Figure 2.5 Transmembrane resting potential in a cardiac cell.
through the membrane. Since sodium ions cannot get inside the cell and the concentration of positively charged sodium ions is higher outside of the cell, a net negative electrical potential can be measured across the cell membrane.
The net negative charge inside the cell also causes potassium to concentrate inside the cell to counterbalance the transmembrane potential difference. However, the osmotic pressure caused by the high concentration of potassium prevents a total balancing of the electrical potential across the membrane.
Since some sodium continually leaks into the cell, maintaining steady state balance requires continual active transport. An active sodium-potassium pump in the cell membrane uses energy to pump sodium out of the cell and potassium into the cell.
Excitability is the ability of a cell to respond to an external excitation. When the cell becomes excited the membrane permeability changes allowing sodium to freely flow into the cell. In order to attempt to maintain equilibrium, potassium that is at a higher concentration inside the cell, flows to the outside. In Fig. 2.6 a cardiac muscle cell is shown depolarizing.
In order to obtain a regulated depolarization, it is crucial that the increases in sodium permeability and in potassium permeability are offset in time. The sodium permeability must increase at the beginning
of depolarization and the potassium channel then increases during repo-larization. It is also important that the potassium channels that open during an action potential are different from the leak channels that allow potassium to pass through the membrane at rest. In cardiac muscle, the action potential is carried mainly by calcium from the extracellular space rather than by sodium. This calcium is then used to trigger the release of intracellular calcium to initiate contraction.
The ability of a cell to respond to excitation depends on the elapsed time since the last contraction of that cell. The heart is refractory to stimulation until it has recovered from the previous stimulation. That is, if you apply stimulation below threshold, before the refractory period has passed, the cell will not give a response. In Fig. 2.7, the effective refractory period (ERP) for a myocardial cell is shown to be approximately 200 ms. After the relative refractory period (RRP) the cell is able to respond to stimulation if the stimulation is large enough. The time for the relative refractory period in the myocardium is approximately another 50 ms.
During a short period following the refractory period, a period of supernormality (SNP) occurs. During the period of supernormality, the cell's transmembrane potential is slightly higher than its resting potential.
The refractory period in heart muscle is much longer than in skeletal muscle, because repolarization is much slower. Ventricular muscle in dogs has a refractory period of 250 to 300 ms at normal heart rates. The refractory period for mammalian skeletal muscle is 2 to 4 ms and 0.05 ms for mammalian nerve fiber.
Automaticity is the ability of a certain class of cells to depolarize spontaneously without external stimulation. All cardiac cells in the conduction system have automaticity. The sinoatrial (SA) node is a small group of cardiac muscle fibers on the posterior wall of the right atrium and the muscle cells that make up the SA node have especially strong auto-maticity. Under normal circumstances, the cells of the SA node control heart rate. They form the pacemaking site of the heart. The atrioventricular node (AV) is located at the lower interatrial septum. The AV node provides a limiting effect on the maximum heart rate. The AV node can only transmit impulses up to about 200 beats per minute. If the atrial rate is higher, as in atrial tachycardia, then some beats will be transmitted to the ventricle and others will not. This condition is known as atrioventricular block.
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