The properties present in other muscle are also shown by the cardiac muscle. But it shows certain special features.
1. Rhythmicity:
One of the main characteristic features of the cardiac muscle is that it can initiate its own impulse rhythmically. This inherent rhythmical property is present throughout the cardiac muscle as evident from the electro-physiological studies of the single fibre from the S.A. node, A.V. node, atrial muscle, Purkinje fibre and also from the ventricular muscle fibre.
If a strip of muscle fibre from the atrium or ventricle is perfused in normal physiological solution with proper ionic concentrations, pH, temperature, etc., then it beats rhythmically, proving the presence of pacemaker activity. We know that the rate of rhythmicity in the S.A. node is 70 to 80 per minute, in A.V. node 40 to 60 per minute, in atrium 60 per minute, in ventricle 20 to 40 per minute.
Due to higher rhythmical property of the S.A. node, it controls the rest of cardiac muscle and thus heart beats at the rhythm of the S.A. node. When the S.A. node fails, the A.V. node takes the charge and if it fails, the atrium and afterwards ventricle take the charge of maintaining heartbeat.
Trans-membrane potentials, re-corded simultaneously from the single fibre of the S.A. node, A.V. node and ventricle during normal beating, vary in their successive phases from those are recorded separately in isolated preparation.
Difference in membrane potential recorded separately in isolated and inside cell membrane is known as trans-membrane potential. Trans-membrane potential can be recorded by inserting micro-electrode (0.2 µ) directly into the single cell and the indifferent electrode is kept outside the cell.
As soon as the micro-electrode penetrates the cell membrane and if the indifferent electrode is kept outside the cell, a potential difference ranging from —80 to -90 mV will be shown in the galvanometer. The resting trans-membrane potential thus recorded in the S.A. node, is -80 mV (Fig. 7.33), but the same, in the A.V node, atrial muscle (Fig. 7.38) and ventricular muscle (Fig. 7.39), is -90 mV.
This resting membrane potential will be maintained until the resting state is disturbed by propagated impulse. With onset of excitation, the steady state is changed rapidly and the membrane potential attains to + 20 mV. After reaching at this level, it maintains steady state for a while and gets down gradually to its initial resting state (Fig. 7.33).
The upward deflection is the de-polarisation phase as the membrane permeability to Na+ is altered due to excitation. In resting state the extracellular Na+ concentration is higher than that of the intracellular and the permeability of Na+ to the cell membrane is hastened during excitation. So during de-polarisation, there is an influx of Na+ and this process is maintained until it reaches + 20 mV.
Here Na+ entry is decreased and K+ begins to come out from the cell. This phase is known as re-polarisation. Heart remains in a state of systole at this stage. K+ efflux decreases after reaching the resting level and reorientation of ions (K+ and Na+) takes place at this stage by pumping against electrochemical gradient and by metabolic energy. This phase is known as slow diastolic de-polarisation.
This phase coincides with the period of diastole. This process is very slow and due to reorientation of ions, the threshold potential (—60m V) is slowly achieved and the membrane is further de-polarised and the process is repeated. This process once started is maintained in the cardiac muscle until death ensues. How this process is initially being started in embryonic cardiac tissue is not yet fully known but it is presumed that certain hypoxic state may have been the cause of excitability in the embryonic stage.
This slow diastolic de-polarisation phase is the characteristic of pacemaker activity. This slow diastolic de-polarisation phase of trans-membrane potentials is absent in other than pacemaker area if the same is recorded simultaneously form single cell in a pacemaker-dominated heart. This phase is however present in a trans-membrane potential recorded from any isolated preparation of cardiac muscle.
Cardiac rhythm is altered following stimulation of vagi or sympathetic nerve supplying the heart. The cause of the slowered heart rate following vagal stimulation is presumably due to prolongation of the slow diastolic de-polarisation phase and also due to hyper-polarisation for increased permeability of K+ to the cells. The rate of firing is decreased and longer time interval is required to achieve the level of threshold potential (Figs 7.34 & 7.35).
Strong vagal stimulation causes the complete disappearance of spontaneous discharge for some time. These effects are in the vagal nerve endings due to liberation of acetylcholine, which causes hyper-polarisation of the cell membrane by increasing the K+ permeability. On the other hand, cardiac sympathetic nerve stimulation or administration of adrenaline induces the membrane potential to fall more rapidly and the rate of spontaneous discharge increases greatly (Fig. 7.36).
