Case Study 2: Atrioventricular Conduction Block

Case Study 2 Atrioventricular Conduction Block

This case involves a 68-year-old male patient, Mr. Charles Doucette, recovering from an acute myocardial infarction. His electrocardiogram (ECG) shows normal PR intervals and QRS complexes, but occasional P-waves are not followed by QRS complexes, indicating a possible atrioventricular (AV) conduction abnormality. The physicians diagnosed him with a Mobitz type II AV block, a form of second-degree heart block attributed to damaged conduction pathways in the AV node or His-Purkinje system. This condition can potentially worsen and lead to critical cardiac output reductions, prompting the plan to implant a pacemaker. The following discussion addresses key aspects of cardiac electrophysiology related to this case, explaining the normal ECG features, the pathophysiology of AV conduction, and the clinical implications of the observed arrhythmia.

1. Describe and explain the physiology of the waves and intervals of the normal ECG.

The normal electrocardiogram (ECG) represents the electrical activity of the heart during each cardiac cycle. It consists of several waves and segments, each reflecting specific electrical events of cardiac depolarization and repolarization. The P wave corresponds to atrial depolarization initiated by the sinoatrial (SA) node, causing the atria to contract. The P wave's polarity and shape are typically upright in standard limb leads, indicating normal atrial conduction. Following the P wave is the PR interval, representing the time from atrial depolarization onset to the onset of ventricular depolarization, encompassing conduction through the atria, AV node, and His-Purkinje system. The QRS complex reflects ventricular depolarization, where the electrical impulse spreads through the interventricular septum, ventricles, and Purkinje fibers, leading to ventricular contraction. The T wave signifies ventricular repolarization and the return of myocardial cells to their resting state. Lastly, the QT interval spans ventricular depolarization and repolarization, vital in assessing cardiac electrical stability. These waves and intervals provide essential information about the heart's rhythm, conduction pathways, and potential abnormalities.

2. What does the PR interval on the ECG represent? What units are used to express the PR interval? What is the normal value?

The PR interval represents the time elapsed from the onset of atrial depolarization (start of the P wave) to the onset of ventricular depolarization (start of the QRS complex). It reflects the conduction time through the atria, the AV node, and the His-Purkinje system. The PR interval is typically expressed in seconds or milliseconds, with 1 millisecond (ms) equal to 0.001 seconds. The normal PR interval ranges from 0.12 to 0.20 seconds (120 to 200 ms). A prolonged PR interval suggests delayed conduction through the AV node, indicative of first-degree AV block, whereas a shortened PR may suggest pre-excitation syndromes such as Wolff-Parkinson-White syndrome.

3. What does the term “conduction velocity” mean, as applied to myocardial tissue? What is the normal conduction velocity through the AV node? How does conduction velocity in the AV node compare with conduction velocity in other portions of the heart?

Conduction velocity refers to the speed at which electrical impulses propagate through cardiac tissue. It is typically expressed in centimeters per second (cm/sec). In myocardial tissue, conduction velocity varies across different regions. The AV node exhibits a markedly slow conduction velocity, roughly 0.05 to 0.1 m/sec, which allows for a delay between atrial and ventricular contraction, facilitating proper ventricular filling. In contrast, conduction velocity through the His-Purkinje system is rapid, about 2 to 4 m/sec, enabling synchronized ventricular depolarization. The slow conduction within the AV node provides a critical functional delay, ensuring the atria contract first, followed by the ventricles, maintaining effective cardiac performance.

4. How does AV nodal conduction velocity correlate with PR interval? Since Mr. Doucette’s physicians believe he has a block in his AV conduction system, why are his PR intervals normal (rather than increased)?

The AV nodal conduction velocity directly influences the duration of the PR interval; slower conduction results in a prolonged PR interval. Conversely, rapid conduction shortens the PR interval. In Mr. Doucette’s case, the normal PR interval indicates that, despite the presence of AV conduction block type II, the conduction time that does occur through the AV node is within normal limits. Mobitz type II AV block is characterized by sudden, unexpected failure of conduction without prolonging the PR interval before theDropped beat, reflecting blockage distal to the AV node, often below the AV node in His-Purkinje fibers. Therefore, his PR intervals remain normal because the delay is not within the portion of the conduction system represented by the PR interval but occurs later in the His-Purkinje pathway, which is not reflected in the PR measurement.

5. What does the QRS complex on the ECG represent? What is implied in the information that the QRS complexes on Mr. Doucette’s ECG had a normal configuration?

The QRS complex represents electrical depolarization of the ventricles, initiating ventricular contraction. Its morphology, duration, and amplitude provide insights into ventricular conduction pathways. A normal QRS complex, typically lasting less than 0.12 seconds (120 ms), indicates that ventricular depolarization occurs efficiently through the His-Purkinje system. On Mr. Doucette’s ECG, the normal configuration of QRS complexes suggests that the ventricles' conduction pathways are functioning properly, and the ventricles depolarize normally when conduction reaches them. This reinforces the idea that the conduction defect resides upstream, perhaps within the His bundle or lower in the conduction pathway, consistent with Mobitz type II AV block.

6. How is it possible to have a P-wave that is not followed by a QRS complex, as seen on Mr. Doucette’s ECG? Propose a mechanism to explain the P-wave that is not followed by a QRS complex.

The phenomenon of P-waves not followed by QRS complexes indicates a failure in conduction from the atria to the ventricles. In Mobitz type II AV block, some impulses fail to pass through the His-Purkinje system due to a conduction block distal to the AV node. This results in a P-wave (atrial depolarization) occurring without subsequent ventricular depolarization (QRS complex). Mechanistically, damaged or diseased His-Purkinje fibers exhibit intermittent conduction failure, perhaps due to ischemic or degenerative changes from the prior myocardial infarction. This leads to non-conducted P-waves, or "blocked" atrial impulses. Such non-conducted P-waves still originate from the SA node but are unable to propagate through the impaired conduction pathways to depolarize the ventricles.

7. Why did Mr. Doucette faint?

Mr. Doucette experienced fainting episodes likely due to transient or intermittent loss of effective ventricular contractions resulting from his AV conduction block. In Mobitz type II AV block, the sudden failure of the conduction of atrial impulses causes a drop in ventricular rate or pauses in ventricular activity, decreasing cardiac output. This brief interruption in effective blood circulation can lead to syncope, especially in individuals with compromised cardiac function or reduced physiological reserve. The episodes of syncope reflect the critical impact of conduction failure on hemodynamics, emphasizing the need for definitive therapy such as pacemaker implantation to maintain consistent ventricular pacing and prevent further fainting episodes.

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