Atrioventricular block (AVB) is a conduction disorder in which the electrical impulse generated by the atria is not properly transmitted to the ventricles through the atrioventricular (AV) node and the His-Purkinje system. The severity of the block ranges from a simple conduction delay to a complete interruption of transmission, with potentially severe hemodynamic consequences.
AVB represents one of the main causes of pathological bradycardia and may be either transient or permanent, depending on the underlying cause. In advanced cases, when atrioventricular conduction is completely interrupted, the ventricular rhythm depends on an escape focus, which may be junctional or ventricular. If these escape rhythms are inadequate, they can lead to syncope, heart failure, and in the most severe cases, sudden cardiac arrest.
It is crucial to distinguish AVB from other forms of conduction disorders, particularly sinoatrial block. In AVB, the impulse is normally generated by the sinus node, but its transmission to the ventricles is delayed or blocked at the level of the AV node or the branches of the His-Purkinje system. In contrast, in sinoatrial block, the issue lies in the generation of the impulse itself or in its transmission to the atria, resulting in pauses where the P wave is absent on ECG. This difference is essential, as the treatment and clinical implications of the two conditions differ significantly.
AVB is classified according to the severity of the conduction disturbance:
Timely recognition of AVB is essential to avoid potentially serious complications, especially in patients at risk of hemodynamic deterioration. Management varies depending on the degree of block and the patient’s clinical condition and may include extended monitoring, pharmacological therapy, or permanent pacemaker implantation.
The causes of atrioventricular block (AVB) can be classified as intrinsic, when the damage directly involves the AV node or the His-Purkinje system, or extrinsic, when the block is due to external factors that temporarily affect conduction.
Intrinsic causes (direct damage to the AV node or conduction system):
Extrinsic causes (external factors that temporarily impair AV conduction):
Atrioventricular block (AVB) occurs when the transmission of the electrical impulse from the atria to the ventricles is slowed or interrupted at the level of the AV node or His-Purkinje system. The underlying mechanism varies depending on the type and degree of block, with different consequences for hemodynamics and heart rhythm.
The causes of AVB can be divided into two main mechanisms:
The progression of the block depends on the site of damage:
The hemodynamic consequences of AVB vary depending on the degree of the block and the heart’s ability to compensate for the reduced heart rate.
In patients with advanced AVB, the reduction in heart rate and loss of atrioventricular synchrony may lead to hypotension, heart failure, and exercise intolerance. Early treatment is essential to avoid serious complications.
Risk factors increase the likelihood of developing atrioventricular block, though they are not direct causes. Recognizing them is essential to identify predisposed patients and implement preventive strategies.
Predisposing factors for AVB:
It is not always possible to prevent atrioventricular block, particularly in cases related to fibrotic degeneration or genetic conditions. However, certain strategies can reduce the risk of developing advanced AV block.
Managing underlying heart disease is crucial, as early treatment of conditions such as heart failure and valvular disorders can help preserve normal AV conduction.
Another key element is monitoring pharmacologic therapy, especially in patients treated with bradycardic drugs, for whom periodic ECG checks are essential to detect early signs of slowed conduction.
Also, correcting metabolic imbalances plays an important role: appropriate management of hypothyroidism, electrolyte abnormalities, and hyperkalemia can prevent the onset of conduction disturbances.
Finally, during cardiac surgery procedures, special care should be taken to preserve conduction structures, thus reducing the risk of iatrogenic injury.
Prevention is particularly important in patients with multiple risk factors, as progression to more advanced forms of AV block may occur insidiously and without symptoms.
The clinical manifestations of atrioventricular block (AVB) depend on the degree of conduction impairment and the heart's ability to compensate for the reduced ventricular rate. In milder cases, the disorder is often asymptomatic and discovered incidentally. In more advanced blocks, reduced cerebral and systemic perfusion may lead to severe symptoms, including syncope.
First-degree AVB is generally well tolerated, as all atrial impulses reach the ventricles, albeit with delayed conduction. Therefore, many patients remain asymptomatic, and the disorder is detected only during routine ECG. However, in cases where the PR interval is markedly prolonged, the patient may report mild fatigue or reduced exercise tolerance due to atrial contraction being desynchronized from ventricular contraction, thereby decreasing cardiac output efficiency.
On physical examination, the heart rhythm appears regular, with no significant frequency abnormalities. The peripheral pulse is consistent, and cardiac auscultation does not reveal notable pauses, making clinical detection of the disorder difficult without an ECG.
In second-degree AVB, some atrial impulses fail to conduct to the ventricles, resulting in pauses in the cardiac rhythm. The clinical picture varies depending on the severity of the block.
In Mobitz I (Wenckebach), the patient is usually asymptomatic due to the AV node's ability to maintain intermittent conduction. However, in individuals with reduced chronotropic reserve, the altered rhythm may manifest as a mild sensation of light-headedness or palpitations. In some cases, particularly in the elderly or those with cardiovascular disease, the slowed heart rate may cause episodes of presyncope.
