Long PR-interval

ECG: Sinus rhythm with a rate of 62 bpm; fixed and very prolonged (480 ms) PR-interval: first-degree AV block;

Comments: The term first degree atrioventricular (AV) block corresponds to a prolongation of the PR-interval beyond physiological values (180 ms in children, 200 ms in adults). The term block is not exactly appropriate since, strictly speaking, it is not a block (interruption of the conduction) but rather a slowdown of conduction. Indeed, on the electrocardiogram, there are an equal number of P-waves and QRS-complexes, each P-wave being conducted after a fixed PR-interval exceeding 200 ms in adults. RR cycles are equal to the PP cycles, the ventricles are therefore at the same rate as the atria and there is no bradycardia if sinus function is normal.

A prolongation of the PR-interval can reflect a slowdown at any level of the “conduction chain” between the first activated atrial cell (beginning of the P-wave) and the first activated ventricular cell. A long PR can therefore be secondary to a slowdown of:

•  Intra-atrial conduction: exceptionally, a pronounced prolongation of intra-atrial conduction time (slowed conduction velocities and/or atrial dilatation) can cause a modest prolongation of the PR-interval; the ECG would thus feature a very widened P-wave;
• Conduction in the atrioventricular node: this is by far the most common case; the slowdown in conduction is usually not secondary to irreversible histological lesions but rather corresponds to an exaggeration of the physiological process of the slowdown of conduction at the atrioventricular node (i.e. a beta-blocker treatment); the longer the PR-interval, the greater the probability that the slowdown is located in the atrioventricular node;
• Distal conduction at the His-Purkinje system; when faced with a patient with bundle branch block (wide QRS) with a long PR, the presence of a first-degree atrioventricular block should evoke the possibility of a low conduction disorder on the branch opposite to the blocked branch; this suggests the presence of a trifascicular block and justifies the implantation of a pacemaker, given the major risk of a complete atrioventricular block with absence of escape rhythm or with very slow and unstable escape rhythm;

Endocardial electrophysiological study (invasive technique with insertion of catheters in the right heart chambers) enables to detect and record the electrical activity which reflects the transit of the excitation wave at the bundle of His (recording of H potential) and to determine the slowdown site by dividing the blocks into:

• Supra-Hisian blocks (slowdown in the atrium and/or the atrioventricular node) with prolongation of the AH interval, measured between the atrial potential and Hisian potential; in the vast majority of cases, the impulse is delayed at the atrioventricular node;
• Intra-Hisian blocks (slowdown in the His bundle) with a prolonged or split His potential which indicates a lesion within the His bundle;
• Infra-Hisian blocks with elective prolongation of the HV, the conduction abnormality  located downstream from the potential corresponding to the recording of the bundle of His;

Various mechanisms can explain the slowdown of atrioventricular conduction:

• A fibrous degeneration can impair conduction throughout the conduction tree from the atrioventricular node to the Purkinje network;
• Inflammatory lesions (viral, rheumatic) mainly reach the atrioventricular node;
• Ischemic lesions can reach the atrioventricular node (often temporary lesions) or the bundle of His and branches (often permanent lesions);
• Certain negative dromotropic drugs (beta-blockers, calcium channel blockers, etc.) primarily act at the atrioventricular node level;

Take-home message: A first-degree atrioventricular block corresponds to a simple prolongation of the PR-interval which exceeds physiological values; there are an equal number of P-waves and QRS-complexes as well as a fixed, constant PR-interval exceeding 200 ms in adults; a first-degree atrioventricular block most often reflects a conduction delay located at the atrioventricular node; the longer the PR-interval, the greater the probability of an intra-nodal slowdown;