow filling)≈ 5–12 mm Hg (steady)≈ 80 mm HgOpenClosed

4. How Pressure Changes Control Valve Motion

  • A valve opens when the pressure behind it exceeds the pressure ahead of it.

  • A valve closes when the reverse pressure gradient develops.

  • Isovolumetric contraction: rising ventricular pressure > atrial pressure → AV valves close; ventricular pressure still < arterial pressure → semilunar valves remain closed.

  • Opening of semilunar valves: ventricular pressure exceeds arterial pressure → pulmonary and aortic valves snap open (produces the “dub” sound when they later close).

  • Isovolumetric relaxation: ventricular pressure falls below arterial pressure → semilunar valves close (“dub”).

  • Opening of AV valves: ventricular pressure falls below atrial pressure → tricuspid and mitral valves open, allowing rapid filling; their closure at the start of systole produces the “lub” sound.

5. Relationship to Blood‑Pressure Measurements

  • Systolic blood pressure (e.g., 120 mm Hg) corresponds to the peak of left‑ventricular pressure when the aortic valve is open.

  • Diastolic blood pressure (e.g., 80 mm Hg) corresponds to the arterial pressure when the ventricles are relaxed and the aortic valve is closed.

  • The arterial pressure curve mirrors the left‑ventricular pressure curve, with a slight delay due to arterial compliance.

6. Clinical Connections (AO2)

  • Mitral (or tricuspid) stenosis – delayed opening of an AV valve reduces rapid ventricular filling, lowering stroke volume and causing a pre‑systolic “opening snap”.

  • Aortic (or pulmonary) regurgitation – back‑flow during diastole raises diastolic arterial pressure and produces a bounding “water‑hammer” pulse.

  • Heart sounds – “lub” = closure of AV valves; “dub” = closure of semilunar valves. Extra sounds (S3, S4) indicate abnormal filling pressures.

Suggested diagram: Simultaneous pressure curves for the left ventricle and aorta plotted against time, with arrows indicating the exact moments each valve opens or closes.

Key Summary Points

  • The cardiac cycle consists of six mechanical phases that generate a repeating pattern of pressure changes.

  • Pressure gradients dictate the sequential opening and closing of the AV and semilunar valves.

  • Systolic pressure is measured when the semilunar valves are open; diastolic pressure when they are closed.

  • Differences in ventricular wall thickness explain the higher systemic (aortic) pressure compared with pulmonary pressure.

  • Any disturbance of normal pressure gradients (valve disease, hypertension) alters valve timing and can compromise cardiac output.