During physical examination, the heart rhythm appears slightly irregular, and auscultation may reveal intermittent absence of a beat, corresponding to the non-conducted atrial impulse.
In Mobitz II, however, the conduction block is less predictable and tends to progress to a more severe form. Patients may complain of more frequent dizziness and presyncope, often accompanied by syncopal episodes due to sudden ventricular pauses. The reduced cardiac output may also cause fatigue and dyspnea, especially during exertion.
Clinically, the pulse is irregular, with missing beats detectable on palpation. Cardiac auscultation reveals abrupt pauses that do not follow the progressive pattern of Mobitz I. In more advanced cases, transient hypotension may be present.
Third-degree AVB is the most severe form, characterized by a complete absence of atrioventricular conduction. The atria and ventricles activate independently, with the ventricles relying solely on an escape rhythm, whose origin determines the clinical severity. If the escape rhythm is junctional (40–60 bpm), the patient may experience only fatigue and occasional dizziness. However, if the escape rhythm is ventricular (<40 bpm), the heart rate becomes insufficient to maintain adequate perfusion of vital organs, leading to recurrent syncopal episodes.
In the most severe cases, the patient may present with Stokes-Adams syncope, characterized by sudden and transient loss of consciousness due to temporary asystole before activation of the escape rhythm. Some patients may also report exertional dyspnea and chest pain, especially if concomitant ischemic heart disease is present.
On physical examination, bradycardia is evident, with a very low ventricular rate unrelated to atrial activity. The jugular pulse may show cannon A waves, caused by atrial contraction against a closed AV valve, highlighting atrioventricular dissociation. In patients with heart failure, signs of pulmonary congestion and severe hypotension may also be present.
Complete AVB constitutes a cardiologic emergency and requires immediate evaluation, as it can rapidly evolve into asystole and cardiac arrest, necessitating urgent permanent pacemaker implantation.
The diagnosis of atrioventricular block (AVB) is based on a careful clinical assessment and electrocardiographic confirmation. Diagnostic suspicion arises from the presence of bradycardia, symptoms of cerebral hypoperfusion, or syncope, particularly in patients with cardiovascular risk factors.
The first step is the medical history, where the clinician investigates episodes of syncope, dizziness, fatigue, or palpitations, evaluating any medications taken and predisposing conditions such as ischemic heart disease or recent surgeries. Physical examination may reveal marked bradycardia, cardiac pauses, and signs of heart failure in more advanced cases.
The 12-lead ECG is the cornerstone diagnostic test for AVB and allows for determination of its degree:
Beyond classification, ECG helps identify possible underlying causes. Signs of myocardial infarction may suggest an ischemic origin, while QRS abnormalities (e.g., bundle branch block) may indicate His-Purkinje system involvement.
In patients with suggestive symptoms but normal ECG or suspected intermittent AVB, prolonged recording methods are used:
These tests are essential for differentiating AVB from other conduction disturbances or paroxysmal arrhythmias.
In some cases, specific tests help clarify the mechanism and severity of the block:
EPS is indicated in patients with second-degree Mobitz II block or uncertain AVB origin to determine the site of block and evaluate pacemaker indication.
An accurate diagnosis allows differentiation between benign forms and those requiring immediate treatment, ensuring the most appropriate patient management.
Treatment of atrioventricular block (AVB) depends on the degree of the block, the presence of symptoms, and the underlying cause. While first-degree AVB and some forms of second-degree AVB can be managed with monitoring and medical therapy, advanced AVB often requires permanent pacemaker implantation to prevent severe complications.
First-degree AVB is generally well tolerated and does not require specific treatment, except in cases where it is secondary to reversible causes such as bradycardic drugs or electrolyte imbalances. In patients with a markedly prolonged PR interval (>300 ms) and symptoms of exercise intolerance, dose reduction or withdrawal of the offending drug may be considered.
The management of second-degree AVB depends on the subtype:
Complete AVB is a potentially life-threatening condition requiring immediate intervention. In hemodynamically unstable patients, the following steps are taken:
In acute myocardial infarction complicated by complete AVB, the need for pacing depends on the infarct location: in inferior post-infarction blocks, the condition may be transient, whereas in anterior infarct-related blocks, degeneration of the His-Purkinje system typically requires a permanent pacemaker.
The prognosis of AVB depends on the severity of the block and the timeliness of treatment. First-degree AVB and Mobitz I generally carry a benign prognosis. However, Mobitz II AVB and complete AVB are associated with a high risk of syncope, heart failure, and sudden cardiac death, making pacemaker therapy essential.
If left untreated, AVB may evolve into serious complications, putting the patient's life at risk.
Appropriate AVB management, including timely pacemaker implantation in high-risk cases, is essential to prevent complications and improve patients’ quality of life.