ARITHMIC

ARITHMIA - heart rhythm disturbances. They can complicate the course of such serious diseases as myocardial infarction, cardiosclerosis , acute myocarditis , valvular rheumatic heart diseases . There are the following basic disturbances of rhythm and conduction: sinus rhythm disturbances, supraventricular (supraventricular) extrasystole, paroxysmal supraventricular tachycardia , fibrillation and atrial flutter; Ventricular extrasystole, paroxysmal ventricular tachycardia , flutter and ventricular fibrillation; Conduction disorders - sinoauric blockade, atrioventricular blockade of I, II and III degree, blockade of the legs of the bundle.

Antiarrhythmic therapy is indicated only with poor subjective tolerance of rhythm disturbances and hemodynamically significant (complicated by the development of syncope, collapse, heart failure) and prognostically significant arrhythmias; These situations are also an indication for hospitalization. It should not be forgotten that antiarrhythmic drug therapy is not always safe. The probability of developing the arrhythmogenic effect (i.e., the development of arrhythmia due to the use of the drug) is on average 10% for each of the antiarrhythmics; Especially often it develops at ventricular arrhythmias and with organic myocardial damage with a violation of left ventricular function. This is probably why, since 1993, anti-arrhythmic drugs have been banned in Germany for the treatment of cardiac rhythm disturbances that do not threaten life.

The use of antiarrhythmic drugs is mainly the prerogative of a doctor; The average medical personnel may be entrusted with monitoring the effectiveness of therapy in the intervals between medical examinations. At the same time, irregularities in the rhythm often require urgent care, as they cause severe circulatory disorders, and sometimes they themselves pose a threat to the life of the patient. Consequence of arrhythmia with violation of hemodynamics can be an attack of angina pectoris, acute heart failure , fainting , collapse or shock , impaired cerebral circulation, thromboembolism . Therefore, in case of impossibility of rendering medical assistance, in emergency situations antiarrhythmic therapy must be performed by a paramedic.

Sinus tachycardia , bradycardia and arrhythmia , constant form of atrial fibrillation and flutter without signs of decompensation, extrasystole (with the exception of ventricular with acute myocardial infarction), atrioventricular blockade of I and II degrees in persons without a history of myocardial infarction, blockade of the bundle of the bundle in most cases in general Do not require medical treatment. Emergency therapy of arrhythmias is performed with paroxysmal supraventricular and ventricular tachycardia, paroxysmal form of atrial fibrillation, and with violations of atrioventricular conduction with the development of syncope (Morgagni-Adams-Stokes syndrome).

Paroxysmal tachycardia is a palpitations with a heart rate of more than 160 in 1 min while maintaining the correct sequence of contractions. In most cases, the cause of paroxysmal tachycardia is circular motion of the pulse - the mechanism of re-entry, less often it is caused by a heterogeneous pacemaker (an unusual focus of excitation located in the atria or ventricles). Paroxysmal tachycardia can occur with myocardial infarction, myocarditis, mitral stenosis, thyrotoxicosis. In the origin of seizures, violations at different levels of nervous regulation of the rhythm of the heart have a certain significance.

The attack begins suddenly. In addition to palpitation, patients often experience a sense of fear, sometimes join in shortness of breath , constricting pain in the heart. The attack lasts from several minutes to several days and stops as suddenly. After this, the patient often feels a pleasant relief, accompanied by a feeling of weakness. After an attack, a large amount of clear urine is usually released.

During the attack, the pallor of the skin, the pulse of small filling, rhythmic, but so frequent that it can not be counted, are revealed. Blood pressure decreases. The heart sounds are loud, the pause between II and I is shortened. With a multi-hour attack of paroxysmal tachycardia, cyanosis develops, cervical veins swell, dyspnea , BP decreases significantly, pulse pressure decreases, angina pains occur more often. The cause of the development of heart failure with prolonged paroxysmal tachycardia are hemodynamic disorders with a shortened diastole time, difficulty in the inflow of blood to the ventricles of the heart, a decrease in the impact and minute volume of the heart, and a worsening of the peripheral and coronary circulation.

