Atrioventricular dissociation. Emergency Care for Cardiac Conduction Disorders ECG News for Incomplete AV Dissociation

Patient K., 21 years old. On the ECG: the PII, III, aVF wave is positive, located at different distances after the non-broadened complex (interval R - P = 0.113-0.20 sec.). Interval P - P = 0.92-0.97 sec. Interval R - R = 0.94 sec. Due to a small sinus arrhythmia of atrial contractions, the P wave either approaches the QRS complex or moves away from it.
Conclusion. Isorhythmic atrioventricular dissociation: sinus rhythm of atrial contractions (63-68 beats per minute) and atrioventricular rhythm of the ventricles (65 beats per minute).

Patient Sh., 62 years old. On the ECG: isorhythmic dissociation during excitation of the atria by impulses from the anterior wall of the left atrium (negative PI, V1-V6. positive PII, III) and excitation of the ventricles from the AV junction with blockade of the right branch of the His bundle and right ventricular hypertrophy in a patient with chronic cor pulmonale. The P wave is located in front of the QRS complex, then approaching it, then moving away from it (P - Q \u003d 0.06-0.13 sec.). The atrial rhythm frequency is 80-85 per minute, the AV connection rhythm frequency is 82 per minute.

Conclusion. Isorhythmic A - V dissociation with the left atrial rhythm of atrial contractions and the rhythm of the AV junction of ventricular contractions. Blockade of the right branch of the His bundle. Hypertrophy of the right ventricle and possibly the right atrium.

A - V dissociation with interference, as well as A - V isorhythmic dissociation, is characterized by two different pacemakers: one for the atria, the other for the ventricles. The difference between dissociation and interference is that, against the background of independent contractions of the atria and ventricles, individual sinus (atrial) impulses periodically propagate from the atria to the ventricles (interference - capture).

Thus, this type of rhythm disturbance is characterized by incomplete A-V dissociation of atrial and ventricular contractions. In the classical form of incomplete A-V dissociation, the rhythm of atrial contractions is less frequent than the frequency of ventricular contractions.

Patient M., 35 years old. On the ECG: atrial contraction frequency is 47-51 per minute. The number of ventricular contractions is 49-55 per minute. The ventricular complex is not widened or deformed, indicating its supraventricular origin (rhythm from the AV junction). The contractions of the atria and ventricles in the first four cycles are independent of each other, since the P wave either coincides with the QRS, or is located directly behind it, or moves away from it, approaching the T wave.

Such painting corresponds to A - V dissociation. After the P wave, a new QRS complex does not follow, since the atrial impulse falls on the refractory period of the AV node. However, due to a lower atrial than ventricular rate, the P wave gradually moves away from the QRS. The fourth P wave layered on the previous T wave and caused contraction of the ventricles, since the AV node had by this time left the refractory state, and the ventricles were “captured” by the atrial impulse with QRS aberrance.

Conclusion. Incomplete A - V dissociation (with interference) due to sinus bradycardia and A - V ventricular rhythm (in the presence of retrograde A - V blockade).

When conductivity is disrupted, different kinds heart block, the conduction of impulses through the conduction system of the heart slows down or completely stops.

AV block

This is a slowdown or cessation of impulse transmission from the atria to the ventricles. AV blocks are divided into congenital and acquired. Also, according to the nature of their occurrence, they are classified into acute, transient and permanent. Depending on the level of impulse conduction disturbance, atrioventricular blocks are:

• proximal
• distal

3 degrees of AV block are distinguished by the severity of AV conduction disorders:

• I degree (extension of the P-P(O) interval more than 200 ms)
• II degree (first and second types)
• III degree (absence of impulse conduction to the ventricles)

Causes of AV block may cause heart disease:

• infiltrative diseases
• cardiomyopathies (including those caused by genetic abnormalities)
• heart defects
• myocardial injury
• electrolyte disturbances
• vagotonia

The etiology may also be in taking medications:

• tricyclic antidepressants
• cardiac glycosides

Atrioventricular blockades often resolve without symptoms. They are found by chance during an ECG. Patients may complain of a feeling of pauses and interruptions in the work of the heart, a disturbance in the rhythm of the heartbeat. With a rare rhythm of ventricular contraction may have the following symptoms:

• general weakness
• dizziness
• poor tolerance to physical activity
• worsening of heart failure and angina pectoris
• Morgagni-Adams-Stokes attacks (considered a serious manifestation of the disease in question)

Treatment of AV block should be aimed at preventing the development of sudden cardiac death, cardiac and coronary failure due to bradyarrhythmia. It is necessary to eliminate or minimize the dose medicines, which impair AV conduction. Drug treatment acute form The disease in question involves the use of β-adrenergic agonists (orciprenaline, isoprenaline) and atropine. If the underlying disease is actively treated, but the symptom of impaired AV conduction remains, the question of implanting a permanent pacemaker should be raised.

