First-degree atrioventricular block

INTRODUCTION — Atrioventricular (AV) block is defined as a delay or interruption in the transmission of an impulse from the atria to the ventricles due to an anatomic or functional impairment in the conduction system. The conduction disturbance can be transient or permanent, with conduction that is delayed, intermittent, or absent. Commonly used terminology includes:

●First-degree AV block – Delayed conduction from the atrium to the ventricle (defined as a prolonged PR interval of >200 ms) without interruption in atrial to ventricular conduction.

●Second-degree AV block – Intermittent atrial conduction to the ventricle, often in a regular pattern (eg, 2:1, 3:2), or higher degrees of block, which are further classified into Mobitz type I (Wenckebach) and Mobitz type II second-degree AV block.

●Third-degree (complete AV) block – No atrial impulses conduct to the ventricle.

●High-grade AV block – Intermittent atrial conduction to the ventricle with two or more consecutive blocked P waves but without complete AV block.

The clinical presentation, evaluation, and management of first-degree AV block will be reviewed here. The etiology of AV block in general, and the management of other specific types of AV block, are discussed separately. (See "Etiology of atrioventricular block" and "Second-degree atrioventricular block: Mobitz type I (Wenckebach block)" and "Second-degree atrioventricular block: Mobitz type II" and "Third-degree (complete) atrioventricular block" and "Congenital third-degree (complete) atrioventricular block".)

DEFINITION — The PR interval, which measures conduction between the atria and the ventricles, includes atrial depolarization (the P wave) and subsequent conduction through the AV node, His bundle, bundle branches and fascicles, and terminal Purkinje fibers (figure 1). The normal PR interval is considered to be between 120 and 200 ms (0.12 to 0.20 s) and tends to shorten with increases in heart rate due in part to rate-related shortening of action potentials. However, some apparently healthy persons have longer PR intervals, with PR intervals as long as 280 ms having been reported in 1.6 percent of healthy aviators [1]. (See "ECG tutorial: Basic principles of ECG analysis", section on 'PR interval'.)

First-degree AV block, defined as a prolonged PR interval (>200 ms at resting heart rates), is not a true block but is rather delayed or slowed AV conduction. Because of this, it is more appropriate to use the term "prolonged AV conduction" rather than AV block. The conduction delay is most frequently in the AV node but may also be in the His-Purkinje system.

ETIOLOGY — Patients who have a slow resting heart rate, such as highly conditioned endurance athletes, may have evidence of first-degree AV block simply due to increased vagal tone and a lower resting heart rate [2]. However, prolongation of the PR interval often represents underlying cardiac pathology. A partial list of pathologic causes of first-degree AV block include the following:

●Underlying structural abnormalities of the node.

●An increase in vagal tone that causes a reduction in the rate of impulse conduction.

●Drugs that impair or slow nodal conduction including digoxin, beta blockers, and non-dihydropyridine calcium channel blocking agents.

●Myocardial infarction – When seen in the setting of an anterior wall myocardial infarction, this finding usually indicates bundle and fascicular block. In comparison, an inferior wall myocardial infarction is more likely to be associated with delay in the AV node since the AV node and inferior wall are usually supplied by the right coronary artery.

●Infiltrative and dilated cardiomyopathies (eg, sarcoidosis).

●Certain muscular dystrophies.

●Myocarditis (eg, Lyme, viral).

●Lev disease and Lenegre disease. (See "Etiology of atrioventricular block", section on 'Idiopathic'.)

LEVEL OF CONDUCTION DELAY — First-degree AV block, or prolonged AV conduction, can occur at a variety of levels within the heart. Clinically, because first-degree AV block is most often asymptomatic and diagnosed by electrocardiogram (ECG), there is usually little clinical significance to the level of conduction delay. However, the presence of additional evidence of conduction abnormalities (eg, bundle branch block) may be an indicator of more widespread conduction disease.

The levels of conduction delay associated with first-degree AV block, and potential related etiologies, includes the following:

The AV node is the most common site of conduction delay in first-degree block. Conduction through the AV node is approximated quite well by the atrial-His (AH) time determined by His bundle ECG. The normal AH time is 60 to 125 ms. Over 90 percent of patients with a PR interval greater than 300 ms have slowed AV nodal conduction [3]. Among the causes of first-degree AV block with a prolonged AH interval are increased vagal tone, calcium channel blockers (which block the inward calcium current responsible for depolarization), digoxin (acting via its vagotonic action), and beta-blockers. PR interval prolongation associated with a narrow or wide P wave but a narrow QRS complex strongly implicates the AV node as the site of the conduction delay. (See "Cardiac excitability, mechanisms of arrhythmia, and action of antiarrhythmic drugs", section on 'Action potential in slow response tissues'.)

