Action potentials in the myocardium
In the myocardium, the action potential is generated by the opening of a voltage-activated fast sodium channel and a completely different set of L-type calcium channels, which are called calcium-sodium channels.
The action potential recorded in a ventricular muscle fibre, on average, is about 105 millivolts, which means that the intracellular potential rises from a very negative value, about -85 millivolts, to a slightly positive value, about + 20 millivolts, in each beat. After the initial peak, the membrane depolarizes for about 0.2 s, represented by a plateau, after the end of the plateau is sudden repolarization. The presence of a plateau in the action potential causes the ventricles to contract for a duration 15 times longer than that of skeletal muscle.
Prolonged action potentials and the appearance of plateaus
Why are the action potentials of the myocardium prolonged and why a plateau appears, while the action potentials of the skeletal muscle have no plateau? but they are better summarized here
Figure. Rhythmic potential features (in millivolts) from Purkinje fibres and from ventricular muscle fibres, recorded with microelectrodes.
There are at least two major differences between the pericardial and skeletal muscle properties that account for the prolonged action potentials and plateaus in the myocardium. First, the action potential of the skeletal muscle is generated almost entirely by the sudden opening of many rapid sodium channels that allow an extremely large amount of sodium ions to enter the skeletal muscle fibres from the extracellular fluid. These channels are called “fast” channels because they open only for a few 1/1000 s and then close abruptly. When this closing is complete, repolarization occurs, and the action potential resumes within a few 1/1000 s.
In the myocardium, action potentials are generated by the opening of two types of channels: (1) voltage-activating fast sodium channels as in skeletal muscle and (2) a completely different set of L-type calcium channels (slow calcium channels). ), they are called calcium-sodium channels. This set of channels is different from the fast sodium channels, they open slowly, and even more importantly, they stay open for only a few tenths of a second. During this time, large amounts of both calcium and sodium ions pass through these channels into the myocardium and remain depolarized for a long time, creating a plateau in the action potential. Furthermore, calcium ions entering the plateau phase trigger muscle contraction, whereas calcium ions that cause skeletal muscle contraction originate in the endoplasmic reticulum.
The second major functional difference between a cardiac and skeletal muscle that helps to account for both the prolonged action potential and the plateau is: immediately after the initiation of the action potential, the permeability of the myocardium to potassium ions decreased by about 5 times, an effect that did not occur in skeletal muscle. The decreased permeability to potassium is probably due to excessive calcium inflow from let-only calcium channels.
Whatever the cause, the drastic decrease in potassium permeability reduces the outflow of positively charged potassium ions during the plateau phase of the action potential and thereby prevents premature repolarization of the action potential to resting level. . When the calcium - sodium channel slowly closes after 0.2 - 0.3 s and the influx of calcium and sodium ions stops entering, the membrane permeability to potassium ions also increases rapidly; The rapid loss of potassium from muscle fibres immediately returns the membrane potential to the resting level, ending the action potential.
The action potential phases of the myocardium
The figure summarizes the phases of action potentials in the myocardium and ionic currents that occur during each phase.
Figure. The action potential phases of ventricular myocytes and ion fluxes involve sodium (Na+), calcium (Ca++) and potassium (K+).
Phase 0 (depolarization), fast sodium channel opening. When cardiac cells are stimulated and depolarized, the membrane potential becomes strongly positive. The fast sodium channel potential gate opens and allows sodium to rapidly enter the cell and depolarize the cell. The membrane potential reaches about +20 millivolts before the sodium channel closes.
Phase 1 (first step of repolarization), rapid sodium channel closure. The sodium channel closes, the cell begins to repolarize, and potassium ions leave the cell by opening the potassium channel.
Phase 2 (plateau), calcium channels open and fast potassium channels close. Initial brief repolarization occurs and the action potential then plateaus as a result of (1) increased calcium ion permeability and (2) decreased potassium ion permeability. The calcium ion channel potential gate opens slowly during phases 1 and 0, and calcium enters the cell. The potassium channel then closes, and the combination of a decrease in outgoing potassium ions and an increase in calcium inflow causes the potential to plateau.
Phase 3 (rapid repolarization), calcium channel closure and slow potassium channel opening. Closing of the calcium channel and increased permeability to potassium ions causes potassium to rapidly exit the cell, ending the plateau and returning the membrane potential to the resting level.
Phase 4 (membrane resting potential) averages about -90 millivolts.
Signal conduction rate in the myocardium
The conduction velocity of the excitatory action potential signal along both atrial and ventricular muscle fibres is about 0.3 to 0.5 m/s or about 1/250 of the speed in the major nerve fibre and about 1/10 of the speed. degree in skeletal muscle fibres. The conduction velocity in a particular conduction system in the heart - the Purkinje fibres - is very fast, about 4 m/s in most parts of the system, which allows for a moderate rate of conduction of the excitatory signal. to different parts of the heart.
The refractory phase of the myocardium
Cardiac muscle is inert like all excitable tissues. Thus, the refractory phase of the heart is the resting period, during which a normal cardiac impulse cannot re-stimulate an already stimulated area of the myocardium. The normal refractory period in the ventricles is 0.25 - 0.3 s, which is the length of time that plateaus in the action potential. There is an additional period of relative inertness of approximately 0.05 s, when the muscle is less excitable than usual, yet can still be stimulated by a strong excitatory signal, as demonstrated by a contraction "Soon". The refractory period of the atrial muscle is very short compared with that of the ventricles (about 0.15 s in the atria versus 0.25 - 0.3 s in the ventricles).
Figure. The force of ventricular contractions also shows the duration of the refractory phase and the relative refractory period, plus the effect of early contraction. Note that the early contractions do not cause synthesis waves, as occurs in skeletal muscle.