Heart rhythm and conduction disorders

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

Any heart disease, including congenital abnormalities of its structure (eg, accessory AV pathways) or function (eg, inherited ion channel disorders), can cause arrhythmia. Systemic etiologic factors include electrolyte disturbances (primarily hypokalemia and hypomagnesemia), hypoxia, hormonal disturbances (such as hypothyroidism and thyrotoxicosis), and exposure to drugs and toxins (particularly alcohol and caffeine).

Anatomy and physiology of cardiac rhythm and conduction disorders

At the entry of the superior vena cava into the upper lateral portion of the right atrium is a collection of cells that generates the initial electrical impulse that drives each heartbeat. This is called the sinoatrial node (SA), or sinus node. The electrical impulse emanating from these pacemaker cells stimulates receptive cells, causing areas of the myocardium to activate in the appropriate sequence. The impulse is conducted through the atria to the atrioventricular (AV) node via the most active internodal pathways and nonspecific atrial myocytes. The AV node is located on the right side of the interatrial septum. It has a low conductivity, so it slows down the conduction of the impulse. The conduction time of the impulse through the AV node depends on the heart rate and is regulated by its own activity and the influence of circulating catecholamines, which allows an increase in cardiac output in accordance with the atrial rhythm.

The atria are electrically isolated from the ventricles by the fibrous ring, with the exception of the anterior septum. Here, the bundle of His (which is a continuation of the AV node) enters the superior portion of the interventricular septum and divides into left and right bundle branches, which terminate in the Purkinje fibers. The right bundle branch conducts the impulse to the anterior and apical portion of the endocardium of the right ventricle. The left bundle branch passes along the left portion of the interventricular septum. The anterior and posterior branches of the left bundle branch stimulate the left portion of the interventricular septum (the first portion of the ventricle to receive the electrical impulse). The interventricular septum thus depolarizes from left to right, resulting in nearly simultaneous activation of both ventricles from the endocardial surface through the ventricular wall to the epicardium.

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Electrophysiology of cardiac rhythm and conduction disorders

Transport of ions across the myocyte membrane is regulated by specialized ion channels that perform cyclic depolarization and repolarization of the cell, called the action potential. The action potential of a functioning myocyte begins with depolarization of the cell from the diastolic transmembrane potential of -90 mV to a potential of about -50 mV. At this threshold potential, Na ⁺ -dependent fast sodium channels open, resulting in rapid depolarization due to the rapid outflow of sodium ions along the concentration gradient. The fast sodium channels are quickly inactivated and the sodium efflux ceases, but other time- and charge-dependent ion channels open, allowing calcium to enter the cell through the slow calcium channels (the depolarization state) and potassium to exit through the potassium channels (the repolarization state). Initially, these two processes are balanced and provide a positive transmembrane potential, prolonging the plateau of the action potential. During this phase, calcium entering the cell is responsible for the electromechanical interaction and contraction of the myocyte. Eventually, calcium influx ceases and potassium influx increases, resulting in rapid repolarization of the cell and its return to the resting transmembrane potential (-90 mV). While in the depolarization state, the cell is resistant (refractory) to the next episode of depolarization; at first, depolarization is impossible (period of absolute refractoriness), but after partial (but not complete) repolarization, subsequent depolarization is possible, although slow (period of relative refractoriness).

There are two main types of tissue in the heart. Fast-channel tissues (functioning atrial and ventricular myocytes, the His-Purkinje system) contain large numbers of fast sodium channels. Their action potential is characterized by a rare or complete absence of spontaneous diastolic depolarization (and therefore very low pacemaker activity), a very high rate of initial depolarization (and therefore high capacity for rapid contraction), and low refractoriness to repolarization (in light of this, a short refractory period and the ability to conduct repeated impulses at a high frequency). Slow-channel tissues (the SP and AV nodes) contain few fast sodium channels. Their action potential is characterized by a more rapid spontaneous diastolic depolarization (and therefore more pronounced pacemaker activity), a slow initial depolarization (and therefore low contractility), and a low refractoriness that is delayed from repolarization (and therefore a long refractory period and inability to conduct frequent impulses).

Normally, the SB node has the highest spontaneous diastolic depolarization rate, so its cells generate spontaneous action potentials at a higher rate than other tissues. For this reason, the SB node is the dominant tissue with automaticity (pacemaker) function in the normal heart. If the SB node does not generate impulses, the pacemaker function is assumed by tissue with a lower level of automaticity, usually the AV node. Sympathetic stimulation increases the excitation rate of the pacemaker tissue, and parasympathetic stimulation inhibits it.

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Normal heart rhythm

The heart rate, influenced by the pulmonary node, is 60-100 beats per minute at rest in adults. A lower rate (sinus bradycardia) may occur in young people, especially athletes, and during sleep. A more rapid rhythm (sinus tachycardia) occurs during physical exertion, illness, or emotional stress due to the influence of the sympathetic nervous system and circulating catecholamines. Normally, there are marked fluctuations in heart rate, with the lowest heart rate early in the morning, before awakening. A slight increase in heart rate during inhalation and a decrease during exhalation (respiratory arrhythmia) is also normal; this is due to changes in the tone of the vagus nerve, which is common in young healthy people. With age, these changes decrease, but do not disappear completely. Absolute correctness of the sinus rhythm can be pathological and occurs in patients with autonomic denervation (for example, in severe diabetes mellitus) or in severe heart failure.