●Atrium – Myocardial disease involving the atria, such as endocardial cushion defects and Ebstein's anomaly of the tricuspid valve.

●AV node – Increased vagal tone, calcium channel blockers (which block the inward calcium current responsible for depolarization), digoxin (acting via its vagotonic action), and beta-blockers.

●Bundle of His – Rare, but drugs that block the sodium channels (eg, quinidine, procainamide, and disopyramide) can slow conduction in the bundle of His.

●Infra-Hisian conduction system (ie, bundle branches, fascicles, Purkinje system) – Rare, but if conduction is equally slowed in the right and left conducting systems, there will be prolongations in the His-ventricular (HV) time and therefore in the PR interval; most commonly due to drugs that block the sodium channels (eg, quinidine, procainamide, and disopyramide).

CLINICAL PRESENTATION — The clinical presentation of first-degree AV block is almost universally benign and only very rarely are symptoms felt to be directly related to first-degree AV block. There are no signs or symptoms that are either sensitive or specific that are related to first-degree AV block, and first-degree AV block cannot be detected from history or physical examination alone. When marked first-degree AV block results in atrial contraction immediately following the preceding ventricular contraction, this may result in signs and symptoms similar to "pacemaker syndrome" and sometimes referred to as "pseudopacemaker syndrome." [4-6]. (See "Modes of cardiac pacing: Nomenclature and selection", section on 'Pacemaker syndrome'.)

DIAGNOSIS AND EVALUATION — The diagnosis of first-degree AV block is typically confirmed using ECG evidence from either a single-lead telemetry strip or a 12-lead ECG. The evaluation of all patients with first-degree AV block identified by ECG includes a thorough history, including medications and recent changes in medications, along with bloodwork (which includes serum electrolytes and thyroid-stimulating hormone [TSH]).

All patients with suspected first-degree AV block should be questioned about any history of heart disease, both congenital and acquired, as well as any recent cardiac procedures or medications that could predispose to AV conduction abnormalities. There is an overlap of cardiac conduction disturbances and other cardiac diseases including infiltrative cardiomyopathies, cardiomyopathies associated with muscular dystrophy, and other dilated cardiomyopathies. Therefore, newly recognized first-degree AV block should include an assessment of patient symptoms and exam findings to exclude these rare but serious conditions. (See "Etiology of atrioventricular block".)

Patients without known or suspected cardiac or systemic disease should be questioned about their level of athletic activities and fitness, as increased vagal tone in a well-conditioned athlete is a relatively common cause of sinus bradycardia and first-degree AV block. Patients without known cardiac disease should also provide a full list of medications and be questioned about any recent changes in dosing, with particular attention paid to drugs that alter AV nodal conduction (ie, beta blockers, non-dihydropyridine calcium channel blockers, digoxin, select antiarrhythmic drugs). Such patients should be questioned about other systemic diseases associated with heart block (eg, amyloidosis, sarcoidosis). Patients who live in an area with endemic Lyme disease should be questioned about any recent outdoor exposure to ticks or known tick bites. (See 'Etiology' above.)

The diagnosis of first-degree AV block can only be made from an ECG in a patient whose PR interval exceeds 200 ms (or >210 ms at slow heart rates). Rarely, first-degree AV block may be seen during an invasive electrophysiology study (EPS) being performed for other indications, but in such instances the surface ECG should provide the diagnosis without the need for invasive EPS.

For patients with isolated first-degree AV block, there is rarely if ever a need to determine the precise level of conduction abnormality which has resulted in first-degree AV block. However, the presence of a wide QRS complex in conjunction with prolongation of the PR interval implies that there is a significant possibility that the conduction delay is below the AV node. There are several clinical approaches to determining the site of first-degree AV block, including surface ECG hints, noninvasive evaluation in response to atropine or vagal maneuvers, and invasive EPS. Recognizing the site of AV block is clinically important because it can determine the potential need for permanent pacing, especially in a patient with syncope or other symptoms that may be due to higher levels of block not previously captured on ECG monitoring.

