heart Arrhythmias

Cardiac arrhythmias - disturbances of frequency, rhythm and sequence of contractions of the heart. Arrhythmias can occur at structural changes in the conduction system of the heart with diseases and (or) under the influence of autonomic, endocrine, and electrolyte, and other metabolic disorders, with intoxication and some medicinal effects. Often, even when expressed structural changes in the myocardium arrhythmia is caused partly or mainly metabolic disorders. The above factors affect the basic function (automaticity, conductivity) of the entire vascular system or its departments, cause the electrical inhomogeneity of the myocardium, leading to arrhythmia. In some cases, arrhythmias are caused by individual congenital anomalies of the conducting system. Severity of arrhythmic syndrome may not reflect the severity of underlying heart disease. Arrhythmias are diagnosed primarily by ECG. Most arrhythmias can be diagnosed and differentiated clinical and electrocardiographic signs. Occasionally you need a special electrophysiological study (or intracardiac electrography intraesophageal with stimulation of departments conducting system), performed in specialized cardiac facilities. Arrhythmias Treatment always includes treatment of the underlying disease and the actual antiarrhythmic action.

The normal rhythm is provided by the automatism of the sinus node is called sinus. The frequency of sinus rhythm in most healthy adults at rest is 60-75 beats / min.

Sinus arrhythmia - sinus rhythm, in which the difference between the RR intervals on ECG greater than 0.1. Respiratory sinus arrhythmia - physiological phenomenon, it is more pronounced (by pulse or ECG) in young individuals, and with slow, but deep breathing. Factors quickens sinus rhythm (physical and emotional stress, sympathomimetics), reduce or eliminate the respiratory sinus arrhythmia. Sinus arrhythmia is not associated with breathing, it is rare. Sinus arrhythmia itself does not require treatment.

Sinus tachycardia - sinus rhythm with a frequency of more than 90-100 in 1 min. In healthy people, it occurs on exertion and emotional excitement. Marked tendency to sinus tachycardia - a manifestation of neuro dystonia, in which case the tachycardia markedly reduced when breath-hold. Temporarily sinus tachycardia occurs under the influence of atropine, sympathomimetic, with a rapid decrease in blood pressure of any nature, after taking alcohol. More persistent sinus tachycardia is in fever, hyperthyroidism, infarction, heart failure, anemia, pulmonary embolism. Sinus tachycardia can be accompanied by palpitations.

Treatment should be directed at the underlying disease. When tachycardia caused by hyperthyroidism, secondary importance is the use of beta-blockers. When sinus tachycardia associated with neuro dystonia may be useful sedatives, beta-blockers (in small doses); Verapamil: tachycardia, caused by heart failure, cardiac glycosides administered.

Sinus bradycardia - sinus rhythm with a frequency of less than 55 in 1 min in healthy fre- quently, especially in physically trained persons at rest, in a dream. It is often combined with marked respiratory arrhythmia, sometimes with arrythmia. Sinus bradycardia can be one of the manifestations of neuro dystonia. Sometimes it occurs in zadnediafragmalnom myocardial infarction, in various pathological processes (ischemic, sclerosis, inflammatory, degenerative) in the sinus node (sick sinus syndrome - see below.), With an increase in intracranial pressure, reduced thyroid function in some viral infections under the influence of certain drugs (cardiac glycosides, beta-blockers, verapamil, sympatholytic, especially reserpine). Sometimes bradycardia it manifested in the form of unpleasant sensations in the heart.

Treatment is directed at the underlying disease. In severe sinus bradycardia caused by neuro dystonia and some other reasons, sometimes effective Belloidum, alupent, aminophylline, which may have a temporary symptomatic effect. In rare cases (severe symptoms) shows a temporary or permanent pacing.

Ectopic rhythms. With the weakening or termination of the activity of the sinus node may occur (temporary or permanent) replacement ectopic beats, that is, reduction of the heart due to the manifestation of automaticity of other parts of the conduction system or myocardium. Their frequency is usually lower than the frequency of sinus rhythm. Typically, the distal source of ectopic rhythm, the less the frequency of its pulse. Ectopic beats may occur in inflammatory, ischemic, sclerotic changes in the sinus node and in other parts of the conduction system, they can be one of the manifestations of sick sinus syndrome (see. Below). Supraventricular ectopic rhythm may be associated with autonomic dysfunction, an overdose of cardiac glycosides.

