Excitability Introduction.
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 in Cardiac Muscle.
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.
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 2msec (0.002 sec). Amplitude of depolarization is about + 20 mV .
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 sodium-calcium pump. Thus, the resting membrane potential is restored.
Action Potential Spreading 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.
Rhythmicity.
Rhythmicity is the ability of a tissue to produce its own impulses regularly. It is also called auto-rhythmicity 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. 18These 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.
Spread of Impulses from SA Node.
Mammalian heart has got a specialized conductive system, by which the14 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 .
3. Atrial muscle : 40 to 60/minute.
4. Purkinje fibers : 35 to 40/minute.
5. Ventricular muscle : 20 to 40/minute.
Pacemaker in Amphibian Heart.
Sinus venosus is the pacemaker in amphibian heart. It is experimentally proved by:
1. Applying Stannius ligatures.
2. When sinus venosus is warmed by warm Ringer solution, heart rate increases.
3. When sinus venosus is cooled by cold Ringer solution, heart rate decreases.
4. Electrical activity starts first in sinus venosus.
Stannius ligature experiment.
Stannius ligature experiment was demonstrated by German biologist Stannius in a pithed frog. Ligature means tying. Pithing is a process by which the brain and spinal cord are severed by using a needle, to abolish all the reflex activities during the experiment. Pithed frog is
technically dead but some of its organs such as heart, continue to function for some time. Chest wall of a pithed frog is opened and heart
is exposed. A bent pin is fixed at the tip of ventricle and attached to a recording device by means of a thread.
After recording the normal heartbeats (normal cardiogram or sinus rhythm), a ligature is applied between the sinus venosus and right auricle. It is called first Stannius ligature. When this ligature is applied, the heart stops beating immediately. It is because the impulses produced by sinus venosus cannot be conducted to the other chambers of the heart. However, the sinus contractions are continued. After sometime, auricular muscle becomes the pacemaker and starts producing the impulses for heartbeat, but at a slower rate.
Auricular contraction occurs first, followed by ventricular contraction. This rhythm of the heart is called auriculoventricular rhythm . When a second ligature is applied between auricles and ventricle, the heart stops beating again, because impulses from auricles cannot reach the ventricle. After few minutes, the ventricle produces its own impulses and starts beating but at a much slower rate. The slow independent ventricular rhythm is called idioventricular rhythm. Thus, all the three parts of the heart, sinus venosus, auricular musculature and ventricular musculature have the property of rhythmicity. However, sinus venosus is the pacemaker because it produces the impulses at a faster rate.
Spread of Impulses from Sinus Venosus.
Amphibian heart does not have any specialized conductive system. Pacemaker in amphibian heart is the sinus venosus and impulses from sinus venosus spreads through the muscles of auricles and ventricle.
Rhythmicity of Different Parts of Amphibian Heart.
1. Sinus venosus : 40 to 60/minute.
2. Auricular muscle : 20 to 40/minute.
3. Ventricular muscle : 15 to 20/minute.
Electrical Potential in SA Node.
Resting Membrane Potential – Pacemaker Potential.
Pacemaker potential is the unstable resting membrane potential in SA node. It is also called prepotential. Electrical potential in SA node is different from that of other cardiac muscle fibers. In SA node, each impulse triggers the next impulse. It is mainly due to the unstable
resting membrane potential. Resting membrane potential in SA node has a negativity of –55 to –60 mV. It is different from the negativity of –85 to –95 mV in other cardiac muscle fibers.
Action Potential.
Depolarization starts very slowly and the threshold level of –40 mV is reached very slowly. After the threshold level, rapid depolarization occurs up to +5 mV. It is followed by rapid repolarization. Once again, the resting membrane potential becomes unstable and reaches the
threshold level slowly .
Ionic Basis of Electrical Activity in Pacemaker.
Pacemaker potential or resting membrane potential.
