In this article we will discuss about:- 1. Meaning of the Cardiac Muscle 2. Properties of the Cardiac Muscle 3. Action Potential.
Meaning of the Cardiac Muscle:
The muscle is involuntary and striated. The muscle fibers repeatedly branch and interdigitate. Wherever these branches come in contact an intercalated disk present, it will maintain continuity with the surrounding fibers through gap junctions. These are the areas which offer least resistance for the passage of electrical current.
Therefore, the process of depolarization, wherever it is produced in the heart, can spread all over (conductivity) the heart causing it to contract as a single unit. Because of this, heart muscle acts like a functional syncitium.
Once the cardiac muscle is depolarized, calcium ions (Ca++) enter into the ICF. This triggers the release of calcium ions from the cisterns of the L tubules. This inturn will bring about excitation contraction coupling of the cardiac muscle.
Properties of the Cardiac Muscle:
6. All or none phenomenon
7. Absolute and relative refractory period.
Excitability: Cardiac Muscle Responds to All Types of Stimuli:
The resting membrane potential of the ventricular muscle fiber is -90 mV. When a threshold stimulus is applied, it initiates the depolarization of the fiber (phase-0). The interior becomes +20 mV. Depolarization is due to influx of sodium ions through sodium channels. When once the interior becomes +20 mV, further influx of Na+ is prevented.
Now there will be opening up of K+ channels and, therefore, K+ efflux (K+ going out from ICF to ECF) is responsible for the initial repolarization (Phase I). This phase is a very short-lived phase, because during this time there is opening of Ca++ channel. Ca++ influx occurs. Further process of repolarization is slowed, giving rise to a plateau (Phase II) phase of action potential.
At the end of this phase, further repolarization becomes faster. This is again due to K+ efflux (Phase III) which is followed by phase IV, during which the resting membrane potential is restored back to normal. The total duration of the action potential is about 200-300 milliseconds. The duration of the action potential is dependent on heart rate.
Factors Influencing the Excitability of the Cardiac Muscle:
1. The ionic composition of the ECF like Na+, K+, Ca++
2. Presence or absence of sympathetic/parasympathetic stimulation
4. Drugs like digitalis, adrenaline/noradrenaline.
Action Potentials from Pacemaker Region:
The resting membrane potential of the pacemaker region is about -60 mV and is not stable. Gradually, it becomes less and less negative. And when this slope reaches the firing level and action potential is pre-potential/pacemaker potential. It is due to Ca++ influx along the T channels (T for transients). The rest of the action potential (the upstroke) is due to Ca++ influx along the L (long-lasting) channels.
The time taken for the prepotential to reach the firing level can be decreased by increasing the temperature or sympathetic stimulation. This in turn produces more number of action potentials in given time and, therefore, increases the heart rate.
The opposite effect is brought about by decreasing the temperature (cold on SA node) or by vagal stimulation. This is how the vagal stimulation (parasympathetic) decreases/stops the heart. Even under resting condition, vagus exerts some amount of inhibitory influence and this is known as vagal tone.
Heart is capable of producing its own impulses at regular intervals. The area concerned with the generation of impulse on its own is known as the pacemaker of heart.
Sinus venosus is the pacemaker of the frog’s heart. This can be proved by Stannius ligature experiments or by applying warm and cold saline on sinus venosus.
The pacemaker of the human heart is the SA node (sinoatrial node). The SA node is located at the junction of the superior vena cava with the right atrium as it opens into the right atrium.
Contractility of the Myocardium:
The contractile mechanism is somewhat similar to the contractile mechanism involved in the contraction of the skeletal muscles. The calcium that is necessary for the excitation-contraction coupling comes from the ECF. This inturn triggers the Ca++ release from the lateral cisterns.
Factors influencing the force of contraction of the cardiac muscle fibers are:
i. The initial length of the fiber depends on the end diastolic volume which in turn depends upon the venous return.
ii. Starling law is applicable to the cardiac muscle fibers also. It states that the force of contraction is directly proportionate to the initial length of the muscle fiber within physiological limits. As the venous return is increased, the ventricle is filled to a greater extent; the initial length of the muscle fiber is increased, resulting in an increase in the force of contraction. This is reflected by an increase in the stroke volume.
Factors Influencing Myocardial Contractility:
1. Sympathetic stimulation: Increases the force of contraction. This is not due to a change in the initial length but sympathetic stimulation increases the Ca++ influx. And this increases the intracellular calcium and increases the excitation- contraction coupling. Hence stroke volume is increased without any increase in end diastolic volume.