Occasionally ectopic rhythm due to increased automaticity of ectopic center; while the heart rate is higher than when the replacement ectopic rhythm (rapid ectopic rhythm). The presence of ectopic rhythm and its source determined by ECG only.

Atrial rhythm characterized by a configuration change P wave diagnostic features of its vague. Sometimes P wave shape and the length P-Q changes from cycle to cycle, which is associated with the migration of the atria pacemaker. Atrio-ventricular rate (rate of atrioventricular connection area) is characterized by the inversion of P-wave, which can be detected near the ventricular complex or superimposed on it. For replacement atrioventricular rhythm characteristic frequency of 40-50 in 1 min for fast-60-100 in 1 min. If ectopic focus a little more active than the sinus node and the opposite impulse conduction is blocked, then there are the conditions for partial atrioventricular dissociation, with periods of sinus rhythm alternating with periods of replacement atrioventricular (rare ventricular) rate, which feature is more rare the rhythm of the atria (P) and independent, but more frequent ventricular rhythm (QRST). Ectopic ventricular rhythm (regular P wave is missing, deformed ventricular complexes, the frequency of 20-50 in 1 min) usually indicates a significant change in the myocardium, at a very low rate of ventricular contractions may contribute to ischemia of vital organs.

Treatment. When the above ectopic rhythms should treat the underlying disease. Atrioventricular rhythm and incomplete atrioventricular dissociation associated with autonomic dysfunction, may be temporarily eliminated by atropine or atropine drug. In rare ventricular rhythm may become necessary temporary or permanent pacing.

Extrasystoles - premature contractions of the heart, caused by the occurrence of the pulse is the sinus node. Extrasystole can accompany any heart disease. No less than half the time beats not associated with heart disease, and is caused by vegetative and psycho-emotional disorders, drug treatment (especially cardiac glycosides), impaired electrolyte balance of different nature, the use of alcohol and stimulants, smoking, reflex influence of the internal organs. Occasionally Extrasystole detected in apparently healthy individuals with high functionality, such as the athletes. Exercise in general provoke arrythmia, associated with heart disease and metabolic disorders, and suppresses extrasystole caused by autonomic dysregulation.

Beats may occur in a row, and two more - pair and group beats. The rhythm at which for each normal systole should extrasystole called bigemia. Particularly unfavorable hemodynamically inefficient early beats that occur simultaneously with the T wave of the previous cycle, or no later than 0.05 seconds after it. If ectopic impulses are generated in different foci, or at different levels, then there politopnye beats, which differ in shape extrasystolic complex on the ECG (within one exhaust) and the largest predekstrasistolicheskogo interval. These beats often caused significant changes in the myocardium. Sometimes it is possible for a long rhythmic functioning ectopic focus, along with the functioning of the sinus pacemaker - parasystole. Parasistolicheskie pulses follow the correct (usually rare) rhythm, independent of the sinus rhythm, but some of them coincides with the refractory period of the surrounding tissue and can not be realized.

The ECG atrial beats are characterized by changes in the shape and direction of the P wave and a normal ventricular complexes. Postextrasystolic interval can be increased. In early premature atrial often observed violation of atrioventricular and intraventricular conduction (often by type of blockade of the right leg) in extrasystolic cycle. Atrioventricular (atrioventricular connection of the field) beats are characterized by an inverted P wave is close to unchanged ventricular complex or superimposed on it. Possible violation of intraventricular conduction in extrasystolic cycle. Postextrasystolic pause usually increased. Ventricular premature beats are more or less pronounced QRST complex deformation, which is not preceded by a P wave (except for very late PVCs in which is recorded normal P wave, but the P-Q interval is shortened). The amount of pre- and postzkstrasistolicheskogo intervals equal to or slightly greater than the length of two intervals between sinus beat. In early beats in the background bradycardia postextrasystolic pause can not be (intercalary beats). Prilevozheludochkovyh arrythmia in the QRS complex in lead the V, is the largest tooth of the R, directed upwards, with the right heart, the S tooth, downward.

Symptoms. Patients do not feel any premature beats or feel them as enhanced push in the heart or sinking of the heart. In the study of premature heart arrythmia corresponds to a weakened pulse wave or loss once the pulse wave, and auscultation -prezhdevremennye heart tones.

