Precardioventricular blockade. When this type of conduction is disrupted, the impulse is blocked at the border of the atria and ventricles. Previously, it was believed that the conduction of impulses through the atrioventricular node was disrupted. However, as has been shown in recent years, impulse conduction, both normally and during blockades, is delayed in two places:
1) at the junction of the atria with the atrioventricular node (less significant)
2) at the junction of the atrioventricular node and the His bundle (more significant). Thus, when talking about atrioventricular blockades, one should keep in mind the slowdown in the conduction of impulses or their blockade in the atrioventricular junction.
Etiology and pathogenesis. One of the common causes of atrioventricular conduction disturbances is ischemic disease hearts. Atrioventricular block of various degrees is detected in 10-15% sick myocardial infarction. The cause of slowing atrioventricular conduction can also be rheumatic carditis, myocarditis of various etiologies, myocardial, atherosclerotic and post-infarction cardiosclerosis, hyperkalemia. There are reports of the development of atrioventricular block in 10% of cases after heart surgery. Sometimes atrioventricular blockade of various degrees occurs due to intoxication with cardiac glycosides, taking various antiarrhythmic drugs (quinidine, beta-blockers, novocainamide, etc.). Cases of congenital complete atrioventricular heart block have been described. In this case, the blockade is sometimes not an isolated disease, but is combined with congenital heart defects. Very rarely, the cause of atrioventricular block is a heart tumor.
Sometimes atrioventricular block (usually incomplete) can be a consequence of increased tone vagus nerve. Vagal stimulation (pressure on the carotid sinus, eyeballs) can cause transient disturbances of atrioventricular conduction. The role of the vagus nerve in the development of atrioventricular block is also confirmed by experimental studies. This factor appears to have great importance in the occurrence of atrioventricular blockade in almost healthy people and among athletes.
The mechanism of atrioventricular blockade is not completely clear. To explain the pathogenesis of atrioventricular blockade, various theories have been put forward: decremental conduction, “hidden” conduction, multiple conduction pathways, etc.
I. A. Chernogorov (1948, 1962) and I. I. Isakov (1953) associate disturbances in atrioventricular conduction with a decrease in the functional lability of the myocardium. At the same time, waves of excitation arriving at the site of reduced lability deepen its parabiotic state.
There are 3 degrees of atrioventricular block.
First degree atrioventricular block- this is an incomplete blockade, characterized by a persistent prolongation of the P-Q interval on the electrocardiogram by more than 0.2 s. In the case of a sharp prolongation of the P-Q interval or when blockade is combined with tachycardia, the P wave merges with the T wave of the preceding complex, which is sometimes incorrectly mistaken for the rhythm of the atrioventricular junction.
Second degree atrioventricular block- This is an incomplete blockade, characterized by periodic loss of ventricular complexes. It comes in two types:
1) Samoilov-Wenckebach type or type I (Mobitz-I); characterized by a gradual lengthening of the P-Q interval on the electrocardiogram and subsequent more or less regular loss of the ventricular complex;
2) type 2 (Mobitz-P); characterized by a normal or constantly prolonged P-Q interval and periodic loss of the ventricular complex.
Atrioventricular block of the second degree, type Mobitz-1, is observed with damage to the proximal parts of the His bundle; type Mobitz-II is observed with damage to the proximal parts of the His bundle. distal sections conducting system hearts at the level of the His bundle branch. Therefore, in the latter case, the complexes on the electrocardiogram are usually widened and deformed.
III degree- complete atrioventricular block, in which not a single sinus impulse is conducted to the ventricles; there are two autonomous rhythms - sinus, or atrial, and ventricular; atrial and ventricular complexes follow independently of each other in the correct rhythm.
Complete atrioventricular block can develop at three levels: with damage to the atrioventricular node or connection (nodular block, proximal block), damage to the trunk of the His bundle (trunk block) and damage to all three branches of the His bundle (three-bundle or trifascicular block, blockade of the distal type).
With nodal block, the pacemaker is located high, in the atrioventricular junction, and therefore bradycardia is least pronounced; with brainstem blockade, bradycardia is more pronounced, since the source of the rhythm is lower; finally, with a three-fascicular block, the ventricular rhythm is the lowest located with the most pronounced bradycardia.
Complete atrioventricular block can also be persistent or permanent, transient and intermittent (intermittent).
Atrioventricular block clinic determined by the nature of the underlying disease and the degree of blockade. Subjective symptoms usually absent as long as there are no violations heart rate. With atrioventricular blockade of the second degree sick complain of interruptions in the functioning of the heart, sometimes slight dizziness. With atrioventricular block of the third degree (complete), in the case of a decrease in ventricular contractions of less than 40 per minute, dizziness, darkening of the eyes, and short-term attacks of blackouts are possible. Against the background of a sharp decrease in rhythm, Morgagni-Edams-Stokes syndrome may develop. Sometimes due to chronic cerebral hypoxia observed mental disorders in the form of a peculiar combination of inadequately elevated mood with motor retardation.
With percussion hearts dimensions cardiac Dullness is determined depending on the underlying disease. On auscultation hearts at sick with atrioventricular block of the first degree, a presystolic three-part rhythm (additional dull tone of atrial contraction) is sometimes heard due to a significant prolongation of the P-Q interval. On auscultation, during a second degree block, the correct rhythm is interrupted by long pauses (loss of ventricular contractions). With complete (III degree) atrioventricular blockade, a rare regular rhythm is heard hearts and changing sonority of the 1st tone. Usually the 1st tone above the top is dull, but from time to time its sonority intensifies, and then the so-called Strazhesko cannon tone appears. N.D. Strazhesko (1908) explained this phenomenon by the simultaneous contraction of the atria and ventricles. However, V.F. Zelenin (1956) and JI. I. Fogelson (1958), based on electrophonocardiographic studies, showed that the “cannon tone” occurs when atrial contraction somewhat precedes ventricular contraction and the closure phases of the atrioventricular valves approach each other. Sometimes atrial sounds together with ventricular ones form a transient three-part rhythm.