Resting membrane potential is not stable in the SA node. To start with, the sodium ions leak into the pacemaker fibers and cause slow depolarization. This slow depolarization forms the initial part of pacemaker potential. Then, the calcium channels start opening.
At the beginning, there is a slow influx of calcium ions causing further depolarization in the same slower rate. It forms the later part of the pacemaker potential. Thus, the initial part of pacemaker potential is due to slow influx of sodium ions and the later part is due to the slow influx of calcium ions.
Depolarization.
When the negativity is decreased to –40 mV, which is the threshold level, the action potential starts with rapid depolarization. The depolarization occurs because of influx of more calcium ions. 1Unlike in other tissues, the depolarization in SA node is mainly due to the influx of calcium ions, rather than sodium ions.
Repolarization.
After rapid depolarization, repolarization starts. It is due to the efflux of potassium ions from pacemaker fibers. Potassium channels remain open for a longer time, causing efflux of more potassium ions.
It leads to the development of more negativity, beyond the level of resting membrane potential. It exists only for a short period. Then, the slow depolarization starts once again, leading to the development of pacemaker potential, which triggers the next action potential.
Conductivity.
Human heart has a specialized conductive system, through which impulses from SA node are transmitted to all other parts of the heart .
Conductive System in Human Heart.
Conductive system of the heart is formed by the modified cardiac muscle fibers. These fibers are the specialized cells, which conduct the impulses rapidly from SA node to the ventricles. Conductive tissues of the heart are also called the junctional tissues.
Components of Conductive System in Human Heart.
1. AV node.
2. Bundle of His.
3. Right and left bundle branches.
4. Purkinje fibers.
SA node is situated in right atrium, just below the opening of superior vena cava. 2AV node is situated in right posterior portion of intra-atrial septum. Impulses from SA node are conducted throughout right and left atria. Impulses also reach the AV node via some specialized fibers called internodal fibers.
There are three types of internodal fibers:
1. Anterior internodal fibers of Bachman.
2. Middle internodal fibers of Wenckebach.
3. Posterior internodal fibers of Thorel.
All these fibers from SA node converge on AV node and interdigitate with fibers of AV node. From AV node, the bundle of His arises. It divides into right and left branches, which run on either side of the interventricular septum. From each branch of bundle of His, many Purkinje fibers arise and spread all over the ventricular myocardium.
Velocity of Impulses at different parts of Conductive System.
1. Atrial muscle fibers : 0.3 meter/second.
2. Internodal fibers : 1.0 meter/second.
3. AV node : 0.05 meter/second.
4. Bundle of His : 0.12 meter/second.
5. Purkinje fibers : 4.0 meter/second.
6. Ventricular muscle fibers : 0.5 meter/second.
Thus, the velocity of impulses is maximum in Purkinje fibers and minimum at AV node.
Contractility of Cardiac Muscle.
Contractility is ability of the tissue to shorten in length (contraction) after receiving a stimulus. Various factors affect the contractile properties of the cardiac muscle.
All-or-None Law.
According to all-or-none law, when a stimulus is applied, whatever may be the strength, the whole cardiac muscle gives maximum response or it does not give any response at all. Below the threshold level, i.e. if the strength of stimulus is not adequate, the muscle doesnot give response. All-or-none law is demonstrated in the quiescent (quiet) heart of frog. Heart is made quiescent by applying the first Stannius ligature in between the sinus venosus and right auricle.
Ventricle is stimulated by placing the electrode at the base of ventricle. First, one stimulus is applied with a minimum strength of 1 volt at the base of ventricle and the contraction is recorded. 3Then, after 20 seconds, the strength of stimulus is increased to 2 volt and the stimulus is applied. The curve is recorded. The procedure is repeated by increasing the strength every time and applying the stimulus with an interval of 20 seconds . Amplitude of all contractions remains the same, irrespective of increasing the strength of stimulus. This shows that cardiac muscle obeys all-or-none law.
Cause for All-or-none law.