The clinical significance of premature beats may be different. Rare beats in the absence of heart disease usually have significant clinical value. Increased extrasystoles sometimes indicates a worsening of existing diseases (coronary heart disease, myocarditis, etc.) Or glycoside intoxication. Frequent atrial premature beats often foreshadow atrial fibrillation. Particularly unfavorable frequent early and politopnye group and PVCs that in acute myocardial infarction and cardiac glycoside intoxication may be harbingers of ventricular fibrillation. Frequent extrasystoles (G 1 or more minutes) may themselves contribute to the aggravation of coronary insufficiency.

Treatment. It is necessary to identify and possibly eliminate the factors leading to arrhythmia. If Extrasystole associated with any particular disease (myocarditis, hyperthyroidism, alcoholism or other.), The treatment of the disease is crucial to eliminate the arrhythmia. If the beats are combined with severe psycho-emotional disorders (regardless of the presence or absence of heart disease), it is important sedative treatment. Extrasystoles in sinus bradycardia tend not require antiarrhythmic treatment, sometimes persists Belloidum (1 tablet 1-3 times a day). Rare extrasystoles without heart disease and usually do not require treatment. If treatment is recognized to show the antiarrhythmic agent is selected taking into account contraindications since smaller doses, bearing in mind that propranolol (10-40 mg 3-4 times a day), verapamil (at 40-80 mg four times a 3- day), quinidine (200 mg 3-4 times a day) are active at supraventricular arrhythmias; lidocaine (w / w, 100 mg), procainamide (inward 250-500 mg 4-6 times a day), phenytoin (100 mg 2-4 times a day), etmozin (100 mg 4-6 times a day ) - with the ventricular extrasystole, Cordarone (200 mg 3 times a day for 2 weeks, followed by 100 mg three times a day) and disopyramide (200 mg 2-4 times a day) - when both.

If the beats occur or become more frequent during treatment with cardiac glycosides, they should be temporarily canceled appoint drugs potassium. In the event of early politopnye PVCs patient need to be hospitalized, the best way (along with intensive treatment of the underlying disease) is the intravenous injection of lidocaine.

Paroxysmal tachycardia - attacks ectopic tachycardia, characterized by a good rhythm with a frequency of about 140-240 in 1 min with a sudden onset and sudden termination. The etiology and pathogenesis of paroxysmal tachycardia are similar to those with arrhythmia.

On the ECG, in most cases possible to distinguish supraventricular (atrial and atrioventricular) and ventricular tachycardia. Atrial paroxysmal tachycardia is characterized by a strict rhythm, the presence of the ECG unchanged ventricular complexes before which may be affected slightly deformed tooth R. atrial tachycardia is often accompanied by a violation of atrioventricular and (or) intraventricular conduction, often by right bundle branch block. Atrio-ventricular tachycardia (atrioventricular connection of the field) is characterized by a negative P wave, which may be located near the QRST complex or often imposed on him. Rhythm strictly regular. Possible violations of intraventricular conduction. Differences in ECG atrial and atrioventricular tachycardia is not always possible. Sometimes in these patients is a paroxysm on the ECG recorded beats that occur at the same level. Ventricular tachycardia is characterized by significant deformation QRST complex. The atria can be excited regardless of the ventricles in the right rhythm, P wave but difficult to see. The shape and amplitude of the complex T ORS and isoelectric contour line slightly vary from cycle to cycle, the rhythm is usually not strictly correct. These features distinguish ventricular tachycardia from supraventricular the blockade bundle branch block. Sometimes for a few days after the paroxysm of tachycardia on ECG recorded negative T waves, at least - with a shift ST- segment changes, referred to as posttahikardialny syndrome. Such patients require observation and exclusion they melkoochagovogo myocardial infarction.

Symptoms. Paroxysm tachycardia is usually felt as a heart attack with a distinct beginning and end, lasting from a few seconds to several days. Supraventricular tachycardias are often accompanied by other manifestations of autonomic dysfunction - sweating, urination abundant at the end of the attack, increasing intestinal peristalsis, a slight rise in body temperature. Prolonged seizures may be accompanied by weakness, faintness, discomfort in the heart, and in the presence of heart disease - angina, occurrence or increase of heart failure. Common to the different types of supraventricular tachycardia is the possibility of at least a temporary normalization of the rhythm in the area of ​​the carotid sinus massage. Ventricular tachycardia is less common and is almost always associated with heart disease. She does not respond to carotid sinus massage, and often leads to disruption of the blood supply to organs and heart failure. Ventricular tachycardia, especially in the acute period of myocardial infarction may be a precursor to ventricular fibrillation.