Obligatory electrocardiography with this symptomatology confirms the presence of paroxysmal tachycardia and allows to establish the localization of the pathological pacemaker. Depending on its location, paroxysmal tachycardia is divided into supraventricular (supraventricular) and ventricular forms. With supraventricular tachycardia, the ECG is overwhelmingly registered with undeformed QRS complexes (sometimes their shape may change due to impaired excitation), the heart rate may be in the range 150 - 250 per minute. With ventricular tachycardia, three or more consecutive wide (more than 0.12 s) QRS complexes with a frequency of 100 to 250 per minute are detected on the ECG with a shift of the ST segment and a T wave in the direction opposite to the main QRS complex tooth. Ventricular tachycardia is more often observed with gross organic pathology of the heart and has a more serious prognosis.

The diagnosis of paroxysmal tachycardia is usually established on the basis of the patient's characteristic complaints, examination data revealing a sharp tachycardia (over 160 beats per minute) with the correct rhythm of contractions of the heart, and an electrocardiographic picture.

Emergency care for an attack of supraventricular paroxysmal tachycardia should begin with an assessment of the state of the circulation. The drop in blood pressure with the development of syncopal conditions is an indication for immediate electroimpulse therapy with a discharge of 100-200 J (performed by a doctor). If the hemodynamics is stable, the patient's consciousness is clear, then the cupping of paroxysm begins with techniques aimed at stimulating the vagus nerve and slowing down through the atrioventricular node. Sometimes it is possible to interrupt an attack with a delay of breathing, a cough, a sharp straining after a deep inspiration (Valsalva test), artificial vomiting, swallowing the crust of bread, immersing the face in ice water. Often, a patient with a recurrent episode of paroxysmal tachycardia himself knows which of the techniques helps him.

The ineffectiveness of reflex techniques requires the urgent hospitalization of a patient or providing him with medical assistance on the spot; If for any reason this is not possible, the anti-arrhythmic therapy is performed by the paramedic. Therapy of paroxysmal supraventricular tachycardia begins with intravenous adenosine (ATP) interrupting the "re-entry" circle due to a short-term slowing of the atrioventricular conduction and often a transient stop of the sinus node. Adenosine is characterized by a rapid onset of action and a short half-life (about 10 s), so its use is safe even in case of an erroneous appointment with ventricular tachycardia. 20 mg (2 ml of a 1% solution) of ATP is administered intravenously struino for 5-10 seconds, in the absence of effect after 2 to 3 minutes, another 20 mg (2 ml of 1% solution) are re-introduced. Side effects (cough, chest discomfort, skin hyperemia, bradycardia) pass independently for 1 min.

If adenosine is ineffective, the use of a calcium antagonist verapamil (isoptin), which also worsens atrioventricular conduction, but which lasts longer (up to 30 min), is indicated. The drug is injected intravenously in a dose of 5-10 mg for 2 minutes. With the initial hypotension (systolic blood pressure less than 100 mm Hg), 500-1000 mg of calcium chloride is preliminarily administered intravenously. Such preparation does not affect the antiarrhythmic activity of verapamil, but prevents its hypotensive effect. Verapamil restores rhythm in paroxysmal supraventricular tachycardia in 90% of cases. With ventricular tachycardia and Wolff-Parkinson-White syndrome, it is contraindicated, since it increases the risk of developing ventricular fibrillation.

Novocainamide , which is administered as a 10% solution of 5 or 10 ml intravenously with 10-15 ml of a 40% glucose solution, remains a reliable agent. In connection with the possibility of reducing blood pressure, novocainamide should be administered in the horizontal position of the patient, having a syringe ready with 1 ml of a 1% solution of mezaton. Introduction is carried out slowly, within 5 - 7 minutes, preferably under the control of auscultation. At the time of restoring the normal rhythm, which often occurs during infusion, literally "under the needle" -, the drug should be discontinued. The advantage of novocainamide is its effectiveness in paroxysmal ventricular tachycardia.

The tactics of treating paroxysmal ventricular tachycardia also depend on the stability of hemodynamics. If the patient does not have a pulse or if there is arterial hypotension, shortness of breath , acute heart failure , stenocardia , the patient is shown emergency electroimpulse therapy - cardioversion with a discharge of 200 J, with inefficiency - a repeated discharge of 360 J.

With stable hemodynamics, the drug of choice for arresting paroxysmal ventricular tachycardia is lidocaine, usually administered intravenously slowly with 4-5 ml of a 2% solution, followed by dropwise administration (6 ml of 2% solution is diluted in 60 ml of sodium chloride solution). Lidocaine is rapidly destroyed and removed from the body, so if necessary, it can be re-administered in the same dose after 20-30 minutes. An additional agent may be magnesium sulfate, 1 - 2 g of the drug is diluted in 100 ml of 5% glucose solution and injected intravenously for 1-2 minutes.