It is practically impossible to distinguish between atrioventricular blockade clinically, nodal (proximal or high), brainstem and t-bundle (distal, or low). Only by heart rate can one guess where the source of the rhythm is: with moderately severe bradycardia - high, t i.e. proximally, with pronounced bradycardia - low, i.e. distally.
IN clinical practice one can observe the transition of incomplete atrioventricular blockade to complete, and vice versa. This alternation of different degrees of blockade can last for a certain period of time and end with the establishment of a persistent complete atrioventricular block.
Big role in clinical course Atrioventricular blockade is played by the addition of other arrhythmias. Most often there is a combination of atrioventricular block with ventricular extrasystole, less often - with atrial fibrillation or flutter (Frederick's syndrome).
Complete atrioventricular block, joining the underlying disease, can cause decompensation or intensify it.
Morgagni-Edams-Stokes syndrome. Complete atrioventricular block is the most common cause appearance of Morgagni-Edams-Stokes syndrome. It is observed in 35-70% of hospitalized patients sick With chronic complete atrioventricular block.
Morgagni-Edams-Stokes attacks can be caused by ventricular asystole during the transition of incomplete atrioventricular blockade to complete, when a long, so-called pre-automatic pause occurs (the activity of the new pacemaker does not occur immediately, but after some time). With complete atrioventricular blockade, extrasystolic arrhythmia can cause post-extrasystolic depression of the ventricular rhythm up to attacks of ventricular asystole. The occurrence of Morgagni-Edams-Stokes attacks can be facilitated by a gradual decrease in the activity of the automaticity of the ventricular conduction system, when the frequency of ventricular contractions decreases to less than 20 beats per minute and attacks appear. Acidosis, hyperkalemia, metabolic disorders in the myocardium and other reasons can inhibit the formation of impulses in the ventricles.
Often Morgagni-Edams-Stokes syndrome occurs with complete atrioventricular block in cases of ventricular fibrillation. Such sick often spontaneously or after one massage hearts without electrical defibrillation the attack stops, which means sick without atrioventricular blockade is observed quite rarely.
Sometimes Morgagni-Edams-Stokes attacks are caused by sick sinus syndrome, ventricular form of paroxysmal tachycardia, etc.
Often periods of ventricular asystole alternate with periods of ventricular tachycardia or ventricular fibrillation in the same patient (mixed form of Morgagni-Edams-Stokes syndrome).
Thus, there are three pathogenetic forms of Morgagni-Edams-Stokes syndrome:
1) oligo- or asystolic (brady-cardiac, adynamic);
2) tachysystolic (tachycardial, dynamic);
3) mixed.
Morgagni-Edams-Stokes syndrome has a characteristic clinical picture. In the midst of complete well-being, suddenly comes severe dizziness, general anxiety, and then loss of consciousness. Along with this, first clonic and then tonic convulsions of the limbs and torso, involuntary urination or defecation appear. During attack pulse is not palpable, sounds hearts are not listened to arterial pressure not detectable, the face is initially pale and then gradually becomes cyanotic, breathing is noisy and uneven. Usually attack goes away on its own or after appropriate therapeutic measures, but sometimes ends in death.
In mild cases, there may be no complete loss of consciousness and there are no convulsions. These attacks occur as not particularly severe states of syncope with sudden pallor, weakness, loss of thinking, dizziness, and slight confusion.
The number and severity of attacks varies sharply, sometimes up to 100 attacks per day are observed.
In all cases of atrioventricular blockade, electrocardiographic examination is of great importance in recognizing it and clarifying the nature and extent.
With first degree atrioventricular block, all electrocardiogram complexes may be normal, only the P-Q interval is increased by more than 0.2 s.
With atrioventricular blockade of the second degree, type Mobitz-I, the P-Q interval gradually lengthens, then after 3-4 complexes the P remains, and the QRST drops out, then everything repeats again.
With second-degree atrioventricular block of the Mobitz-II type, the P-Q interval is normal or prolonged, QRST complexes periodically fall out, and the P wave remains.
With complete (III degree) atrioventricular blockade P complexes are recorded in their own more frequent rhythm, and QRST complexes are also recorded in their own, but rare rhythm. The P wave on the same curve either precedes the QRST complexes at different intervals, then follows them, or is layered in various parts ventricular complex, deforming it.
Complete nodal (proximal) atrioventricular block is characterized by slight bradycardia and no changes in QRS complexes. For brainstem blockade, accurate diagnosis can be established based on the His bundle electrogram, since there are no clear changes on the electrocardiogram. Complete atrioventricular block of the distal type (trifascicular) is characterized by widening of the QRS complex (0.12 s or more) and its deformation, as well as significantly pronounced bradycardia.
Diagnostics. Put diagnosis incomplete atrioventricular blockade based on auscultatory data is rarely possible. First degree atrioventricular block can be assumed based on the three-part rhythm. However, such a rhythm is also detected with blockades of the legs and may be absent with atrioventricular blockade of the first degree. Correct diagnosis diagnosed on the basis of an electrocardiographic study. With sinoauricular block, the P wave and the associated QRST complex are absent on the ECG, and with atrioventricular block of the second degree, loss of the QRST complex is noted (with or without a gradual lengthening of P-Q). The P wave remains.
It is necessary to differentiate between complete atrioventricular block and sinus bradycardia. Complete blockade is diagnosed on the basis of the variable sonority of the 1st tone, the periodic appearance of Strazhesko’s “gun tone”, a rare pulse, the frequency of which does not change under the influence of an injection of atropine. However, it must be remembered that the pulse may remain rare after an injection of atropine for sick sinus syndrome. Therefore, to establish a final diagnosis, it is necessary to perform an electrocardiographic study.