Treatment. During the attack necessary to stop the load, it is important to reassure the patient, use, if necessary sedation. Always exclude comparatively rare exceptions, when the paroxysm of tachycardia associated with intoxication with cardiac glycosides or sinus node weakness (see below). such patients should be immediately hospitalized in the cardiology department. If these situations are excluded, then the supraventricular tachycardia in the first minutes of the attack requires stimulation of the vagus nerve - a vigorous massage of the carotid sinus region (contraindicated in older persons) alternately left and right, evoking gagging, pressure on the abdominal muscles or the eyeballs. Sometimes the patient himself ceases to attack the delay of breath, straining determined by turning the head and other techniques. In case of failure it is advisable to repeat the maneuvers vagotropic and later, on the background of drug treatment. Reception 40-60 mg propranolol at the beginning of the attack sometimes relieves him 15-20 minutes. Faster and more reliable valid / introduction verapamil (4.2 ml of 0.25% solution) or propranolol (5 ml of 0.1% solution) or procainamide (5.10 ml of a 10% solution). These drugs should be administered slowly over a few minutes, constantly monitoring blood pressure. One patient can not enter the verapamil, the propranolol. When significant hypotension previously administered subcutaneously or intramuscularly mezaton. In some patients, effective digoxin administered intravenously (if the patient has not received cardiac glycosides in the days before the attack). If the attack is not stopped, and the patient's condition worsens (which is rare with supraventricular tachycardia), the patient is sent to the hospital for the relief of cardiac attack by frequent intraatrial or transesophageal atrial pacing or use cardioversion. Treatment of ventricular tachycardia should, as a rule, be carried out in a hospital. The most effective in / lidocaine (e.g., 75 mg / in repetition at 50 mg every 5-10 min, monitoring ECG and blood pressure, up to a total dose of 200-300 mg). In severe the patient's condition associated with tachycardia, can not be postponed electropulse treatment. As with supraventricular or ventricular tachycardia at effective reception can be etatsizina 50-75 mg (daily dose of 75 to 250 mg), and ventricular tachycardia effective etmozin - 100-200 mg (1400-1200 mg daily dose).

After a paroxysm of tachycardia is shown receiving antiarrhythmic agents in small doses to prevent a relapse, it is best to apply this into a drug that took paroxysm.

Fibrillation and atrial flutter (atrial fibrillation). Atrial fibrillation - a chaotic contraction of individual groups of muscle fibers of the atria, while the atrium as a whole is not reduced, but due to the variability of the atrioventricular ventricles arrhythmic, usually at a frequency of about 100-150 in 1 min. Atrial flutter is a regular atrial contraction with a frequency of about 250-300 in 1 min; ventricular rate is determined by the atrioventricular conduction, the ventricular rate may be at the same regular or irregular. Atrial fibrillation can be persistent or parokoizmalnym. Paroxysms it is often preceded by persistent form. Atrial flutter occurs in 10-20 times less than the flicker, and usually in the form of paroxysms. Sometimes flutter and atrial fibrillation alternate. Atrial fibrillation may occur with mitral heart defects, coronary heart disease, thyrotoxicosis, alcoholism. Transient atrial fibrillation is sometimes observed in myocardial infarction, cardiac glycoside intoxication, alcohol.

The ECG atrial fibrillation teeth P no, instead they are registered irregular waves, which are best seen in lead V1; followed by ventricular complexes in the wrong rhythm. Frequent ventricular rhythm may cause blockade legs, usually right bundle branch block. In the presence of atrial fibrillation, along with violations of atrioventricular conduction or under the influence of treatment of ventricular rate may be lower (less than 60 in 1 min - bradisistolicheskoe atrial fibrillation). Occasionally atrial fibrillation combined with complete atrioventricular blockade. When atrial flutter instead of P waves recorded regular atrial waves, without a pause, with a distinctive saw-like appearance; ventricular complexes follow rhythmically after every 2nd, 3rd, and so on. d. atrial arrhythmic waves or, if you frequently change the conductivity.