With I degree AV block, no treatment is needed. Indications for pacemaker implantation are:

• the need to prescribe drugs that inhibit conduction through the AV junction
• III degree AV block or II degree AV block of any level in combination with clinical manifestations of bradycardia
• the same degrees of AV block in patients with no symptoms and heart rate less than 40 per minute.

Intraventricular blocks

They arise due to a disturbance in the conduction of impulses along the left or right bundle branch. The branches of the left bundle branch may also be blocked. Types: permanent blockade and transient.

Since different numbers of bundle branches may be involved, intraventricular blocks can be:

• single-bundle (in turn divided into blockade of the posterior branch of the left bundle branch, the anterior branch of the left bundle branch; and the right bundle branch)
• double-bundle (blockade of the right bundle branch and the anterior branch of the left bundle branch, combined blockade of the anterior and posterior branches of the left bundle branch, the right bundle branch and the posterior branch of the left bundle branch)
• three-bundle (with complete or incomplete AV block)

Complete blockade of the right bundle branch is recorded more often than the left bundle branch. May occur in healthy people who do not have heart disease. The cause is divided into acquired and congenital. Congenital defects also include atrial septal defect.

Blockade of the branches of the left bundle branch can be caused by the following reasons:

• cardiomyopathy
• transient hyperkalemia
• calcification aortic valve

Combined blockade of the anterior and posterior branches of the left bundle branch is in many cases a manifestation of organic heart damage. Among the causes are long-term hypertension, ischemic heart disease, cardiomyopathy and aortic valve defects. It should be taken into account that the sudden occurrence of blockade of the left bundle branch may be one of the manifestations of myocardial infarction. Often bundle branch blocks (if they do not reach the degree of complete three-bundle block) resolve without clinical manifestations.

In most cases, therapy for these types of conduction disorders is not needed. But with 2 and 3 fascicle blockade, pacemaker implantation may be necessary. For people with chronic heart failure and manifestations of dyssynchrony of ventricular excitation, doctors can perform a permanent 2-chamber pacemaker.

AV dissociation (atrioventricular dissociation)

AV dissociation, as a rule, is not an independent pathology. It accompanies other heart rhythm disorders. It appears when there are two independent heart pacemakers. Typical for AV dissociation are confluent complexes and so-called ventricular capture.

The causes of the disease in question may be an increase in the activity of the underlying center of automaticity or severe sinus bradycardia in the form of an escape rhythm from the AV junction. Treatment consists of eliminating the cause of AV dissociation. Bradycardia should be eliminated, and antiarrhythmic drugs may be used.

Ion channel dysfunctions

Hereditary arrhythmic diseases:

• elongated syndrome O-T interval
• catecholamine-dependent polymorphic ventricular tachycardia
• shortened O-T interval syndrome

Long 0-T syndrome- a hereditary disease in which the duration of 0,-TII increases, life-threatening ventricular arrhythmias develop in stressful situations. The cause may be congenital or acquired. Extended 0-G syndrome has the following diagnostic criteria:

• history of episodes of loss of consciousness
• prolongation of the corrected O-T interval more than 440 ms
• alternation of T waves on the ECG
• bradycardia in children
• congenital sensorineural hearing loss, etc.

Long 0-T syndrome requires treatment only if there are clinical manifestations. Patients and their close relatives are advised to avoid heavy physical activity, any kind of sports, and diving in water. low temperatures, exposure to unexpected sound stimuli.

Brugada syndrome on the ECG it is manifested by signs of right bundle branch block, recurrent syncope and a tendency to malignant arrhythmias causing sudden cardiac death. People with this condition also have an increased tendency to develop atrial fibrillation. Most often, the disease is recorded in men aged 30 to 40 years, while the heart is structurally normal. Among the clinical manifestations of the syndrome, syncope dominates.

If flutter and ventricular fibrillation occur, electrical defibrillation and resuscitation should be performed. To prevent sudden death caused by paroxysmal ventricular fibrillation, a cardioverter-defibrillator is implanted in patients:

After a paroxysm of polymorphic ventricular tachycardia;

With a history of fainting;

Survivors after resuscitation;

If there are cases of sudden cardiac death at a young age in the family.

Short 0-T interval syndrome is a genetic disease of the electrophysiological system structurally normal heart. Symptoms include:

• dizziness
• heart failure
• atrial fibrillation

The following symptoms are typical for this syndrome:

• Reducing the threshold for atrial and ventricular fibrillation during programmed pacing
• Tall and pointed T wave
• The presence of a shortened O1-T interval in some family members

TO diagnostic criteria There are also cases of SCD in the family at a young age. Treatment consists of implantation of a cardioverter-defibrillator. Indications: documented episodes of ventricular fibrillation and sustained paroxysms of VT.

Catecholamine-dependent polymorphic ventricular tachycardia

This is a genetic disease characterized by episodes of bidirectional or polymorphic VT caused by adrenergic stimulation and developing in the absence of structural changes in the heart. cases of the disease are rarely recorded - one case per 10,000. Inheritance occurs in a recessive or autosomal dominant manner. Patients are mostly teenagers or young children.

Symptoms first appear between the ages of two and 36 years. Patients with this tachycardia come to the doctor with complaints of fainting. The reasons for fainting are emotional or exercise stress. There are no specific signs on the ECG at rest in patients with catecholamine-dependent polymorphic ventricular tachycardia; they are noted only during physical activity. Without treatment, the prognosis of the disease is unfavorable. According to statistics, 79% of people under the age of 40 experience fainting or air force. And the mortality rate is, according to various sources, from 30 to 50%.

All persons with confirmed or probable (family history, genetic analysis, presence of syncope) catecholaminergic polymorphic VT should be prescribed β-blockers:

• (1-3 mg/kg per day)
• or (1-3 mg/kg per day)

In resuscitated patients and patients with episodes of hemodynamically unstable VT, fainting, despite taking β-blockers, the issue of implanting a cardioverter-defibrillator is decided.

CHARACTERISTICS
Atrial and ventricular rhythms are generated independently of one another - caused by many mechanisms; found in many arrhythmias; is not an electrocardiographic diagnosis.

CAUSES
Digoxin intoxication
Myocarditis
Cardiomyopathy
· Chronic failure valves
Congenital (congenital) heart disease
anesthesia with halotane in cats

RISK FACTORS: Same reasons as

PATHOPHYSIOLOGY
· Possible reasons- complete pathological interruption of impulse conduction between the atrium and ventricle (complete AV block), temporary psychological interruption, and variable refractoriness in AV conduction.
A combination of two or 3 of the following mechanisms causes AV dissociation:
· Reduced automaticity of the sinus node - allows the connecting AV or ventricular center to slip out and control the ventricles independently;
· Increased automaticity of the AV or ventricular junction - in this case, the ectopic center controls the ventricle and the sinus node controls the atria.
· Confusion in AV impulse conduction - blockade of the AV node allows the action of two independent rhythms, one in the atrium and the other below the area of ​​impulse conduction delay.
· Hemodynamic disturbances caused by reduced cardiac output can be detected by slowing of junctional and ventricular escape rhythms or by the presence of variable tachyarrhythmias.

SYSTEMS AFFECTED: Cardiovascular

Susceptibility: Dogs and cats

CLINICAL SIGNS

History data
· Without clinical signs
ZSN (CHS)
· Fast fatiguability with physical load
· Syncopation

General Clinical Study Data
Jugular vein pulsation
regular or irregular rhythm
· Gallop rhythm
Clinical signs of congestive heart failure

DIFFERENTIAL DIAGNOSIS
Atrial or ventricular premature complexes
Ventricular tachycardia
· Complete AV block - Atrial frequency is faster than ventricular or at the AV junction; in AV dissociation, the atrial frequency is slower than the frequency in the AV connection.

VISUALIZATION
Echocardiography and Doppler ultrasound to determine the structure and function of the heart.

ECG CHARACTERISTICS
· Sinus P waves do not have a constant connection with QRS complexes.
· P waves - may precede, be in the middle of, or follow QRS complexes without changing their usually normal shape.
P wave frequency - usually slower than the QRS complex frequency
· Ventricular capture complex - sometimes the P wave and QRS complex look like they are conducting an impulse in the time of regular sinus rhythm; always appears when a sinus or ectopic supraventricular impulse arrives when the AV connecting and/or ventricular pathways are restored from the previous impulse; this is called complete AB dissociation
· Ventricular mixed complexes - sometimes appear as premature complexes during AV dissociation; always preceded by P waves; The QRS complex of the mixed contraction of the heart has a configuration similar to that characteristic of the normal sinus complex and the ventricular ectopic complex; called incomplete AV (AV) dissociation.