The electrical activity of the heart is mainly displayed on the electrocardiogram, although the depolarization of the SA, AV nodes and the His-Purkinje system by itself does not involve a sufficient volume of tissue to be clearly visible. The P wave reflects atrium depolarization, the QRS complex reflects ventricular depolarization, and the QRS complex reflects ventricular repolarization. The PR interval (from the beginning of the P wave to the beginning of the QRS complex) reflects the time from the beginning of atrial activation to the beginning of ventricular activation. Most of this interval reflects the slowing of impulse conduction through the AV node. The RR interval (the interval between two R complexes) is an indicator of ventricular rhythm. The interval (from the beginning of the complex to the end of the R wave) reflects the duration of ventricular repolarization. Normally, the duration of the interval is somewhat longer in women, and it also lengthens with a slowing rhythm. The interval changes (QTk) depending on the heart rate.

Pathophysiology of cardiac rhythm and conduction disorders

Rhythm disturbances are the result of disturbances in impulse formation, conduction, or both. Bradyarrhythmias occur as a result of decreased internal pacemaker activity or conduction block, primarily at the level of the AV node and the His-Purkinje system. Most tachyarrhythmias occur as a result of the re-entry mechanism, some are the result of increased normal automatism or pathological mechanisms of automatism.

Re-entry is the circulation of an impulse in two unrelated conduction pathways with different conduction characteristics and refractory periods. Under certain circumstances, usually created by premature contraction, re-entry syndrome results in prolonged circulation of the activated excitation wave, which causes tachyarrhythmia. Normally, re-entry is prevented by tissue refractoriness after stimulation. At the same time, three conditions contribute to the development of re-entry:

• shortening of the tissue refractoriness period (for example, due to sympathetic stimulation);
• lengthening of the impulse conduction pathway (including in the case of hypertrophy or the presence of additional conduction pathways);
• slowing of impulse conduction (for example, during ischemia).

Symptoms of cardiac rhythm and conduction disorders

Arrhythmias and conduction disturbances may be asymptomatic or cause palpitations, hemodynamic symptoms (eg, dyspnea, chest discomfort, presyncope or syncope), or cardiac arrest. Polyuria occasionally occurs due to release of atrial natriuretic peptide during sustained supraventricular tachycardia (SVT).

Heart rhythm and conduction disorders: symptoms and diagnosis

Drug treatment of rhythm and conduction disorders

Treatment is not always required; the approach depends on the manifestations and severity of the arrhythmia. Asymptomatic arrhythmias that are not associated with high risk do not require treatment, even if they occur with worsening examination data. In case of clinical manifestations, therapy may be needed to improve the patient's quality of life. Potentially life-threatening arrhythmias are an indication for treatment.

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

Most antiarrhythmic drugs are divided into four main classes (Williams classification) depending on their effect on 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 vagotonic, as a result of which it prolongs conduction through the AV node and its refractory period. Adenosine phosphate slows or blocks conduction through the AV node and can terminate tachyarrhythmias that pass through this node during impulse circulation.

Heart rhythm and conduction disorders: medications

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Implantable cardioverter defibrillators

Implantable cardioverter-defibrillators perform cardioversion and defibrillation of the heart in response to VT or VF. Modern ICDs with an emergency therapy function involve connecting the pacemaker function in the development of bradycardia and tachycardia (in order to stop sensitive supraventricular or ventricular tachycardia) and recording an intracardiac electrocardiogram. Implantable cardioverter-defibrillators are sutured subcutaneously or retrosternally, the electrodes are implanted transvenously or (less often) during thoracotomy.

Implantable cardioverter defibrillators

Direct cardioversion-defibrillation

Transthoracic direct cardioversion-defibrillation of sufficient intensity depolarizes the entire myocardium, causing immediate whole-heart refractoriness and re-depolarization. The fastest intrinsic pacemaker, usually the sinus node, then resumes control of the heart rhythm. Direct cardioversion-defibrillation is very effective in terminating re-entry tachyarrhythmias. However, the procedure is less effective in terminating automatic arrhythmias, since the restored rhythm is often an automatic tachyarrhythmia.

Direct cardioversion-defibrillation

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Artificial pacemakers

Artificial pacemakers (APs) are electrical devices that generate electrical impulses sent to the heart. Permanent pacemaker leads are implanted via thoracotomy or transvenous access, but some temporary emergency pacemakers can have leads placed on the chest.

Artificial pacemakers

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Surgical treatment

Surgical intervention to remove the focus of tachyarrhythmia has become unnecessary 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 require valve replacement or VT require cardiac revascularization or excision of an LV aneurysm.

Radiofrequency ablation

If the development of tachyarrhythmia is due to the presence of a specific conduction pathway or an ectopic rhythm source, this zone can be ablated by a low-voltage, high-frequency (300-750 MHz) electrical impulse delivered by an electrode catheter. This energy damages and necrotizes an area < 1 cm in diameter and approximately 1 cm deep. Before the moment of application of the electrical discharge, the corresponding zones must be identified by electrophysiological examination.

Radiofrequency ablation