Symptoms. Atrial fibrillation may not feel sick or feels like a heartbeat. When atrial fibrillation and flutter with irregular ventricular rhythm aritmichen pulse, heart sounds changeable sonority. Filling pulse also variable and part of the heart rate does not give the pulse wave (pulse deficit). Atrial flutter with regular ventricular rate can only be diagnosed by ECG. Atrial fibrillation with a rapid ventricular rhythm contributes to the emergence or growth of heart failure. As proof, and especially paroxysmal atrial fibrillation causes a tendency to thromboembolic complications.

Treatment. In most cases, if atrial fibrillation is associated with fatal heart disease, the goal of treatment is a rational slowing of ventricular rate (up to 70-80 in 1 min), which is used for systemic administration of digoxin with the addition if necessary of small doses of propranolol, potassium preparations. In some cases, cure the underlying disease or acute (surgical removal of blemish, thyrotoxicosis compensation, successful treatment of myocarditis, the termination of reception of alcohol) can lead to the restoration of sinus rhythm.

Some patients with persistent atrial fibrillation lasting up to 2 years of arrhythmia can be eliminated in a hospital drug or electric pulse treatment. The results of the treatment the better, the shorter the duration of arrhythmias, lower the value of the atria and the severity of heart failure. Defibrillation is contraindicated in a significant increase in atrial thromboembolic complications in the near history of myocarditis, a rare ventricular rhythm (not associated with the treatment), expressed conduction disorders, cardiac glycoside intoxication, various states, preventing the anticoagulant treatment. Frequent paroxysms of atrial fibrillation in the past also point to the prospect of a small sinus rhythm.

In the treatment of persistent atrial fibrillation, usually for 2-3 weeks before defibrillation and for the same time after the prescribed anticoagulants. In most cases, effective treatment of quinidine. With good tolerability test dose (0.2 g) increasing drug administered in a daily dose of, for example: g 0,6-0,8-1,0-1,2-1,4 daily dose given fractionally with 0.2 g interval 2-2.5 hours under ECG control. For defibrillation can be used zlektroimpulsnuyu therapy, especially in serious condition of the patient, caused arrhythmia. The immediate effect of cardioversion slightly higher at flutter than in atrial fibrillation. After the restoration of sinus rhythm is necessary for a long and persistent supports antiarrhythmic treatment, usually quinidine dose of 0.2 g every 8 hours, or other antiarrhythmic drugs.

Paroxysms of atrial fibrillation often terminated spontaneously. They can be eliminated intravenous verapamil, procainamide or digoxin. frequent intraatrial or transesophageal atrial electrical stimulation may be used for relief of paroxysmal atrial fibrillation. With frequent paroxysms requires systematic receiving antiarrhythmic drug as a prophylactic measure. Systematic receiving digoxin sometimes promotes translation of paroxysmal atrial fibrillation in a permanent form, which after reaching a rational frequency of ventricular rate is usually better tolerated than frequent paroxysms. If you often poorly tolerated paroxysms not preventable drug treatment can be effective in the partial or complete cut bundle of His (typically at cardiac catheterization and use of electrocautery or laser coagulation), followed by permanent pacing, if necessary. This intervention is carried out in specialized institutions.

Blink and ventricular flutter, ventricular asystole may occur in any severe heart disease (most commonly in the acute phase of a myocardial infarction), and pulmonary embolism, with an overdose of cardiac glycosides, antiarrhythmics, when zlektrotravme, anesthesia, with intracardiac manipulation, in severe general metabolic disorders .

Symptoms - sudden cessation of blood circulation, the pattern of clinical death: no pulse, heart sounds, consciousness, hoarse agonal breathing, sometimes convulsions, dilated pupils (starts in 45 seconds after the cessation of blood flow). Differentiate flicker and flutter and ventricular asystole may ECG (virtually - at zlektrokardioskopii). When ventricular fibrillation ECG looks messy waves of different shapes and sizes. Krupnovolnovoe flicker (2-3 mV) somewhat easier reversible with appropriate treatment, melkovolnovoe indicates a profound hypoxic myocardium. If ventricular fibrillation is similar to an electrocardiogram ECG during ventricular tachycardia, but the rhythm more often. ventricular flutter hemodynamically inefficient. Asystole (t. E. The absence of cardiac electrical activity) corresponds to the ECG straight line. Some auxiliary diagnostic value is previous arrhythmia: politopnye early ventricular premature beats and ventricular tachycardia often precede flickering and fluttering of the ventricles, increasing the blockade - asystole.

