Absolute and relative refractoriness. Refractoriness

Compared with electrical impulses originating in nerves and skeletal muscles, the duration of the cardiac action potential is much longer. This is due to a long refractory period, during which the muscles are unresponsive to repeated stimuli. These long periods are physiologically necessary, since at this time blood is released from the ventricles and their subsequent filling for the next contraction.

As shown in Figure 1.15, there are three levels of refractoriness during an action potential. The degree of refractoriness initially reflects the number of fast Na+ channels that have emerged from their inactive state and are able to open. During phase 3 of the action potential, the number of Na+ channels that emerge from the inactive state and are able to respond to depolarization increases. This, in turn, increases the likelihood that stimuli will trigger the development of an action potential and lead to its propagation.

The absolute refractory period is the period during which cells are completely insensitive to new stimuli. The effective refractory period consists of the absolute refractory period, but extending beyond it also includes a short phase 3 interval during which the stimulus excites a local action potential that is not strong enough to propagate further. The relative refractory period is the interval during which stimuli excite an action potential, which can propagate, but is characterized by a slower development rate, lower amplitude and lower conduction velocity due to the fact that at the moment of stimulation the cell had a less negative potential than the resting potential .

After a relative refractory period, a short period of supernormal excitability is distinguished, in which stimuli whose strength is lower than normal can cause an action potential.

The refractory period of atrial cells is shorter than that of ventricular myocardial cells, therefore the atrial rhythm can significantly exceed the ventricular rhythm in tachyarrhythmias

Impulse conduction

During depolarization, the electrical impulse propagates through the cardiomyocytes, quickly passing to neighboring cells, due to the fact that each cardiomyocyte connects to neighboring cells through low-resistance contact bridges. The rate of tissue depolarization (phase 0) and the velocity of conduction through the cell depends on the number of sodium channels and the magnitude of the resting potential. Tissues with a high concentration of Na+ channels, such as Purkinje fibers, have a large, fast inward current that spreads quickly within and between cells and allows for rapid impulse conduction. In contrast, excitatory conduction velocity will be significantly slower in cells with a less negative resting potential and more inactive fast sodium channels (Figure 1.16). Thus, the magnitude of the resting potential greatly influences the rate of development and conduction of the action potential.

Normal sequence of cardiac depolarization

Normally, the electrical impulse that causes cardiac contraction is generated in the sinoatrial node (Fig. 1.6). The impulse propagates into the atrium muscles through intercellular contact bridges, which ensure continuity of impulse propagation between cells.

Regular atrial muscle fibers are involved in the propagation of electrical impulses from the SA to the AV node; in some places, a denser arrangement of fibers facilitates impulse conduction.

Due to the fact that the atrioventricular valves are surrounded by fibrous tissue, the passage of an electrical impulse from the atria to the ventricles is possible only through the AV node. As soon as the electrical impulse reaches the atrioventricular node, there is a delay in its further conduction (approximately 0.1 seconds). The reason for the delay is the slow conduction of the impulse by small-diameter fibers in the node, as well as the slow pacemaker type of action potential of these fibers (it must be remembered that in pacemaker tissue, fast sodium channels are constantly inactive, and the speed of excitation is determined by slow calcium channels). A pause in impulse conduction at the site of the atrioventricular node is useful, as it gives the atria time to contract and completely empty their contents before the ventricles begin to excite. In addition, this delay allows the atrioventricular node to act as a pylorus, preventing the conduction of too frequent stimuli from the atria to the ventricles in atrial tachycardias.

Having left the atrioventricular node, the cardiac action potential propagates along the rapidly conducting bundles of His and the Purkinje fibers to the bulk of the cells of the ventricular myocardium. This ensures coordinated contraction of ventricular cardiomyocytes.

Refractory periods reflect the ability of tissues to conduct two successive impulses. The second impulse is the result of ongoing stimulation; the first one can be spontaneous or artificially caused. Assessment of refractory periods does not directly determine the timing of the procedure. The differences between conduction time and the duration of refractory periods are shown in Fig. 5.7. As an example, it shows the AV node as part of the conduction system. Electrical activity is recorded by electrodes located near the input and output of this system. For the AV node, both the input (inferior atrial potential) and output (His bundle potential) are recorded by one electrode. Other tissues may require separate electrodes. The conduction interval represents the absolute time required for a single impulse (Si) to travel through a portion of the conduction system; in the case of the AV node this is the interval A-H (A\-Hi).

