1. Introduction

First-degree AV block (more precisely, first-degree AV delay) describes slowed conduction from atria to ventricles. Unlike second- or third-degree AV block, conduction is not intermittently or completely interrupted: each P wave is followed by a QRS complex, but the PR interval is prolonged.

It is commonly an incidental ECG finding and may occur with increased vagal tone or athletic training. It can also accompany myocardial ischaemia, myocardial inflammation, structural or postoperative disease, electrolyte disturbance, or drugs that slow AV nodal conduction.

2. Electrophysiology and Pathophysiology

After atrial depolarisation, the impulse travels through the AV node, His bundle, bundle branches, and Purkinje system before activating the ventricles. The PR interval spans from the beginning of the P wave to the beginning of the QRS complex and reflects atrial conduction plus conduction through the AV junction and His–Purkinje system.

In first-degree AV delay, conduction time is prolonged at one or more points in this pathway, most often within the AV node. The delay may be influenced by autonomic tone, medications, ischaemia, inflammation, infiltrative or degenerative disease, and electrolyte abnormalities. A surface ECG establishes the prolonged atrioventricular conduction time but does not, by itself, localise the site of delay with certainty.

Common settings and potential causes

• Increased vagal tone and athletic conditioning.
• Inferior myocardial infarction or myocardial ischaemia.
• Myocarditis, including Lyme carditis in an appropriate epidemiological context.
• After mitral valve surgery or other cardiac procedures.
• Electrolyte disturbance, particularly hyperkalaemia.
• AV nodal/conduction-slowing medicines, including beta-blockers, non-dihydropyridine calcium-channel blockers, digoxin, and amiodarone.

These causes are listed in the supplied reference; the clinical context determines which are relevant in an individual patient.

3. Characteristic ECG Features

Marked first-degree AV delay

A PR interval of approximately 300 ms or longer is commonly described as marked or markedly prolonged. At this degree of prolongation, the P wave may fall within the preceding T wave and become difficult to identify. Marked PR prolongation can impair atrioventricular timing and, in selected patients, produce exertional intolerance or symptoms resembling pacemaker syndrome.

4. Systematic ECG Interpretation

1. Assess rate and rhythm. Determine the ventricular rate and whether the rhythm is regular. Identify sinus P waves or another atrial rhythm.
2. Find the P waves. Inspect multiple leads and the rhythm strip. In marked PR prolongation, a P wave can be partly buried in the preceding T wave.
3. Check atrioventricular association. Confirm that every P wave is followed by a QRS complex (1:1 conduction). Do not label first-degree delay if atrial impulses are intermittently non-conducted.
4. Measure the PR interval. Measure from the earliest onset of the P wave to the earliest onset of the QRS. At standard paper speed of 25 mm/s, one small square is 40 ms and five small squares are 200 ms.
5. Check consistency. Confirm that the PR interval is prolonged and generally similar from beat to beat. Consider physiologic variation with changing sinus rate.
6. Review QRS and the rest of the ECG. Note bundle branch block, QRS widening, ischaemic changes, or other abnormalities that may indicate associated disease.
7. Correlate clinically. Review symptoms, medications, prior ECGs, acute illness, and reversible causes before deciding whether further evaluation is needed.

5. Diagnostic Criteria

• Essential: prolonged PR interval greater than 200 ms.
• Essential: no dropped ventricular response; each identifiable P wave is followed by a QRS.
• Supportive: stable atrial-to-ventricular relationship with prolonged AV conduction.
• Marked prolongation: PR interval around or above 300 ms; this is a descriptor of severity, not a separate degree of AV block.

At 25 mm/s, 200 ms corresponds to five small squares. At 50 mm/s, it corresponds to ten small squares. Confirm the ECG paper speed and calibration before measuring.

Limitations: A single lead may obscure P-wave onset or QRS onset. Atrial ectopy, changing sinus rate, fusion of P and T waves, or intermittent higher-grade AV block can complicate interpretation. If a P wave is not followed by a QRS, reassess for second-degree AV block rather than calling the tracing uncomplicated first-degree AV delay.

6. Differential Diagnosis

The defining distinction from second-degree AV block is that first-degree AV delay has no dropped P waves: every atrial impulse is conducted.

