Initiation of the heartbeat

The heartbeat is controlled by the propagation of action potentials leading to coordinated contraction of the cardiac muscle (Figure 30.1). The heartbeat is initiated by the sinoatrial node (SAN), which is the pacemaker, as it has the highest intrinsic rate of depolarisation. The pacemaker is set by Na⁺ influx via the I_f current. This leads to an initial depolarization (from −60mV) which takes the membrane to threshold (−45mV) and leads to the opening of voltage-operated Ca²⁺ channels, resulting in slow depolarization as there is no involvement of fast Na⁺ channels. This is followed by repolarization as the Na⁺ current switches off and K⁺ channels open with K⁺ efflux. The spread of depolarization from the SAN leads to atrial contraction.

To drive the ventricles, depolarisation is conducted across the atrioventricular (AV) node and the time required for this to occur leads to a delay (the AV delay). The depolarisation then spreads down the Purkinje fibres of the bundle of His. The Purkinje fibres are specialised conducting fibres that convey the spread of excitation to the ventricular muscle. The excitation-contraction coupling starts in the septum and spreads from the apex to the base of the ventricles. The spread of depolarisation is then followed by a wave of repolarisation.

The action potential in ventricular cells is prolonged compared with that in atrial cells and this ensures sufficient time for Ca²⁺ influx to couple to forceful contraction. The initial depolarisation is driven via voltage-operated (‘fast’) Na⁺ channels and the plateau of depolarisation lasts typically 200 msec and is associated with Ca²⁺ influx via voltage-operated L-type Ca²⁺ channels, which leads to contraction of the ventricular mass. The spread of electrical activity between myocytes is mediated via gap junctions composed of connexins at the intercalated discs which join the cells.

The electrocardiogram (ECG)

The ECG is used to detect the electrical activity of the heart as conducted to the surface of the body via the body’s salt solutions. It indicates electrical activity and is not a measure of mechanical events. The recording electrodes can be placed on the limbs and/or on the chest. The ‘classical’ ECG is referred to as lead II (recorded by an inferior lead, Figure 30.2) and is divided into the following.

• P-waves: atrial depolarisation. These are relatively small, reflecting the small mass of the atria.
  
• P-R interval (sometimes referred to as P-Q) (120–200 msec): a period due to conduction delay across the atrioventricular node.
  
• QRS complex an initial dip reflects the septal depolarisation and this is then followed by the spread of depolarisation from the apex to the base.
  
• T wave: ventricular repolarisation.

The ST length corresponds with ejection and the T-P interval corresponds with cardiac filling.

A positive deflection on the ECG reflects a wave of depolarisation towards (or a wave of repolarisation away from) the positive electrode. By comparing the relative magnitudes of ventricular QRS waveforms from different leads (e.g. I, II, III), vectoral analysis determines the ‘cardiac axis’ of depolarisation. This can be shifted to the right (e.g. pulmonary hypertension) or to the left (e.g. systemic hypertension).

Clinically, the ECG identifies disorders of rate, conduction (e.g. heart block where AV conduction is either slowed or completely blocked), rhythm (e.g. atrial flutter and fibrillation) and ischaemic heart disease (where the ST segment is elevated in myocardial infarction or depressed in ischaemia associated with angina).