There are cases when, with complete atrioventricular block, there is one QRST complex for every 2-3 P waves. It seems that this is atrioventricular blockade) of the first degree, i.e. incomplete, with an atrial and ventricular rhythm of 2:1 or 3:1. These two blockades can be distinguished by recording an electrocardiogram with an artificially accelerated atrial rhythm (physical activity, atropine injection). With complete atrioventricular blockade, the correct alternation of the P and QRST waves will disappear, i.e., the P wave will occupy a different position in relation to the QRST (in front of it, merging with it, behind it). With incomplete atrioventricular block, the P and QRST waves will remain in the same bundle, but with an increased rhythm.
Treatment of atrioventricular block should be aimed primarily at eliminating the etiological factor. Thus, in case of intoxication with drugs (cardiac glycosides, beta-blockers, etc.), their withdrawal is indicated. For rheumatism, infectious-allergic myocarditis or ischemic illnesses hearts- appropriate treatment underlying disease.
Atropine and sympathomimetic drugs are used to restore impaired atrioventricular conduction. facilities- stimulants of beta-adrenergic receptors. Atropine is administered intravenously or subcutaneously in 0.75-1 ml of 0.1% solution. Under the influence of atropine, in 25-30% of cases with atrioventricular blockade of the second degree of the Mobitz-1 type and complete (III degree) blockade, a temporary restoration of conduction is observed. With second-degree blockade of the Mobitz-II type, the administration of atropine can even lead to a slowdown in the ventricular rhythm due to increased atrial rate and an increase in the degree of blockade, therefore atropine should not be used with this form of blockade.
Due to the fact that the effect of atropine is short-lived, every ephedrine, adrenaline. These drugs improve conductivity due to increased tone of the sympathetic nervous system, increase myocardial excitability and increase ventricular automaticity.
However, it should be noted that adrenaline and ephedrine have side effect: increase arterial pressure, cause pain in the heart, increase the excitability of ectopic foci with the possible development of ventricular fibrillation, which significantly limits its use in atrioventricular blockades. Therefore, they are more often used drugs isopropylioradrenaline group (isadrin, orciprenaline, etc.).
Izadrin is prescribed under the tongue, 1/2-1 tablet 3-4 times or more per day. Orciprenaline sulfate can be carefully administered intravenously (0.5-1 ml of 0.05% solution), intramuscularly or subcutaneously (1-2 ml of the same solution), orally (1 tablet of 0.02 g 5-10 times a day) .
It must be remembered that sympathomimetic amines (beta-adrenergic receptor stimulants) increase myocardial oxygen demand; against the background of their administration, extrasystolic arrhythmia and ventricular tachycardia may appear or become more frequent.
There are reports of the successful use of corticosteroid drugs for atrioventricular conduction disorders.
Prednisolone is prescribed orally at 0.04-0.06-0.08 g per day, intravenously at 0.06-0.12 g for acute atrioventricular block.
Positive Effect prednisolone for blockades that developed against the background of various myocarditis and heart attack myocardium, can be explained by its anti-inflammatory and anti-edema effects. To a certain extent Effect corticosteroids is caused by loss of intracellular potassium.
For treatment atrioventricular block at one time potassium-removing drugs(dichlorothiazide or hypothiazide). Their action is associated with a decrease in the concentration of potassium ions and a corresponding increase in the resting membrane potential. The drug is prescribed at 0.025-0.2 g per day.
In some cases, sodium lactate improves the rhythm and conductivity (intravenous 150-200 ml of 5-10% solution), the mechanism actions which is to reduce hyperkalemia and acidosis (see also “Antiarrhythmics”).
Despite the therapy for atrioventricular block (especially complete), it is not always possible to avoid Morgagni-Edams-Stokes attacks. Therefore, in some cases they resort to temporary or permanent electrical stimulation of the heart, or pacing. Temporary cardiac pacing is performed when transient disorders rhythm and conductivity, constant - with its persistent forms.
Indications for temporary electrical pacing for atrioventricular blockade in sick acute myocardial infarction: Morgagni-Edams-Stokes attacks, progressive circulatory failure, ventricular contraction rate less than 40 per minute, combination of atrioventricular block with other rhythm disturbances.
In some cases attack Morgagni-Edams-Stokes stops after a punch to the sternum in the region of the heart. If there is no effect, begin a closed massage hearts and artificial ventilation. If the patient is under monitoring and asystole is recorded on the electrocardiogram, the most effective endocardial electrical stimulation is used; 1-2 hour injections must be repeated. In addition, atropine is contraindicated in glaucoma and can cause mental disorders and urinary retention.
From sympathomimetic drugs apply isadrin (isoproterenol, novodrin, euspiran, isuprel), orciprenaline (alupent), heart line; if the reason attack is ventricular fibrillation - electrical pulse therapy.
Prognosis for atrioventricular block I degree favorable. With second degree blockade, as well as with complete blockade (111th degree), the prognosis depends on the underlying disease, the frequency of ventricular contraction and the condition of the myocardium. In the case of complete atrioventricular block, the prognosis is always unfavorable. However, currently, with implantation of an artificial pacemaker, the prognosis is improving.
Prevention- this is, first of all, active, adequate and comprehensive treatment underlying disease. It is almost impossible to predict the occurrence of a particular blockade. However, it should be borne in mind that atrioventricular blockade of the first degree can develop into a blockade of the second degree, and a blockade of the second degree into a blockade of the third degree. To prevent life-threatening complete atrioventricular block, it is important to achieve the elimination of second-degree blockade of the Mobitz-1 type, and even more so of the second-degree blockade of the Mobitz-II type. Since this is often impossible to achieve with medication, it is necessary to insert an electrode for prophylactic purposes and, in the event of a complete blockade, immediately begin temporary cardiac stimulation.
