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Conceptual Overview

The P wave represents atrial depolarization - the electrical activation of both atria. In normal sinus rhythm, the impulse originates from the sinoatrial (SA) node in the high right atrium and spreads through the atrial myocardium to reach the AV node.

Understanding P wave morphology is fundamental to rhythm interpretation. The shape, size, and direction of the P wave in different leads reveals:

  • Origin of impulse: Sinus node, ectopic atrial focus, or AV junction
  • Atrial chamber abnormalities: Enlargement or hypertrophy
  • Conduction pathways: Normal interatrial conduction or abnormal patterns
  • Rhythm classification: Supraventricular vs ventricular
Key concept: The P wave is the "signature" of atrial activity. No P wave or abnormal P waves change your entire differential diagnosis for the rhythm.
Normal P Wave Characteristics

Sinus P Wave Criteria

  • Upright in leads I, II, and aVF: Indicates depolarization traveling inferiorly and leftward from SA node
  • Inverted in aVR: As impulse travels away from right shoulder
  • Variable in III, aVL: Depending on heart axis
  • Biphasic in V1: Initial positive deflection (right atrium) followed by negative (left atrium)
  • Upright in V2-V6: Anterior and leftward spread

Normal Measurements

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Parameter Normal Range Clinical Significance
Duration <0.12 seconds (less than 3 small boxes) Prolonged >0.12 sec suggests atrial enlargement or intra-atrial conduction delay
Amplitude (limb leads) <2.5 mm >2.5 mm in lead II suggests right atrial enlargement
Amplitude (precordial) <1.5 mm Increased amplitude may indicate atrial abnormality
P wave axis 0° to +75° Outside this range suggests ectopic atrial rhythm
Remember: P waves in V1 are normally biphasic. An initial small positive deflection represents right atrial depolarization, followed by a deeper negative deflection from left atrial activation.
P Wave Abnormalities

Right Atrial Enlargement (P Pulmonale)

  • Criteria: P wave amplitude >2.5 mm in leads II, III, or aVF
  • Mechanism: Increased right atrial muscle mass
  • Causes: Pulmonary hypertension, chronic lung disease (COPD, cor pulmonale), tricuspid stenosis, pulmonary stenosis
  • Morphology: Tall, peaked P waves best seen in inferior leads

Left Atrial Enlargement (P Mitrale)

  • Criteria in limb leads: P wave duration >0.12 seconds with notched, bifid appearance (M-shaped)
  • Criteria in V1 (Morris index): Negative terminal deflection ≥1 mm deep AND ≥0.04 seconds (1 small box) in duration
  • Mechanism: Delayed left atrial activation due to increased chamber size
  • Causes: Mitral valve disease (stenosis or regurgitation), left ventricular failure, systemic hypertension, aortic valve disease

Biatrial Enlargement

  • Criteria: Features of both RAE and LAE present
  • P wave characteristics: Tall (>2.5 mm) AND wide (>0.12 sec) with notching
  • V1 morphology: Tall initial positive component with deep terminal negative deflection
  • Causes: Advanced valvular disease, cardiomyopathy, congenital heart disease
Clinical pearl: "P pulmonale" and "P mitrale" are named for their classic associations (pulmonary disease and mitral valve disease), but these patterns can occur in other conditions affecting atrial chamber size or conduction.
Ectopic P Waves & Non-Sinus Rhythms

Identifying Ectopic Atrial Activity

When the P wave doesn't match normal sinus morphology, consider an ectopic atrial rhythm:

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P Wave Finding Rhythm Interpretation
Inverted P in II, III, aVF; upright in aVR Low atrial or junctional rhythm (retrograde atrial activation)
Varying P wave morphology (≥3 forms) Multifocal atrial tachycardia (MAT) or wandering atrial pacemaker
Sawtooth flutter waves Atrial flutter (typically 2:1, 3:1, or variable block)
Irregular, chaotic baseline without discrete P waves Atrial fibrillation
No P waves, narrow QRS Junctional rhythm or atrial fibrillation with controlled rate
P waves following QRS (retrograde) Junctional tachycardia or AVNRT

Premature Atrial Complexes (PACs)

  • P wave morphology: Different from sinus P waves; shape depends on ectopic focus location
  • Timing: Occurs earlier than expected sinus P
  • PR interval: May be shorter, normal, or longer than sinus PR; very premature PACs may not conduct (blocked PAC)
  • QRS: Typically narrow and identical to sinus beats; aberrantly conducted PACs can be wide
Technique tip: Look for P waves hiding in the preceding T wave. Comparing the T wave of a PAC beat to normal sinus T waves often reveals a "buried" premature P.
Quick Reference
  • Normal P wave duration: <0.12 seconds (less than 3 small boxes)
  • Normal P wave amplitude: <2.5 mm in limb leads
  • Normal sinus P wave: Upright in leads I, II, aVF; inverted in aVR
  • P wave represents: Atrial depolarization from SA node through atrial myocardium
  • First half: Right atrial activation
  • Second half: Left atrial activation
  • Key pearl: P wave morphology tells you where the impulse originated
Clinical Pearls
"No P wave, no problem... sometimes": Absence of clear P waves can indicate atrial fibrillation, junctional rhythm, or artifact obscuring P waves. Context matters - irregular narrow-complex tachycardia without P waves = Afib; regular narrow complex without P = junctional.
"V1 is your friend": Lead V1 is the best lead to evaluate atrial activity. Its proximity to the atria makes P waves and flutter waves most prominent here. When in doubt about the rhythm, examine V1 carefully or use a Lewis lead.
"P wave axis unlocks ectopic rhythms": A negative P in lead II (where it should be positive) immediately tells you the impulse is NOT from the SA node - think low atrial or junctional origin.
Don't miss flutter waves: Atrial flutter can be subtle, especially with 2:1 conduction at rates around 150 bpm. The "flutter" portion may hide in the T wave or QRS. Use vagal maneuvers or calipers to unmask the rhythm.
Biatrial enlargement = advanced disease: When you see both tall AND wide P waves, think severe, chronic structural heart disease. These patients often have significant valvular pathology or cardiomyopathy.
References
  1. Farkas, Josh MD. (2015). Table of Contents - EMCrit Project. EMCrit Project. https://emcrit.org/ibcc/toc/
  2. Khan, M. G. (2007). Rapid ECG Interpretation. Humana.
  3. Sigg, D. C., Iaizzo, P. A., Xiao, Y.-F., Bin He, & Springerlink (Online Service). (2010). Cardiac Electrophysiology Methods and Models. Springer Us.
  4. Wang, K. (2012). Atlas of Electrocardiography. JP Medical Ltd.
  5. ECG Library • LITFL • ECG Library Basics. (2018). Life in the Fast Lane • LITFL • Medical Blog. https://litfl.com/ecg-library/
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