How is the arrhythmia manifested?
Arrhythmia is clinically divided into the following types:
The sinus node is the most important element of the myocardium, it provides the formation of the electropulse transfer. This is an excessively active contraction of the muscle, exceeding the prescribed 90 beats per minute. Subjectively, such an arrhythmia is felt as an intensified heartbeat. To provoke a tachycardia the stress, intensive, unusual physical loading can. Less often, tachycardia causes internal diseases.
The frequency of contraction of the heart muscle decreases, sometimes decreases to 50 beats per minute. Bradycardia does not necessarily signal problems of the cardiovascular system, at times it can manifest in absolutely healthy people during complete relaxation or sleep. Also, bradycardia is characteristic of hypotension and for those who suffer from hypothyroidism. Subjective feelings can manifest weakness, a feeling of pressure in the heart, dizziness.
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Typical for young children and children in the puberty period. Alternation of cardiac strokes can be associated with the active growth of organs and systems, as well as with breathing. This type of arrhythmia does not require therapeutic intervention.
This is an unplanned violation of rhythmic muscle contraction. The rhythm seems to be lost. This kind of arrhythmia provokes an unhealthy lifestyle, smoking, alcohol abuse. It is also often associated with a basic somatic disease, if the cause is eliminated, or goes into the stage of remission or disappears. Subjectively manifested sudden heart beats or the same sudden fading of the heart.
This is an excessive activity of the heart, which beats rhythmically, but too quickly. The frequency of impacts sometimes exceeds the rate of 200 beats per minute. It is often accompanied by vegetative reactions, sweating, dizziness, reddening of the facial skin.
Atrial fibrillation (atrial fibrillation)
This kind of arrhythmia is provoked by cardiosclerosis, rheumatic carditis, thyroid gland diseases. Often the cause of atrial fibrillation is heart disease. Individual parts of the heart muscle begin to randomly shrink against a background of incomplete contraction of the atrium itself. The auricles may be "trembling", subjective sensations are similar - flutter, dyspnea. The main clinical sign of atrial fibrillation is the pulse, which is noticeably behind the frequency of contractions of the heart muscle. On prognostic values this is the most dangerous arrhythmia, which can result in loss of consciousness, cramps, and cardiac arrest.
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Blockade of the heart is characterized by a complete loss of heart rate. This is because impulses cease to be carried out on the structures of the myocardium in the right rhythm, sometimes this process slows down so much that the patient hardly feels a pulse. It is also a life-threatening arrhythmia, because besides convulsions and fainting, it can end with heart failure until death.
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Disorders of cardiac rhythm and myocardial conductivity that occur in the periarest period (i.e., before the circulatory arrest and after its restoration) pose a significant danger to the patient's life (in the English-language literature they were called periarrest arrhythmias). This arrhythmia can dramatically worsen central hemodynamics and quickly lead to a stop of blood circulation.
Cardiac arrhythmias and conduction disorders can occur as a result of a variety of pathological conditions, but changes in heart punctures, such as automatism, excitability and conductivity, are at the heart of it.
Among the factors responsible for the development of arrhythmia, pain syndrome, ischemia, electrolyte balance disorders, elevated levels of catecholamines, angiotensin, metabolic acidosis, arterial hypo- and hypertension are more important. These factors not only predispose to the development of arrhythmias, but also reduce the activity of antiarrhythmic drugs.
Pain, ischemia and electrolyte imbalance are reversible causes of life-threatening tachyarrhythmias, they define a risk group for potential arrhythmic events.
All arrhythmias that precede the arrest of blood circulation and arrhythmia that occurs after the restoration of spontaneous circulation require intensive intensive therapy to prevent cardiac arrest and stabilize hemodynamics after successful resuscitation.
At the heart of the gradation of periarest arrythmia lies the presence or absence of the patient of unfavorable signs and symptoms associated with a violation of the rhythm of the cardiac activity, and indicative of instability of the condition. The main features are listed below.
- Clinical symptomatology of reduced cardiac output. Signs of activation of the sympathoadrenal system: pallor of the skin, increased sweating, cold and wet extremities, increased signs of impaired consciousness due to a decrease in cerebral blood flow, Morgagni-Adam-Stokes syndrome, arterial hypotension (systolic pressure less than 90 mm Hg).
- Severe tachycardia. Excessive heart rhythm (more than 150 per 1 minute) decreases coronary blood flow and can cause myocardial ischemia.
- Heart failure. Left ventricular failure is indicated by pulmonary edema, and increased pressure in the jugular veins (swelling of the jugular veins) and enlarged liver indicate a lack of the right ventricle.
- Pain syndrome. The presence of pain in the chest means that arrhythmia, especially tachyarrhythmia, is caused by myocardial ischemia. The patient may, at the same time, present or not complain about the rapidity of the rhythm.
Threatening arrhythmia - violations of the heart rhythm, immediately preceding and transforming into fibrillation and asystole of the ventricles. Long-term electrocardiographic monitoring showed that ventricular fibrillation is most often preceded by paroxysms of ventricular tachycardia with a gradual increase in the rhythm, which translates into a flutter of the ventricles. A dangerous form of ventricular tachycardia is the "tachycardia of a vulnerable period," a characteristic feature of which is the onset of early ventricular extrasystoles.
The most threatening are episodes of polytopic ventricular tachycardia, in particular, bidirectional-spindle-shaped "pirouette" ventricular tachycardia (torsades de pointes - is rare enough). This kind of polymorphic, pause-dependent ventricular arrhythmia occurs under conditions of an elongated QT interval. There are two main forms of this tachyarrhythmia: acquired arrhythmia (provoked by medications) and congenital arrhythmia. Antiarrhythmic drugs with these forms can act as causal agents and as agents of proarrhythmia. For example, pirouette ventricular tachycardia can be triggered by drugs that increase the duration of the membrane potential of the action of cardiomyocytes (antiarrhythmic drugs of class IA, III and others). However, in itself, prolonging the QT interval does not necessarily cause arrhythmia.
Among the factors influencing the development of torsades de pointes, there are:
- treatment with diuretics;
- increased plasma concentration of antiarrhythmic drugs (with the exception of quinidine);
- rapid intravenous administration of the drug;
- conversion of atrial fibrillation into a sinus rhythm with the appearance of a pause or bradycardia;
- prolongation of QT interval, lability of Gili's tooth, its morphological changes, increase in QT dispersion during therapy;
- congenital syndrome of the extended QT interval.
Intracellular calcium overload can significantly increase the risk of torsades de pointes. Genetic anomalies in the coding of transmembrane ion channels increase the risk of torsades de pointes due to metabolic disturbance of drugs.
The use of cordarone, which contributes to the elongation of the QT interval, does not lead to the appearance of torsades de pointes. In patients with hypokalemia. Hypomagnesemia and bradycardia (especially in females), the heterogeneity of the drug effect of antiarrhythmic drugs at different levels of the myocardium increases. There is evidence that this heterogeneity can be reduced by blockade of arrhythmogenic currents with cordarone.