PATHOLOGICAL CHANGES: Variable - depends on the reasons described.

TREATMENT
Operating principles
· Urgent or Inpatient - depends on the severity of clinical signs
· Treat described congestive heart failure or other causes.
· ECG is not a diagnosis; the description of the phenomenon is secondary, due to different types electrical deviations from the norm that require various methods treatment (eg, if AV dissociation is caused by AV block, a pacemaker may be the treatment of choice; if caused by junctional rate acceleration, the animal may be sensitive to digoxin or have myocarditis)

HOSPITAL CARE: Varies depending on underlying causes

PHYSICAL ACTIVITY: Limit if there are clinical symptoms.

DIETS: Only changes needed to treat underlying conditions (eg, sodium-reduced diet, for congestive heart failure)

INFORMING CLIENTS: additional may be necessary diagnostic studies to determine the causes and prescribe appropriate therapy.

SURGICAL ACCOUNTS
If AV dissociation is caused by AV block, pacemaker implantation may be treatment.

MEDICATIONS OF CHOICE
· Correct disturbances in electrolyte and acid-base balance.
· Treat the underlying heart disease adequately.
· See the section that describes treatment for complete AV block and for ventricular tachycardia.

PATIENT MONITORING: monitor heart rate and rhythm through serial ECGs.

SYNONYMS
Complete AV dissociation
· Incomplete AV dissociation

CM. ALSO
Idioventricular rhythm
· Atrioventricular block, Complete (Third-Degree)
Ventricular (ventricular) tachycardia

ABBREVIATIONS
AV = atrioventricular
CHF = Chronic (congestive) heart failure

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Sinoatrial block (SAB)

In sinus rhythm, the impulse from the sinus node (SU) must be conducted into the atrium to stimulate heart contractions. A delay in the release of impulses from the sinus node or blockade of their propagation through the atria indicates the presence of a sinoatrial block. There are three degrees of sinoatrial block.

In first-degree SAB, the conduction of the impulse from the sinus node to the atrium is delayed; this condition cannot be recognized on a clinical ECG.

In second-degree SAB, some impulses exit the SA, while the rest are blocked. A second-degree block can be suspected if the expected P wave and corresponding QRS complex are absent on the ECG. In variant SAB II (Wenckebach variant), the P wave appears after a period of increasing increase in the time of impulse conduction from the SA to the atrium, which is again poorly defined on the clinical ECG. However, another ECG sign characteristic of the Wenckebach phenomenon may be observed: progressive shortening of the P-P intervals before the disappearance of the P wave.

With a permanent form of second-degree SAB, the sinoatrial conduction time remains unchanged before and after impulse blocking. Under these conditions, the interval that includes the dropped contraction exactly (or almost exactly) corresponds to the duration of the cardiac cycle.

SAB of the third degree is observed with complete blockade of the impulse emanating from the sinus node; in this case, the P wave originating from the SU is absent.

True, there are three more reasons for the absence of sinus R waves on the ECG:

• weakness of the sinus node;
• the stimulus arising in the suture system turns out to be inadequate to activate the atrium;
• atrial non-reactivity.

Clinical significance

SAB usually occurs due to myocardial disease (acute rheumatism, acute inferior myocardial infarction, other myocarditis) or drug intoxication (digitalis, atropine, quinidine, salicylates, propranolol). In rare cases, SAB can be caused by stimulation of the vagus nerve.

Treatment

• Treatment depends on the myocardial lesion causing SAB, associated arrhythmias, and the presence of symptoms of hypoperfusion.
• The frequency of impulses coming from the SG and sinoatrial conduction can be adjusted with atropine or isoproterenol (if necessary).
• For recurrent or persistent symptomatic bradycardia, cardiac pacing is indicated.

Stopping the sinus node (sinus pause)

During a sinus pause, the sinus impulse is not able to form in the sinus system. When the sinus node stops, the R-R interval cannot be mathematically correlated with the initial frequency of discharges in the sinus node.

