Properties Of Cardiac Muscle Notes

Excitability Definition

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

Electrical Potentials In Cardiac Muscle: The basics of electrical potentials in the muscle.

Read And Learn More: Medical Physiology Notes

Resting Membrane Potential

The resting membrane potential in:

• Single cardiac muscle fiber: – 85 to – 95 mV
• SA node: -55 to-60mV
• Purkinje fiber:-90to-100mV

Action Potential

Action potential in a single cardiac muscle fiber occurs in 4 phases:

1. Initial depolarization
2. Initial repolarization
3. A plateau- final depolarization
4. Final repolarization.

The approximate duration of the action potential in cardiac muscle is 250-350 msec (0.25-0.35 sec)

1. Initial Depolarization: The depolarization is very rapid and it lasts for about 2 msec (first phase of depolarization). The amplitude of the 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 – Final Depolarization

• Afterward, the muscle fiber remains in the depolarized state for some time before further repolarization.
• It forms the plateau (stable period) in the action potential curve. The plateau lasts for about 200 msec (0.2 sec) in atrial muscle fibers and for about 300 msec (0.3 sec) in ventricular muscle fibers.
• Due to the long plateau in action potential, the contraction time is longer in cardiac muscle by about 5-15 times than in skeletal muscle.

4. Final Repolarization: Final repolarization occurs after the plateau. it is a slow process and it lasts for about 50-80 msec (0.05-0.08sec) before the re-establishment of resting potential.

Ionic Basis Of Action Potential

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

2. Initial Repolarization

• The initial repolarization just before the plateau 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 a slow influx of a low quantity of sodium ions.

3. Plateau – Final Depolarization

• During the plateau, the slow calcium channels open. These channels are kept open for a longer period and cause an influx of a large number of calcium ions.
• Already the slow sodium channels are opened through which the slow influx of sodium ions continues.
• The entry of both calcium and sodium ions into the muscle fiber makes the inside of the cell positive.
• Thus, the positivity is maintained inside the muscle fiber producing prolonged depolarization, i.e. plateau.
• The calcium ions entering the muscle fiber play an important role in the contractile process.

4. Final Repolarization

• Final repolarization starts at the end of the plateau. Now, the efflux of potassium ions increases.
• And, the 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. The efflux of potassium ions continues until the end of repolarization.

Restoration of Resting Membrane Potential

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

Spread Of Action Potential Through Cardiac Muscle

• The action potential spreads through the cardiac muscle or rapidly. It is because of the presence of gap junctions between the cardiac muscle fibers.
• The gap junctions are permeable junctions and allow free movement of ions.
• Due to this, the action potential spreads rapidly from one muscle fiber to another fiber.
• The action potential is transmitted from the atria to the ventricles through the fibers of the specialized conductive system.

Rhythmicity Definition

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

Pacemaker

• A pacemaker is defined as the part of the heart from which the impulses for the heartbeat are produced normally.
• It is formed by the pacemaker cells called P cells. In the mammalian heart, the pacemaker is the sinoatrial node (SA node).
• It was Lewis Sir Thomas who named the SA node the pacemaker of the heart in 1918.
• SA node is a small strip of modified cardiac muscle situated in the superior part of the lateral wall of the right atrium, just below the opening of the 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 the atria.

Even though the other parts of the heart like the AV node, atria, and ventricle can produce the impulses, the SA node is called the pacemaker because the rate of production of impulses (rhythmicity) is more in the SA node than in other parts.

Experimental pieces of evidence

The experimental evidence to prove that the SA node is the pacemaker in the mammalian heart:

1. Stimulation of the SA node accelerates the heart rate
2. Destruction of the SA node causes immediate stoppage of the heartbeat. After some time, the atrioventricular node becomes the pacemaker and starts generating the impulses. So the heart starts beating, but the ran is slow.
3. Local cooling of the SA node decreases the heart rate-
4. Local warming of the SA node increases the heart rate
5. The electrical activity starts first in the SA node.

Spread of Impulses from SA Node: The mammalian heart has got a specialized conductive system by which, the impulses from the SA node spreads to other parts of the heart.

Rhythmicity of Other Parts of the Heart: Though the SA node is the pacemaker in the mammalian heart, other parts of the heart also have the property of rhythmicity.