In the treatment of tachycardia of an unknown nature with a wide complex of QRS (ventricular, or supraventricular with disruption or blockade of the bundle of the bundle of His), treatment is started with novocaineamide, effective for all paroxysmal tachycardias.

In case of ineffectiveness of urgent measures or the appearance of symptoms of heart failure (swelling of the veins of the neck, dyspnea, cyanosis , enlargement of the liver, falling blood pressure) and other signs of unstable hemodynamics, the patient must be hospitalized in a therapeutic hospital. Transportation should be carried out in ambulance transport, on stretchers.

Prevention of paroxysms of supraventricular tachycardia is indicated in patients in whom they occur frequently or are accompanied by painful subjective sensations. To this end, use verapamil, beta-blockers, less often - quinidine , novocainamide . In the prevention of paroxysms of ventricular tachycardia, quinidine, novocaineamide , mexitylene, amiodarone ( cordarone ) are effective ; Beta-blockers are less effective.

Extrasystolia is a violation of the heart rhythm associated with the appearance of additional foci of excitation, generating extraordinary pulses with premature contraction of the heart. Localization of the focus of excitation distinguishes between supraventricular (supraventricular) and ventricular extrasystole. Because after contraction the myocardium remains insensitive for some time (refractory) to the next pulse from the sinus node, there is a long (compensatory) pause between cardiac contractions. With ventricular extrasystole, an extra wide (more than 0.12 s) deformed QRS complex, a discordant displacement of the ST segment and a T wave, a complete compensatory pause (the interval between pre- and postextrasystolic denticles P is equal to twice the normal PP interval) is recorded on the ECG. Potentially life-threatening can be considered ventricular extrasystole in acute myocardial infarction (when even a single extrasystole may cause ventricular fibrillation) and frequent group extrasystole in patients with organic myocardial damage (for example, postinfarction cardiosclerosis). With acute myocardial infarction, the drug of choice for arresting ventricular arrhythmias is lidocaine; In case of its inefficiency Novocaineamide can be used . In other cases, beta-blockers, cordarone, mexiletine , propafenone are more often used .

Atrial fibrillation (atrial fibrillation) is a disorder of the rhythm, in which there is no one-stage contraction of them - systole of the atria, there are indiscriminate contractions of certain groups of muscle fibers of the myocardium of the atria. The consequence of this is a violation of the work of the heart ventricles coordinated with atrium contractions, the duration of the diastole becomes unstable, the correct sequence of contractions of the heart and, accordingly, pulse waves is violated, which is defined as absolute arrhythmia.

The paroxysmal form of atrial fibrillation most often complicates the course of severe organic heart diseases. Most often it is observed with rheumatic mitral heart defects, cardiosclerosis, myocardial infarction, thyrotoxicosis. Atrial fibrillation may occur periodically as paroxysms or be permanent; The prescription of arrhythmia is always subject to specification, since it largely determines the therapeutic tactics.

Clinic of paroxysm of atrial fibrillation resembles a picture of paroxysmal tachycardia. The attack begins suddenly, accompanied by the same painful subjective sensations. Objectively reveal a sharp irregularity of gaps between individual contractions of the heart, tachycardia with a frequency of abbreviations of more than 160 in 1 min. The pulse wave frequency at the periphery is usually much lower than the number of heartbeats, that is, the pulse deficit is determined. Sometimes it is possible to distinguish the paroxysm of atrial fibrillation from paroxysmal tachycardia only on the basis of an electrocardiographic study. On the ECG with atrial fibrillation there are no atrial complexes, the intervals RR are different.

Atrial fibrillation paroxysm significantly worsens hemodynamics, intensifies manifestations of heart failure, accompanied by a marked decrease in blood pressure. Frequently repeated atrial fibrillation paroxysms usually precede the development of a persistent form of atrial fibrillation.

Atrial fibrillation with a low heart rate does not require emergency therapy. With paroxysm of atrial fibrillation and unstable hemodynamics, cardioversion is performed (beginning with a discharge of 100 J). If the arrhythmia with a high heart rate is tolerated well, drug therapy is indicated. Therapy begins with the introduction of intravenously slowly 10 ml of a 10% solution of Novocainamide in 20 ml of a 5% solution of glucose or isotonic sodium chloride solution.