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Atrioventricular (atrioventricular) block(AV block) - a disorder of conduction function, expressed in slowing down or stopping the passage of an electrical impulse between the atria and ventricles and leading to a disorder of heart rhythm and hemodynamics. AV block may be asymptomatic or accompanied by bradycardia, weakness, dizziness, attacks of angina and loss of consciousness. Atrioventricular block is confirmed using electrocardiography, Holter ECG monitoring, and EPI. Treatment of atrioventricular block can be medication or cardiac surgery (implantation of a pacemaker).
General information
Atrioventricular block is based on a slowdown or complete cessation of the passage of the impulse from the atria to the ventricles due to damage to the AV node itself, the His bundle or the branches of the His bundle. Moreover, the lower the level of damage, the more severe the manifestations of the blockade and the more unsatisfactory the prognosis. The prevalence of atrioventricular block is higher among patients suffering from concomitant cardiac pathology. Among people with heart disease, I degree AV block occurs in 5% of cases, II degree - in 2% of cases, III degree AV block usually develops in patients over 70 years of age. Sudden cardiac death, according to statistics, occurs in 17% of patients with complete AV block.
The atrioventricular node (AV node) is part of the conduction system of the heart, providing sequential contraction of the atria and ventricles. The movement of electrical impulses coming from the sinus node is slowed down in the AV node, allowing the atria to contract and pump blood into the ventricles. After a short delay, the impulses spread along the His bundle and its legs to the right and left ventricles, promoting their excitation and contraction. This mechanism ensures alternate contraction of the atria and ventricles myocardium and maintains stable hemodynamics.
Classification of AV blocks
Depending on the level at which the disturbance of electrical impulse conduction develops, proximal, distal and combined atrioventricular blockades are distinguished. With proximal AV blockade, impulse conduction may be disrupted at the level of the atria, AV node, and His bundle branch; at distal – at the level of the branches of the His bundle; with combined ones, multi-level conduction disturbances are observed.
Taking into account the duration of development of atrioventricular block, it is divided into acute (with myocardial infarction, drug overdose, etc.), intermittent (intermittent - with ischemic heart disease, accompanied by transient coronary insufficiency) and chronic forms. According to electrocardiographic criteria (slowness, periodicity, or complete absence of impulse conduction to the ventricles), three degrees of atrioventricular block are distinguished:
- I degree– atrioventricular conduction through the AV node is slowed down, but all impulses from the atria reach the ventricles. Clinically not recognized; on the ECG the P-Q interval is prolonged > 0.20 seconds.
- II degree– incomplete atrioventricular block; not all atrial impulses reach the ventricles. The ECG shows periodic loss of ventricular complexes. There are three types of second-degree AV block according to Mobitz:
- Mobitz type I - the delay of each subsequent impulse in the AV node leads to a complete delay of one of them and loss of the ventricular complex (Samoilov-Wenckebach period).
- Mobitz type II - critical impulse delay develops suddenly, without a previous prolongation of the delay period. In this case, the absence of conduction of every second (2:1) or third (3:1) impulse is noted.
- III degree- (complete atrioventricular block) - complete cessation of the passage of impulses from the atria to the ventricles. The atria contract under the influence of the sinus node, the ventricles contract at their own rhythm, less than 40 times per minute, which is not enough to ensure adequate blood circulation.
Atrioventricular blocks of the 1st and 2nd degrees are partial (incomplete), blockades of the 3rd degree are complete.
Reasons for the development of AV blockades
According to etiology, functional and organic atrioventricular blockades are distinguished. Functional AV blockades are caused by an increase in the tone of the parasympathetic nervous system. Atrioventricular block of the first and second degrees is observed in isolated cases in young physically healthy individuals, trained athletes, and pilots. It usually develops during sleep and disappears during physical activity, which is explained by increased activity of the vagus nerve and is considered a normal variant.
AV blockades of organic (cardiac) origin develop as a result of idiopathic fibrosis and sclerosis of the conduction system of the heart in various diseases. The causes of cardiac AV blockade can be rheumatic processes in the myocardium, cardiosclerosis, syphilitic heart disease, infarction of the interventricular septum, heart defects, cardiomyopathies, myxedema, diffuse diseases connective tissue, myocarditis of various origins (autoimmune, diphtheria, thyrotoxic), amyloidosis, sarcoidosis, hemochromatosis, heart tumors, etc. With cardiac AV blockade, a partial blockade may initially be observed, however, as the cardiopathology progresses, a third-degree blockade develops.
Various surgical procedures can lead to the development of atrioventricular blockade: aortic valve replacement, plastic surgery of congenital heart defects, atrioventricular RFA of the heart, catheterization of the right side of the heart, etc.
With second degree atrioventricular block, patients feel a loss of the pulse wave as interruptions in the heart area. With type III AV block, Morgagni-Adams-Stokes attacks occur: a decrease in heart rate to 40 or less beats per minute, dizziness, weakness, darkening of the eyes, short-term loss of consciousness, pain in the heart, cyanosis of the face, and possibly convulsions. Congenital AV block in patients of childhood and adolescence can be asymptomatic.
Complications of AV block
Complications from atrioventricular blockade are mainly caused by a pronounced slowdown in rhythm that develops against the background of organic heart damage. Most often, the course of AV block is accompanied by the appearance or worsening of chronic heart failure and the development of ectopic arrhythmias, including ventricular tachycardia.
The course of complete atrioventricular block may be complicated by the development of Morgagni-Adams-Stokes attacks associated with cerebral hypoxia as a result of bradycardia. The onset of an attack may be preceded by a feeling of heat in the head, attacks of weakness and dizziness; During an attack, the patient turns pale, then cyanosis and loss of consciousness develop. At this point, the patient may need chest compressions and mechanical ventilation, since prolonged asystole or the addition of ventricular arrhythmias increases the likelihood of sudden cardiac death.