Clinical significance

Sinus node arrest may be due to the same causative factors that cause SAB; this is especially true for digitalis intoxication. The combination of digitalis therapy and carotid sinus massage can lead to a prolonged sinus pause, which is well known. Short periods of sinus node arrest can also be observed in healthy people when the tone of the vagus nerve increases. During prolonged sinus pause, escape rhythms originating from the AV junction often occur.

Treatment

• Treatment depends on the causative factor of sinus node arrest, associated cardiac arrhythmias, and the presence of symptoms of hypoperfusion.
• In symptomatic sinus arrest, atropine usually increases the frequency of impulses originating in the sinus node.

For recurrent or symptomatic bradycardia, pacing is indicated.

Atrioventricular dissociation

Atrioventricular dissociation is a condition in which the atria and ventricles contract under the influence of separate and independent pacemakers. It is not a rhythm disorder and occurs as a result of other conduction and rhythm disorders. There are two forms of AV dissociation: passive (default, or “escape”) and active (usurpation).

Passive AV dissociation occurs when the impulse fails to reach the AV node due to sinus node weakness or block. In such cases, the escape rhythm takes over and stimulates the ventricles. When the sinus node is restored, atrial activity is also restored, but this can occur during the period when ventricular contraction is controlled by the extrasystolic pacemaker, so P waves and QRS complexes appear on the ECG independently of each other.

The active form of AV dissociation occurs when the underlying pacemaker accelerates the rhythm to usurp the sinus node and capture the ventricles; the atria are still stimulated.

In both forms of AV dissociation, fused excitations are not uncommon. Often both pacemakers operate at almost the same speed, perhaps as a result of mechanical or electrical influences causing them to somehow stay in phase with each other; this condition is called isorhythmic dissociation.

Clinical significance

Passive AV dissociation occurs when the frequency of impulses in the sinus node decreases due to sinus bradycardia, sinus arrhythmia, SA block or sinus pause. Her common reasons include the following:

• IHD (especially acute lower myocardial infarction);
• myocarditis (especially rheumatic carditis);
• drug intoxication (especially digitalis);
• vagal reflexes.

Passive AV dissociation may also occur in highly trained athletes.

Active AV dissociation occurs when the automaticity of the downstream pacemaker increases. It is often caused by myocardial ischemia and intoxication. medicines(especially digitalis).

Treatment

• In most cases, the heart rate during AV dissociation is quite acceptable and well tolerated by patients.

Therapy (if carried out) is aimed at eliminating the causative factor of AV dissociation.

Atrioventricular block

The clinical classification of AV blocks was proposed a long time ago, before modern ideas about conduction mechanisms and locations of disturbances in the conduction of impulses between the atria and ventricles. Unfortunately, this classification is too simplified and does not take into account all the problems associated with impaired AV conduction. However, it is used almost everywhere.

First-degree AV block is characterized by slowing of AV conduction and is manifested by an increase in the PR interval on the ECG. Second-degree AV block is characterized by intermittent AV conduction, with some atrial impulses reaching the ventricles while others are blocked. Third degree AV block is characterized by complete cessation of AV conduction.

The exact localization of AV blocks can be determined by His bundle electrocardiography. Although application of this method in the emergency department appears unrealistic, a correlation can be made between the clinical ECG, the approximate location of the block, and the risk of further progression.

AV blocks can be divided into nodal and infranodal; this is an important distinguishing feature since clinical significance and prognosis depend on the location of the block. AV nodal blocks are usually caused by reversible inhibition of conduction, often self-resolving; however, as a rule, there is a stable infranodal escape pacemaker stimulating the ventricles, so the prognosis cannot be reliable.

Infranodal blocks are usually associated with organic disease of the His bundle or its branches; the damage is often irreversible, and there is usually a slow and unstable ventricular escape rhythm that stimulates the ventricles; the prognosis can be quite severe depending on the clinical circumstances.

First degree AV block

With this blockade, each atrial impulse is conducted into the ventricles, but more slowly than normal. On the ECG this is recognized by a PR interval exceeding 0.2 s. Conduction delay occurs at the AV node, although it can occur at any infranodal level.

Clinical significance

First-degree AV block sometimes occurs in a healthy heart. Common causes include increased vagal tone, digitalis toxicity, acute infarction of the lower posterior wall of the heart, and myocarditis.

Treatment

• Treatment is usually not required.
• Prophylactic pacing for acute myocardial infarction is not indicated unless there are more serious conduction abnormalities at the infranodal level.