In those cases when the paroxysm of atrial fibrillation lasts more than 2 days, or it is difficult to establish the timing of the occurrence of paroxysm (tachycardia in a patient with a constant form of atrial fibrillation can not be excluded), cardiac glycosides become the means of reducing heart rate. Intravenously, 1 ml of a 0.025% solution of digoxin is injected strontaneously. Indication for the use of cardiac glycosides is also heart failure , usually rapidly increasing with atrial fibrillation. With Wolff-Parkinson-White syndrome, verapamil and digoxin are contraindicated.

Patients with a prolonged paroxysm of atrial fibrillation, as well as signs of decompensation of blood circulation against a background of constant atrial fibrillation, are hospitalized in a therapeutic hospital on ambulance transport, on stretchers.

Atrioventricular blockade - a violation of atrioventricular (from the atrium to the ventricles) conduction - is more common in patients with atherosclerotic cardiosclerosis, with inflammatory heart diseases - myocarditis of rheumatic or other etiology, with digitalis intoxication (foxglove poisoning) or overdose of other drugs that affect conductivity. Atrioventricular blockade requires urgent therapy in case of fainting (Morgagni-Adams-Stokes syndrome).

A sudden loss of consciousness occurs more often:

• With atrioventricular blockade II degree II type. Individual impulses from the sinus node do not reach the ventricles at this time and cause only a contraction of the atria; On the ECG, abaissement of the ventricular complex after the P wave is recorded in the normal or extended PQ interval;

• At the transition of incomplete atrioventricular blockade to full, when all impulses from the sinus node do not reach the ventricles, which have to develop their own rhythm; The frequency of ventricular contractions is usually 20-40 beats per minute, which is not sufficient for adequate blood supply to the brain. На ЭКГ полная поперечная блокада проявляется правильным ритмом предсердных комплексов — интервал РР одинаковый, отсутствием стабильного интервала PQ, периодическим наслоением зубцов Р на комплекс QRS, постоянным интервалом RR, комплекс QRS не изменен или уширен.

При этих нарушениях проводимости у некоторых пациентов во время паузы между сокращениями миокарда возникают и спонтанно прекращаются эпизоды фибрилляции желудочков, что еще более ухудшает прогноз.

Morgagni-Adams-Stokes syndrome is characterized by a sharp appearance of sudden pallor with subsequent loss of consciousness, swelling of the veins of the neck, acrocyanosis, twitching of the facial muscles, and then tonic general cramps in combination with a periodic lack of pulse. Auscultation reveals rare muffled tones, at times a loud I tone is heard, caused by a simultaneous contraction of the atria and ventricles. These symptoms are explained by the fact that the absence of ventricular contraction and the flow of blood into the aorta and pulmonary trunk leads to the development of acute brain ischemia and increasing tissue hypoxia. Attacks rarely last more than 2 minutes, after the restoration of consciousness, there is skin hyperemia. Attacks Morgani-Adams-Stokes, as a rule, do not lead to neurologic complications, in some patients, confusion may persist for a long time.

However, this detailed picture of the seizure is far from always observed. Often there are reduced, abortive forms, expressed in short-term fainting, a sense of failure with loss of consciousness for just a moment. The duration of such attacks sometimes does not exceed 15 to 20 seconds. Appearance of a patient with a heart pathology of complaints of frequent fainting, short-term loss of consciousness should always be alarming, since such symptoms may be a manifestation of the Morgagni-Adams-Stokes syndrome.

Medical treatment of hemodynamically significant bradycardia is primarily aimed at increasing the frequency of ventricular contractions. To this end, atropine is slowly intravenously injected atropine (0.5-1.0 mg), the administration is repeated every 3 to 5 minutes until a total dose of 2 mg is reached. In acute myocardial infarction, the introduction of atropine requires particularly careful monitoring, as it can increase myocardial ischemia and provoke ventricular rhythm disturbances; In addition, atropine is contraindicated in chronic urinary retention and glaucoma.

The patient with complete transverse blockade and the first appearance of Morgagni-Adams-Stokes syndrome is subject to compulsory admission to the cardiology department, where necessary examination and observation and, if necessary, permanent or temporary cardiostimulation. Transportation is carried out according to the rules of transportation of patients with myocardial infarction.