Repeated episodes of loss of consciousness in elderly patients can lead to the development or worsening of intellectual-mnestic disorders. Less commonly, with AV blockade, the development of arrhythmogenic cardiogenic shock is possible, more often in patients with myocardial infarction.
In conditions of insufficient blood supply during AV blockade, phenomena are sometimes observed cardiovascular failure(collapse, fainting), exacerbation of coronary heart disease, kidney disease.
Diagnosis of AV blocks
When assessing the patient's medical history in case of suspicion of atrioventricular block, they find out the fact of previous myocardial infarction, myocarditis, other cardiopathologies, taking medicines that disrupt atrioventricular conduction (digitalis, β-blockers, calcium channel blockers, etc.).
When auscultating the heart rhythm, a correct rhythm is heard, interrupted by long pauses, indicating loss of ventricular contractions, bradycardia, and the appearance of Strazhesko's cannon I tone. An increase in pulsation of the neck veins is determined compared to the carotid and radial arteries.
On the ECG, AV block of the first degree is manifested by prolongation P-Q interval> 0.20 sec.; II degree - sinus rhythm with pauses, as a result of loss of ventricular complexes after the P wave, the appearance of Samoilov-Wenckebach complexes; III degree – a decrease in the number of ventricular complexes by 2-3 times compared to atrial complexes (from 20 to 50 per minute).
Carrying out additional laboratory research in case of AV blockade, it is indicated in the presence of concomitant conditions and diseases (determination in the blood of the level of electrolytes in case of hyperkalemia, the content of antiarrhythmics in case of their overdose, enzyme activity in case of myocardial infarction).
Treatment of AV blocks
With atrioventricular block of the first degree, occurring without clinical manifestations, only dynamic observation is possible. If AV block is caused by taking medications (cardiac glycosides, antiarrhythmic drugs, β-blockers), dose adjustment or complete discontinuation is necessary.
In case of AV blockades of cardiac origin (myocardial infarction, myocarditis, cardiosclerosis, etc.), a course of treatment with β-adrenergic stimulants (isoprenaline, orciprenaline) is carried out, and then implantation of a pacemaker is indicated.
First aid drugs for the relief of Morgagni-Adams-Stokes attacks are isoprenaline (sublingual), atropine (intravenous or subcutaneous). For symptoms of congestive heart failure, diuretics, cardiac glycosides (with caution), and vasodilators are prescribed. As symptomatic therapy at chronic form AV blockade is treated with theophylline, belladonna extract, nifedipine.
A radical method of treating AV block is the installation of an electrical pacemaker (pacemaker), which restores normal rhythm and heart rate. Indications for implantation of an endocardial pacemaker are a history of Morgagni-Adams-Stokes attacks (even a single one); ventricular rate less than 40 per minute and periods of asystole of 3 or more seconds; AV block II degree (Mobitz type II) or III degree; complete AV block, accompanied by angina pectoris, congestive heart failure, high arterial hypertension, etc. To decide on surgery, consultation with a cardiac surgeon is necessary.
Forecast and prevention of AV blocks
The influence of developed atrioventricular block on the patient’s future life and ability to work is determined by a number of factors and, above all, the level and degree of blockade and the underlying disease. The most serious prognosis is for grade III AV block: patients are unable to work, and the development of heart failure is noted.
The prognosis is complicated by the development of distal AV blocks due to the threat of complete blockade and rare ventricular rhythm, as well as their occurrence against the background of acute myocardial infarction. Early implantation of a pacemaker can increase the life expectancy of patients with AV block and improve their quality of life. Complete congenital atrioventricular blocks have a more favorable prognosis than acquired ones.
As a rule, atrioventricular block is caused by an underlying disease or pathological condition, therefore, its prevention is the elimination of etiological factors (treatment of cardiac pathology, exclusion of uncontrolled use of drugs that affect the conduction of impulses, etc.). To prevent worsening of the degree of AV block, implantation of a pacemaker is indicated.
Atrioventricular blockade is a conduction disorder at the level of the atrioventricular junction, i.e., the atrioventricular node and adjacent structures, including the atrioventricular bundle.
First degree atrioventricular block can only be diagnosed by ECG. Atrioventricular block of the second degree can be suspected if regular loss of every third, fourth, etc. expected systole or irregular loss is detected pulse waves and heart sounds. Sometimes the patient feels a sinking heart during the prolapse. If, with incomplete blockade, every second impulse is carried out, then the resulting picture is indistinguishable from bradycardia of a different nature. With third-degree blockade, pronounced bradycardia (sometimes bradyarrhythmia) is combined with uneven sonority of 1 tone. Blockades with severe bradycardia or isolated extended diastolic pauses may manifest as signs of impaired blood supply to organs, primarily the brain and heart. Sometimes brain hypoxia manifests itself as attacks that suddenly occur in any position with loss of consciousness, respiratory failure and convulsions (Morgagni-Adams-Stokes attacks), which can spontaneously stop or result in the death of the patient.
On an ECG with 1st degree block (slowing of atrioventricular conduction), the PQ interval is extended to 0.21 s or more, but all atrial impulses reach the ventricles.
In case of second degree block (incomplete atrioventricular block), individual atrial impulses are not conducted to the ventricles, the corresponding ventricular complex disappears, and a timely but isolated P wave appears on the ECG. Proximal type blockade is distinguished at the level of the atrioventricular node (Wenckenbach type, Mobitz type I) and blockade of the distal type at the level of the atrioventricular bundle or more distally (Mobitz type P). With a proximal type blockade, the loss of the ventricular complex is preceded by a progressive lengthening of the PQ interval in a series of 2–8 (usually 3–4) cycles; these periods are sometimes regularly repeated (Samoilov–Wenckebach periods). With a distal type blockade, there is no gradual lengthening of the OC interval before prolapse; prolapses can be regular or irregular. If an incomplete atrioventricular block with 2:1 conduction is recorded on the ECG, then classifying it as a proximal or distal type based on indicated signs impossible. This issue can presumably be resolved if it is known what disorder preceded the incomplete block: a proximal block is usually preceded by a slowdown in atrioventricular conduction, and a distal block is preceded by the occurrence of intraventricular block. In addition, some diseases are characterized by a certain level of blockade.