Treatment reduces the immediate external cardiac massage, artificial respiration, which should continue to achieve the effect (spontaneous heart sounds and heart rate), or for the time necessary to prepare for cardioversion (with blink and flutter) or temporary pacing (with asystole). Intracardiac administration of drugs (potassium chloride at the blink of adrenaline when asystole) may be effective in some patients, if the nature of the arrhythmia is installed. During resuscitation important excess oxygenation, administration of sodium bicarbonate. For the prevention of recurrence of life-threatening ventricular tachyarrhythmias is necessary for several days to enter in / lidocaine, potassium chloride, intensively treat the underlying disease.

Cardiac blockade - cardiac abnormalities associated with delay or termination of the pulse on the conducting system. Localization distinguish sinoatrial blockade (at the level of the atrial myocardium), atrio-zhepudochkovye (at the level of the atrioventricular node) and intraventricular (at the level of His and its branches beam). In the words of distinguished conduction slowing (each pulse slowed held in the lower divisions of the conduction system, the blockade of 1 degree), partial blockades (carried out only part of the pulse, II of the degree of blockage) and full blockade (pulses are not held, cardiac activity is supported ectopic center of reference rate, the blockade III degree).

Violations of sinoatrial and atrioventricular conduction may occur when myocarditis, kardiosklerosis, focal and degenerative diseases of the myocardium, especially in the field of zadnediafragmalnoy wall, intoxications, for example, cardiac glycosides, with an increase in vagal tone, under the action of beta-blockers, verapamil. Violations of intraventricular conduction often caused by necrotizing, sclerotic or inflammatory processes. Non-severe conduction disturbances (sinoatrial and atrioventricular blockade 1 and II degree, the blockade of right bundle branch block, or one of the branches of the left leg) occasionally occur in healthy individuals. Congenital complete transverse blockade is very rare. In general, the distal and expressed the blockade, the greater its clinical significance. All of the blockade may be persistent or transient, transient blockade sometimes show an aggravation of heart disease. The location and severity of the siege are determined by ECG, more reliably when intracardiac conduction system of registration of potentials.

Sinoatrial block - diagnosed only incomplete blockade: in sinus rhythm or sinus arrhythmia observed loss of individual complexes PQRST c appropriately (twice, sometimes three times or more) extension diastolic pause.

Atrioventricular block of 1 degree, the interval P - Q is extended to more than 0.21 B, but all atrial impulses reach the ventricles. Atrioventricular block II degree: some atrial impulses are not conducted to the ventricles, ventricular complexes corresponding fall (isolated on ECG P wave). When blockade proximal type (at the atrioventricular node) such loss precedes progressive elongation interval P Q cycles 2-8 in a series, and these periods are repeated, sometimes regularly. When the blockade of the distal type (in the distal branch block and beam level) loss of individual cycles are not preceded by a gradual lengthening of the interval P Q. Blockade distal type case with more severe myocardial damage, it often turns into a complete transverse blockade. Atrioventricular blockade III Grade-atrium and the ventricles are driven in the right, but independent of one another rhythm. It may also be isolated proximal block type (narrow QRS, ventricular rate 40-50 1 min preceded incomplete blockade proximal type) type and distal (wide QRS, ventricular rate of about 20-40 1 min precedes s, sometimes very short, incomplete blockade of the distal type). The most accurate determination of the level of blockade is possible at registration intracardiac potentials of the conduction system.

Intraventricular blocks relate to one, two or all three branches of the intraventricular conduction system (mono-, bi- and trifastsikulyarnye blockade). The blockade of the front or rear of the branches left bundle branch is characterized by a significant deviation of electrical axis of the heart to the left or right (the latter feature is less specific: should be excluded other, more common causes of ECG right type). In right bundle branch block the initial part of the QRS complex is stored, the final expanded and jagged, QRS duration is usually increased; in lead V ^ is usually enlarged and serrated tooth R, ST segment is omitted negative T wave; on the frontal plane axis is projected electric poor (ECG S-Type in standard leads). The combination of the blockade of the right leg to the blockade of one of the branches of the left leg (bifastsikulyarnaya blockade) is characterized by the presence of ECG signs of blockade of the right leg and a significant deviation of electrical axis. Blockade of both branches of the left leg, the blockade of the left leg: QRS complex is widened to 0.12 and more serrated; in the left chest leads prevails tooth R, ST4acTO segment is omitted, negative T wave. Trifastsikulyarnaya blockade corresponds atrioventricular blockade III extent of distal type (see. Above).

