Cardiac activation

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Chapter 2 Cardiac activation


As a foundation from which to explore the responses of the circulation to exercise and environment, it is worthwhile to review the characteristics that the heart requires in order to fulfil its role as a pump. At least most of the material covered in this first section is probably familiar to you from earlier courses, but it may be helpful to have it set out again. As you read through the first section of this chapter, use the simulated records in Figure 2.1 to remind yourself of the sequences of electrical and mechanical events that make up the cardiac cycle.

Rhythmic excitation

For a muscular pump to provide continuous blood flow through the circulation there must be a system that guarantees generation of muscle action potentials at regular intervals. The normal rhythm generator or pacemaker is a small group of cells that lies high in the wall of the right atrium, constituting the so-called sinoatrial node. The membranes of these cells have an unusually high sodium conductance and contain metabolic pumps that progressively reduce potassium conductance. These two properties together result in the membrane potential depolarizing gradually towards zero in what is termed the pacemaker potential, rather than them having a stable resting membrane potential of around −70 mV as is characteristic of the normal cardiac muscle cells. Since the threshold membrane potential for action potential initiation is around −40 mV, the pacemaker cells fire an action potential as soon as they depolarize to this threshold. As in any excitable cell, the action potential activates a delayed potassium efflux and this repolarizes the cells to around −70 mV but, once these voltage-gated potassium channels close, the membrane starts to depolarize once more and initiates another action potential.

The period between successive action potentials in a sinoatrial node cell at 37° C (98.5° F) is around 600 ms, giving an inherent frequency of cardiac excitation of about 100 beats/min. In the intact body, however, the slope of the pacemaker potential is subject to tonic influences by thoracic sympathetic nerves that increase the slope and speed up heart rate (tachycardia) and vagal parasympathetic nerves that reduce the slope and slow the heart down (bradycardia). In a resting subject, both of these neural inputs are continuously active but the bradycardic effect of the parasympathetic input predominates, so that resting heart rate is normally less than 100 beats/min and typically around 65–75 beats/min.

Guaranteed time for filling

After ventricular contraction finishes and the heart relaxes, there must be time for the ventricles to relax completely so that they can refill. Thus, a safety mechanism must exist to guard against another action potential causing re-excitation while some muscle cells are still contracted. To achieve this the voltage-gated calcium channels in the endocardial muscle cells nearest to the conducting system have longer cycle times than those in the more superficial muscle layers, with correspondingly longer plateau phases and refractory periods. Thus, the cells that are coupled to the Purkinje system will remain electrically non-excitable until the rest of the ventricular muscle has repolarized and relaxed. The difference in channel cycle time between endocardium and epicardium is due at least partly to the higher pressure that is exerted on membranes of the endocardial cells when the heart wall contracts.

An additional safety factor is that the action potential plateau of the Purkinje fibres themselves is significantly longer than that of any ventricular myocardial cell, so that a second impulse is unlikely even to reach the ventricular myocardium until this has relaxed entirely.

Existence of a finite relaxation period is a prerequisite for nutritional perfusion of the ventricular myocardium. The coronary arteries that supply the heart arise from the aorta and so the pressure gradient responsible for coronary blood flow is essentially identical to that generated by the left ventricle. Because ventricular ejection must involve at least equivalent pressure being developed within the left ventricular wall, the left coronary arteries are mechanically occluded during the ejection phase of the cardiac cycle (termed systole) and nutritional perfusion can occur only during the relaxation phase (termed diastole). As will be discussed in Chapter 8 (p. 95), coronary perfusion of the right ventricle is more continuous, since the ventricular pressure developed there is much lower than systemic arterial pressure, and so the vasculature is perfused during systole as well as diastole.

Coordination of right and left outputs

Since the systemic and pulmonary circulations are in series, they must each pump identical volumes of blood per unit time. It is, therefore, essential that both ventricles eject blood simultaneously. This coordinated timing is ensured by the fact that the Purkinje system conveys action potentials simultaneously to the apices of both ventricles. Even with exact timing, however, the left ventricle needs to generate a far greater ejection pressure than the right ventricle in order to eject the same volume of blood, because the systemic vasculature has a much higher resistance than does the pulmonary vasculature. To provide the extra degree of pressurization, the left ventricle is wrapped with an additional spiral layer of muscle.

Increased venous return, for example in response to lying down, will produce a corresponding rise in end-diastolic ventricular volume. If the volume of blood ejected with each systolic contraction (the stroke volume) remained constant, there would be progressive pooling of blood in the heart and a progressive fall in cardiac output, so it is important that stroke volume can be matched automatically to ventricular filling. This is achieved by the resting length of all ventricular muscle fibres being substantially below the length that would correspond to optimal actin/myosin crossbridging and development of maximal active shortening. With increased filling, the increased resting sarcomere length that results from passive stretch of the ventricular wall will therefore result in increased active tension. This phenomenon is known as the Frank-Starling relationship.