Patient: 63-year-old man, asymptomatic, electrocardiogram made during regular check-up;
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First-degree atrioventricular block
ECG: Sinus rhythm (positive P waves in leads I, II, V5, V6, negative in aVR); fixed and prolonged PR interval (300 ms): first-degree atrioventricular block; narrow QRS with no abnormality; the isolated negative T wave in lead III is physiological and does not signify inferior ischemia;
Comments: The PR interval corresponds to the delay between the depolarization of the first atrial cells and the depolarization of the first ventricular cells. The PR interval can be divided between P wave, whose width represents the depolarization time of both atria, and the PR segment, measured between the end of the P wave and the beginning of the R wave, which reflects the conduction delay in the atrioventricular node and the His-Purkinje network. The PR segment is most often isoelectric, the traversed structures do not generate sufficient amplitude to be detected on the surface electrocardiogram.
Within a patient, the PR interval may vary throughout the day and exhibit physiological variations (shortened during exercise, prolonged upon increased vagal activity). Indeed, conduction velocities and refractory periods in the atrioventricular node are dependent on calcium channels and vary according to various parameters (influence of the autonomous nervous system, of certain drugs and certain metabolic abnormalities). In spite of these physiological variations, it is not usual to index and correct the value of the PR interval as a function of heart rate (unlike the QT interval).
The term first-degree atrioventricular (AV) block corresponds to a prolongation of the PR interval beyond physiological values. The term ‘block’ is actually not appropriate since, strictly speaking, it is not a block (interruption of conduction) but rather a slowing of conduction. Indeed, on the electrocardiogram, there are an equal number of P waves and QRS complexes (each P wave being conducted) and a fixed PR interval exceeding 200 ms in adults.
A prolongation of the PR interval can reflect a slowing at any level of the “conduction chain” between the first activated atrial cell (onset of the P wave) and the first activated ventricular cell. A long PR may occur as a result of: 1) a delay in atrial conduction (rare); a marked prolongation of intra-atrial conduction time (slowed conduction velocities and/or dilatation of the atrium), revealed by a very wide P wave on the electrocardiogram, can lead to a modest prolongation of the PR interval; 2) a conduction delay in the atrioventricular node (the most common); the longer the PR interval, the greater the likelihood that the deceleration is located in the atrioventricular node; 3) a delay in distal conduction in the His-Purkinje network; most often associated with the presence of a wide QRS, this condition reflects the presence of a trifascicular block and justifies implantation of a pacemaker.
In this asymptomatic patient, the P wave is normal, the QRS is narrow, making the hypothesis of an intra-atrial conduction slowing or a distal conduction slowing in the His-Purkinje network very unlikely. A 24-hour Holter-ECG and an exercise test showed a reduction of the PR interval on exertion, a preserved exercise capacity and the absence of second- or third-degree atrioventricular block episodes. This pattern is likely benign and does not justify implantation of a pacemaker.
Take-home message: A first-degree AV 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 and a fixed, constant PR interval exceeding 200 ms in adults; if sinus function is normal, there is no bradycardia (ventricular and atrial rates rate are the same).
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Regarding this ECG, which answer(s) is(are) true?
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