When measuring refractory periods, the difference in the conduction of two successive impulses is assessed: S\(spontaneous or artificial) and Ss(artificial). In this case, the absolute conduction time is not determined; rather, the delays between the impulses at the exit and entrance to the conducting tissue are compared. The closer the coupling of two impulses, the greater the likelihood of slow conduction of the second impulse due to tissue refractoriness. As a result of refractoriness, the length of the S1-S2 interval measured at the output is longer than at the input. In the case of the AV node, the exit delay (H1-H2) compared with the coupling interval at the input (A1-A2). If there is no effect of refractoriness, then there is no difference in the conduction of two successive pulses and the interval A1-A2 equal to the interval H1-H2. This is usually observed with relatively large coupling intervals between S1 and S2. When the second impulse occurs earlier, it enters partially refractory tissue, as a result of which its conduction through the AV node slows down. As a result Hi-LF getting bigger A1-A2, or, in other words, the interval A-N impulse S2 exceeds that of S1. Longest adhesion interval (A1-A2), at which this is observed corresponds to the period of relative refractoriness of the tissue being studied. The above is illustrated by a graph of the dependence of the coupling intervals at the output and input (Fig. 5.8). At the coupling interval at the exit from the AV node (H1-H2) influences the degree of premature impulses (shortening H1-H2) due to a decrease A1-A2 and the degree of refractoriness of the AV node (lengthening H1-H2 as a result of a delay in conduction with an increase A2-H2). As can be seen in Fig. 5.8, with greater premature impulses, a decrease in the interval H1-H2 continues, but it occurs more slowly due to increasing refractoriness. A point is often reached at which the increase in conduction delay exceeds the rate of decrease in impulse prematurity, resulting in the duration of the interval H1-H2 becomes greater than observed with less premature impulses. This is well represented by the ascending part of the refractory period curve. A point may be noted at which complete refractoriness exists. The second impulse is then blocked within the AV node and is not recorded at the output (H2). The effective refractory period (ERP) corresponds to the longest coupling interval (A1A2), in which there is no conduction. Analysis of the curve shows that for a number of conducted premature impulses there is a minimum interval at the output (H1-H2); it corresponds to the functional refractory period (FRP).

Rice. 5.7. Conduction intervals and refractory periods.

Rice. 5.8. Dependence of intervals Hi-Hiorintervals A\-Ai obtained during electrography of the His bundle in order to determine the refractory periods of the AV nodes (AVN).

The relative refractory period (RRP) is determined when the graph deviates from the line of equal interval values. The functional refractory period of the AV node (FRP) corresponds to the minimum H1-H2 interval. The effective refractory period of the AV node (ERP) corresponds to the shortest A1-A2 interval at which conduction through the His bundle is maintained.

Refractory periods were determined for various cardiac tissues when carried out in both the anterograde and retrograde directions. The parameters measured at the input and output necessary for assessing refractory periods are listed in Table. 5.13. In table Figure 5.14 presents the ranges of normal values ​​for commonly defined refractory periods. Different cardiac tissues differ not only in the magnitude of the absolute refractory periods, but also in the shape of the refractory period curve. The AV node is characterized by a pronounced rise in the curve, and its ERP significantly exceeds the ERP. The refractory period curves of the atria and ventricles usually approach a line of equal values, with the ERP often being only 10-30 ms greater than the ERP.

It should be noted that the ORP and ERP are determined by the value of the coupling interval at the input of the system (at the point of critical changes in conduction), while the FRP is determined by the value of the interval at the output. Thus, to fully characterize tissue refractory periods, it is necessary to determine electrical events at both the input and output. This can be difficult in many situations. Refractory periods of the AV node are determined by the difference between A1A2 And H1H2, however, atrial refractoriness should not be limited during application of a premature stimulus. If the atrial ERP exceeds the ERP of the AV node, an accurate determination of the latter is impossible, since atrial refractoriness limits the degree of premature impulses at the entrance to the AV node; this is observed in 36% of patients. It is often difficult to assess retrograde conduction using the His-Purkinje system, which in many cases is associated with the inability to record the retrograde potential of the His bundle. Refractoriness is influenced by many factors. The measured values ​​can be significantly affected by medications and changes in autonomic tone (see Table 5.8). The frequency of the main heart rhythm, at which tissue refractoriness is assessed, also has a certain influence. With increased heart rate, the refractory periods of the atria, the His-Purkinje system and the ventricles decrease, and the AV node increases.

