The heart’s rhythm is coordinated by an electrical system that ensures the upper chambers (atria) contract just before the lower chambers (ventricles), allowing for efficient blood pumping. The Atrioventricular (AV) node is a relay station that receives the electrical signal from the atria and transmits it to the ventricles. A heart block occurs when this signal is delayed or interrupted at or below the AV node. Mobitz I (Wenckebach) and Mobitz II are both second-degree AV blocks, meaning some atrial signals fail to reach the ventricles, resulting in a “dropped” beat. Despite this shared classification, their underlying causes, locations, and clinical importance differ significantly, making their distinction necessary for proper management.
Location and Mechanism of the Block
The difference between the two types of second-degree heart block lies in the location and nature of the resistance encountered by the electrical signal. Mobitz I (Wenckebach) typically involves a block occurring within the AV node itself. This area of the conduction system exhibits “decremental conduction,” meaning its ability to transmit signals decreases with successive impulses.
The mechanism for Mobitz I is a progressive fatigue of the AV nodal cells. The electrical signal is delayed longer with each impulse until the signal fails to pass through completely, resulting in a dropped ventricular beat. After this dropped beat, the AV node rests, and the cycle of increasing delays begins again. This block is often temporary and can be caused by reversible factors like high vagal tone, common in athletes, or the side effects of certain medications.
In contrast, Mobitz II is generally a block that occurs below the AV node, usually in the Bundle of His or the bundle branches (the His-Purkinje system). This system does not exhibit progressive fatigue. The mechanism is characterized by an “all-or-nothing” failure of conduction. Signals that successfully pass through are conducted normally, but occasionally, the signal fails entirely without any prior warning or progressive slowing.
This abrupt failure in Mobitz II often signals structural damage to the heart’s electrical wiring, such as fibrosis. The His-Purkinje fibers are not designed to recover gradually like AV node cells. Consequently, the signal either passes quickly and efficiently or is suddenly blocked, representing a more unstable malfunction of the conduction system.
Visualizing the Difference: ECG Patterns
The distinct mechanisms of Mobitz I and Mobitz II create recognizable patterns on an Electrocardiogram (ECG), the primary diagnostic tool. The segment of interest is the PR interval, which represents the time the electrical impulse takes to travel from the atria (P wave) through the AV node to the ventricles (QRS complex).
In Mobitz I, the progressive AV node fatigue translates into the Wenckebach phenomenon. With each successive conducted beat, the PR interval gets progressively longer, reflecting the increasing delay. This lengthening continues until a P wave is generated but is not followed by a QRS complex, indicating a dropped ventricular beat. The cycle then resets, and the first PR interval after the dropped beat is the shortest, beginning the lengthening sequence anew.
Mobitz II presents a different visual pattern because the block occurs lower in the system. When a signal is successfully conducted, the PR interval remains constant, showing no progressive lengthening. The signal passes through the AV node normally but suddenly fails at the His-Purkinje system. The hallmark of Mobitz II is the sudden, unpredictable appearance of a P wave that is not followed by a QRS complex, without any preceding change in the PR interval.
The constancy of the PR interval in conducted beats differentiates Mobitz II from Mobitz I. This visual distinction between predictable, progressive lengthening and the sudden, unheralded drop is fundamental for interpreting the ECG tracing.
Clinical Implications and Treatment Pathways
The difference in location and mechanism leads to vastly different patient outcomes and required medical intervention. Mobitz I is generally considered a more stable and benign condition, especially in asymptomatic patients. Since the block is high in the AV node and often caused by reversible factors, the risk of progression to a complete heart block is low.
For Mobitz I, treatment often involves monitoring the patient, particularly if they are asymptomatic. If symptoms like dizziness or fainting are present, the first step is to identify and remove underlying causes, such as discontinuing medication or treating an electrolyte imbalance. Permanent pacing is rarely necessary and is reserved for patients with persistent, severe symptoms attributable to the block.
Mobitz II is considered an unstable rhythm that requires proactive management. The block is located in the His-Purkinje system, the heart’s final electrical connection to the ventricles, and failure here indicates significant underlying structural disease. This form of heart block has a high risk of progressing suddenly to a third-degree (complete) heart block.
Progression to complete heart block can cause dangerously slow heart rates, resulting in fainting, severe symptoms, or sudden cardiac death. Due to this substantial risk, the standard of care for Mobitz II typically involves the insertion of a permanent pacemaker, often regardless of current symptoms. The pacemaker provides a reliable electrical backup to ensure the ventricles continue to contract, mitigating the danger posed by the unstable block.