With third-degree block (complete atrioventricular block), atrial impulses are not conducted to the ventricles, cardiac activity is maintained by a replacement ventricular rhythm. The atria and ventricles are excited in a regular, but independent rhythm. In this case, proximal blockade is also distinguished (narrow QRS complex, ventricular rate 40 - 50 beats per minute; it is preceded by an incomplete block of the proximal type) and distal (wide QRS complex, ventricular rate 18 - 40 beats per minute; preceded by - sometimes very short-term, incomplete distal blockade) type.
All disturbances of atrioventricular conduction can be persistent, but more often they are transient. The severity (degree) of the blockade is usually very labile: often on one electrocardiographic curve you can see transitions of the blockade from one degree to another. Sometimes repeated conduction disturbances are very short-lived and can only be noticed during cardiac monitoring. If the ECG shows the transition of incomplete distal blockade to complete, then an unusually long pause before the establishment of the replacement ventricular rhythm attracts attention. This pause can reach several seconds (in fact, it is a short-term cardiac arrest) and is accompanied by signs of organ hypoxia, Morgagni-Adams-Stokes attacks, or even a picture of clinical death.
Determining the level of blockade based on the ECG is conditional. The same prolongation of the PQ interval, caused in most cases by impaired conduction through the atrioventricular node, in some patients may be associated with a slowdown in conduction in the branches of the atrioventricular bundle. More precise definition the level of blockade is possible with electrography of the atrioventricular bundle: with proximal blockade, the bundle signal (H) precedes ventricular depolarization (V), the HV interval is normal (about 0.05 s); with distal blockade, depolarization of the atrioventricular bundle and ventricles occurs independently of each other.
Clinical significance
The meaning of proximal and distal blockades is different. In general, the more distal and severe the blockade, the more serious its clinical significance.
Slowing of atrioventricular conduction and (rarely) incomplete block of the proximal type can be observed in apparently healthy individuals, even athletes. This blockage usually disappears after exercise. Proximal blockades occur in individuals with neurocirculatory dystonia with high vagal tone. They can develop due to intoxication with cardiac glycoside, as well as under the influence of b-blockers, verapamil. Quite often, a short-term (within a few days) disturbance of atrioventricular conduction occurs with a posterior phrenic infarction. Atrioventricular blockades can accompany myocarditis, and in persistent form - cardiosclerosis. Rarely, congenital complete transverse blockade at this level occurs. In general, proximal-type blocks usually have little hemodynamic deterioration, rarely lead to a noticeable deterioration in organ perfusion, and thus generally have a favorable prognosis. The appearance of a blockade may have diagnostic value, for example, in myocarditis that is asymptomatic.
Blockade of the distal type is especially characteristic of extensive, anteroseptal myocardial infarction, in which it can occur and quickly (over several hours, days) progress until the development of complete blockade. The appearance of a distal blockade indicates the extent of the pathological focus.
This may be one of the reasons (along with large sizes heart attack) severe course of the disease and death of the patient in acute period heart attack. Distal blockade also occurs with other sclerotic, inflammatory, degenerative changes in the His bundle and its branches, being a poor prognostic sign. As a rule, it adversely affects hemodynamics and is often accompanied by signs of organ hypoxia (Morgagni–Adams–Stokes attacks are characteristic of blockades of this level), heart failure; difficult to reversible and prone to rapid progression.
Rational treatment of the underlying disease (myocardial infarction, myocarditis, etc.) can lead to the disappearance of the blockade. It is necessary to discontinue medications that contribute to atrioventricular conduction disturbances - cardiac glycosides, b-blockers, verapamil and other antiarrhythmic drugs, potassium preparations. For incomplete and complete transverse blockade of the proximal type, atropine, belladonna, belloid, isoproterenol, aminophylline are sometimes used, but the effect of using these drugs is inconsistent, in best case scenario they have a temporary effect. For distal blockades, these drugs are contraindicated as they can increase the degree of blockade. All blockades that led to violations peripheral circulation, Morgagni-Adams-Stokes attacks, heart failure, as well as incomplete and complete blockade of the distal type are indications for the use of permanent or temporary ventricular pacemaker.
The process of conduction disturbance in which a complete or partial cessation of nerve impulse transmission occurs is known as heart block.
It has the ability to form in different departments hearts.
The choice of therapeutic therapy depends on its location and severity.
The essence of the disease
The heart muscle has nodes on its surface, presented in the form of clusters nerve cells. It is in these nodes that nerve impulses are formed, which are transmitted along nerve fibers through the myocardium to the cardiac atria and ventricles, causing their contraction.
In the atrium there is one type of node - the sinus-atrial node, where an electrical impulse occurs and enters the atrioventricular node. As a result of this, the heart is able to contract.
Violation of the conduction process is heart block. If the impulses are not partially transmitted, we can talk about a partial blockade, and if the transmission stops completely, we can talk about a complete heart block. But regardless of the type of pathology, the patient’s heart contraction process is disrupted.
When the passage of the nerve impulse slows down, the patient lengthens the pause that occurs between the contraction of the ventricles and atria. When impulse transmission completely stops, contractions of the ventricles and atria do not occur. In this case, the patient develops ventricular or atrial asystole.
A disturbance in the transmission of electrical impulses may be different stages, which leads to the formation of blockades of various forms. In case of complete cessation of NI transmission, blood does not pass through blood vessels, which leads to a decrease in pressure and insufficient supply internal organs human body oxygen.