On gradual lowering of temperature the spontaneous rhythmicity of the space-maker area is depressed. The slow diastolic de-polarisation phase of the muscle fibre is prolonged. The slope of the slow diastolic de-polarisation phase is decreased. The resting trans-membrane potential is decreased (Fig. 7.37).
2. Trans-Membrane Potential:
Characteristic features of trans-membrane potential recorded simultaneously from the S.A. Node, Atrial Muscle, Purkinje fibres and ventricular muscle in normal beating heart:
Trans-membrane potential recorded from the single cell of S.A. node shows certain characteristic features which are absent in the same of the atrial muscle, Purkinje fibres and ventricular muscle fibres. In the trans-membrane potential of S.A. node, there are slow de-polarisation phase, re-polarisation phase and also slope of slow diastolic de-polarisation phase (Fig. 7.33).
The peak of the action potential is rounded and the re-polarisation is slow but uninterrupted. But in atrial and ventricular muscle fibres and also in Purkinje fibres, the de-polarisation phase is very sharp, the peak is mostly pointed. Besides these, there are interrupted fall of re-polarisation phase and the slope in the diastolic de-polarisation phase is absent.
Thus in S.A. node-dominated heart, pacemaker activity of the atrial muscle (Fig. 7.38), ventricular muscle (Fig. 7.39) and Purkinje fibres are depressed due to higher rhythmical activity of the S.A. node and this is evident from the absence of slope of slow diastolic de-polarisation phase in those muscles.
If the trans-membrane potential is recorded in isolated fibres, then the slope of slow diastolic de-polarisation phase or the instability of the membrane resting potential is observed. This indicates that in the S.A. node-dominated heart, before achieving the threshold potential, the cell membrane of the atrial muscles, Purkinje fibres or the ventricular muscle fibres are de-polarised by the propagated impulse of the S.A. node.
Relationship between Trans-Membrane Potential and Electrocardiogram:
There is a direct relationship between the trans-membrane potential recorded from the single ventricular muscle fibre by micro-electrode techniques and the unipolar electrocardiogram recorded from an electrode placed on the surface on the heart in close proximity to the micro-electrode. It shows that the R wave of the electrocardiogram (E.C.G.) synchronises with the upstroke of the de-polarisation wave of the trans-membrane potential.
During the plateau of the re-polarisation phase of trans-membrane potential, the base line of the electrocardiogram returns quickly to the isoelectric line followed by smaller biphasic T waves. This T wave actually represents the re-polarisation wave of the ventricle. The E.C.G. actually represents the electrical activities of multicellular units but not of unicellular unit.
For this reason the amplitude and shape of the R and T waves of an electrocardiogram are mostly dependent upon the amount of electrical activities offered by the multicellular units and also upon the different configurations of the membrane potentials of the multicellular units than that of an individual cell unit (Fig. 7.40).
3. Conductivity:
The impulse originated at the S.A node spreads over the atria and reaches the A. V. node through the internodal fibres. There is no special connecting tissue between the two nodes, demonstrated histologically but from electrophysiological studies, the existence of such tissue has been reported by Carvalho and others (1961).
The A.V. node transmits the impulse through the bundle of His and its branches to the ventricles. From the apex of the heart through the Purkinje fibres the impulse is conducted to the base. Conduction in the bundle of His and the Purkinje fibres is 1 meter per second, still less in the ventricular muscles 0.4 metre per second and least in the S.A. node 0.05 metre per second and A.V. node 0.1 metre per second.
4. Excitability and Contractility:
Like other muscles, the cardiac muscle is excitable by adequate stimuli and responds by contraction. The fundamental contractile unit of the cardiac muscle is myofibril which contains the protein units, actin and myosin. During contraction these two units are associated in presence of ATP and thus the fibre is shortened, but during rest these are dissociated again with the re-synthesis of ATP.
Myosin itself is an enzyme ‘ATP-ase’ capable of dephosphorylation of ATP. Ca++ ion activates the ATP -ase activity—favouring prompt association of acto-myosin and ADP complex. Excess calcium always keeps the muscle unit in contracting state (calcium rigor) due to association of more contractile units. K+ ions do not favour association of actin and myosin. So if excess K+ is added in the extracellular fluid then the heart muscle gradually stops in diastole.
5. All-or-None Response:
If a quiescent heart muscle is stimulated at widely spaced electrical shocks of increasing strength then muscle contracts as a whole only when the threshold strength is reached. But there was no such increasing amplitude of contraction with increasing intensities of stimulation. This was observed by Bowditch (1871). Single skeletal muscle fibre behaves like this but if the entire muscle is stimulated with graded intensities of stimuli then graded responses are encountered.
