The Cardiac Cycle.
The cardiac cycle
(Fig. 18a) describes the events that occur during one beat of the heart. These are shown in the
figure for the left side of the heart, together with the pressures and volumes
in the chambers and main vessels. At the start of the cycle, towards the end of
diastole, the whole of the heart is relaxed. The atrioventricular (AV)
valves are open (right, tricuspid; left, mitral), because the
atrial pressure is still slightly greater than the ventricular pressure. The pulmonary
and aortic valves are closed, as the pulmonary artery and aortic
pressures are greater than that in the ventricles. The cycle starts when the sinoatrial
node (SA node) initiates atrial systole (Chapter 19).
Atrial systole (A). At rest, atrial contraction only contributes
the last ∼15–20% of the final ventricular volume, as most of the filling has
already occurred due to venous pressure. The atrial contribution 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 atrial systole
causes a small pressure rise in the great veins (a wave). The
ventricular volume after filling is complete (end-diastolic volume, EDV)
is ∼120–140 mL in humans. The end-diastolic pressure (EDP) is less
than 10 mmHg, and is higher in the left ventricle than in the right due to the
thicker and therefore stiffer left ventricular wall. EDV strongly affects the
strength of ventricular contraction (see Starling’s law; Chapter 20).
Atrial depolarization causes the P wave of the electrocardiogram (ECG);
it should be noted that atrial repolarization is too diffuse to be seen
on the ECG.
Ventricular systole (B, C). The ventricular pressure
rises sharply during contraction, and the AV valves close as soon as this is
greater than the atrial pressure. This causes a vibration which is heard as the
first heart sound (S1). Ventricular depolarization is associated
with the QRS complex of the ECG. For a short period, while force is
developing, both the AV and outflow (semilunar) valves are closed and there is
no ejection, as the ventricular pressure is still less than that in the
pulmonary artery and aorta. This is called isovolumetric contraction (B),
as the ventricular volume does not change. The increasing pressure makes the AV
valves bulge into the atria, causing a small atrial pressure wave (c wave),
followed by a fall (x descent).
Ejection. Eventually, the ventricular pressure exceeds
that in the aorta or pulmonary artery, the outflow valves open and blood is
ejected. The flow is initially very rapid (rapid ejection phase, C)
but, as contraction wanes, ejection is reduced (reduced ejection phase, D).
During the second half of ejection, the ventricles stop actively contracting,
and the muscle starts to repolarize; this is associated with the T wave of
the ECG. The ventricular pressure during the reduced ejection phase is slightly
less than that in the artery, but initially blood continues to flow out of the
ventricle because of momentum. Eventually, the flow briefly reverses, causing
the closure of the outflow valve, a small increase in aortic pressure (dicrotic
notch) and the second heart sound (S2). The amount of blood
ejected in one beat is the stroke
volume, ∼70 mL.
About 50 mL of blood is therefore left in the ventricle at the end of systole (end-systolic volume, ESV).
The proportion of EDV that is ejected (stroke volume/EDV) is the ejection
fraction; this is normally ∼0.6, but
is reduced below 0.5 in heart failure.
Diastole. Immediately after the closure of the outflow
valves, the ventricles rapidly relax. The AV valves remain closed, however,
because the ventricular pressure is initially still greater than that in the
atria (isovolumetric relaxation, E). This is called isometric
relaxation because again the ventricular volume does not change. Meanwhile, the
atrial pressure has been increasing due to filling from the veins (v wave).
When the ventricular pressure falls sufficiently, the AV valves open and the atrial
pressure falls (y descent) as the ventricles rapidly refill (rapid filling
phase, F). This is assisted by elastic recoil of the ventricular
walls, essentially sucking blood into the ventricle. Filling during the last
two-thirds of diastole is slower and due to venous flow alone (reduced
filling phase, G). Diastole is twice the length of systole at rest,
but decreases as the heart rate increases.
Ventricular pressure–volume loop
The ventricular pressure plotted
against volume generates a loop (Fig. 18b), the area of which represents the
work performed. Its shape is affected by the force of ventricular contraction
(contractility), factors that alter refilling (EDV) and the pressure
against which the ventricle has to pump (e.g. aortic pressure, afterload).
An estimate of stroke work
is calculated from the mean
arterial pressure × stroke volume.
The pulse
The peripheral arterial pulse reflects
the pressure waves travelling down through the blood from the heart; these move
much faster than the blood itself. The shape of the pulse is affected by the
compliance (stretchiness) and diameter of the artery; stiff (e.g.
atherosclerosis) or small arteries have sharper pulses because they cannot
absorb the energy so easily. Secondary peaks are due to reflections of the
pressure wave at bifurcations of the artery. The jugular venous pulse reflects
the right atrial pressure, as there is no valve between the jugular vein and
right atria, and has corresponding a, c, and v waves.
Heart sounds
Heart sounds are caused by vibrations
in the blood due, for example, to closure of the cardiac valves (see above).
Normally, only the first and second heart sounds are detectable
(S1, S2), although a third sound (S3) can occasionally be heard in fit young
people. When the atrial pressure is raised (e.g. in heart failure), both a
third and fourth sound may be heard, associated with rapid filling and atrial
systole, respectively; this sounds like a galloping horse (gallop rhythm).
Cardiac murmurs are caused by turbulent blood, and a benign murmur is
sometimes heard in young people during the ejection phase. Pathological murmurs
are associated with the narrowing of valves (stenosis), or regurgitation
of blood backwards through valves that do not close properly (incompetence).