Table 5.13. Measurable drugs needed to assess refractory periods

Retrograde His potential; S - stimulus artifact; A - atrial electrogram; N - His bundle potential; V- ventricular electrogram; index 1 - first impulse; index 2 - second impulse.

Table 5.14. Normal values ​​of refractory periods

"The ERP of the AV node is limited by the ERP of the atrium in 36% of patients. AVN - AV node; SGP - His-Purkinje system.

The refractory period that occurs after coitus reflects sexual, but not general physical exhaustion.

This is clearly evidenced by the fact that when changing sexual partners, even the male quickly restores libidinal activity. In domestic animals, as well as wild ones, repeated matings with a short break are common. Thus, a bull, when released after isolation to a current cow, performs 5-6 coitus in a row with ejaculation. A stallion can perform up to 10 mounts in a row at short intervals. Boars make up to 10 matings per day. In a special test, each of three boars placed in a herd of nine sows showing signs of estrus produced eight successful matings over a 25-hour period. According to J. O. Almquist and E. V. Hale (1956), in a 5-hour sexual exhaustion test, a bull produced 75 ejaculations. However, rams still have the greatest sexual endurance. It is estimated that in large flocks with a large number of females in estrus, the stud ram maintains high sexual activity for several months and performs an average of about 45 coitus per week.

After the “lock,” dogs develop a refractory period, during which both the male and female carefully lick their genitals for 10-15 minutes. As a rule, after recovery, the bitch “mates” with another male. The duration of the refractory period of a male is significantly longer compared to the duration of the refractory period of a female. These sexual differences ensure that several males participate in the sexual process.

Coital receptivity of females as a general biological phenomenon has been studied to a lesser extent compared to the sexual activity of males. The literature indicates that when kept freely, ewes and ewes allow rams to cage no more than 6 times during the entire period of sexual heat. Approximately the same figures are given for cows.

Researchers of the sexual behavior of domestic animals note that when animals are kept separately during the year and males and females unite during the sexual season, animals tend to form temporary “family” pairs. After the first successful coitus, bulls remain in close proximity to the female until the end of her estrus. In this case, the animals occupy a “parallel or opposite” position relative to each other.

On horses, it is shown that a couple is formed after the mare exposes her butt to the stallion and performs demonstrative urination. This is followed by the ritual of the stallion biting the mare and the mare kicking the stallion. In horses, an indicator of the formation of a mating pair is the position of the partners, in which they stand nose to nose.

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The excitability of the cardiac cell changes during certain periods of the cardiac cycle. During systole, the heart cell is not excited, i.e. it is refractory to irritation. During diastole, the excitability of the cardiac cell is restored. Refractoriness is the inability of an activated cardiac cell to become activated again with additional stimulation. A cardiac cell, covered by the process of electrical excitation and possessing an action potential, cannot create another additional electrical excitation, another action potential. Electrical excitation completely involves the cell's sodium ion system in the process, as a result of which there is no ionic substrate that could respond to additional stimulation.

There are three degrees of refractoriness, respectively. period: absolute, effective and relative (relative) refractory period (Fig. 12).

Refractoriness of the heart muscle.

ARP- absolute refractory period; ERP - effective refractory period; O^P- relative refractory period; VP - vulnerable (vulnerable) period; SNF - supernormal phase.

During the absolute refractory period, the heart cannot activate and contract, regardless of the strength of the stimulus applied.

