EKG: PR Interval Abnormalities

I. Problem/Condition.

The normal PR interval is from 0.12-0.2 seconds and is measured on the EKG from the beginning of the P wave to the beginning of the QRS complex. This interval represents the onset of atrial depolarization to the onset of ventricular depolarization and consists of:

-Atrial depolarization

-Electrical conduction from the atria to the ventricles via the AV node (end of the P to the beginning of the R wave)

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-Conduction through the His-Purkinje System

Aleterations in the PR interval may be physiologic or may represent abnormal progression of electrical conduction from the atria to the ventricles through the AV node. They are manifest in either prolongation (PR>= 0.2 s) or shortening (PR<= 0.12s).

II. Diagnostic Approach.

A. What is the differential diagnosis for this problem?

The differential for an abnormal PR interval begins with exclusion of abnormality due to normal PR variability. Following this, the diagnositic algorithm is based on the length of the PR interval – divided into shortened PR or prolonged PR.

Normal PR Variability:

In normal physiologic states the PR interval may vary with heart rate due to variations in sympathetic tone; increased tone mediates increased conduction through the AV node at faster heart rates (shortened PR), and withdrawal of sympathetic tone or increased vagal inputs will slow conduction through the AV node at slower heart rates (lengthened PR). In the majority of cases, despite physiologic variability, the PR interval should be between 0.14 and 0.2 s. Rarely, some individuals without known cardiac disease (young adults, well conditioned athletes) may present with a PR >0.2s that is physiologic. In this clinical presentation, administration of atropine invariably shortens the PR interval. This is not the case in patients with underlying cardiac pathophysiologic disease.

PR Interval < 0.12 s (see Wolff Parkinson White Syndrome (WPW)):

The differential for a PR interval less than 0.12 s is short and largely limited to the diagnosis of an accessory bypass tract between the atria and ventricles. In this clinical scenario the PR interval is shortened as electrical conduction has “bypassed” the normal route of conduction through the AV node and the cardiac current travels directly between the atria and ventricles. The accessory conducting tissue may be between the atria and ventricles (WPW), between the atria and the AV node (atriofasicular pathways) or between the AV node and the ventricle (nodoventricular).

PR Interval > 0.2 s (see Heart Block):

Patients with isolated prolonged PR intervals are rarely symptomatic. However, prolonged PR intervals associated with a higher grade AV block (see below) can present wtih symptoms ranging from fatigue, to decreased exercise tolerance to frank syncope. Overall, patients with prolonged PR intervals that present with symptoms tend to be older and have a history of cardiovascular disease. Occasionally, young adults or well conditioned athletes with high vagal tone will present with asymptomatic PR prolongation.

The differential of a prolonged PR interval is based on the EKG and can be divided into:

1. First Degree Heart Block: Prolonged PR interval

2. Second Degree Heart Block (Higher grade AV block): Mobitz Type I, Mobitz Type II

B. Describe a diagnostic approach/method to the patient with this problem.

Diagnostic Approach PR <0.12s

Accurate history taking may help differentiate a shortened PR due to physiologic variant (no associated bypass tract, accelerated conduction through AV node) versus a shortened PR due to accelerated conduction associated via a bypass tract. Patients with physiologic variants are asymptomatic and come to clinical attention largely through EKG analysis. Thus, a patient with a shortened PR and a history of sudden palpitations should be considered to have a physiologic variant only as a diagnosis of exclusion. However, not all patients with bypass tracts are symptomatic, thus the lack of symptoms cannot be used to exclude the diagnosis of a bypass tract associated with a shortened PR interval.

In addition to accurate history taking, key to appropriate diagnosis is examination of the EKG to determine if the short PR is associated with other EKG abnormalities:

1. Wolf Parkinson White Syndrome: short PR, slurring of the QRS complex (delta wave), widened QRS (see WPW)

2. Atriofasciular or Nodofasicular Pathways: short PR interval, normal width QRS (see WPW)

Diagnostic Approach PR > 0.2s

The appropriate diagnosis of a prolonged PR is based on EKG analysis to determine the severity of the AV nodal dysfunction from simple delay in conduction to complete lack of conduction through the AV node (complete heart block). In addition, the EKG should be examined for other abnormalities that may be associated with the prolonged PR.

