McKenna's Pharmacology for Nursing, 2e

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C H A P T E R 4 2 Introduction to the cardiovascular system

Conductivity Normally, the SA node sets the pace for the heart rate because it depolarises faster than any cell in the heart. However, the other cells in the heart are capable of generating an impulse if anything happens to the SA node, which is another protective feature of the heart. As mentioned earlier, the SA node is said to be the pace­ maker of the heart because it acts to stimulate the rest of the cells to depolarise at its rate. When the SA node sets the pace for the heart rate, the person is said to be in sinus rhythm. The specialised cells of the heart can conduct an impulse rapidly through the system so that the muscle cells of the heart are stimulated at approximately the same time. This property of cardiac cells is called con­ ductivity . The conduction velocity, or the speed at which the cells can pass on the impulse, is slowest in the AV node and fastest in the Purkinje fibres. A delay in conduction at the AV node, between the atria and the ventricles, accounts for the fact that the atria contract a fraction of a second before the ventricles contract. This allows extra time for the ven­ tricles to fill completely before they contract. The almost simultaneous spread of the impulse through the Purkinje fibres permits a simultaneous and powerful contraction of the ventricle muscles, making them an effective pump. After a cell membrane has conducted an action potential, there is a span of time, called the absolute refractory period, in which it is impossible to stimulate that area of membrane. The absolute refractory period is the minimal amount of time that must elapse between two stimuli applied at one site in the heart for each of these stimuli to cause an action potential. This time reflects the responsiveness of the heart cells to stimuli. Cardiac drugs may affect the refractory period of the cells to make the heart more or less responsive. Autonomic influences The heart can generate action potentials on its own and could function without connection to the rest of the body. However, the autonomic nervous system (see Chapter 29) can influence the heart rate and rhythm and the strength of contraction. The parasympathetic nerves—primarily the vagus or tenth cranial nerve—can slow the heart rate and decrease the speed of conduction through the AV node. This allows the heart to rest and conserve its strength. In addition, the parasympathetic influence on the SA node is the dominant influence most of the time, keeping the resting heart rate at 70 to 80 beats per minute. The sympathetic nervous system stimulates the heart to beat faster, speeds conduction through the AV node and causes the heart muscle to contract harder. This action is important during exercise or stress, when the body’s cells need to have more oxygen delivered.

• Phase 1 is the very short period when the sodium ion concentrations are equal inside and outside the cell. • Phase 2, or the plateau stage, occurs as the cell membrane becomes less permeable to sodium. Calcium slowly enters the cell and potassium begins to leave the cell. The cell membrane is trying to return to its resting state, a process called repolarisation. • Phase 3 is a period of rapid repolarisation as the gates are closed and potassium rapidly moves out of the cell. • Phase 4 occurs when the cell comes to rest as the sodium–potassium pump returns the membrane to its previous state, with sodium outside and potassium inside the cell. Spontaneous depolarisation begins again. Each area of the heart has an action potential that appears slightly different from the other action poten­ tials, reflecting the complexity of the cells in that particular area. Because of these differences in the action potential, each area of the heart has a slightly different rate or rhythm. The SA node generates an impulse about 90 to 100 times a minute, the AV node about 40 to 50 times a minute and the complex ventricular muscle cells only about 10 to 20 times a minute (Figure 42.3).

0 –20 +20 –40

phase 0

phase 3

phase 4

–60

A SA node action potential Membrane potential (mV) –80

phase

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1 phase 2

phase 0

phase 3

Stimulation Resting membrane potential

phase 4

RMP

Membrane potential (mV) –80 –100

B Ventricular muscle cell action potential

FIGURE 42.3  Action potentials recorded from a cell in the sinoatrial (SA) node (A) showing diastolic depolarisation in phase 4 and recorded from a ventricular muscle cell (B) . In phase 0, the cell is stimulated, sodium rushes into the cell, and the cell is depolarised. In phase 1, sodium levels equalise. In phase 2, the plateau phase, calcium enters the cell (the slow current), and potassium and sodium leave. In phase 3, the slow current stops, and sodium and potassium leave the cell. In phase 4, the resting membrane potential (RMP) returns and the pacemaker potential begins in the SA node cell.