Symptoms. When partial cross blockades marked loss of pulse and heart sounds. Intraventricular blocks are sometimes accompanied by splitting tones, often - the blockade of the right bundle branch block. Full transverse blockade is characterized by stable bradycardia, heart sounds changing sonorities, convulsions (seizures TAPS - Stokes - Morgagni). Angina pectoris, heart failure, sudden death can occur when the full cross-section blockade, particularly the distal type.

Treatment. Treat the underlying disease, eliminate the factors that led to the blockade. With incomplete and complete transverse blockade proximal type sometimes used atropine, isoproterenol, aminophylline, but the efficacy of these agents is variable and unreliable, at best, they have a temporary effect. Blockade, leading to heart failure and (or) peripheral circulation, as well as partial and complete blockade of the distal type is an indication for the use of temporary or permanent ventricular electrical stimulation.

sick sinus syndrome (SSS) is associated with a weakening or cessation of sinus node automaticity. SSS may be due to ischemia unit area (often in myocardial infarction, especially zadnediafragmalnom as transient or persistent complication), kardiosklerosis (atherosclerotic, postmiokarditicheskim, especially after diphtheria), myocarditis, cardiomyopathy and infiltrative lesions of the myocardium. SSS can also be a manifestation of the inherent features of the conduction system. The process of contributing to the SSS, sometimes spreading to other segments of the vascular system.

Symptoms. The most characterized by a combination of sinus bradycardia or bradyarrhythmias with paroxysms tahisistolicheskoy and ectopic arrhythmias. Other manifestations of the syndrome: the replacement periods ectopic rhythm and sometimes complete asystole, pacemaker migration, atrial fibrillation (more common with a rare ventricular rate, which indicates the involvement of the atrioventricular node), sinoatrial block, arrhythmia and tachycardia, supraventricular often. It is significant that immediately after tachycardia pause is especially great, unusual increase in the pause can be markedly after the beats. Many patients with sick sinus syndrome is not accompanied by any unpleasant sensations. In some cases it may be signs of insufficient blood supply to the brain, heart, heart failure is possible. Patients can not tolerate vagotropic impact.

Treatment. Many patients do not need treatment. With frequent changes of rhythm, with signs of circulatory disorders of vital organs is a constant alektrokardiostimulyatsiya. Sympathomimetics and antiarrhythmics generally contraindicated, since they can dangerously intensify respectively tahikardichesky or bradycardic component of the syndrome. The forecast is highly dependent on the disease, which led to the development of the syndrome.

Syndrome of premature ventricular excitation (Wolff - Parkinson - White) - electrocardiographic syndrome with shortening P- Q interval and the extension of the QRS complex due to start so-called delta - wave. The syndrome may be persistent or transient. It is based on an inherent feature of the conduction system (the presence of accessory pathways). The syndrome may show up at birth or manifest later diagnosed by ECG only. Some leads can check the Q-wave, changes in S - T, which sometimes leads to erroneous diagnosis of coronary heart disease, myocardial infarction, ventricular hypertrophy. Approximately half of the patients have varying frequency and duration of paroxysmal supraventricular tachycardia, rarely - atrial fibrillation (occasionally with very frequent ventricular rate - about 200 in 1 min). The syndrome may randomly be combined with any heart disease.

Treatment in the absence of paroxysmal arrhythmias are not required to avoid impacts that might provoke them (eg, alcohol). Drug treatment and prevention of paroxysmal tachycardia is carried out in substantially the same manner as in paroxysmal supraventricular tachycardia other nature. Verapamil is effective more often. Digoxin is considered contraindicated, if the syndrome is combined with atrial fibrillation. If drug treatment is ineffective paroxysm, and the patient's condition is getting worse, resort to the electric pulse treatment. If attacks are frequent and associated with severe symptoms, the attacks carried out preventive treatment, choosing an effective antiarrhythmic agent. With frequent attacks and poorly tolerated and ineffective prevention of drug use cut an additional pathway (usually using transvenous electrocautery or laser coagulation), followed by permanent pacing when necessary.