Second degree AV block, Mobitz I (Wenckebach)

With this block, there is a progressive increase in the duration of AV conduction (and the PR interval on the ECG) until the atrial impulse is completely blocked.

The conduction ratio is used to express the ratio of atrial and ventricular depolarizations. So, with its value 3:2, two out of three atrial impulses are conducted to the ventricles. Usually only one atrial impulse is blocked. After unconducted excitation, AV conduction returns to normal and the cycle usually repeats either with the same conduction ratio (fixed ratio) or with a different ratio (variable ratio). This type of block is almost always observed at the level of the AV node and is often caused by reversible inhibition of AV nodal conduction.

The Wenckebach phenomenon contains an apparent paradox. Although PR intervals progressively lengthen before the loss of excitation, the extent of their lengthening decreases with subsequent cardiac contractions, resulting in progressive shortening R-R interval immediately before the missed excitation. Based on this, we can assume that the Wenckebach phenomenon occurs even in cases where the conduction delay cannot be seen on the ECG, as with Wenckebach SA block.

Wenckebach block is believed to occur because each subsequent depolarization leads to an increase in the refractory period of the AV node. When the subsequent atrial impulse arrives at the node, it is still in the relative refractory period, so conduction is slower relative to the preceding stimulus. This process progresses until the atrial impulse reaches the AV node during the absolute refractory period and conduction is completely blocked. The ensuing pause allows the AV node to recover, and the process can be repeated again.

Clinical significance

This blockade is often transient and is usually combined with acute inferior myocardial infarction, digitalis intoxication, myocarditis, or observed after cardiac surgery. Wenckebach block can also occur when a normal AV node is exposed to very frequent impulses coming from the atria.

Treatment

• Specific treatment is not necessary until slow ventricular contractions cause signs of hypoperfusion.
• 0.5 mg of atropine is administered intravenously; if necessary, the dose is repeated every 5 minutes, titrated until the desired effect is obtained or until a total dose of 2.0 mg is achieved. In almost all cases, a positive response is noted.
• The administration of isoproterenol during acute myocardial infarction or digitalis intoxication is very risky, so its use should be avoided.
• If atropine does not help, it is necessary to install a transvenous ventricular pacemaker (as required).

Second degree AV block Mobitz II

With this type of block, the PR interval remains constant both before and after unconducted atrial impulses. It is possible that one or more impulses may not be carried out at a time.

Mobitz II block usually occurs in the infranodal conduction system, often with associated bundle or bundle branch blocks, so the QRS complexes are usually widened. But even with narrow QRS complexes, the block is usually localized in the infranodal system.

With second-degree AV block, which occurs with a fixed conduction ratio of 2:1, differentiation of Mobitz type I (Wenckebach) and Mobitz type II blocks is impossible. If the QRS complexes are narrow, then localization of the block in the AV node or in the infranodal system is equally likely. With wide QRS complexes, infranodal localization of the block is more likely.

Clinical significance

The second type of block assumes the presence of structural damage to the infranodal conduction system; it is usually persistent and can progress unexpectedly to complete heart block, especially during acute myocardial infarction.

Treatment

• If slow ventricular contractions cause symptoms of hypoperfusion, emergency treatment is necessary. Atropine should be used first: almost 60% of patients have a positive response. Isoproterenol is effective in almost 50% of cases, but it is potentially dangerous during acute myocardial infarction or digitalis intoxication, so its use should be avoided. In patients who do not respond to atropine, transcutaneous cardiac stimulation is advisable.

In most cases, especially with acute myocardial infarction, continuous transvenous cardiac pacing is required.

Third degree AV block (complete)

With third-degree AV block, there is no atrioventricular conduction. The ventricles are stimulated by the escape pacemaker at a rate lower than that of the atria. Conduction disturbances can be localized at the nodal or infranodal level.

If AV block occurs in the AV node, then the work of the ventricles is controlled by the escape pacemaker in the AV junction, while the ventricular contraction rate ranges from 40 to 60 beats/min; Because the rhythm occurs above the bifurcation of the His bundle, the QRS complexes are narrow.

If third-degree AV block occurs at the infranodal level, the ventricles are stimulated by a ventricular escape rate of less than 40 beats/min.

Clinical significance

Nodal third-degree AV block develops in almost 8% of patients with acute inferior myocardial infarction; it is usually transient, although it may persist for several days.

Third-degree infranodal AV block indicates structural damage to the infranodal conduction system, as occurs in large acute myocardial infarction of the anterior wall. The ventricular escape pacemaker usually fails to maintain adequate cardiac output and appears unstable during periods of ventricular asystole.

