Pacemaker cells cardiac conduction system

General definitions relating to action potentials are given in Section 9. This section deals specifically with action potentials within the cardiac pacemaker cells and conducting system. 

The cardiac conduction system of the horse shares many features with other species but also has some important differences. The function of the heart relies upon the presence of cells capable of spontaneous activity these form the pacemaker areas of the heart. These nodal areas generate the normal cardiac rhythm. The electrical activity of the... 

As with the normal cardiac conducting system and its propagation of impulses through the His Purkinje network, electrostimulation by an artificial cardiac pacemaker depends on the depolarization of a single or a group of myocyte cell membranes which can then act as pacemaker cells. In order for these cells to depolarize, the electric field of the applied artificial pacemaker stimulus must exceed a threshold voltage. This initiates a complex cascade of ionic currents both in and out of the cell membrane referred to as the action potential. The impulse or wave of depolarization then propagates away from the site of stimulation from cell to cell across gap junctions or intercalated disks, which with normal cells provide very low resistance to depolarization. 

The sinoatrial (SA) node is innervated by both the sympathetic (beta and parasympathetic (vagus) nervous systems. Sympathetic activation increases the discharge rate of the SA pacemaker cells, and thereby increases heart rate (a positive chronotropic effect). Sympathetic nerves also innervate adrenergic receptors (betaj) on cardiac ventricular cells leading to an increase in stroke volume (a positive inotropic effect). Vagal activation, on the other hand, has the opposite effect and decreases heart rate and conduction velocity. In normal adults, cardiac vagal innervation is functionally predominant, so abolition of vagal activity results in a pronounced tachycardia (increased heart rate). 

In the myocardium, automaticity is the ability of the cardiac muscle to depolarize spontaneously (i.e., without external electrical stimulation from the autonomic nervous system). This spontaneous depolarization is due to the plasma membrane within the heart that has reduced permeability to potassium (K+) but still allows passive transfer of calcium ions, allowing a net charge to build. Automaticity is most often demonstrated in the sinoatrial (SA) node, the so-called pacemaker cells. Abnormalities in automaticity result in rhythm changes. The mechanism of automaticity involves the pacemaker channels of the HCN (Hyperpolarization-activated, Cyclic Nucleotide-gated) family14 (e.g., If, "funny" current). These poorly selective cation channels conduct more current as the membrane potential becomes more negative, or hyperpolarized. They conduct both potassium and sodium ions. The activity of these channels in the SA node cells causes the membrane potential to slowly become more positive (depolarized) until, eventually, calcium channels are activated and an action potential is initiated. 

The basic rhythm of heart rate is maintained by a part of the heart known as the pacemaker or sinoatrial (SA) node. This is a group of cardiac muscle cells in the right atrium that depolarize spontaneously. Depolarization of cardiac muscle cells brings about contraction. The pacemaker forms part of a conduction system that transmits electrical activity through the heart by means of action potentials so that contractions are coordinated and the heart can function as an efficient pump. The conduction pathway of electrical activity goes from the SA node to the atrioventricular (AV) node between atria and ventricles, then down the septum between the two ventricles to the apex of the heart and finally round the ventricles themselves. The conduction pathway in the heart is shown in Figure 4.2. 

In the SA node, each normal cardiac impulse is initiated by the spontaneous depolarization of the pacemaker cells (see Chapter 34). When a threshold is reached, an action potential is initiated and conducted through the atrial muscle fibers to the AV node and thence through the Purkinje system to the ventricular muscle. ACh slows the heart rate by decreasing the rate of spontaneous diastolic depolarization (the pacemaker current) and by increasing the repolarizing current at the SA node (a direct effect of fiy subunits of G/G, ) in sum, the membrane potential is more negative and attainment of the threshold potential and the succeeding events in the cardiac cycle are delayed. 

---