●Surface ECG – The ECG is usually of limited value in indicating the site of first-degree AV block, but there may be some helpful clues.

•A PR interval duration of 300 ms or greater with a normal QRS complex is most often due to delay in the AV node (waveform 1), while a PR interval of 200 to 300 ms is less specific.

•First-degree AV block coupled with a wide QRS complex can be due to infranodal disease (waveform 2) [7-10]. (See 'Level of conduction delay' above.)

●Vagal maneuvers – Increased vagal tone slows conduction in the AV node but has little effect on the infranodal conduction system. Vagal maneuvers (eg, Valsalva maneuver, carotid sinus massage, etc) tend to slow conduction in the AV node. However, this effect may be obscured because of concurrent slowing of the sinus rate, which allows more time for both the AV node and infranodal conduction systems to recover excitability and to conduct more normally. (See "Vagal maneuvers".)

Atropine, a vagolytic drug, can have a variable effect on first-degree AV block depending on the level of the block. The direct vagolytic effect of atropine will enhance AV node conduction and shorten the PR interval in patients whose block is at the level of the AV node. However, atropine also increases heart rate by accelerating sinoatrial nodal output; this accelerated heart rate can encroach on the refractory period and exacerbate the AV conduction delay in persons with infranodal conduction delays.

●Invasive EPS – Conduction through the AV node is approximated quite well by the atrial-His (AH) time determined by His bundle ECG as part of invasive electrophysiology studies (EPS). The normal AH time is 60 to 125 ms. Over 90 percent of patients with a PR interval greater than 300 ms have slowed AV nodal conduction [3]. Atrial pacing, during EPS or by means of a previously implanted pacemaker, can worsen first-degree block in patients with AV nodal conduction delay and, less commonly, infranodal conduction delay. The most common EPS finding in patients with first-degree AV block is prolongation of the AH interval.

MANAGEMENT — Asymptomatic patients with first-degree AV block do not require any specific therapy. A general principle in considering the use of pacemakers for AV block of any severity is whether symptoms will be relieved and/or survival prolonged. We agree with the professional society guidelines which do not recommend a pacemaker for most cases of first-degree AV block [11,12]. Prior to considering placement of a permanent pacemaker, any reversible causes of AV block (ie, ischemia, prior administration of AV nodal blocking medications) should be identified and treated (ischemia) or withdrawn (offending medications).

Patients with first-degree AV block and symptoms consistent with the loss of AV synchrony, a situation referred to as "pseudopacemaker syndrome," are potential candidates for a pacemaker [11,12]. Pacemaker syndrome describes the uncomfortable awareness of one's heart beat due to atrial contraction against a closed mitral valve or when atrial contraction occurs shortly after ventricular systole with incomplete atrial filling that can occur with single-chamber ventricular pacing. Pseudopacemaker syndrome refers to a similar constellation of symptoms that can occur with first-degree AV block and other heart rhythms that have AV dissociation. There has been a case described where pseudopacemaker syndrome was effectively treated with modification of the slow pathway [5]; however, this is an extremely uncommon indication for catheter ablation. Likewise, implantation of a permanent pacemaker strictly for pseudopacemaker syndrome from first-degree AV block is exceedingly rare.

Other situations in which a pacemaker may be considered include [12]:

●First-degree AV block with concurrent neuromuscular disease or Lamin A/C associated cardiomyopathy (eg, myotonic muscular dystrophy, Kearns-Sayre syndrome, Erb dystrophy [limb-girdle], and peroneal muscular atrophy) due to the unpredictable risk of progressive AV conduction disturbances.

●Patients with a wide QRS complex in conjunction with prolongation of the PR interval, which implies a significant possibility of conduction delay below the AV node. Given the unpredictability of progression to second- and third- degree heart block, we consider His bundle ECG and the use of a permanent pacemaker in patients with marked prolongation of the HV interval (>70 ms).

