Rhythmicity is the ability of a tissue to produce its own impulses regularly. It is also called autorhythmicity or self-excitation. Property of rhythmicity 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 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 sinoatrial node (SA node). It was Lewis Sir Thomas, who named SA node as pacemaker of heart in 1918.
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 to prove that SA node is the pacemaker in mammalian heart:
- Stimulation of SA node accelerates the heart rate.
- 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.
- Local cooling of SA node decreases the heart rate.
- Local warming of SA node increases the heart rate.
- 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 (see below).
Rhythmicity of Different Parts of Human Heart:
- SA Node : 70 to 80/minute
- AV Node : 40 to 60/minute
- Atrial Muscle : 40 to 60/minute
- Purkinje fibers : 35 to 40/minute
- Ventricular Muscle : 20 to 40/minute.
Pacemaker In Amphibian Heart:
Sinus venosus is the pacemaker in amphibian heart. It is experimentally proved by:
- Applying Stannius ligatures.
- When sinus venosus is warmed by warm Ringer Solution, heart rate increases.
- When sinus venosus is cooled by cold Ringer solution, heart rate decreases.
- 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. s 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:
- Sinus Venosus : 40 to 60/minute
- Auricular Muscle : 20 to 40/minute
- 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.
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.
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.
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. Unlike in other tissues, the depolarization in SA node is mainly due to the influx of calcium ions, rather than sodium ions.
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.