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PR interval

The PR interval is a fundamental measurement in electrocardiography (ECG), representing the duration from the beginning of the P wave, which marks the onset of atrial depolarization, to the start of the QRS complex, indicating the initiation of ventricular depolarization.^[1] This interval encompasses the time for electrical impulse conduction through the atria, across the atrioventricular (AV) node, and along the bundle of His, serving as a key indicator of AV conduction integrity.^[1] In clinical practice, it provides essential insights into cardiac rhythm and conduction system function, helping to identify both normal physiology and potential abnormalities.^[2] The PR interval is typically measured on a standard 12-lead ECG tracing at a paper speed of 25 mm per second, where each small square equals 40 milliseconds.^[1] The normal range for adults is 120 to 200 milliseconds (0.12 to 0.20 seconds), corresponding to approximately three to five small squares on the ECG grid.^[2] Variations can occur due to factors such as age, heart rate, autonomic tone, and certain medications, but values outside this range often warrant further evaluation.^[1] For instance, in pediatric populations, the normal PR interval is shorter than in adults and age-dependent, with ranges typically 80-160 ms in neonates and increasing toward adult values with age, reflecting differences in cardiac maturation.^[3] Prolongation of the PR interval beyond 200 milliseconds defines first-degree AV block, a common conduction delay that may be benign or associated with underlying conditions like degenerative AV node disease, electrolyte imbalances, or drug effects (e.g., beta-blockers).^[1] Conversely, a shortened PR interval below 120 milliseconds can signal accelerated AV conduction, as seen in pre-excitation syndromes such as Wolff-Parkinson-White (WPW) syndrome, where an accessory pathway bypasses the AV node.^[1] Both extremes have prognostic implications; prolonged PR intervals are linked to increased risks of atrial fibrillation, heart failure, and mortality in population studies, while short intervals may predispose to supraventricular tachycardias.^[4] Accurate assessment of the PR interval thus plays a critical role in diagnosing and managing arrhythmias and conduction disorders.^[1]

Definition and Basics

Definition

The PR interval is the duration from the onset of the P wave, representing atrial depolarization, to the onset of the QRS complex, representing ventricular depolarization, as observed on an electrocardiogram (ECG).^[5] This measurement captures the temporal span between these key electrophysiological events in the cardiac cycle.^[6] The PR interval was first described in the early 20th century as part of the standardization of ECG interpretation, building on Willem Einthoven's foundational work on the electrocardiogram, which he developed and published around 1903.^[1] Einthoven's innovations, including the naming of the P wave for atrial activity and the recognition of the interval to the QRS complex, enabled precise analysis of conduction timing.^[7] It is typically expressed in milliseconds (ms), though it can be reported in seconds, with conversions such as 0.12 seconds equating to 120 ms.^[1]

Components of the PR Interval

The PR interval on an electrocardiogram (ECG) is composed of two primary waveform elements: the P wave and the PR segment. The P wave represents the electrical depolarization of the atria, typically lasting approximately 80 milliseconds, during which the impulse originates from the sinoatrial node and spreads through the atrial myocardium. This initial upward deflection marks the beginning of the PR interval. The PR segment follows the P wave and appears as an isoelectric line, reflecting the conduction delay through the atrioventricular (AV) node, with a duration of about 50-100 milliseconds. This segment excludes the QRS complex, which signifies ventricular depolarization and is not part of the PR interval itself. Visually, on a standard 12-lead ECG tracing recorded at 25 mm/second, the PR interval is demarcated from the onset of the P wave's initial deflection—where the baseline first deviates upward—to the point just before the QRS complex's initial sharp downward or upward deflection, often appearing as a straight line returning to the isoelectric baseline after the P wave. This measurement captures the temporal span of atrial activation and AV nodal conduction without including ventricular activity. For optimal assessment, the PR interval is primarily evaluated in the inferior leads II, III, and aVF, where the P wave morphology is most prominent and reliable due to the anatomical orientation of atrial depolarization vectors. Variations may occur in other leads, such as precordial leads V1-V6, where P wave amplitude or PR segment slope can differ slightly owing to differing electrode perspectives, potentially affecting visual interpretation but not the fundamental interval components.