Questions for appropriate EKG analysis:

1. Is the PR interval uniformly prolonged before each QRS? (First degree heart block)

2. Does the PR interval become progressively prolonged until there is no P wave before a QRS? (Mobitz Type I, site of block is usually in the AV node and proximal to the bundle of His)

3. Is the PR interval following the dropped beat shorter than the PR interval prior to the dropped beat? (Mobitz I, in all cases of Mobitz I this should be true).

4. Do QRS complexes tend to cluster together? (Mobitz I)

5. Is a normal PR interval followed by a nonconducted P wave (Mobitz II, site of block is usually infranodal)

6. Are there pathologic Q waves on EKG?

7. Are there changes on EKC suggestive of active ischemia? (Inferior MI is associated with Mobitz I, Anterior wall MI is associated with Mobitz II)

The differential can also be approached based on the etiology of the prolonged PR:

Underlying cardiac disease (previous MI, cardiomyopathy, myocarditits, electrical degeneration with age)

Ongoing active ischemia (acute inferior wall MI, acute anterior wall MI)

Medication effect (Amiodarone, Digitalis, beta blockers, calcium channel blockers)

Electrolyte abnormalities (hyperkalemia)

High vagal tone (young adults, well conditoned athletes)



1. Historical information important in the diagnosis of this problem.

Historical Information PR <.12s

Patients with shortened PR intervals due to bypass tracts may present with paroxysmal supraventricular tachycardias. Thus, history taking should be targeted at eliciting a history of papitations, light headedness, near loss of consciousness, syncope or unexpected death in patients and their family members.

Historical questions to ask:

1. Have you ever experienced palpitations or the sensation of your heart racing?

2. Have you ever suddenly lost consciousness?

3. Does anyone in your family have a history of sudden cardiac death, palpitations or sudden loss of consciousness?

Historical Information PR > 0.2s

History taking should be targeted at determining if the prolonged PR is associated with higher grade AV block (Mobitz I or II). Is the delay in nodal conduction significant enough to impair cardiac output and cause syncope or lightheadedness? Adjunct to this is probing the patient’s history for possible etiologies of their conduction disease.

1. Have you ever had an episode where you lost consciousness or felt as if you were going to pass out? If so, when?

2. Have you ever had an episode of sudden onset of dizziness?

3. What medications are you currently taking? Have you recently started or stopped any medications?

4. Have you ever been told that you have cardiac disease? To your knowledge have you had an MI in the past?

2. Physical Examination maneuvers that are likely to be useful in diagnosing the cause of this problem.

Physical Examination PR<0.12 s

Examination in patients with a suspected bypass tract should include a full cardiac exam. In general patients with bypass tracts do not have other associated cardiac abnormalities, however attention should be paid to auscultation as in rare cases, a bypass tract is associated with congenital heart disease (Ebstein’s Anomaly), heritable cardiomyopathies (glycogen storage disease) or mitral valve proloape (See WPW).

Physical Examination PR> 0.2 s

Examination of patients with a prolonged PR should include a full cardiac exam with emphasis on the pulse looking for an irregular pulse with dropped beats (Mobitz I) or an irregular pulse with occasional dropped beats (Mobitz II). In addition, evaluation of the patient for evidence of co-existing heart disease such cardiomyopathy or valvular disease is of value.

3. Laboratory, radiographic and other tests that are likely to be useful in diagnosing the cause of this problem.

Laboratory testing PR <0.12s

In specialized scenarios genetic testing may be appropriate to diagnose a heritable form of WPW. In general, laboratory testing is not helpful in the diagnosis of an accessory tract.

Laboratory testing PR> 0.2 s

The type of PR abnormalities can be diagnosed via EKG analysis and the etiology is usually determined by history. Occasionally the etiololgy can be determined via laboratory testing – generally in the setting of medication induced abnormality or severe hypothyroidism. In these cases measuring the drug level (e.g., digitalis) or TSH is useful in determining the diagnosis.

C. Criteria for Diagnosing Each Diagnosis in the Method Above.

Diagnosis of shortened PR associated bypass tracts (See WPW)

EKG criteria alone are insufficient for diagnosis of a bypass tract associated with a shortened PR as the findings may be intermittent (WPW) or the shortened PR may represent a physiologic variant consistent with enhanced AV conduction. However, WPW may be associated with the presence of a delta wave and or widened QRS (WPW).

In general, patients with a suspected bypass tract should be referred to a cardiac electrophysiologist for further evaluation.

Diagnosis of prolonged PR (see Heart Block)

Any PR>= 0.2 s is considered prolonged. Criteria to differentiate between first degree heart block (simple PR prolongation) and second degree heart block (Mobitz I and II) include the following:

1. First degree heart block: PR >= 0.2 s, PR interval uniformly prolonged before each QRS.

2. Second degree heart block, Mobitz I: PR >= 0.2 s, gradual prolongation of the PR interval until there is failed conduction (P with no subsequent QRS), shortened PR following the dropped QRS, presence of group beating.

3. Third degree heart block Mobitz II: PR >= 0.2s, fixed duration of PR interval with abrupt appearance of the P without a subsequent QRS.

D. Over-utilized or “wasted” diagnostic tests associated with the evaluation of this problem.


III. Management while the Diagnostic Process is Proceeding.

A. Management of Clinical Problem PR Interval Abnormalities.

Management PR < 0.12s (see WPW)


Patients with an accessory bypass tract may present with supraventricular tachycardias. In particular, during atrial fibrillation in patients with atrioventricular reentrant tachycardia due to conduction through the bypass tract (AVRT) the ventricles may become pre-excited, posing a risk of degeneration into ventricular fibrillation. As a result , patients with a known history of preexcitation or evidence of preexcitation as seen on EKG should not be given nodal agents to control their heart rate when presenting with atrial fibrillation as this may exacerbate their arrhythmia. For full details please see the ACLS guidelines (https://www.acls.net/aclsalg.htm).


Patients may present with a shortened PR interval diagnosed soley by EKG. In this setting the emphasis is placed on determining if the patient has associated symptomatic tachycardias suggestive of a bypass tract. Patients with symptomatic tachycardias should be referred to cardiology for evaluation and possible treatment with radiofrequency ablation of the bypass tract if appropriate. While the overall risk of sudden cardiac death in asymptomatic patients with a known bypass tract is low, asymptomatic patients should be referred to cardiology for evaluation and determination of risk.

Management PR >0.2s (see Heart Block)

The management of a prolonged PR is determined by the degree of AV nodal blockade.

1. First degree AV block: no intervention

2. Second degree heart bock, Mobitz I: This is generally due to reversible causes (active ischemia, medication effect) and emergency management is aimed at increasing the heart rate while the underlying cause is managed. Please see ACLS guidelines for details of this approach – http://www.acls.net/acls-bradycardia-algorithm.htm.

>>If the HR is greater than 40 and the patient is asymptomatic, no intervention is needed to increase the HR.

>>If the HR is less than 40 and the patient is symptomatic, Atropine 0.5 mg may be given as needed up to 3 doses every 3-5 minutes to increase conduction through the AV node. Alternative medications to increase the HR may also be given (See ACLS guidelines at http://www.acls.net/acls-bradycardia-algorithm.htm).

>>Symptomatic patients with reversible causes may require the insertion of a temporary pacemaker while the reversible cause is addressed.

>>Symptomatic patients with an irreversible cause will require insertion of a permanent pacemaker.

3. Second degree heart block Mobitz II: This generally represents severe infra AV nodal conduction disease and is less likely to be due to reversible cause. Emergency management is the same as that for symptomatic Mobitz I, however as Mobitz II is more likely to progress to complete heart block, these patients usually require insertion of a permanent pacemaker.

B. Common Pitfalls and Side-Effects of Management of this Clinical Problem.


IV. What's the evidence?

Goldberger. Clinical Electrocardiography: A Simplified Approach.

Ferri. Ferri's Clinical Advisor. 2011.

Sgarbossa, EB, Wagner, G.. Electrocardiography. Textbook of Cardiovascular Medicine. pp. 978-1012.