Physiology
Lec: 2 Cardiovascular System د. زيــد الاطرقجيThe specialized non contractile cardiac cells capable of auto rhythmicity form 1% of the heart muscle. They are as follow:
1. The sino-atrial node [SA-node] discharge 70-80 per minute.
2. atrio-ventricular node [AV-node] discharge 40-60 per minute.
3. The bundle of Hiss [atrio ventricular bundle]
4. Purkinje fibers.
Discharge rate of bundle of His and Purkinje fibers 20-40 per minute.
The heart cells with the faster rate of action potential initiation are localized in the S-A node. Once an action potential occurs in any cardiac muscle cell it is propagated throughout the rest of myocardium via gap junctions and the specialized system.
Therefore the S-A node which normally has the fastest rate of auto rhythmicity at 70-80 action potential per minute drives the rest of the heart at this rate and thus is known as the pace-maker of the heart. That is the entire heart becomes excited, triggering the contractile cells to contract and the heart to beat at the pace or the rate set by S-A node auto rhythmicity normally at 70-80 beats per minute.
The other auto rhythmic tissues cannot assume their own naturally slower rates because they are activated by action potentials originated in the S-A node before they can reach threshold at their own slower rhythm.
The spread of action potential is coordinated to ensure efficient pumping. Once initiated in the S-A node an action potential spreads throughout the rest of the heart.
For efficient cardiac function the spread of excitation should satisfy three criteria
1. Atrial excitation and contraction should be complete before the onset of ventricular contraction. The atria must become excited and contract before ventricular excitation and contraction. During a normal heart beat atrial contraction occurs about 160 msec before ventricular contraction.
Excitation of cardiac muscle fibers should be coordinated to ensure that each heart chamber contracts as a unite to pump efficiently. If the muscle fibers in a heart chamber become excited and contracted randomly rather than contracting simultaneously in a coordinated fashion they would be unable to eject blood .
A smooth uniform ventricular contraction is essential to squeeze out the blood.
Contraction of isolated cardiac muscle fibers is not successful in pumping blood .such random uncoordinated excitation and contraction of the cardiac cells is known as fibrillation.
The pair of atria and pair of ventricles should functionally coordinate so that both members of the pair contract simultaneously this coordination permits synchronized pumping of blood into the pulmonary and systemic circulation.
Atrial excitation
An action potential originating in the S-A node spread rapidly throughout both atria primarily from cell to cell via gap junction; in addition several poorly delineated specialized conduction pathways spreads up conduction of the impulse through the atria.
Inter-atrial pathway:
Extends from the S-A node within the right atrium to the left atrium. This pathway rapidly transmits the action potential from the S-A node to the pathways termination in the left atrium. A wave of excitation can spread across the gap junctions throughout the left atrium at the same time excitation is similarly spreading throughout the right atrium this ensure that atria become depolarized to contract simultaneously.
Inter- nodal pathway:
Extends from the S-A node to the A-V node. The A-V node is the only point of electrical contact between the atria and ventricles because atria are separated by non conductive fibrous tissue. The inter-nodal conduction pathway directs the spread of an action potential originating at the S-A node to the A-V node to ensure sequential contraction of the ventricles following atrial contraction. Hastened by this pathway the action potential arrives at the A-V node within 30 msec after the S-A node firing.
The action potential is conducted relatively slowly through the A-V node. This slowness is advantageous because it allows time for complete ventricular filing. The impulse is delayed about 100 mesc[the A-V nodal delay]which enables the atria to become completely depolarized and to contract emptying their contents into the ventricles before ventricular depolarization and contraction occur.
Ventricular excitation:
After the A-V nodal delay the impulse travels rapidly down the septum to the right and left branches of the bundle of Hiss and throughout the ventricular myocardium via the purkinje fibers. The network of fibers in this ventricular conduction system is specialized for rapid propagation of action potentials. Its presence hastens and coordinates the spread of ventricular excitation to ensure that the ventricles contract as a unit. The action potential is transmitted through the entire purkinje fiber system within 30 msec.
Although this system carries the action potential rapidly to a large number of cardiac muscle cells it does not terminate on every cell. The impulse quickly spreads from the excited cells to the rest of the ventricular muscle cells by means of gap junctions. Purkinje fibers can transmit an action potential six times faster than the ventricular syncytium of contractile cells could. If the entire ventricular depolarization process depends on cell to cell spread of the impulse via gap junctions the ventricular tissue immediately next to the A-V node would become excited and contract before the impulse have even passed to the heart apex this of course would not allow efficient pumping.
Rapid conduction of the action potential down the bundle of Hiss and its swift diffuse distribution throughout the purkinje network lead to almost simultaneous activation of the ventricular myocardial cells in both ventricular chambers which ensures a single, smooth, coordinated contraction that can efficiently eject blood into both the systemic and pulmonary circulation at the same time.
Action potential of contractile muscle cells:
Unlike the membrane of auto rhythmic cells the membrane of contractile cells remains essentially at rest at about -90 mV until excited by electrical activity propagated from the pace-maker of the heart.
Phases of action potential in myocardial contractile cell:
1. Rising phase of action potential up to +30mV as a result of activation of voltage gated Na+ channels and Na+ subsequently rapidly entering the myocardial cell.
2. plateau-phase is maintained by two voltage dependent permeability changes. These are the activation of slow L-type Ca+ channels and marked decrease in K+ permeability in the contractile cell membrane.
3. The rapid falling of the action potentials results from inactivation of the Ca+ channels and delayed activation of voltage gated K+-channels. So the return to its resting level as the K+ leaves the cell.
Effect of elevated K+ ion on the heart:
Normally there is substantially more K+ inside the cells than in the ECF. But with elevated ECF K+ levels this gradient is reduced. Associated with this change is a reduction in resting membrane potential [that is the membrane is less negative on the inside than normal because less K+ leaves]. Among the consequences is tendency to develop ectopic foci , prolongation in conduction , weak cardiac muscle as well as cardiac arrhythmias.
Effect of ECF Ca+ on the heart:
Elevated ECF calcium concentration augments the strength of cardiac contraction by prolonging the plateau phase of action potential and by increasing the cytosolic concentration of Ca+.
Contraction tends to be of longer duration with little time to rest between contractions.
Calcium channel blockers block Ca+ influx during an action potential reducing the force of cardiac contraction.
Effect of temperature on the heart
Increased temperature as occurs when one has fever, causes greatly increased heart rate, sometimes it reach as great as double the normal . Decreased temperature causes greatly decrease heart rate falling to as low as a few beats per minute when a person is near death from hypothermia. These effects result from the fact that heat cause increased permeability of the muscle membrane to the ions, resulting in acceleration of the self-excitation process.
Contractile strength of the heart is often enhanced temporarily by a moderate increase in temperature, but prolonged elevation of the temperature exhausts the metabolic system of the heart and cause weakness.