PROGNOSIS — The prognosis related to first-degree AV block remains uncertain, with mixed results reported from a variety of population-based studies. Several studies of first-degree AV block have suggested a benign prognosis, while other cohort studies have suggested an adverse prognosis related to PR prolongation [13-20]. In a 2016 meta-analysis that included 14 studies and over 400,000 patients, first-degree AV block was associated with a higher risk of mortality (risk ratio [RR] 1.2, 95% CI 1.0-1.5) as well as heart failure or left ventricular dysfunction (RR 1.4, 95% CI 1.2-1.7) and atrial fibrillation (RR 1.5, 95% CI 1.2-1.7) but was not associated with a higher risk of cardiovascular mortality, coronary heart disease, myocardial infarction, or stroke [21].

As examples of the individual studies performed in different populations:

●In a prospective cohort of 10,785 Finnish persons aged 30 to 59 years who received a baseline 12-lead ECG and were followed for an average of 30 years, a baseline PR interval >200 ms was present in 222 people (2.1 percent) [18]. Compared with those with a PR interval <200 ms, individuals with first-degree AV block had no significant differences in mortality or cardiovascular morbidity.

●In a prospective community-based study of 7575 individuals from the Framingham Heart Study (only 2 percent with prior myocardial infarction or heart failure), a baseline PR interval ≥200 ms was present in 124 people (1.6 percent) [15]. Compared with those with a PR interval <200 ms, individuals with first-degree AV block were significantly more likely to develop atrial fibrillation (adjusted hazard ratio [HR] 2.1, 95% CI 1.4-3.1) or to need a permanent pacemaker (adjusted HR 2.9, 95% CI 1.8-4.6), and had a higher all-cause mortality (adjusted HR 1.4, 95% CI 1.1-1.9).

●In a prospective study of 938 patients with stable coronary heart disease (history of myocardial infarction, greater than 50 percent coronary stenosis by angiography, exercise-induced ischemia on stress testing, or prior revascularization) from the Heart and Soul Study, a baseline PR interval ≥220 ms was present in 87 people (9.3 percent) [17]. Compared with those with normal AV conduction (PR interval <220 ms), persons with first-degree AV block had a higher risk of hospitalization for heart failure (adjusted HR 2.3, 95% CI 1.5-3.7), cardiovascular mortality (adjusted HR 2.3, 95% CI 1.3-4.2), and all-cause mortality (adjusted HR 1.6, 95% CI 1.1-2.2).

As such, the presence of first-degree AV block in healthy persons portends an uncertain prognosis, although there appears to be an increase in some cardiovascular risks but not others. Meanwhile, in those with underlying coronary heart disease, there appears to be a higher risk of morbidity and mortality. In nearly all patients, however, there is rarely if ever a need to provide permanent pacing for isolated first-degree AV block. (See 'Management' above.)

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SUMMARY AND RECOMMENDATIONS

●Definition – First-degree atrioventricular (AV) block, defined as a prolonged PR interval (>200 ms at resting heart rates), is not a true block but is rather delayed or slowed AV conduction. Because of this, it is more appropriate to use the term "prolonged AV conduction" rather than AV block. The conduction delay is most frequently in the AV node but may also be in the His-Purkinje system. (See 'Definition' above.)

●Etiology – A variety of conditions can result in first-degree AV block, but it is most commonly seen in cases of increased vagal tone (eg, highly conditioned endurance athletes) or as a result of medications that slow AV node conduction (eg, digoxin, beta blockers, and non-dihydropyridine calcium channel blockers). (See 'Etiology' above.)

●Clinical presentation – The clinical presentation of first-degree AV block is almost universally benign, and only very rarely are symptoms felt to be directly related to first-degree AV block. There are no signs or symptoms that are sensitive or specific for first-degree AV block, and this condition cannot be detected from history or physical examination alone.

●Diagnosis – The diagnosis of first-degree AV block is typically confirmed using ECG evidence from either a single-lead telemetry strip or a 12-lead ECG. (See 'Clinical presentation' above.)

●Management – Asymptomatic patients with first-degree AV block do not require any specific therapy. The rare patient with first-degree AV block and symptoms consistent with the loss of atrioventricular synchrony, a situation sometimes referred to as "pseudopacemaker syndrome," is a potential candidate for a pacemaker. Other situations in which a pacemaker may be considered for first-degree AV block due to unpredictable progression of conduction disease include patients with concurrent neuromuscular disease and patients with a wide QRS complex with suspected conduction delay below the AV node. (See 'Management' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Leonard Ganz, MD, FHRS, FACC, who contributed to earlier versions of this topic review.