The rhythmicity of different parts:

1. SA node: 70-80/minute
2. AV node: 40-60/minute
3. Atrial muscle: 40-60/minute
4. Purkinje fibers: 35-40/minute
5. Ventricular muscle: 20-40/minute

Pacemaker in Amphibian Heart: The sinus venosus is the pacemaker in the amphibian heart.

It is experimentally proved by:

1. Applying Stannius ligatures
2. When sinus venosus is warmed by warm Ringer’s solution, the heart rate increases
3. When sinus venosus is cooled by cold Ringer’s solution, the heart rate decreases
4. While recording the electrical activity, it is observed that the electrical activity starts from the sinus venosus.

Stannius ligature experiment

• It is an experiment done in a pithed frog demonstrated by German biologist Stannius.
• 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.
• The pithed frog is technically dead. But some of its organs continue to function for some time.
• The chest wall of the pithed frog is opened and the heart is exposed. A bent pin is fixed at the tip of the 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 the right auricle. It is called the first Stannius ligature.
• When the ligature is applied, the heart stops beating immediately. It is because the impulses produced by smus venosus cannot be conducted to the other chambers of the heart.
• However, the sinus contractions are continued. After some time, the auricular muscle becomes the pacemaker and starts producing the Impulses for a heartbeat but at a slower rate.
• The auricles contract first and then it is followed by ventricular contraction. This rhythm of the heart is called auriculo- ventricular rhythm.
• When a second ligature is applied between the auricles and ventricle, the heart stops beating again, because the impulses from the auricles cannot reach the ventricle.
• After a 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 three parts of the heart – sinus venosus, auricular musculature, and ventricular musculature have the property of rhythmicity.
• However, the sinus venosus is the pacemaker because it produces the impulses at a faster rate.

Spread of Impulses from Sinus Venosus

• The amphibian heart does not have any specialized conductive system.
• The pacemaker in the amphibian heart is the sinus venosus and, impulses from the sinus venosus spread through the muscles of the auricles and ventricles.
• Rhythmicity of Different Parts of the Heart in Amphibians

The rhythmicity of different parts of the frog’s heart:

1. Sinus venous: 40-60/minute
2. Auricular muscle : 20-40/minute
3. Ventricular muscle: 15-20/minute

Resting Membrane Potential – Pacemaker Potential

Pacemaker potential is the unstable resting membrane potential in the SA node. It is also called prepotent.

• The electrical potential in the SA node is different from that of other cardiac muscle fibers.
• In the SA node, each impulse triggers the next impulse. It is mainly due to the unstable resting membrane potential.
• The resting membrane potential in the 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

• The 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

• The 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. In the beginning, there is a slow influx of calcium ions causing further depolarization at the same slower rate.

It forms the later part of the pacemaker potential.

• Thus, the initial part of pacemaker potential is due to the slow influx of sodium ions and the later part is due to the slow influx of calcium ions.
• When the negativity is decreased to – 40 mV, which is the threshold level, the action potential starts with rapid depolarization.
• Depolarization occurs because of the influx of more calcium ions.
• Unlike in other tissues, the depolarization in the SA node is mainly due to the influx of calcium ions rather than sodium ions.
• After the rapid depolarization, the repolarization starts. It is due to the efflux of potassium ions from the pacemaker fibers.
• The potassium channels remain open for a longer time, causing the 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: The human heart has a specialized conductive system through which the impulses from the SA node are transmitted to all other parts of the heart.

Conductive System In Human Heart

• The 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 the SA node to the ventricles.
• The conductive tissues of the heart are also called the junctional tissues.

The conductive system in the human heart comprises:

1. AV node
2. Bundle of His
3. Right and left bundle branches
4. Purkinje fibers.

SA node is situated in the right atrium just below the opening of the superior vena cava. The AV node is situated in the right posterior portion of the intra-atrial septum.

The impulses from the SA node are conducted throughout the right and left atria. The impulses also reach the AV node via some specialized fibers called intermodal filers.

There are three types of intermodal fibers:

1. Anterior internodal fibers of Bachman
2. Middle internodal fibers of Wenckebach
3. Posterior internodal fibers of Thorel.

• All these fibers from the SA node converge on the AV node and interdigitate with the fibers of the AV node.
• From the 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 the Bundle of His, many Purkinje fibers arise and spread all over the ventricular myocardium.