7. Clinical Significance and Prognosis

Isolated first-degree AV delay is often benign, particularly in otherwise healthy people without structural heart disease. The supplied reference describes it as generally benign when isolated and notes that no specific treatment is usually required. The prognosis is generally favourable in the absence of structural heart disease, and progression to higher-grade block is uncommon.

Clinical significance changes with the degree of PR prolongation, symptoms, associated ECG abnormalities, underlying cardiac disease, and the suspected cause. A very long PR interval can cause atrioventricular dyssynchrony, reducing effective ventricular filling and producing fatigue, exertional intolerance, dyspnoea, or presyncope in selected patients.

Red flags that warrant prompt assessment

• Syncope, presyncope, hypotension, acute heart failure, chest pain, or other evidence of haemodynamic compromise.
• New or rapidly changing PR prolongation in the setting of acute myocardial infarction, myocarditis, or suspected Lyme carditis.
• Marked PR prolongation with persistent symptoms plausibly related to AV dyssynchrony.
• Coexisting bundle branch block, QRS widening, pauses, or evidence of intermittent second-/third-degree AV block.
• Potential drug toxicity or a significant electrolyte abnormality, particularly hyperkalaemia.

8. Clinical Evaluation and Management Principles

Initial evaluation

• Assess haemodynamic status and symptoms; obtain a 12-lead ECG and compare with previous tracings.
• Review prescribed and non-prescribed medicines that slow AV conduction; assess for recent dose changes, interactions, or toxicity.
• Investigate clinically suspected reversible causes, such as acute ischaemia, myocarditis/infection, and electrolyte or metabolic disturbance.
• Use echocardiography when history, examination, or ECG suggests structural heart disease.
• Consider ambulatory ECG monitoring when intermittent symptoms need rhythm correlation. Exercise testing may be useful in selected patients with exertional symptoms or to assess conduction behaviour during increased heart rate.

Management

Asymptomatic, isolated first-degree AV delay: generally observation and clinical follow-up are appropriate; a pacemaker is not routinely indicated. Address reversible causes and review medications when appropriate.

Marked PR prolongation with symptoms: evaluate whether symptoms are attributable to AV dyssynchrony. The 2021 ESC pacing guideline states that permanent pacing should be considered in patients with persistent symptoms resembling pacemaker syndrome that are clearly attributable to first-degree AV block with PR >300 ms (Class IIa, Level C). Symptom correlation is essential.

Acute or unstable presentation: manage the underlying cause and the patient's haemodynamic state urgently. Reassess the rhythm for progression to higher-grade AV block; do not manage a symptomatic unstable patient as uncomplicated incidental first-degree AV delay.

9. ECG Interpretation Examples

The following are the three authentic ECG examples included in the supplied PDF. The descriptions below retain the source's reported findings; no additional patient history or unreported measurements have been inferred.

Example 1 — Marked first-degree AV block

Reasoning: The key teaching point is that a P wave may be difficult to recognise when the PR interval is markedly prolonged. Inspect the rhythm strip and multiple leads rather than assuming the T-wave contour is purely ventricular repolarisation.

Example 2 — Sinus bradycardia with first-degree AV block

Reasoning: Bradycardia and prolonged AV conduction are two separate ECG observations. Report both rather than treating the slow rate as the defining feature of AV delay.

Example 3 — Sinus rhythm with PR interval 260 ms

Reasoning: A PR interval of 260 ms exceeds the adult diagnostic threshold of 200 ms. The source labels the rhythm as normal sinus rhythm with first-degree AV block.

10. Common Interpretation Pitfalls

• Calling it a true block: every P wave is conducted; the abnormality is delayed conduction.
• Failing to measure the PR interval: visual estimation alone can miss modest prolongation.
• Missing a concealed P wave: in marked delay, a P wave may overlap the preceding T wave.
• Ignoring dropped beats: any non-conducted P wave should prompt assessment for second-degree or higher-grade AV block.
• Equating a long PR with infranodal disease: surface ECG alone does not reliably localise the delay.
• Assuming all cases are harmless: isolated asymptomatic delay is often benign, but symptoms, acute disease, marked prolongation, or additional conduction abnormalities change the assessment.
• Implanting a pacemaker based on PR duration alone: pacing is not routinely indicated for asymptomatic first-degree AV delay.

11. ECG Pearls and Red Flags

12. Quick Reference Summary

13. References