PR interval

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The PR duration depends on the conduction velocity in the atria, AV node, His bundle, bundle branches and Purkinje fibers.

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Overview

The PR interval starts at the beginning of the atrial excitation (beginning of the P wave and ends at the beginning of the ventricular excitation (beginning of the QRS complex. It is termed the PQ interval if a Q wave is present. The PR interval measures the time required for an electrical impulse to travel from the atrial myocardium adjacent to the sinoatrial (SA) node to the ventricular myocardium adjacent to the fibers of the Purkinje network.

The duration of the PR interval is normally from 0.10 to 0.21 s. A major portion of the PR interval reflects the slow conduction of an impulse through the AV node, which is controlled by the balance between the sympathetic and parasympathetic divisions of the autonomic nervous system. Therefore, the PR interval varies with the heart rate, being shorter at faster rates when the sympathetic component predominates, and vice versa. The PR interval tends to increase with age ^{[1] [1]};

• In childhood: 0.10 - 0.20 sec
• In adolescence: 0.12 - 0.16 sec
• In adulthood: 0.14 - 0.21 sec

Changes in PR interval

A prolonged PQ interval is a sign of delayed conduction through the atrium and AV node. Pathophysiologically, this can be due to 1st, 2nd or 3rd degree AV block, increased vagal tone [Bezold-Jarisch reflex; described as an eponym for a triad of responses (apnea, bradycardia, and hypotension) following intravenous injection of veratrum alkaloids in experimental animals], or it can be pharmacologically induced.^{[1] [1]}

A short PR interval can be seen in the WPW syndrome in which a faster connection exists between the atria and the ventricles.

• Shortens up to a rate of 140 to 150 beats per minute through a withdrawal of parasympathetic tone ^{[1] [1]}.
  
• PR may increase with increasing rate in the presence of digoxin or if the conducting system is diseased.
  
• If the atria are artificially paced the PR increases as the paced rate increases ^[1].
  
• Children have shorter PR intervals (0.11 at 1 year).
  
• Prolongation can be a normal variant: 67.000 healthy airmen studied and 0.52% found to have a prolonged PR.

80% of the PR prolongations ranged from 0.21 to 0.24 ^[1]. In a second study 59 of 19.000 (0.31%) airmen had a PR of 0.24 or more ^[1].

• In healthy middle aged men, a prolongation of the PR in the presence of a normal QRS does not affect prognosis and is not related to ischemic heart disease ^[1].
  
• PR prolongation often signifies a delay in the AV node but may reflect intra atrial or His Purkinje disease.
  
  

Differential Diagnosis of the Shortened PR Interval:

• AV junctional and low atrial rhythms.
  
• Wolff Parkinson White syndrome ^[1]
  
• Lown Ganong Levine syndrome
  
• Glycogen storage disease ^[1]
  
• Hypertension
  
• Normal variant
  
• Fabry's disease
  
• Pheochromocytoma
  
  

Differential Diagnosis of a Prolonged PR Interval

• Beta blocker therapy
• AV block due to coronary artery disease, rheumatic disease
• Hyperthyroidism
  
• Normal variant
  
  

Differential Diagnosis of the Depressed PR Interval:

• Acute pericarditis
  
• Atrial infarction
  

References

Additional resources

• ECGpedia: Course for interpretation of ECG
• The whole ECG - A basic ECG primer
• 12-lead ECG library
• Simulation tool to demonstrate and study the relation between the electric activity of the heart and the ECG
• ECG information from Children's Hospital Heart Center, Seattle
• ECG Challenge from the ACC D2B Initiative
• National Heart, Lung, and Blood Institute, Diseases and Conditions Index
• A history of electrocardiography
• EKG Interpretations in infants and children

Acknowledgement and Attribution Regarding Sources of Content

Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .