The heart is a pump which together with the vascular system supplies the tissues with blood containing oxygen and nutrients, and removes waste products.
The flow of blood around the body is as follows:
- Deoxygenated blood from body tissues reaches the right atrium through the systemic veins (the superior and inferior venae cavae).
- Blood flows into the right ventricle, which then pumps the deoxygenated blood via the pulmonary artery to the lungs, where the blood becomes oxygenated before reaching the left atrium via the pulmonary vein.
- Blood flows from the left atrium into the left ventricle. From here it is pumped into the systemic circulation via the aorta, to supply the tissues of the body.
Cardiac rate and rhythm
The sinoatrial node (SAN) and the atrioventricular node (AVN) govern the rate and timing of the cardiac action
The SAN is located in the superior part of the right atrium near the entrance of the superior vena cava; the AVN is located at the base of the right atrium. The SAN discharges at a frequency of 80 impulses/min; it is the pacemaker for the heart and as such determines the heart rate. The action potential generated by the SAN spreads throughout both atria, reaching the AVN.
The AVN delays the action potential arising from the SAN to encourage the complete emptying of the atria before the ventricles contract.
The secondary action potential generated by the AVN descends into the interventricular septum via the
bundle of His. The bundle of His splits into left and right branches making contact with the Purkinje fibres, which conduct the impulse throughout the ventricles, causing them to contract.
Cardiac action potential
The shape of the action potential is characteristic of the location of its origin (i.e. whether from nodal tissue, the atria or the ventricles).
The resting membrane potential across the ventricular cell membrane is approximately 85 mV; this is because the resting membrane is more permeable to potassium than to other ions.
Four phases occurring at the ventricular cell membrane are:
- Phase 0 or depolarization: Occurs when the membrane potential reaches a critical value of 60 mV.
The upstroke of the action potential is due to the transient opening of voltage-gated sodium channels,
allowing sodium ions into the cell. In addition, potassium conductance falls to very low levels.
- Phase 1 (partial repolarization): Occurs as a result of the inactivation of the sodium current, and a transient outward potassium current.
- Phase 2 (plateau phase): The membrane remains depolarized at a plateau of approximately 0 mV. This is due to the activation of a voltage-dependent slow inward calcium current (conducting positive charge into the cell) and a delayed rectifier potassium current conducting positive charge out of the cell.
- Phase 3 (repolarization): Repolarization is due to the inactivation of the calcium current and an increase in potassium conductance.
The resting membrane potential of nodal cells is approximately 60 mV.
In nodal cells, there is no fast sodium current. Instead, the action potential is initiated by an inward calcium current, and, because calcium spikes conduct
slowly, there is a delay of approximately 0.1 s between atrial and ventricular contraction.
Nodal cells have a phase known as phase 4 (the pacemaker potential). This phase involves a gradual depolarization that occurs during diastole and is known as the f current (If0 funny). The f current
is activated by hyperpolarization at 45 mV, and consists of sodium and calcium ions entering the cell.
Autonomic control of the heart
Both the parasympathetic and sympathetic nervous systems influence the heart, though parasympathetic
This explains why the heart rate is lower than the inherent firing frequency of the sinoatrial node (SAN).
The sympathetic nervous system mediates its effects through the cardiac nerve, and activation of b1-adrenoceptors.
These are linked to adenylyl cyclase and their activation causes increased levels of cyclic adenosine monophosphate (cAMP), and a subsequent increase
in intracellular calcium levels.
The parasympathetic nervous system mediates its effects through the vagus nerve, and activation of M2
receptors. These are also linked to adenylyl cyclase, but their activation causes decreased levels of cAMP, and a
subsequent decrease in intracellular calcium levels.
The effects of the sympathetic and parasympathetic nervous systems on the heart are summarized
in Figure 2.5.
Myocardial contraction is the result of calcium entry through L-type channels, giving rise to an increase in cytosolic calcium in the myocytes (Fig. 2.6).
The calcium is derived from two sources:
- The sarcoplasmic reticulum within the cell
- The extracellular medium.
Extracellular calcium enters the cell, triggering larger amounts of calcium to be released from the sarcoplasmic reticulum, a process known as calcium-induced calcium release.
During contraction, the intracellular levels of calcium increase to levels 10 000 times greater than those at rest.
Calcium binds to troponin C, thereby modifying the position of actin and myosin filaments, and allowing the cell to contract.
Contraction ceases only once calcium has been removed from the cytoplasm. This occurs through two mechanisms:
- Calcium is pumped out of the cell via the electrogenic Na2+/Ca2+ exchanger, which pumps one calcium ion out for every three sodium ions in.
- Calcium is re-sequestered into sarcoplasmic reticulum stores by a Ca2+ ATPase pump.