Physiology

Atrioventricular Conduction Pathway

The atrioventricular conduction pathway begins with the sinoatrial (SA) node, a cluster of specialized pacemaker cells located in the superior right atrium near the entrance of the superior vena cava, which generates the initial electrical impulse that initiates atrial depolarization.^[8] This impulse spreads rapidly through the atrial myocardium via internodal pathways, including Bachmann's bundle, to ensure coordinated atrial contraction before reaching the atrioventricular (AV) node.^[9] The AV node, situated in the triangle of Koch at the base of the right atrium near the coronary sinus, serves as the sole electrical bridge between the atria and ventricles, introducing a deliberate delay to allow complete atrial emptying.^[10] From the AV node, the impulse penetrates the fibrous annulus via the penetrating portion of the atrioventricular bundle, known as the bundle of His, which lies along the crest of the interventricular septum.^[11] The bundle of His then bifurcates into the right and left bundle branches, which extend downward along the septal endocardium—the left branch dividing further into anterior and posterior fascicles—to distribute the signal efficiently.^[12] These branches terminate in an extensive network of Purkinje fibers, subendocardial strands that ramify throughout the ventricular myocardium, particularly dense on the left side, to synchronize ventricular activation from apex to base.^[13] This hierarchical structure of specialized conductive tissues ensures orderly propagation without direct atrial-ventricular muscular connections, minimizing arrhythmic risks.^[14] Conduction velocities vary markedly along the pathway to optimize timing in the cardiac cycle. In the atrial myocardium, impulses travel at approximately 0.4-0.5 m/s, facilitating swift atrial synchronization.^[15] Within the AV node, velocity slows dramatically to about 0.05 m/s, resulting in a conduction delay of 0.06-0.12 seconds that permits atrial contraction to contribute to ventricular filling before ventricular systole begins.^[15]^[16] In contrast, the His-Purkinje system conducts rapidly at 1-4 m/s, with the bundle of His and branches at around 2 m/s and Purkinje fibers reaching up to 4 m/s, enabling near-simultaneous ventricular depolarization for efficient pumping.^[15] These velocity gradients, arising from differences in cell coupling, ion channel density, and gap junction expression, underpin the pathway's role in maintaining rhythmic cardiac output.^[17]

Physiological Role and Timing

The PR interval serves a critical physiological role in ensuring atrioventricular (AV) synchrony, which coordinates the timing of atrial and ventricular contractions to optimize cardiac efficiency. By introducing a deliberate delay in impulse transmission primarily at the AV node, the PR interval allows atrial systole to complete before ventricular depolarization initiates, thereby maximizing ventricular preload through the atrial kick. This atrial contribution propels additional blood into the ventricles during late diastole, enhancing end-diastolic volume and stroke volume by approximately 20-30% under normal conditions.^[18]^[15] The normal timing of the PR interval, typically ranging from 120 to 200 ms, reflects this essential conduction delay that prevents simultaneous atrial and ventricular contractions. This interval encompasses the time for the electrical impulse to travel from the sinoatrial node through the atria, pause at the AV node for about 80-100 ms, and then proceed via the His-Purkinje system to the ventricles. Such sequential activation supports effective sequential pumping, where atrial contraction boosts ventricular filling without interfering with ventricular ejection, thereby contributing to overall hemodynamic stability and cardiac output optimization.^[19]^[15] Autonomic influences dynamically adjust the PR interval to adapt to physiological demands; enhanced vagal (parasympathetic) tone prolongs the interval by slowing AV nodal conduction, while sympathetic activation shortens it to facilitate faster heart rates during stress or exercise. These modulations help maintain AV synchrony across varying conditions, such as rest or activity. Furthermore, age-related changes lead to a slight prolongation of the PR interval, attributed to progressive alterations in AV nodal tissue and conduction velocity, which become more pronounced in the elderly.^[20]^[21]

Measurement

ECG Measurement Technique

The PR interval is measured manually on a standard electrocardiogram (ECG) tracing by identifying the onset of the P wave, which represents atrial depolarization, and the onset of the subsequent QRS complex, which marks the beginning of ventricular depolarization. The measurement begins at the initial deflection of the P wave upward from the baseline and ends at the first sharp deflection of the QRS complex, typically the Q wave or the initial R wave if no Q is present. To perform this accurately, use ECG calipers to span the distance between these two points, or count the number of small squares on the ECG grid paper, where each small square represents 0.04 seconds (40 milliseconds) at the standard paper speed of 25 mm/s. For irregular rhythms, average the PR interval over at least three consecutive beats in sinus rhythm to account for natural variability, ensuring the selected beats are representative of the overall conduction pattern.^[22]^[23] When using grid paper or calipers, align the tool precisely to avoid over- or underestimation, and verify the measurement in the lead that provides the clearest distinction between the P wave and QRS complex, such as lead II, which often shows optimal atrioventricular (AV) transition. If the ECG paper speed differs from the standard 25 mm/s—such as 50 mm/s used in some stress tests—adjust the calculation accordingly by halving the time per millimeter (e.g., 1 mm = 0.02 seconds at 50 mm/s) to maintain accuracy. Manual verification is recommended even with automated systems, particularly in leads exhibiting the most distinct P-QRS relationship, to confirm consistency across multiple cardiac cycles.^[22]^[24] Digital ECG machines typically auto-calculate the PR interval using algorithmic detection of waveform onsets, providing global measurements reported in milliseconds, which enhances reproducibility compared to purely manual methods. These systems adhere to standardization guidelines recommending routine inclusion of PR interval values in ECG reports for clinical review. However, manual override or confirmation remains essential in cases of ambiguity.^[24]^[23] Common pitfalls in PR interval measurement include artifacts from patient movement, muscle tremor, or poor electrode contact, which can distort the baseline and obscure wave onsets, leading to erroneous readings. Measurements should be avoided during premature atrial or ventricular beats, as these can alter conduction timing and do not reflect baseline AV node function; instead, focus on sinus beats for reliability. In sinus rhythm, selecting the longest measurable PR interval among consecutive beats helps assess the true extent of conduction delay without overemphasizing shorter transients. Additionally, single-lead analysis may introduce errors if P wave morphology varies across leads, so cross-verification in multiple views is advised to mitigate inter-lead discrepancies.^[25]^[22]^[23]