Velocity Of Impulses At Different Parts Of The 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: 0.5 meter/second

Ventricular muscle fibers Thus, the velocity of impulses is maximum in Purkinje fibers and minimum at the AV node.

Contractility

• Contractility is the ability of the tissue to shorten in length (contraction) after receiving a stimulus.
• Various factors affect the free contractile properties of the cardiac muscle.

The contract properties are:

1. Ac or none law
2. Staircase phenomenon
3. Summation of subliminal stimuli
4. Refractory period

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 the stimulus is not adequate, the muscle does not give a response.
• All or none law is demonstrated in the quiescent (quiet) heart of the frog. To make the heart quiescent, the first Stannius ligature is applied between the sinus venosus and the right auricle.
• Ventricle is stimulated by placing the electrode at the base of the ventricle.
• First, one stimulus is applied with a minimum strength of 1 volt at the base of a ventricle and the contraction is recorded.
• Then, after 20 seconds the strength of the stimulus is increased to 2 volts and the stimulus is applied.
• The curve is recorded. The procedure is repeated by increasing the strength every time and applying the stimulus at an interval of 20 seconds.
• The amplitude of all contractions remains the same irrespective of increasing the strength of the stimulus. It 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 the 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 a frog is stimulated at an interval of two seconds without changing the strength, the force increases gradually for the first few contractions, and then it remains the same.
• Gradual increase in the force of contraction is called the staircase phenomenon.

Cause for Staircase Phenomenon

The staircase phenomenon occurs because of the beneficial effect which facilitates the force of successive contraction. So, there is a gradual increase in the 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 a few stimuli with the same subliminal strength are applied in succession, the heart shows a response by contraction. It is due to the summation of the stimuli.

Refractory Period

The refractory period is the period in which the muscle does not show any response to a stimulus.

It is of two types:

1. Absolute refractory period
2. Relative refractory period.

1. Absolute Refractory Period

• The 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 lie-polarization is not possible.

Relative Refractory Period

• The relative refractory period is the period during which the muscle shows a response if the strength of the stimulus is increased to maximum.
• It is the stage at which the muscle is in the repolarizing state.

Refractory Period in Skeletal Muscle

In the case of skeletal muscle, the refractory period is short. The absolute refractory period extends during the first half of the latent period measuring about 0.005 sec and the relative refractory period during the second half of the latent period measuring 0.005 sec. So, the total refractory period is 0.01 sec.

Refractory Period in Cardiac Muscle

• Compared to skeletal muscle, the cardiac muscle has a long refractory period.
• The absolute refractory period extends throughout the contraction period of cardiac muscle.
• It is for 0.27 sec and the relative refractory period extends during the first half of the relaxation period which is about 0.26 sec. So, the total refractory period is 0.53.sec.

Significance of Long Refractory Period in Cardiac Muscle

The 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: The refractory period is demonstrated in the heart of a pithed frog. The refractory period can be recorded in the beating heart as well as the quiescent heart.

The refractory period in the beating heart

• First, a normal cardiogram is recorded with the heart of a pithed frog. The impulses for the heartbeat arise from the sinus venosus.
• An electrical 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 the systole.
• When a stimulus is applied during diastole, the heart contracts because the diastole is the relative refractory period.
• This contraction of the heart is called extrasystole or premature contraction.
• The extrasystole is followed by the stoppage of the heart in diastole for a while.
• This diastole is longer than the diastole after regular contraction. The temporary stoppage of the heart before it starts contracting is called a compensatory pause.
• The duration of the extrasystole and the compensatory pause is equivalent to the duration of two cardiac cycles.

Cause for compensatory pause

• A natural impulse from the sinus venosus arrives at the time of the contraction period of the extrasystole.
• As this period is an absolute refractory period, the natural impulse cannot cause contraction of the heart, and the heart has to wait for the arrival of the next natural impulse from sinus venosus.
• Till the arrival of the next impulse, the heart stops in diastole.

The refractory period in the quiescent heart

• The frog’s heart is made quiescent by applying the first Stannius ligature.
• The electrode is placed over the base of the ventricle. When two stimuli are applied successively in such a way that the second stimulus falls during the contraction period, the heart contracts only once.
• U is because of the first stimulus. There is no response to the second stimulus because the systole is the absolute refractory period.
• However, when a second stimulus is applied during diastole, the heart contracts again and the second contraction superimposes over the first one.
• It shows that the relative refractory period extends during diastole.