Violation of the rhythm and conductance of the heart

Normally, the heart contracts in a regular, coordinated rhythm. This process is provided by the generation and carrying out of electrical impulses by myocytes possessing unique electrophysiological properties, which leads to an organized reduction of the entire myocardium. Arrhythmias and conduction disorders occur due to impaired formation or carrying out of these impulses (or both).

Any heart disease, including congenital anomalies of its structure (for example, additional AV-ways of carrying out) or functions (for example, hereditary pathology of ion channels), can lead to rhythm disturbance. Systemic etiological factors include electrolyte disturbances (mainly hypokalemia and hypomagnesemia), hypoxia, hormonal disorders (such as hypothyroidism and thyrotoxicosis), the effects of drugs and toxins (in particular, alcohol and caffeine).

Anatomy and physiology of cardiac arrhythmias and conduction

At the site of the confluence of the superior vena cava in the upper lateral part of the right atrium, a cluster of cells is located, which generates an initial electrical impulse providing each cardiac contraction. It is called the sinus-atrial node (JV), or sinus node. An electrical impulse originating from these pacemaker cells stimulates susceptible cells, leading to activation of the myocardium in the appropriate sequence. The impulse is conducted through the atrium to the atrioventricular (AB) node through the most active conducting interstitial pathways and nonspecific atrial myocytes. The AV node is located on the right side of the interatrial septum. It has a low conductive capacity, so it slows down the pulse. The time of the impulse through the AV-node depends on the heart rate, is regulated by the self activity and the influence of circulating catecholamines, which allows to increase the cardiac output in accordance with the rhythm of the atria.

The atria are electrically isolated from the ventricles by a fibrous ring, with the exception of the anterior part of the septum. At this point, the bundle of the Gis (which is the extension of the AV node) enters the upper part of the interventricular septum, there it is divided into left and right legs, which terminate with Purkinje fibers. The right leg conducts an impulse to the anterior and apical parts of the right ventricular endocardium. The left leg passes along the left side of the interventricular septum. The anterior and posterior branches of the left bundle branch of the bundle stimulate the left part of the interventricular septum (the first part of the ventricle that must receive the electrical impulse). Thus, the interventricular septum performs depolarization from left to right, which leads to the practically simultaneous activation of both ventricles from the endocardial surface through the ventricular wall to the epicardium.

[1], [2], [3], [4], [5], [6], [7], [8]

Electrophysiology of cardiac arrhythmia and conduction

Transport of ions through the membrane of the myocyte is regulated by special ion channels, which carry out cyclic depolarization and repolarization of the cell, called the action potential. The potential of the functioning of the myocyte begins with the depolarization of the cell from the diastolic transmembrane potential of -90 mV to a potential of about -50 mV. At the level of this threshold potential, Na ⁺ -dependent fast sodium channels are opened , which leads to a rapid depolarization due to the rapid outflow of sodium ions along the concentration gradient. Fast sodium channels are quickly inactivated, and sodium outflow stops, but other time- and charge-dependent ion channels open, allowing calcium to enter through the slow calcium channels into the cell (depolarization state), and potassium - to exit through the potassium channels (repolarization state). First, both these processes are balanced and provide a positive transmembrane potential, which extends the plateau of the action potential. During this phase, calcium entering the cell is responsible for electromechanical interaction and reduction of the myocyte. Eventually, calcium intake ceases, and the flow of potassium increases, which leads to a rapid repolarization of the cell and its return to the transmembrane resting potential (-90 mV). Being in a state of depolarization, the cell is stable (refractory) to the subsequent episode of depolarization; first, depolarization is impossible (the period of absolute refractoriness, but after partial (but not complete) repolarization, subsequent depolarization is possible, although it proceeds slowly (the period of relative refractivity).