During the effective refractory period, the heart is able to activate, but the resulting electrical impulse is weak and does not spread, as a result of which myocardial contraction does not occur. The effective refractory period covers the absolute refractory period and that period during which weak electrical activation occurs without impulse propagation. During the relative, relative or, also called partial, refractory period, the heart can be activated by irritation that is stronger than usual. The resulting electrical impulse spreads, although more slowly than normal, and can cause the heart muscle to contract. The sum of the effective and relative refractory periods gives the total refractory period. The total refractory period corresponds to the Q-T interval on the electrocardiogram - electrical ventricular systole. It corresponds to the entire action potential of the cell. The absolute refractory period corresponds to the QRS complex and the initial and middle part of the S-T segment on the electrocardiogram. It covers the action potential from its onset until approximately -50 mV repolarization. The end of the absolute refractory period is defined as the moment of repolarization, after which, with additional stimulation, a weak, non-propagating electrical impulse can occur. The effective refractory period corresponds to the QRS complex and the entire S-T segment on the electrocardiogram. It covers the action potential from its onset until approximately -60 mV of repolarization. The end of the effective refractory period is defined as the moment of repolarization, after which, with additional stimulation, a slowly propagating electrical impulse can occur. Therefore, the difference between the absolute and effective refractory period is that the effective refractory period also covers the part of the repolarization, approximately between -50 and -60 mV, when a weak, non-propagating electrical impulse can be generated with additional stimulation. The relative refractory period is very short and corresponds to the T wave on the electrocardiogram. It covers the final part of the repolarization and is located approximately between -60 mV and the end of the action potential.

The extra-refractory period corresponds to diastole of phase 4 of the transmembrane potential. During this period, the conduction system and the heart muscle restore excitability and are capable of normal activation.

The duration of the refractory period is different in individual parts of the conduction system and the contractile myocardium. The longest refractory period is in the atrioventricular node. The middle place in terms of the duration of the refractory period is occupied by the ventricular muscle, and the atrial muscle has the shortest refractory period. The right bundle branch has a longer refractory period than the left.

The duration of the refractory period is not constant. It changes under the influence of many factors, but the most important among them is the frequency of cardiac activity and autonomic innervation. Accelerating cardiac activity shortens the refractory period, and slowing it down has the opposite effect. The vagus nerve increases the duration of the refractory period of the atrioventricular node, but shortens the refractory period of the atria. The sympathetic nerve shortens the refractory period of the entire heart.

There are two relatively short phases of the cardiac cycle during which the excitability of the heart is increased: the vulnerable (vulnerable) period and the supernormal phase.

The vulnerable period is located in the final part of repolarization and is a component of the relative refractory period. During the vulnerable period, the threshold potential is lowered and the excitability of the cell is increased. As a result, under the influence of even relatively weak stimuli, ventricular tachyarrhythmias and their fibrillation can occur. The ionic mechanism of this period is not clear. This period approximately coincides with the peak of the T wave on the electrogram and corresponds to a small part of phase 3 of cellular repolarization.

The supernormal phase follows immediately after the end of the relative refractory period, resp. repolarization. It is located at the beginning of diastole and often coincides with the U wave on the electrocardiogram. The excitability of the cardiac cell in this phase is increased. Minor stimuli can cause unusually strong electrical activation and tachyarrhythmias. This period is detected only with functional depression of the heart.

Refractory periods. Relative refractory period. Absolute refractory period.

Another important consequence of inactivation of the Na+ system is the development membrane refractoriness. This phenomenon is illustrated in Fig. 2.9. If the membrane depolarizes immediately after the development of an action potential, then excitation does not occur either at the potential value corresponding to the threshold for the previous action potential, or at any stronger depolarization. This state of complete non-excitability, which lasts about 1 ms in nerve cells, is called absolute refractory period. Followed by relative refractory period, when through significant depolarization it is still possible to cause an action potential, although its amplitude is reduced compared to normal.

An action potential of normal amplitude at normal threshold depolarization can be evoked only a few milliseconds after the previous action potential. The return to the normal situation corresponds to the end of the relative refractory period. As noted above, refractoriness is due to inactivation of the Na+ system during the preceding action potential. Although the inactivation state ends with membrane repolarization, such restoration is a gradual process lasting several milliseconds, during which the Na """ system is not yet able to activate or is only partially activated. The absolute refractory period limits the maximum frequency of generation of action potentials. If, As shown in Fig. 2.9, the absolute refractory period ends 2 ms after the onset of the action potential, then the cell can be excited with a frequency of a maximum of 500/s. There are cells with an even shorter refractory period, in which the excitation frequency can reach 1000/s. However, most cells have a maximum action potential frequency below 500/s.