Normal Values and Variations

The normal PR interval in adults at rest is typically 120-200 milliseconds (ms).^[26] In children, the range is shorter, generally 80-160 ms, varying with age and heart rate, with newborns exhibiting values around 90-160 ms that gradually lengthen toward adult norms by adolescence.^[27]^[28] Physiological variations in the PR interval are influenced by autonomic tone, metabolic factors, and heart rate. Enhanced vagal tone, common in athletes, often prolongs the PR interval up to 400 ms without pathology, reflecting adaptive high parasympathetic activity.^[29] Hypothermia prolongs the PR interval due to slowed atrioventricular conduction, as does hyperkalemia through impaired cellular depolarization.^[30]^[31] The interval is rate-dependent, shortening with faster heart rates (e.g., during exercise) and prolonging at slower rates due to extended atrioventricular nodal recovery time.^[32] Demographic factors also contribute to variations. The PR interval increases with age, potentially reaching up to 220 ms in the elderly due to progressive conduction system fibrosis.^[33] Sex differences are minimal, though women tend to have slightly shorter PR intervals than men, possibly related to differences in ventricular mass and conduction pathways.^[34]

Abnormalities

Prolonged PR Interval

A prolonged PR interval, also known as first-degree atrioventricular (AV) block, is defined as a consistent extension of the PR interval beyond the normal range of 120-200 milliseconds, typically exceeding 200 milliseconds in adults, without any interruption in atrioventricular conduction or dropped beats.^[35]^[36] This condition represents a delay in the conduction from the atria to the ventricles, where every P wave is followed by a QRS complex, distinguishing it from higher degrees of AV block.^[37] It is classified as "marked" first-degree AV block when the PR interval surpasses 300 milliseconds, at which point the P wave may overlap with the preceding T wave.^[38]^[35] Common causes of a prolonged PR interval include intrinsic diseases of the AV node, such as those resulting from myocardial ischemia or degenerative changes in the conduction system.^[36] Enhanced vagal tone, often seen in athletes or during sleep, can physiologically prolong the interval, while pharmacological agents like beta-blockers, calcium channel blockers, and digoxin commonly induce this delay by slowing AV nodal conduction.^[37]^[35] Electrolyte imbalances, particularly hyperkalemia or hypomagnesemia, and acute myocardial infarction—especially of the inferior wall—also contribute by affecting nodal excitability and conduction velocity.^[35]^[36] On electrocardiography, a prolonged PR interval appears as a uniform extension across consecutive beats, with P waves consistently preceding QRS complexes but separated by an elongated segment greater than 200 milliseconds.^[38] This "marching out" of P waves ahead of the QRS maintains a 1:1 atrioventricular relationship, and the QRS morphology typically remains narrow if the delay is nodal in origin, indicating the site of conduction slowing within the AV node rather than the His-Purkinje system.^[35] In cases of marked prolongation, the ECG may show partial superposition of the P wave on the T wave of the prior beat, yet conduction proceeds without block.^[36]

Shortened PR Interval

A shortened PR interval is defined as a duration less than 120 milliseconds on the electrocardiogram (ECG), contrasting with the normal range of 120 to 200 milliseconds in adults.^[39] This abnormality typically indicates accelerated atrioventricular (AV) conduction and is most commonly associated with pre-excitation syndromes such as Wolff-Parkinson-White (WPW) syndrome.^[40] In WPW syndrome, the shortened PR interval results from an accessory pathway, such as the bundle of Kent, that connects the atria directly to the ventricles, bypassing the AV node's inherent delay.^[41] This early ventricular activation produces a characteristic delta wave on the ECG, appearing as a slurred upstroke of the QRS complex.^[42] The mechanism allows for rapid conduction, predisposing affected individuals to re-entrant tachyarrhythmias like supraventricular tachycardia.^[40] A short PR interval with a normal QRS complex (without delta wave) may indicate enhanced AV nodal conduction. This pattern was historically described as Lown-Ganong-Levine (LGL) syndrome in 1952 but is not recognized as a distinct clinical entity in contemporary cardiology, as no specific anatomical substrate such as atrio-His fibers has been consistently identified.^[43]^[44] It is now viewed as a variant of accelerated conduction that may increase the risk of paroxysmal supraventricular tachyarrhythmias. Both WPW syndrome and enhanced AV nodal conduction highlight the clinical importance of identifying shortened PR intervals to assess arrhythmia risk.