There are two main types of tissue in the heart. Fabrics with fast channels (functioning atrial and ventricular myocytes, the His-Purkinje system) contain a large number of fast sodium channels. Their action potential is characterized by a rare or total absence of spontaneous diastolic depolarization (and, as a result, very low pacemaker activity), a very high rate of initial depolarization (and therefore a high ability to rapidly reduce) and low refractoriness to repolarization (in the light of this short refractory period and ability to conduct repeated pulses with a high frequency). Fabrics with slow channels (SP- and AV-nodes) contain a small number of fast sodium channels. Their action potential is characterized by a more rapid spontaneous diastolic depolarization (and, as a result, more pronounced pacemaker activity), slow initial depolarization (and therefore low ability to contract) and low refractoriness, which is delayed from repolarization (and as a result a long refractory period and inability to conduct frequent impulses ).

Normally, the SP node has the highest frequency of spontaneous diastolic depolarization, so its cells generate a spontaneous action potential with a higher frequency than other tissues. For this reason, the SP node serves as the dominant tissue possessing the function of automatism (pacemaker) in the normal heart. If the SP node does not generate pulses, the pacemaker's function takes on a tissue with a lower level of automatism, usually an AV node. Sympathetic stimulation increases the frequency of stimulation of pacemaker tissue, and parasympathetic stimulation inhibits it.

[9], [10], [11], [12]

Normal heart rhythm

The heart rate that occurs under the influence of the joint node, at rest in adults is 60-100 per minute. A lower frequency (sinus bradycardia) can occur in young people, especially athletes, and during sleep. A more frequent rhythm (sinus tachycardia) occurs during physical exertion, during illness or emotional stress due to the effects of the sympathetic nervous system and circulating catecholamines. Normally, there are pronounced fluctuations in the heart rate with the lowest heart rate early in the morning, before awakening. Normal also there is a slight increase in heart rate during inspiration and a decrease during exhalation (respiratory arrhythmia); this is associated with a change in the tone of the vagus nerve, which is often found in young healthy people. With age, these changes decrease, but do not disappear at all. Absolute correctness of sinus rhythm is abnormal and occurs in patients with autonomous denervation (for example, in severe diabetes mellitus) or in severe heart failure.

Basically, the electrical activity of the heart is displayed on an electrocardiogram, although the depolarization of CA-, AV-nodes and the His-Purkinje system does not involve sufficient tissue volume to be clearly seen. The tooth P reflects atrial depolarization, QRS- depolarization of the ventricles, and the tooth-repolarization of the ventricles. The PR interval (from the beginning of the P wave to the start of the QRS complex) reflects the time from the onset of atrial activation to the onset of ventricular activation. Most of this interval reflects the slowing down of the pulse through the AV node. The RR interval (the interval between the two R complexes) is an indicator of the rhythm of the ventricles. The interval (from the beginning of the complex to the end of the R wave) reflects the duration of repolarization of the ventricles. Normally, the duration of the interval is somewhat larger in women, and it also lengthens when the rhythm slows down. The interval varies (QTk) depending on the heart rate.

Pathophysiology of cardiac arrhythmia and conduction

Violations of the rhythm - a consequence of violation of the formation of momentum, its conduct or both violations. Bradyarrhythmias occur due to a decrease in internal pacemaker activity or blockade, primarily at the level of the AV node and the His-Purkinje system. Most tachyarrhythmias are due to the mechanism of re-entry, some are the result of increased normal automatism or pathological mechanisms of automatism.

Re-entry - pulse circulation in two unconnected conductive paths with different conductivity characteristics and refractory periods. Under certain circumstances, usually caused by premature contraction, the reentry syndrome leads to a prolonged circulation of the activated excitation wave, which causes tachyarrhythmia. Normally, re-entry is prevented by refractory tissue after stimulation. At the same time, three states contribute to the development of re-entry:

• shortening of the period of tissue refractoriness (for example, due to sympathetic stimulation);
• lengthening the path of the impulse (including hypertrophy or the presence of additional conductive pathways);
• slowing the pulse (for example, with ischemia).

