Refractory period is the phase during which re-excitation of neurons is not possible after the arrival of an action potential. These refractory periods prevent retrograde propagation of excitation in the human body. In cardiology, a disturbance of the refractory period is present, for example, in phenomena such as ventricular fibrillation.
What is refractory period?
The refractory period is the phase during which re-excitation of neurons is not possible after the arrival of an action potential. In biology, the refractory period, or refractory phase, is the recovery time of depolarized neurons. This recovery time corresponds to the period during which no new action potential can be triggered at a nerve cell that has just been depolarized. Thus, the neuron cannot respond anew to a stimulus during the refractory period. In connection with the refractory period of neurons, a distinction is made between the absolute and relative refractory periods, which directly follow each other. The triggering of an action potential is only limited during the relative refractory period, but not impossible. In a narrower sense, therefore, only the absolute refractory period and the associated impossibility of a new action potential are to be understood as actual refractory periods. Outside of medicine, the refractory period plays a role mainly with regard to stimulus-reactive aggregates and meets the medical definition in this context. In cardiology, refractory period may additionally mean a different context. Cardiac pacemakers must not stimulate themselves and must support the still existing intrinsic rhythm of the heartbeat. For this purpose, signal detection in pacemakers is deactivated for fixed periods of time. These periods of deactivation are also refractory periods from a cardiological point of view.
Function and Purpose
Neurons respond to excitation by generating action potentials. This generation occurs through elaborate biochemical and bioelectrical processes in the lacing rings of neurons. The action potential is passed from lacing ring to lacing ring and accordingly jumps along the neural pathways. This process is described by the term saltatory excitation conduction. The transmission of an action potential depolarizes the membrane of the downstream neuron. When the membrane is depolarized beyond its resting potential, the neuron’s voltage-gated sodium channels open. Only the opening of these channels generates the action potential in the next neuron, which depolarizes the downstream neuron again. After opening, the channels close independently. After this process, they are not ready to open again for some time. The nerve cell must first allow potassium ions to escape and thus repolarize its own membrane back below -50 mV. Only this repolarization enables a repeated depolarization. Thus, the sodium channels cannot be reactivated until repolarization is complete. Therefore, the cell can no longer respond to stimuli before complete repolarization. During the absolute refractory period, no action potential can be triggered regardless of the stimulus strength. All voltage-gated channels are in an inactivated and closed state during this time, which lasts for about two ms. This phase is followed by the relative refractory period, during which some sodium channels have regained an activatable state due to the repolarization that has begun, although they are still closed. During this phase, action potentials can be triggered if a correspondingly high stimulus strength is present. However, the amplitude of the action potentials and the depolarization slope are low even then. The refractory period limits the maximum frequency of action potentials. Thus, the body prevents retrograde propagation of neuronal excitation. For example, the heart is protected by the refractory period from too rapid a succession of contractions that could collapse the cardiovascular system.
Diseases and ailments
Probably the best-known complaint associated with refractory period is ventricular fibrillation of the heart muscle. Unlike skeletal muscle, failure to maintain refractory period in cardiac muscle leads to life-threatening consequences. When current is injected into a skeletal muscle, it contracts. As the current strength increases, so does the contraction. A strong stimulus therefore triggers an equally strong reaction in the skeletal muscle.This connection does not apply to the heart muscle. It only contracts if the stimulus is strong enough. If it is not strong enough, no contraction takes place. When the current is raised, the heartbeat does not increase at the same time, and once a heartbeat has occurred, a refractory period of 0.3 seconds occurs. Thus, skeletal muscles can contract or be permanently tense in rapid succession, while the cardiac muscle is unable to do so. During the refractory period, the chambers of the heart fill with blood. During the subsequent contraction, this blood is expelled again. If the refractory period of the heart falls below the duration of about 0.3 seconds, insufficient blood is flowing into the ventricles. During the next heartbeat, correspondingly little blood is ejected again. Shortly before the refractory period is completed, the muscle fibers of the cardiac excitation conduction system are already partially excited. If a stimulus reaches the myocardium during this time, the heart responds with a racing heartbeat. Ventricular fibrillation sets in. The frantic heartbeat hardly moves any more blood through the organism. A pulse beat can no longer be detected. The refractory period of the heart also plays a role with regard to various drugs. For example, the class III antiarrhythmic drug amiodarone prolongs the refractory period of the ventricular and atrial myocardium.