Treatment

• Nodal third-degree AV blocks are treated in the same way as second-degree Mobitz I AV blocks with atropine or, if necessary, a ventricular pacemaker (on-demand type).
• Infranodal AV blocks of the third degree require the installation of the above pacemaker. To temporarily accelerate the ventricular escape rate, isoproterenol can be used or external cardiac pacing can be performed before installing a transvenous pacemaker.

All the same. With a rhythm from the AV junction, both the atria and ventricles contract under the influence of impulses generated in the AV junction, i.e. impulses to the ventricle are conducted through the His-Purkinje system (as is normal), but to the atria they are retrograde. The presence of retrograde conduction, i.e. “atrial capture” occurs (i.e., a negative P wave is formed after the QRS complex, or the P wave is absent due to overlap with the QRS complex). This excludes AV dissociation and argues in favor of a rhythm from the AV connection.

“Atrial capture” is a rhythm from the AV junction.

“Ventricular capture” - AV dissociation.

With complete AV dissociation, the ECG usually shows a “flirting” of the P wave with the QRS complex, i.e. The P wave moves close to the QRS complex, being located slightly in front or behind it, or completely located on the QRS complex, while it is always positive.

With complete AV dissociation (i.e. in the absence of ventricular “captures”), isorhythmia may be observed, i.e. the frequency of P waves and QRS complexes on the ECG may become the same, BUT the P waves are not conducted to the ventricles. In this case, a fixed position of the P waves in relation to the QRS complex is observed. This is the so-called isorhythmic AV dissociation. Some authors believe that this is a kind of compensatory phenomenon, somehow synchronizing the work of the atria and ventricles.

Conditions causing AV dissociation:

• surgical interventions, anesthesia (including intubation),
• conditions in which the level of catecholamines increases (including infusions of drugs with a positive inotropic effect) and drugs that block catecholamines,
• sinus node damage
• glycoside intoxication
• IM and others organic lesions hearts,
• hyperkalemia
• vagotonia (neurogenic syncope, nausea),
• ventricular tachycardia or pacemaker in the ventricles.
• AV dissociation can be observed after radiofrequency ablation of the slow pathway in AV nodal reentry tachycardia, with damage to the vagus nerve fibers.
• After electric shock, AV dissociation occurs against the background of an escape rhythm, this may be a normal phenomenon.

The reasons leading to increased automaticity of centers of the 2nd and 3rd order can be remembered using mnemonics dr(doctor). Eric

D - digitalis intoxication

E – electrolyte disorders (hypokalemia, hypercalcemia)

P – stretching of the myocardium and conduction pathways (dilatation of the heart chambers)

I – myocardial ischemia

K – catecholamines, ASR disorders

Regardless of the cause, AV dissociation is usually secondary, i.e. may be a consequence of some other cause.

Anamnesis

AV dissociation may be asymptomatic, but when symptoms are present, they are usually due to bradycardia, tachycardia, AV dyssynchrony, or loss of atrial pump and include the following symptoms:

• Severe dyspnea
• dizziness
• sensation of strong pulsation in the neck
• heartbeat
• weakness, malaise

Physical examination

Physical findings are due to bradycardia, tachycardia, AV dyssynchrony, or at least transient loss of atrial pumping.

• General inspection– variable pulse or variable blood pressure, caused by a change in the ratio between contractions of the atria and ventricles.
• Pulse– pulse rate is variable. A fast or slow pulse may occur, depending on the underlying cause.
• HELL– low with idioventricular rhythm (VT).
• Jugular venous pulse - Periodically occurring gun waves a , which are noted at the moment when simultaneous contraction of the atria and ventricles occurs. Wavesa change when the interval changesPR or if the complexQRS occurs immediately after the toothP.
• Heart sounds:
• variable volume of the first tone,
• periodic intensification of the first tone, occurring as the PR interval shortens, reaching a very loud sound (cannon shot); occurs when the ventricular rate exceeds the atrial rate and the QRS appears immediately following the P wave
• beat-to-beat variability of systolic murmur.

Causes

The main causes of AV dissociation are VT, nonparoxysmal tachycardia from the AV junction, escape rhythm from the AV junction, and accelerated idioventricular rhythm.

• Ventricular tachycardia,
• non-paroxysmal junctional tachycardia,
• rhythm from the AV junction/tachycardia occurs with a rhythm exceeding the sinus frequency in the absence of retrograde atrial capture.