Classification
As mentioned earlier, the blockade tends to form at different levels. Based on the location of its localization, the following classification is used:
- Proximal. Disruption of nerve impulse conduction occurs at the level of the atria, the atrioventricular bundle of His or its trunk.
- Distal. The blockage forms in the area where the branches of the His bundle are located.
- Combined. In this case, the violation may have a variety of localizations.
When classifying blockades, experts also focus on its electrocardiographic indicators:
The most accurate determination of the degree of development of the disease will help determine the course of treatment.
Causes and symptoms
There are many factors that can provoke a disruption in the transmission of nerve impulses. The degree of the disease has a direct relationship with the cause that provoked it.
For example, 1st degree heart block, which is considered an incomplete block, often does not have any symptomatic manifestations and can be considered normal. As a rule, it appears during sleep or complete rest, and goes away with increased physical activity.
Often the cause of 1st degree block is the patient’s vegetative-vascular dystonia. In children or young people, the disease can be triggered by the presence of mitral valve prolapse or OO foramen. The development of minor anomalies in the functioning or development of the heart can also lead to the formation of pathology.
If we talk about blockades of 2 or 3 degrees, then they are formed in the presence of any disturbance in the structure or functioning of heart tissue, which leads to the formation of scars, as well as inflammatory processes myocardium. These include the following diseases:
- myocarditis;
- cardiomyopathy;
- cardiosclerosis;
- myocardial infarction;
- heart defect (congenital or acquired);
- hypertension, etc.
Incomplete first-degree blockade, as a rule, occurs without visible symptoms. Its presence can be determined by the results of an electrocardiogram during a routine examination of the patient.
Complete blockades (2nd and 3rd degrees) manifest themselves in the form of symptoms of arrhythmia or concomitant disease. Signs may appear instantly or may occur over a long period of time.
Some of the most common symptoms include:
- rapid fatigue and loss of ability to work;
- interruptions in the rhythm of the heart. The patient experiences a sensation of short-term cardiac arrest;
- pain in the sternum;
- dizziness, fainting;
- nausea or ringing in the ears;
- the human body may suddenly break out in cold sweat, while the pulse becomes thread-like and rare;
- convulsions.
If we talk about signs concomitant diseases of cardio-vascular system, such as cyanosis of the skin, pain behind the sternum, swelling of the upper or lower limbs, nausea or vomiting, increased body temperature up to 37.5 degrees, etc.
If you detect one or more of the above signs of the disease, you should immediately contact a specialist for comprehensive survey.
Diagnostics
When first examining a patient, specialists must first determine the patient’s previous diseases of the cardiovascular system (myocardial infarction, cardiopathy, arrhythmias, etc.).
During auscultation, the patient can hear a normal heart rhythm, which is interrupted from time to time by long interruptions, which is associated with loss of contractions of the ventricles of the heart, bradycardia or the development of Strazhesko's 1st cannon sound.
Signs of blockade are clearly visible during Holter monitoring throughout the day.
For getting additional information To determine the presence of parallel diseases, laboratory examinations of the patient’s blood and urine are carried out. Based on their results, it is possible to determine the level of electrolytes, arrhythmics, potassium and magnesium in the blood.
Only after a comprehensive examination can you not only make an accurate diagnosis, but also decide on the choice of effective treatment therapy.
Treatment
When diagnosing a first degree block, the patient does not need drug treatment. It is enough to go 2-3 times a year medical examination, and also be under the supervision of specialists.
In the event that the disease was provoked by taking medications (glycosides, antiarrhythmic drugs, beta blockers), specialists must adjust the dose and schedule of their administration. It is possible that there will be a need to completely stop taking them.
When treating 2nd and 3rd degree blockades, beta-agonists are prescribed. In more complex cases of the disease, implantation of a pacemaker may be recommended.
In order to quickly stop the first attacks of blockade, it is recommended to use drugs such as isadrin or atropine.
One of the radical methods of treating 3rd degree blockade is the implantation of a pacemaker, which will help restore the heart rhythm.
When treating a blockade, there is no way to do without adjusting the patient’s lifestyle, including his diet. It is recommended to introduce foods rich in plant proteins into your diet and limit foods enriched with animal proteins and simple carbohydrates.
It is advisable to adjust the intensity of physical activity and the duration of the rest period.
With incomplete blockade, experts give a fairly positive prognosis.
As for pathologies of degrees 2 and 3, the success of their treatment fully depends on factors such as the patient’s age, his general condition, as well as the presence of concomitant diseases of the cardiovascular system.
We should also not forget about the positive impact on the success of treatment of timely access to specialists.
1st degree AV block is a prolongation of the PQ interval by more than 0.20 s. It is found in 0.5% of young people without signs of heart disease. In the elderly, 1st degree AV block is most often the result of an isolated disease of the conduction system (Lenegra's disease).
Etiology and pathogenesis
- Etiology of atrioventricular blocks
Atrioventricular block can develop when various diseases(both cardiovascular and non-cardiac), and also be a consequence of taking medications.
Reasons for the development of AV block:
IHD.
- Myocarditis.
- Postmyocardial cardiosclerosis.
- Non-ischemic degenerative and infiltrative diseases with damage to the conduction system of the heart.
- Degenerative changes in the AV node or bundle branches (fibrosis, calcification).
- Hypothyroidism.
- Organic heart diseases of non-ischemic origin.
- Congenital complete AV block.
- Surgical or various therapeutic procedures.
- Systemic connective tissue diseases.
- Neuromuscular diseases.
- Medicines.
- AV block in healthy people.
- Pathogenesis of atrioventricular blockades
AV block of the first degree and second degree of the Mobitz type I (proximal) occurs mainly as a result of a delay in the conduction of excitation at the level of the atrinodal (atrium-AV node) pathways.