2. Parasympathetic stimulation brings about the opposite effect.
3. Effect of electrolytes: A decrease in Na+ concentration decreases the force of myocardial contraction.
4. An increase in ECF potassium stops the heart completely.
5. Increase in ionic calcium increases the force of contraction. If the ionic calcium level is further increased, the cardiac muscle fiber contracts even more and remains in a state of contraction. This is known as calcium rigor.
6. Temperature also affects the force of contraction. Increased temperature increases the force of contraction.
7. Drugs: Adrenaline, noradrenaline, digitalis bring about an increase in the force of contraction (positive inotropic effect).
Distensibility of the cardiac muscle fibers is limited because of the pericardium. This fibrous sheath covers the entire heart. Distensibility of the cardiac chambers is further decreased, if fluid/blood accumulates in the pericardial cavity.
Absolute and Relative Refractory Periods of Cardiac Muscle:
Heart muscle has long absolute refractory period. It extends throughout the duration of ventricular systole (Fig. 3.3). Due to its long absolute refractory period, cardiac muscle fiber cannot be tetanized. During the relative refractory period, cardiac muscle responds to a second stimulus, provided the second stimulus is of a higher intensity.
The response obtained is known as an extra-systole or premature contraction and this is followed by a compensatory pause. Following which the rhythm is brought back to normal.
All or None Law:
The entire heart (all the cardiac muscles) obeys this law. If the stimulus strength is of threshold value, the entire heart responds maximally. A further increase in the strength of stimulus will not alter the response of the cardiac muscle. If the stimulus strength is not adequate, it does not respond at all.
Action Potential of Cardiac Muscle:
Cardiac muscle is also an excitable tissue. Accordingly, the membrane potential of cardiac muscle will also be in the polarized state at resting condition. This is known as resting membrane potential.
While discussing the electrical activity of cardiac muscle, the representative part of the muscle that is considered will be taken from the ventricular region. The atrial, ventricular and Purkinje fibers demonstrate a fast response. In myocardial infarction, the fast response becomes a slow response.
In slow response, the action potential gets conducted more slowly than the fast response. The conduction is more likely to get blocked compared to fast response.
i. Under normal resting conditions, the resting membrane potential of the cardiac muscle fiber will be around -90 mV.
ii. The action potential recorded from the single cardiac muscle fiber differs from the one that is recorded from a bulk of the cardiac muscle.
iii. The configuration of the single fiber recording will be entirely different from the one that is recorded from the whole of cardiac muscle.
iv. The whole of the cardiac muscle recording is a summated recording and is known as electrocardiogram (ECG).
v. The configuration and ionic basis of cardiac muscle fiber action potential is different from the action potential recorded from either the single skeletal muscle fiber or a nerve fiber.
vi. There is lot of correlation between the cardiac muscle action potential duration with that of the contractile process that is occurring in the ventricular muscle fibers (Fig. 3.8).
The action potential has 5 phases, numbered from 0 to 4 (Fig. 3.9).
a. Fast depolarization phase is 0.
b. The slight falling phase is 1 (early repolarization).
c. The plateau phase of depolarization is 2.
d. The steep repolarization which follows phase 2 is phase 3.
e. Restoration of the resting membrane potential is phase 4.
vii. RMP is -90 mV.
viii. On application of the effective stimulus, there will be production of propagated action potential.
ix. Net amount of ionic diffusion depends on the permeability of the membrane for a given ion, transmembrane concentration difference, and transmembrane potential difference.
Ionic Basis of the Action Potential (Fig. 3.10):
i. It is almost due to an increase in permeability to sodium ions.
ii. There will be sudden increase of sodium influx.
iii. Sodium enters through fast sodium channels (this channel can be blocked by tetradotoxin).
i. Immediate repolarization.
ii. Due to transient outward current carried by potassium efflux.
iii. Aminopyridine blocks the potassium channels.
i. Following phase I, the further process of repolarization becomes much slower (plateau phase).
ii. The “L” channels refer to the long-lasting calcium channels.
iii. There will be increased permeability of the membrane throughout the duration of this phase for calcium ions from ECF to ICF.
iv. Therefore, there will be calcium influx.
v. Calcium also takes part in excitation-contraction coupling.
vi. Calcium conduction is increased by catecholamine, isoproterenol and is decreased by acetylcholine.
vii. Calcium channel antagonists, like verapamil, diltiazem, etc., decrease calcium conductance.
viii. Increased calcium conductance increases the force of contraction of the muscle.
i. Starts when the efflux of potassium becomes more than the calcium influx.
ii. The duration of the plateau is less in atrial muscle because at phase 2, potassium efflux is greater than calcium influx. In addition to this, outward potassium current is also greater in atrial muscle and, therefore, the duration of action potential is less in atrial muscle fiber.
i. The excess of sodium that has entered the cell is pumped out by sodium-potassium ATPase.
ii. For every three sodium ions transported out, there will be transport of two potassium ions into the cell.
iii. Calcium that has entered will also be transported out by sodium-calcium exchanger.
iv. It exchanges three sodium ions for one calcium ion transported out by an ATP-driven calcium pump.
