Decoding Bradyarrhythmias and Heart Block: An MRCP (UK) Part 1 Guide

Welcome to MEDIT & CME Academy's dedicated blog post, meticulously crafted to assist you in your preparation for the MRCP (UK) Part 1 examination.

Today, we're tackling a crucial Cardiology topic: Bradyarrhythmias and Heart Block. This is a frequently tested area, so a solid understanding is essential. This guide will provide a comprehensive overview of bradyarrhythmias and heart blocks, ensuring you're well-equipped to tackle related questions on the exam.

Learning Outcomes:

By the end of this post, you should be able to:

1. Recall the anatomy and physiology of the cardiac conduction system, including the sinoatrial (SA) node, atrioventricular (AV) node, and His-Purkinje network.

2. Describe the pathophysiological mechanisms leading to bradyarrhythmias and different degrees of heart block.

3. Recognize ECG patterns characteristic of sinus bradycardia, first-degree AV block, second-degree AV block (Mobitz Type I and II), and complete heart block.

4. Outline the pharmacology of medications that can cause bradyarrhythmias (e.g., beta-blockers, calcium channel blockers).

5. Understand the initial management of symptomatic bradycardia, including indications for atropine and temporary pacing.

6. Differentiate between physiological bradycardia (e.g., in athletes) and pathological causes such as myocardial infarction or hypothyroidism.

Understanding the Cardiac Conduction System

Before delving into bradyarrhythmias, let's revisit the fundamental anatomy and physiology of the cardiac conduction system. A strong foundation here will significantly aid your understanding of the different types of heart block.

The heart's electrical activity originates in the sinoatrial (SA) node, often called the heart's natural pacemaker, located in the right atrium. From the SA node, the electrical impulse spreads through the atria, causing atrial contraction. This impulse then reaches the atrioventricular (AV) node, which acts as a crucial gatekeeper, delaying the signal slightly to allow for complete atrial emptying before ventricular contraction begins.

Finally, the impulse travels down the His-Purkinje network, rapidly spreading through the ventricles and triggering ventricular contraction.

Bradyarrhythmias: What are they?

Bradyarrhythmias are defined as heart rhythms with a rate slower than 60 beats per minute (bpm). While not all bradycardia is pathological, it's crucial to differentiate between physiological and pathological causes.

Physiological Bradycardia is common in well-trained athletes due to increased vagal tone and can also be seen during sleep. It is usually asymptomatic.

Pathological Bradycardia can arise from a variety of underlying conditions, including:

• Sinus Node Dysfunction (Sick Sinus Syndrome): Impaired SA node function leads to inappropriate sinus bradycardia, sinus pauses, or alternating bradycardia and tachycardia.

• Atrioventricular (AV) Block: Impairment in the conduction of impulses from the atria to the ventricles. This is further classified into different degrees of heart block.

• Medications: Beta-blockers, calcium channel blockers, digoxin, and amiodarone can all slow the heart rate. Remember to consider drug history when evaluating a patient with bradycardia.

• Underlying Medical Conditions: Hypothyroidism, myocardial infarction (particularly inferior MI affecting the right coronary artery, which supplies the SA and AV nodes), and electrolyte imbalances (e.g., hyperkalaemia) can all contribute to bradyarrhythmias.

Heart Block: A Deeper Dive

Heart block, also known as atrioventricular (AV) block, is a condition where the electrical signals from the atria to the ventricles are delayed or blocked entirely. It is classified into three degrees:

AV Conduction Blocks

🫀First-Degree AV Block

First-degree AV block is characterised by a prolonged PR interval (>0.20 seconds or 200 milliseconds) on the ECG. Every P wave is followed by a QRS complex, meaning all atrial impulses are still conducted to the ventricles, but the conduction is simply slowed. It is generally asymptomatic and usually requires no specific treatment. Think "PR is prolonged."

🫀Second-Degree AV Block

Second-degree AV block is characterised by intermittent failure of atrial impulses to conduct to the ventricles. There are two main types:

• Mobitz Type I (Wenckebach): Progressive prolongation of the PR interval on consecutive beats, followed by a dropped QRS complex. The PR interval then resets and the cycle repeats. Usually occurs proximal to the Bundle of His. This type is generally benign and often asymptomatic. Think "Longer, longer, longer, DROP! Then you have a Wenckebach."

• Mobitz Type II: Sudden, intermittent failure of atrial impulses to conduct to the ventricles without progressive PR interval prolongation. This is more serious than Mobitz Type I, as it often progresses to complete heart block. It usually occurs within or distal to the Bundle of His. Think "Type II is trouble for you!".

  
  

🫀Third-Degree AV Block (Complete Heart Block)

Third-degree AV block, or complete heart block, is the most severe form. There is complete dissociation between the atrial and ventricular activity. The atria and ventricles beat independently of each other. The P waves bear no relation to the QRS complexes. The ventricular rate is typically slow, usually less than 40 bpm, and is determined by an escape rhythm originating from either the AV node or the ventricles. This condition is usually symptomatic and requires urgent treatment, often with a permanent pacemaker.

Management of Bradyarrhythmias

The management of bradyarrhythmias depends on the underlying cause and the presence of symptoms.

• Asymptomatic Bradycardia: May not require any treatment, especially if it's physiological.

• Symptomatic Bradycardia:

• Initial Management: Assess airway, breathing, and circulation (ABC). Monitor ECG and blood pressure. Identify and address any reversible causes (e.g., medication side effects, electrolyte imbalances).

• Atropine: An anticholinergic medication that blocks vagal stimulation, increasing heart rate. It is often the first-line treatment for symptomatic bradycardia.

• Temporary Pacing: If atropine is ineffective or contraindicated, temporary pacing (transcutaneous or transvenous) may be necessary.

• Permanent Pacemaker: Indicated for symptomatic bradycardia due to irreversible causes, such as advanced heart block or sick sinus syndrome.

Further Learning

To further enhance your understanding of Cardiology and other vital topics for the MRCP (UK) Part 1, consider enrolling in our comprehensive short course: Cardiology MRCP Part 1.