Electric Potentials

EXCITABILITY

DEFINITION

Excitability is defined as the ability of a living tissue to give response to a stimulus. In all the tissues, initial response to a stimulus is electrical activity in the form of action potential. It is followed by mechanical activity in the form of contraction, secretion, etc.

ELECTRICAL POTENTIALS

Resting Membrane Potential

Resting membrane potential in:

Single cardiac muscle fiber : – 85 to – 95 mV

Sinoatrial (SA) node : – 55 to – 60 mV

Purkinje fibers : – 90 to – 100 mV.

ELECTRICAL POTENTIALS Resting Membrane Potential

 

Action Potential

Action potential in cardiac muscle is different from that of other tissues such as skeletal muscle, smooth muscle and nervous tissue. Duration of the action potential in cardiac muscle is 250 to 350 msec (0.25 to 0.35 sec).

Phases of action potential

Action potential in a single cardiac muscle fiber occurs in four phases:

1. Initial depolarization

2. Initial repolarization

3. A plateau or final depolarization

4. Final repolarization.

1. Initial Depolarization

Initial depolarization is very rapid and it lasts for about 2 msec (0.002 sec). Amplitude of depolarization is about + 20 mV (Fig. 90.1).

2. Initial Repolarization

Immediately after depolarization, there is an initial rapid repolarization for a short period of about 2 msec. The end of rapid repolarization is represented by a notch.

3. Plateau or Final Depolarization

Afterwards, the muscle fiber remains in depolarized state for sometime before further repolarization. It forms the plateau (stable period) in action potential curve. The plateau lasts for about 200 msec in atrial muscle fibers and for about 300 msec in ventricular muscle fibers. Due to long plateau in action potential, the contraction time is also longer in cardiac muscle by 5 to 15 times than in skeletal muscle.

4. Final Repolarization

Final repolarization occurs after the plateau. It is a slow process and it lasts for about 50 to 80 msec before the re-establishment of resting membrane potential.

IONIC BASIS OF ACTION POTENTIAL

1. Initial Depolarization

Initial depolarization (first phase) is because of rapid opening of fast sodium channels and the rapid influx of sodium ions, as in the case of skeletal muscle fiber.

2. Initial Repolarization

Initial repolarization is due to the transient (short duration) opening of potassium channels and efflux

of a small quantity of potassium ions from the muscle fiber. Simultaneously, the fast sodium channels close suddenly and slow sodium channels open, resulting in slow influx of low quantity of sodium ions.

3. Plateau or Final Depolarization

Plateau is due to the slow opening of calcium channels. These channels are kept open for a longer period and cause influx of large number of calcium ions. Already the slow sodium channels are opened, through which slow influx of sodium ions continues. Because of the entry of calcium and sodium ions into the muscle fiber, positivity is maintained inside the muscle fiber, producing prolonged depolarization, i.e. plateau. Calcium ions entering the muscle fiber play an important role in the contractile process.

4. Final Repolarization

Final repolarization is due to efflux of potassium ions. Number of potassium ions moving out of the muscle fiber exceeds the number of calcium ions moving in. It makes negativity inside, resulting in final repolarization. Potassium efflux continues until the end of repolarization.

Restoration of Resting Membrane Potential

At the end of final repolarization, all sodium ions, which had entered the cell throughout the process of action potential move out of the cell and potassium ions move into the cell, by activation of sodium-potassium pump. Simultaneously, excess of calcium ions, which had entered the muscle fiber also move out through sodiumcalcium pump. Thus, the resting membrane potential is restored.

SPREAD OF ACTION POTENTIAL

THROUGH CARDIAC MUSCLE

Action potential spreads through cardiac muscle very rapidly because of the presence of gap junctions

between the cardiac muscle fibers. Gap junctions are permeable junctions and allow free movement of ions and so the action potential spreads rapidly from one muscle fiber to another fiber. Action potential is transmitted from atria to ventricles through the fibers of specialized conductive system, which is explained later in this chapter.

RHYTHMICITY

DEFINITION

Rhythmicity is the ability of a tissue to produce its own impulses regularly. It is also called autorhythmicity or self-excitation. Property of rhythmicity is present in all the tissues of heart. However, heart has a specialized excitatory structure, from which the discharge of impulses is rapid. This specialized structure is called pacemaker. From here, the impulses spread to other parts through the specialized conductive system.

PACEMAKER

Pacemaker is the structure of heart from which the impulses for heartbeat are produced. It is formed by the pacemaker cells called P cells. In mammalian heart, the pacemaker is sinoatrial node (SA node). It was Lewis Sir Thomas, who named SA node as pacemaker of heart, in 1918.

Sinoatrial Node

Sinoatrial (SA) node is a small strip of modified cardiac muscle, situated in the superior part of lateral wall of right atrium, just below the opening of superior vena cava. The fibers of this node do not have contractile elements. These fibers are continuous with fibers of atrial muscle, so that the impulses from the SA node spread rapidly through atria. Other parts of heart such as atrioventricular (AV) node, atria and ventricle also can produce the impulses and function as pacemakers. Still, SA node is called the

pacemaker because the rate of production of impulse (rhythmicity) is more in SA node than in other parts. It is about 70 to 80/minute.

Experimental Evidences

Experimental evidences to prove that SA node is the pacemaker in mammalian heart:

1. Stimulation of SA node accelerates the heart rate

2. Destruction of SA node causes immediate stoppage of the heartbeat. After sometime, atrioventricular node becomes the pacemaker and starts generating the impulses. So the heart starts beating, but the

rate is slow.

3. Local cooling of SA node decreases the heart rate

4. Local warming of SA node increases the heart rate

5. Electrical activity starts first in SA node.

Spread of Impulses from SA Node

Mammalian heart has got a specialized conductive system, by which the impulses from SA node spreads to other parts of the heart.

Rhythmicity of Different Parts of Human Heart

1. SA node : 70 to 80/minute

2. AV node : 40 to 60/minute

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