Biophysical Aspects of Circulation:
Blood vessels are a closed system of conduits that carry blood from the heart to the tissues and back to the heart. Blood flows through the blood vessels primarily because of the forward motion imparted to it by pumping ability of the heart, although in the case of systemic circulation diastolic recoil of the walls of the arteries, compression of veins by skeletal muscles during exercise and negative intrapleural pressure also move blood towards the heart.
The resistance to flow is affected by many factors but one of the most important being the diameter of the blood vessels. The resistance offered by the blood vessels to flow of blood is predominantly provided by the arterioles.
The blood flow to each organ or tissue is regulated by local, neural and humoral mechanisms. These factors either dilate or constrict the vessels to adjust the flow according to the needs of the concerned part of body.
In pulmonary circulation, all the blood flows to lungs, whereas in systemic circulation, it is made up of numerous different circuits. The arrangement permits wide variation in regional blood flow without changing the total systemic flow.
The design of the various parts of the vascular system is in conformity to the dynamics of circulation. The intraluminal diameter, the wall thickness, the histological structure of the walls are designed in such a way that the circulation in the overall parts of the body is smooth with specific basic functions to be complied with.
The wall of arteries are made up of three layers, namely:
i. The outer most connective tissue layer, the tunica adventitia
ii. The middle layer is made up smooth muscle, the tunica media
iii. And the innermost layer is made up of endothelial cell, the tunica intima.
The walls of the aorta and other large diameter arteries contain relative large amount of elastic tissue (Fig. 3.11) that permit distensibility and collagen fibers. Collagen prevents overstretching; elastic fibers recoil and act as secondary pump in facilitating blood flow during ventricular diastole. They are stretched during ventricular systole and recoil during ventricular diastole.
The smooth muscles present in the blood vessels are innervated by sympathetic noradrenergic fibers, which bring about the constriction of the blood vessels. The parasympathetic innervations to the smooth muscle are almost insignificant. The arterioles are the major site of resistance to the blood flow.
Blood always flows from areas of higher pressure to areas of lower pressure except in certain situations when momentum transiently sustains flow (forward flow of blood in aorta during protodiastole phase of ventricular diastole. In this phase, in spite of semilunar valves being in the open state and the pressure being more in the aorta than in left ventricle, there will not be back flow of blood into the ventricle from the aorta).
i. Flowing blood creates a force on the endothelium that is parallel to the long axis of the vessel.
ii. This shear stress is proportionate to the viscosity (ƞ) times the shear rate.
iii. Shear rate is the rate at which the axial velocity increases from the vessel wall towards the lumen.
i. It is important to distinguish between velocity and flow.
ii. Velocity is rate of displacement per unit time, whereas flow is rate of volume flow per unit time.
iii. Velocity is proportionate to
V = Q/A
V = velocity;
Q = flow;
A = area of the conduit
Hence Q = A × V
The average velocity of blood is inversely proportional to the total cross-sectional area. Therefore, the average velocity of blood flow is high in aorta, decreases gradually in the arterial compartment and is least at the level of capillaries (the cross-sectional area of capillaries will be few thousands of times to that of the aorta). The average velocity of blood again increases slight in the veins.
Viscosity and Resistance:
i. The resistance to flow is determined not only by the radius of blood vessels but also by viscosity of blood.
ii. Blood is about 5-6 times more viscous to that of water.
iii. In large vessels, increase in hematocrit causes appreciable increase in viscosity.
iv. In small vessels, the change in hematocrit does not affect the viscosity much. This is because of change in the type of blood flow.
v. That is why changes in hematocrit will have relatively no effect in the change of viscosity.
vi. Apart from hematocrit, the other factors of blood which contribute for viscosity are fibrinogen and immunoglobulin in plasma. Hence, any increase in fibrinogen and immunoglobulin levels in circulation affects viscosity.
Critical Closing Pressure or Critical Opening Pressure (Fig. 3.12):
i. Critical closing pressure is the minimum pressure that should be exerted by blood in order to maintain the patency of vessels in the arterial compartment.
ii. Normally, it is around 20 mm Hg.
iii. Since blood vessels are collapsible, when the blood pressure is less than 20 mm Hg, the walls of the blood vessels get collapsed and there will be no flow of blood through the blood vessel.