Clinical Significance

Associated Cardiac Conditions

Prolongation of the PR interval is associated with several cardiac conditions that impair atrioventricular (AV) conduction. Rheumatic heart disease, resulting from streptococcal infection and subsequent autoimmune response, can cause inflammation and fibrosis of the AV node, leading to delayed conduction.^[36] Lyme disease, an infectious condition caused by Borrelia burgdorferi transmitted via tick bites, frequently involves Lyme carditis that infiltrates the AV conduction system, manifesting as AV block (often starting as first-degree) in up to 90% of cases with cardiac involvement.^[45] Congenital AV block, often linked to maternal autoantibodies crossing the placenta or structural heart defects, may present with prolonged PR interval as a milder form of conduction delay from birth.^[36] Myocarditis, encompassing inflammatory processes from viral, bacterial, or autoimmune etiologies, disrupts AV node function and is a recognized cause of PR prolongation.^[36] Additionally, drug-induced effects, such as digoxin toxicity in patients treated for heart failure or arrhythmias, elevate vagal tone and slow AV nodal conduction, resulting in extended PR intervals.^[46] Shortening of the PR interval is linked to conditions involving accelerated AV conduction or accessory pathways. Ebstein's anomaly, a congenital defect characterized by apical displacement of the tricuspid valve, is associated with accessory atrioventricular pathways in approximately 10% of cases, leading to a short PR interval and Wolff-Parkinson-White (WPW) pattern on ECG.^[47] Glycogen storage diseases, particularly those involving cardiac glycogen accumulation like PRKAG2-related cardiomyopathy, promote abnormal proliferation of accessory pathways, causing pre-excitation and shortened PR intervals.^[48] Familial forms of WPW syndrome, inherited through mutations in genes such as PRKAG2 or those affecting ion channels, result in congenital accessory pathways that bypass the AV node, consistently producing a short PR interval.^[49] PR interval deviations commonly coexist with broader cardiac comorbidities and systemic factors. In ischemic heart disease, coronary artery occlusion can damage the AV nodal blood supply, leading to conduction delays and prolonged PR intervals.^[50] Post-cardiac surgery, particularly valve or congenital repairs, transient PR prolongation occurs due to edema or direct trauma to conduction tissues in approximately 20% of patients.^[51] Systemically, hypothyroidism slows cardiac metabolism and enhances vagal effects, associating with PR prolongation, whereas hyperthyroidism increases sympathetic drive and AV nodal acceleration, often shortening the PR interval.^[52]

Diagnostic and Prognostic Implications

The analysis of the PR interval plays a crucial role in diagnosing atrioventricular (AV) conduction disturbances, particularly in identifying the degree of AV block. A prolonged PR interval greater than 200 ms is diagnostic of first-degree AV block, while progressive prolongation or associated symptoms can indicate higher-degree blocks requiring further evaluation.^[4] In symptomatic patients with first-degree AV block, PR interval assessment guides decisions for pacemaker implantation, as permanent pacing is reasonable for symptoms attributable to AV block, per 2018 ACC/AHA/HRS guidelines.^[53] Additionally, a short PR interval less than 120 ms in young patients presenting with palpitations prompts screening for Wolff-Parkinson-White (WPW) syndrome through electrocardiographic features like delta waves.^[54] Prognostically, deviations in the PR interval are associated with adverse cardiovascular outcomes. A prolonged PR interval exceeding 200 ms is linked to an increased risk of atrial fibrillation, with studies showing an absolute risk increase of 1.04% per person-year and a hazard ratio of 2.06 (95% CI, 1.36-3.12) compared to normal intervals.^[4] It also correlates with higher rates of pacemaker implantation (absolute risk increase of 0.53% per person-year) and all-cause mortality.^[4] Conversely, a shortened PR interval signals vulnerability to arrhythmias, particularly in WPW syndrome, where the annual risk of sudden cardiac death is approximately 0.25% in symptomatic individuals and low (less than 0.1%) in asymptomatic individuals.^[55] In clinical monitoring, serial electrocardiograms are essential during acute settings such as myocardial infarction to detect dynamic PR interval changes that may signal progression to higher-degree AV block or worsening conduction.^[56] Holter monitoring complements this by capturing intermittent PR variations over 24-48 hours, aiding in the assessment of arrhythmia risk in patients with suspected conduction abnormalities.^[36]

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