The cardiac cycle is the sequence of events that occurs during a heart beat (Figure 16a). The amount of blood ejected by the ventricle in this process is the stroke volume (SV), ∼70 mL, and cardiac output is the volume ejected per minute (SV × heart rate).
Towards the end of diastole (G) all chambers of the heart are relaxed. The valves between the atria and ventricles are open (AV valves: right, tricuspid; left, mitral), because atrial pressure remains slightly greater than ventricular pressure until the ventricles are fully distended. The pulmonary and aortic (semilunar) outflow valves are closed, as pulmonary artery and aortic pressure are greater than the respective ventricular pressures. The cycle begins when the sinoatrial node initiates the heart beat (see Chapter 11).
Atrial systole (A)
Contraction of the atria completes ventricular filling. At rest, the atria contribute less than 20% of ventricular volume, but this proportion increases with heart rate, as diastole shortens and there is less time for ventricular filling. There are no valves between the veins and atria, and some blood regurgitates into the veins. The a wave of atrial and venous pressure traces reflects atrial systole. Ventricular volume after filling is known as end-diastolic volume
(EDV), and is ∼120–140 mL. The equivalent pressure (end-diastolic pressure, EDP) is <10 mmHg, and is higher in the left ventricle than in the right due to the more muscular and therefore stiffer left ventricular wall. EDV is an important determinant of the strength of the subsequent contraction (Starling’s law; see Chapter 17). Atrial depolarization causes the P wave of the ECG.
Ventricular contraction causes a sharp rise in ventricular pressure, and the atrioventricular (AV) valves close once this exceeds atrial pressure. Closure of the AV valves causes the first heart sound (S1; see below). Ventricular depolarization is associated with the QRS complex of the ECG. During the initial phase of ventricular contraction pressure is less than that in the pulmonary artery and aorta, so the outflow valves remain closed. This is isovolumetric contraction (B), as ventricular volume does not change. The increasing pressure causes the AV valves to bulge into the atria, resulting in the small atrial pressure wave (c wave), followed by a fall (x descent). Note the jugular venous pulse reflects the right atrial pressure, and has corresponding a, c and v waves, and x and y descents.
The outflow valves open when pressure in the ventricle exceeds that in its respective artery. Note that pulmonary artery pressure (∼15 mmHg) is considerably less than that in the aorta (∼80 mmHg).
Flow into the arteries is initially very rapid (rapid ejection phase,C), but as contraction wanes ejection is reduced (reduced ejection phase, D). Rapid ejection can sometimes be heard as a murmur. Active contraction ceases during the second half of ejection, and the muscle repolarizes. This is associated with the T wave of the ECG. Ventricular pressure towards the end of the reduced ejection phase is slightly less than that in the artery, but blood continues to flow out of the ventricle because of momentum. Eventually the flow briefly reverses, causing closure of the outflow valve and a small increase in aortic pressure, the dicrotic notch. Closure of the semilunar valves is associated with the second heart sound (S2).
The ventricle ejects ∼70 mL of blood (SV), so if EDV is 120 mL, 50 mL is left in the ventricle at the end of systole (end-systolicvolume). The proportion of EDV that is ejected (stroke volume/ EDV) is the ejection fraction. During the last two-thirds of systole atrial pressure rises as a result of filling from the veins (v wave).
Diastole – relaxation and refilling
Following closure of the outflow valves the ventricles are rapidly relaxing. Ventricular pressure is still greater than atrial pressure, however, and the AV valves remain closed. This is isovolumetric relaxation (E). When ventricular pressure falls below atrial pressure, the AV valves open, and atrial pressure falls (y descent) as the ventricles refill (rapid ventricular refilling, F). This is assisted by elastic recoil of the ventricular walls, essentially sucking in the blood. A third heart sound (S3) may be heard. As the ventricles relax completely refilling slows (reduced refilling, G). This continues during the last two-thirds of diastole due to venous flow. At rest, diastole is twice the length of systole, but decreases proportionately during exercise and as heart rate increases.
The pressure–volume loop
Ventricular pressure plotted against volume generates a loop (Figure 16b). The shape of the loop is affected by contractility (see Chapters 12 and 17) and compliance (‘stretchiness’) of the ventricle, and factors that alter refilling or ejection (e.g. central venous pressure, afterload). The bottom dotted line shows the passive elastic properties of the ventricle (compliance). If compliance was decreased as a result of fibrotic damage following an infarct, the curve would be steeper. The area of the loop (Δ pressure × Δ volume) is a measure of work done during a beat, and is an indicator of cardiac function. A clinical estimate of stroke work is calculated from mean arterial pressure × stroke volume.
Heart sounds and murmurs
Heart sounds are caused by vibrations in the blood. S1 and S2 are each formed of two components (one for each valve). Normally, these may not be distinguishable, but they can ‘split’, so two dis- tinct sounds are heard. S1 is comprised of M1 and T1, due to closure of the mitral and tricuspid valves, respectively. Splitting of S1 is always pathological, and commonly due to conduction defects (see Chapter 13). S2 is comprised of A2, and P2, closure of aortic and pulmonary valves, respectively. A2 slightly precedes P2, and a split is often heard in healthy young people, especially during inspiration and exercise. A large split may relate to conduction defects or high outflow pressures. S3 is due to rapid ventricular filling, and is often heard in young healthy people and also when EDP is high (e.g. heart failure). S4 (not shown) is associated with atrial systole, and rarely heard unless EDP is high.
Murmurs are caused by turbulence. Valve stenosis (narrowing; see Chapter 52) increases blood velocity and thus turbulence. Stenosis of the AV valves causes a soft diastolic murmur during ventricular filling. Semilunar valve stenosis causes a loud systolic murmur during ejection. Valve leakage (regurgitation, incompetence) also causes murmurs. AV valve regurgitation causes a pansystolic murmur (throughout systole) as blood leaks back into the atria, whereas semilunar valve regurgitation causes early diastolic murmurs as arterial blood leaks back into the ventricle.