This is observed in such clinical situations as digoxin intoxication; sinus bradycardia with an escape rhythm from the AV junction; after heart surgery, in particular valve surgery.

§ Long post-ectopic cycle, allowing the emergence of an escape rhythm from the AV junction.

Laboratory research

digoxin level

Other tests

§ ECG is the most common method for diagnosing this pathology. An escape rhythm and P wave morphology are detected. With complete AV dissociation, the P waves and QRS complexes do not have a fixed time relationship with each other. P wave morphology depends on the source of atrial activation.

§ The relationship between atrial and ventricular rhythms is important for understanding AV dissociation. The ventricular rate is equal to or greater than the atrial rate.

§ There are times when other methods are required to determine atrial and ventricular activation. The figure shows the diagnostic approach.

§ Determining whether P waves are conducted can be difficult. In order to distinguish AV dissociation from AV block, tests that change the frequency of atrial and ventricular rhythms can be used. While connected to the monitor, the patient can rise, sit, or perform any exercises.

Treatment

The choice of treatment depends on the cause of this pathology and its severity. When treating patients with AV dissociation, it is important to consider its hemodynamic status and determine the underlying pathology.

§ In hemodynamically unstable patients, such as those with VT, the treatment of choice is in-situ cardioversion or intravenous administration drugs, depending on the patient's stability. Treatment of glycoside intoxication should also be continued.

§ It is important to ensure that AV conduction is not impaired in patients with AV dissociation due to an accelerated rhythm from the AV junction after cardiac surgery. Rarely, patients experience complete AV block with an accelerated rhythm from a site distal to the level of the block; if the accelerated focal rhythm becomes constant, then we are dealing with complete AV block.

Surgery

The need to implant a permanent pacemaker is rare.

Medicines

The goal of pharmacotherapy is to reduce mortality and prevent complications.

Anticholinergic drugs

Competitive inhibitors of autonomic, postgangliolar and cholinergic receptors.

o Atropine i.v. or i.m. – increases heart rate due to the vagolytic effect, contributing to an increase in CO.

Adrenergic receptor agonists

Stimulate the myocardium and improve coronary blood flow.

o Isoproterenol: has beta1 and beta2 adrenergic activity. Binds to beta receptors of the heart, bronchial smooth muscles, skeletal muscles, muscles of the vascular wall and gastrointestinal tract. Has a positive inotropic and chronotropic effect.

In case of “capitulation” of the SA node (SA blockade), sinus rhythm should be restored. You should not prescribe drugs that can cause depression of physiological (replacement) centers. This can lead to cessation of blood circulation. It is enough to carry out ECS during SSSU.

For digitalis intoxication - potassium preparations.

After the operation - potassium supplements, oxygen therapy, normalization of blood hormone levels, if necessary (VT) - cordarone.

Antidotes

Used to treat digitalis intoxicadia

· Digoxine immune Fab (Digibind) – is a fragment of immunoglobulin with a specific and high affinity for both digoxin and digitoxin molecules. Removes digoxin and digitoxin from tissues by binding to them. Each vial (ampule) of digibind contains 40 mg of purified digoxin-specific antibody fragments that bind approximately 0.6 mg of digoxin or digitoxin. The dose of antibodies depends on the total loading dose of digoxin, which can be calculated in three ways:

1) determine the amount of digoxin administered “acutely” (acute, in the sense of quickly), taking into account 80% bioavailability (amount of digoxin administered in mg X 0.8 = loading dose of digoxin);

2) determine the concentration of digoxin in the blood plasma and, using the pharmacokinetic formula, multiply by the volume of distribution of digoxin (Vd – volume of distribution) and the patient’s body weight in kg (Digoxin loading dose = digoskin level in plasma (ng/ml) X 6l/ kg X body weight in kg);

3) use an empirical dose, taking as a basis the average doses of drugs that cause acute or chronic overdose in adults and children.

If the amount of digoxin administered cannot be accurately determined empirically (it is safer to use the highest amount), an alternative option is to be prepared to increase the dose if the effect is insufficient.

Injectable solution

Literature

Okorokov A.N. "Diagnosis of diseases internal organs» Volume 10

Kushakovsky M.S. “Arrhythmias of the heart”

Roitberg G.E., Strutynsky A.V. “Diseases of the Cardiovascular System”.

Modest comments from a clinical resident.