Symptoms of rhythm and conduction of the heart

Arrhythmias and conduction abnormalities may occur asymptomatically or cause a palpitations, symptoms of hemodynamic disorders (eg, dyspnea, chest discomfort, pre-syncope or fainting) or cardiac arrest. Sometimes polyuria occurs due to the release of the atrial natriuretic peptide during prolonged supraventricular tachycardia (CBT).

Violation of the rhythm and conductivity of the heart: symptoms and diagnosis

Drug therapy for rhythm and conduction disorders

Treatment is not always required; The approach depends on the manifestations and danger of arrhythmia. Asymptomatic arrhythmias, not accompanied by high risk, do not require treatment, even if they occur with deterioration of survey data. At clinical displays therapy can be necessary for improvement of quality of a life of the patient. Potentially life-threatening arrhythmias are an indication for treatment.

Therapy depends on the situation. If necessary, an antiarrhythmic treatment is prescribed, including antiarrhythmic drugs, cardioversion-defibrillation, implantation of ECS, or a combination thereof.

Most antiarrhythmic drugs are divided into four main classes (Williams classification), depending on their effect on the electrophysiological processes in the cell / digoxin and adenosine phosphate are not included in the Williams classification. Digoxin shortens the refractory period of the atria and ventricles and is a vagotonik, as a result of which it lengthens the conduction along the AV node and its refractory period. Adenosine phosphate slows or blocks conduction on the AV node and can stop tachyarrhythmias that pass through this node during circulation of the pulse.

Violation of the rhythm and conductivity of the heart: drugs

[13], [14]

Implantable cardioverter-defibrillators

Implantable cardioverter-defibrillators perform cardioversion and heart defibrillation in response to VT or VF. Modern ICDF with the emergency therapy function involves the connection of the rhythm driver function in the development of bradycardia and tachycardia (with the aim of stopping sensitive supraventricular or ventricular tachycardia) and recording an intracardial electrocardiogram. Implantable cardioverter-defibrillators are sutured subcutaneously or retrosternally, electrodes are implanted transvenously or (more rarely) during thoracotomy.

Implantable cardioverter-defibrillators

Direct cardioversion-defibrillation

Transthoracic direct cardioversion-defibrillation of sufficient intensity depolarizes the entire myocardium as a whole, leading to instantaneous refractoriness of the entire heart and repetition of depolarization. After this, the fastest internal pacemaker, usually a sinus node, resumes control of the heart rhythm. Direct cardioversion-defibrillation very effectively stops tachyarrhythmias arising from re-entry. At the same time, the procedure is less effective for stopping arrhythmias due to automatism, since the restored rhythm is often automatic tachyarrhythmia.

Direct cardioversion-defibrillation

[15], [16], [17], [18], [19], [20], [21], [22]

Artificial pacemakers

Artificial pacemakers (IWR) are electrical appliances that produce electrical impulses sent to the heart. Permanent electrodes of artificial rhythm drivers are implanted with thoracotomy or by excessive access, but electrodes of some temporary emergency artificial pacemakers can be applied to the chest.

Artificial pacemakers

[23], [24], [25], [26], [27], [28], [29]

Surgery

Surgical intervention to remove the focus of tachyarrhythmia is no longer necessary after the introduction of a less traumatic technique of radiofrequency ablation. However, this method is sometimes used if the arrhythmia is refractory to radiofrequency ablation or there are other indications for cardiac surgery: most often, if patients with AF need to replace the valves or if VT is necessary, revascularization of the heart or excision of an aneurysm of the LV.

Radiofrequency ablation

If the development of tachyarrhythmia occurs due to the presence of a specific pathway or ectopic source of rhythm, this zone can be ablated with a low-voltage high-frequency (300-750 MHz) electric pulse supplied by an electrode catheter. Such energy damages and necroticizes the zone <1 cm in diameter and approximately 1 cm in depth. Before the moment of exposure to an electric discharge, the corresponding zones should be identified by electrophysiological examination.

Radiofrequency ablation