All-or-none law is applicable to whole cardiac muscle. It is because of syncytial arrangement of cardiac muscle. In the case of skeletal muscle, all-or-none law is applicable only to a single muscle fiber.
Staircase Phenomenon.
When the ventricle of a quiescent heart of frog is stimulated at a short interval of 2 seconds, without changing the strength, the force of contraction increases gradually for the first few contractions and then it remains same. Gradual increase in the force of contraction is called staircase phenomenon.
Cause for Staircase Phenomenon.
Staircase phenomenon occurs because of beneficial effect , which facilitates the force of successive contraction. So, there is a gradual increase in force of contraction .
Summation of Subliminal stimuli.
When a stimulus with a subliminal strength is applied, the quiescent heart does not show any response. When few stimuli with same subliminal strength are applied in succession, the heart shows response by contraction, due to the summation of stimuli.
Refractory Period.
Refractory period is the period in which the muscle doesnot show any response to a stimulus. It is of two types:
1. Absolute refractory period.
2. Relative refractory period.
Absolute Refractory Period.
Absolute refractory period is the period during which the muscle does not show any response at all, whatever may be the strength of the stimulus. It is because, the depolarization occurs during this period. So, a second depolarization is not possible.
Relative Refractory Period.
Relative refractory period is the period during which the muscle shows response if the strength of stimulus is increased to maximum. It is the stage at which the muscle is in repolarizing state.
Refractory Period in Skeletal Muscle.
In skeletal muscle, the refractory period is short. Absolute refractory period extends during the first half of latent period, measuring about 0.005 sec. Relative refractory period extends during the second half of latent period measuring 0.005 sec. So, the total refractory period is 0.01 sec.
Refractory Period in Cardiac Muscle.
Cardiac muscle has a long refractory period compared to skeletal muscle. Absolute refractory period extends throughout the contraction period of cardiac muscle and its duration is 0.27 sec. Relative refractory period extends during first half of relaxation period, which is about 0.26sec. So, the total refractory period is 0.53 sec.
Significance of Long Refractory Period in Cardiac Muscle.
Long refractory period in cardiac muscle has three advantages:
1. Summation of contractions does not occur.
2. Fatigue does not occur.
3. Tetanus does not occur.
Demonstration of Refractory Period in Heart.
Refractory period is demonstrated in the heart of a pithed frog. Refractory period can be recorded in beating heart as well as the quiescent heart.
Refractory period in beating heart.
First, normal cardiogram is recorded with the heart of a pithed frog. The impulses for heartbeat arise from the sinus venosus. An electrical (external) stimulus is applied by keeping the electrode at the base of the ventricle. When the stimulus is applied during systole, the heart does not show any response. It is because the absolute refractory period extends throughout systole.
When a stimulus is applied during diastole, the heart contracts because, diastole is the relative refractory period. This contraction of the heart is called extrasystole or premature contraction. extrasystole is followed by the stoppage of heart in diastole for a while. This diastole is longer than the diastole after regular contraction. Temporary stoppage of the heart before it starts contracting is called compensatory pause. Duration of extrasystole and compensatory pause is equivalent to the duration of two cardiac cycles.
Cause for compensatory pause.
A natural impulse from sinus venosus arrives at the time of contraction period of extrasystole. As this period is absolute refractory period, the natural impulse cannot cause contraction of heart. And the heart has to wait for the arrival of next natural impulse from sinus venosus. Till the arrival of next impulse, the heart stops in diastole.
Refractory period in quiescent heart.
Frog’s heart is made quiescent by applying the first Stannius ligature. Electrode is placed over the base of ventricle. When two stimuli are applied successively in such a way that the second stimulus falls during contraction period, the heart contracts only once. It is because of the first stimulus.
There is no response to second stimulus because systole is the absolute refractory period. However, when a second stimulus is applied during diastole, the heart contracts again and second contraction superimposes over the first one. This shows that the relative refractory period extends during diastole .
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