Conductivity in this zone significantly depends on the tone of the sympathetic and parasympathetic parts of the autonomic nervous system.
Epidemiology
Sign of prevalence: Rare
First-degree AV block is uncommon in young healthy adults. According to research, it occurs only in 0.65-1.1% of young people over 20 years of age. The highest prevalence rate was observed in athletes (8.7%). Prevalence also increases with age; a reported prevalence of about 5% among men over 60 years of age. The overall prevalence is 1.13 cases per 1000 people. In total, first-degree AV block occurs in 0.45-2% of people; in people aged 60 years and older, it is registered in 4.5-14.4% of cases; in people over 70 years old, it is found in almost 40% of cases (P-R interval> 0.20s).
Risk factors and groups
Athletic training - Well-trained athletes may experience first-degree (and sometimes higher-degree) AV block due to increased vagal tone.
- Ischemic disease hearts
- In acute myocardial infarction, first-degree AV block is observed in less than 15% of patients receiving adequate therapy. AV block is more common in cases of established inferior myocardial infarction.
Idiopathic degenerative diseases of the conduction system:
Lev's disease. Expressed by degenerative progressive fibrosis and calcification of adjacent cardiac structures, “sclerosis of the fibrous skeleton of the heart,” including the mitral annulus, central fibrous body, septum, base of the aorta and crest of the interventricular septum. Lew's disease begins in the fourth decade and is thought to be secondary to wear and tear of these structures due to the force of the ventricular musculature. As a result, conduction in the proximal branches of the branch is disrupted and bradycardia and varying degrees of severity of blockade of the AV node appear.
Lenegra's disease, which is an idiopathic, fibrodegenerative disease with limited involvement of the His-Purkinje system. Accompanied by fibrous-calculous changes in the mitral ring, septum, aortic valve and crest of the interventricular septum. These degenerative and sclerotic changes are not associated with inflammatory changes or adjacent ischemic areas of the myocardium. Lenegra's disease involves conduction disturbances in the middle and distal part of the arborization and, unlike Lev's disease, affects a younger generation.
Medicines. Calcium channel blockers, beta blockers, digoxin, amiodarone can cause first degree AV block. Although the presence of first-degree AV block is not an absolute contraindication to the use of these drugs, extreme caution should be exercised when using these drugs in these patients, as the risk of developing higher degrees of AV block increases.
Calcification of the mitral and aortic valve rings. The main branches of the His bundle are located at the base of the anterior leaflets of the mitral valve leaflets and the non-coronary leaflet of the aortic valve. Calcium deposits in patients with calcification of the aortic or mitral valve annulus are associated with increased risk AV block.
Infectious diseases. Infectious endocarditis, diphtheria, rheumatism, Chagas disease, Lyme disease, tuberculosis can cause first-degree AV block.
The spread of infection in infective endocarditis to the native or artificial valve (for example, a valve ring abscess) and adjacent areas of the myocardium can lead to AV block.
Acute myocarditis caused by diphtheria, rheumatism, or Chagas disease can lead to AV block.
Systemic collagenoses with vascular damage. Rheumatoid arthritis, systemic lupus erythematosus, scleroderma can lead to AV block.
Infiltrative diseases such as amyloidosis or sarcoidosis
Myotonic dystrophy
First degree AV block can occur after heart surgery. Transient, temporary AV blocks may result from right-sided cardiac catheterization.
Clinical picture
Clinical diagnostic criteria
Decreased exercise tolerance
Symptoms, course
First degree AV block is usually asymptomatic at rest. With a significant increase in the duration of the PR interval, tolerance to physical activity in some patients with left ventricular systolic dysfunction. Syncope may be a result of or a sign of progression to a higher degree of AV block, primarily accompanied by intranodal block and a wide QRS complex.
Objective research:
In patients with first-degree AV block, the intensity and sonority of the first heart sound decreases.
A short, soft "blowing" diastolic murmur may also be heard at the apex of the heart. This diastolic murmur is not due to diastolic regurgitation of the mitral valve, since it reaches its peak even before the onset of regurgitation. Diastolic murmur is thought to be due to return flow through the closing mitral valve leaflets, which are stiffer than normal. The use of atropine can shorten the duration of this murmur by shortening the PR interval.
Diagnostics
ECG criteria:
Prolongation of P-Q intervals on the ECG by more than 0.22 s with bradycardia; more than 0.18 s with tachycardia
- The size of the P-Q intervals is constant, each P is followed by a QRS complex.
- With a very pronounced prolongation of the PQ interval (more than 0.30-0.36 seconds), a small tooth concordant with the P wave can be detected along its length, which reflects the process of atrial repolarization and is normally superimposed on the QRS complex.
- With proximal blockade of the first degree, the shape of the ventricular complex is not changed. With a distal blockade, it is usually expanded and deformed.
- Sometimes when the interval lengthens P-Q tooth P overlaps the T wave of the previous ventricular complex, which requires differential diagnosis with various ectopic arrhythmias.
Complications
Complications of atrioventricular block occur in a significant proportion of patients with acquired high-degree atrioventricular block and complete AV block.
Complications of atrioventricular block are caused mainly by a significant slowdown in ventricular rhythm against the background of severe organic heart disease.
Main complications of AV block:
- Morgagni-Adams-Stokes attacks.
The most common complications include Morgagni-Adams-Stokes attacks and the onset or worsening of chronic heart failure and ectopic ventricular arrhythmias, including ventricular tachycardia.
A Morgagni-Adams-Stokes attack usually develops at the moment of transition of incomplete atrioventricular blockade to complete, before the start of stable functioning of the pacemaker of the 2nd - 3rd order, or with persistent AV block of the 3rd degree, usually distal, with a sudden decrease in the frequency of the impulses generated by it.
After multiple episodes of loss of consciousness, despite their short duration, in elderly patients a violation of intellectual-mnestic functions may develop or worsen.