6. Staircase:
In a Stannius preparation if the ventricular muscle is stimulated with inducted current, the first few contractions gradually increase in size and then it becomes steady. This is known as treppe or staircase phenomenon. This staircase phenomenon is only observed in quiescent heart but not in active normal heart.
Bowditch (1871) have described that contractions of ventricular muscle following a stoppage are weaker, but the heart regains its full strength gradually in the subsequent contractions, which on the record form a kind of staircase.
In other words, every contraction leaves a condition more favourable than it found, but this favourable condition deteriorates in time. From the experiments on staircase phenomenon of Hajdu and Szent-Gyorgyi (1952) it can be suggested that it is caused by the decrease of internal potassium.
After analysis of ion Hajdu (1953) has reported that this favourable condition following a contraction is mostly related with the release of potassium from the cell, which re-enters during rest at a speed depending on the condition of the membrane.
Equilibrium of these two processes will decide the internal ion content and through this, the height of tension. His quantitative measurement leaves very little doubt that the change in tension during the staircase is related to the change in the internal ionic content. Visco-elastic properties or the accumulation of metabolic products have got little role on the staircase phenomena.
Besides this, change in internal ionic content acts on the contractile proteins directly rather than indirectly through some other mechanism. He has further claimed that actomyosin goes from full dissociated (un-contracted) to full associate (contracted) form if there is a change of 10% or even less in the ionic concentration.
Loss of 3 mEq potassium out of 106.8 mEq internal Na and K, increases tension from 0-100% (Fig. 7.41). With digitalis the staircase phenomenon is shortened by blocking K+ re-entry into the cells so that intracellular K+ concentration is decreased very rapidly.
Thus it can be assumed that during quiescent state excess K+ is accumulated within the cell and the association of actin and myosin is being depressed. With the excitation, reductions in intracellular K+ accompanied with successive increased contractions are taken place.
Height of contraction is associated with the parallel loss of intracellular. Maximum tension is developed after the loss of 3 mEq of intracellular K+. But heart muscle remains in contracting states following release of intracellular K+ more than 10 mEq.
7. Refractory Period:
This is another characteristic property of the heart muscle.
The refractory period of the heart is long and can be divided into three parts:
i. Absolute Refractory Period:
This period extends throughout the whole period of contraction. Any stimulus, however strong, will fail to elicit a response if it falls within this period. For this reason, heart muscle cannot be tetanised. This long refractory period ensures enough time for recovery of the cardiac muscle. This is the reason why cardiac muscle cannot be fatigued. This period coincides the period from the onset of de-polarisation phase to the re-polarisation up to the threshold potential (Fig. 7.42).
ii. Relative Refractory Period:
This starts immediately after the absolute refractory period and involves the first part of relaxation. Only a very strong stimulus will be effective. This period begins when the trans-membrane potential during re-polarisation phase has just reached the threshold potential (-60 mV) and ends just before the re-polarisation phase is ceased.
iii. Supernormal Period:
There is another type of refractory period observed after the relative refractory period which is known as supernormal period. This period is limited from the point of termination of re-polarisation to the beginning of slow diastolic re-polarisation phase.
The refractory period is longest in the A.V. node, intermediate in the ventricles and least in the atria. Drugs like digitalis and quinidine prolong the absolute refractory period. Stimulation of the vagus reduces the systole and as such, diminishes the refractory period.
The length of the refractory period is directly proportional to the duration of systole and inversely to that of the diastole of the heart. Hence, it will depend upon the heart rate. For rates up to 100 per minute, the absolute refractory period is about 0.2 second.
8. Tone:
Heart muscle possesses tone. This tone is independent of nerves and can be adjusted. In this way, it can maintain a fairly constant tension upon its varying contents.
It has been observed that the different properties of cardiac muscles (Table 7.1) are not developed in all the tissues of heart in the same order. Certain properties have developed specially in certain tissues while others are not. It is also seen that these functions are related to the size and chemical composition of the muscle cells.
Hence, cardiac muscle can be divided into four groups:
i. The smallest fibres with least glycogen at the nodes.
ii. The broader fibres with more glycogen in the ventricles.
iii. The still broader fibres with more glycogen in the atria.
iv. The broadest fibres with abundant glycogen in the Purkinje fibres, bundle of His and its branches. As the size of the fibres increases, the rate of conduction and the glycogen content also increase. But the duration of systole, the refractory period and the rhythmicity increase in the reverse order.