ECG criteria
- P wave ≥2.5 mm (0.25 mV) in lead II, tall and peaked — P pulmonale; this criterion is most applicable in lead II, but can also be seen in III and aVF
- In V1, a supportive sign is an initial positive P-wave phase with an amplitude of >1.5 mm; "peakedness" or phase "dominance" on its own is not a standalone standardized criterion
- The electrical axis of the heart (derived from limb leads) is deviated to the right or vertical; an "indeterminate" (northwest) axis is also possible
- Low QRS voltage: amplitude <5 mm in all six limb leads and/or <10 mm in all chest leads at standard 10 mm/mV calibration; reduced amplitude in only some leads of a group does not meet the formal criterion
- SI-SII-SIII pattern (S wave in I, II, and III) is a nonspecific sign of a vertical heart position and axis deviation, which can also occur as a normal variant; there is no standardized S-wave amplitude threshold
- Poor R-wave progression in the chest leads with a late transition zone (up to V5–V6); this sign is nonspecific, and incorrect electrode placement, prior myocardial infarction, and hypertrophy must be ruled out
- Signs of heart position (right axis deviation, R/S >1 in V1, incomplete right bundle branch block) are often caused by verticalization and rotation of the heart and do not by themselves confirm right ventricular hypertrophy or strain
- Multifocal atrial tachycardia or frequent atrial extrasystoles against the background of hypoxia may occur
What it looks like on ECG
A classic yet inconstant marker is P pulmonale: the P wave in lead II is tall (≥2.5 mm), peaked, and of normal width (duration is not increased, unlike P mitrale); an equally tall P wave may appear in III and aVF. In V1, the initial positive P phase with an amplitude of >1.5 mm is considered a supportive sign. P pulmonale reflects right atrial overload, but is often absent even in severe emphysema; its absence does not rule out COPD, and the sign itself is nonspecific and does not indicate the cause or degree of overload.
The electrical axis (assessed via limb leads I, II, III, aVL, aVF) shifts vertically or to the right due to lung hyperinflation and a low diaphragm; in severe cases, the axis becomes indeterminate (northwest). A pattern of clockwise rotation of the heart around its longitudinal axis is typical, evaluated by the transition zone and R-wave progression in chest leads V1–V6: the transition zone shifts to the left, as far as V5–V6, meaning poor R-wave progression persists from V1 to V4. Such a late transition zone and poor R progression are nonspecific on their own, and when detected, improper chest electrode placement and other causes (prior infarction, hypertrophy) must be excluded.
The SI-SII-SIII pattern (S wave in I, II, and III) is another nonspecific sign of a vertical heart position or axis deviation and possible cardiac rotation; there is no universally accepted standardized threshold based solely on the presence of an S wave, and by itself it does not confirm clockwise rotation, COPD, or cor pulmonale.
QRS voltage may be reduced (amplitude <5 mm in all limb leads and/or <10 mm in all chest leads) due to increased distance between the heart and electrodes, changes in heart position, and attenuation of the recorded electrical field in lung hyperinflation. This sign is not always pronounced; amplitude reduction in only isolated leads within a group does not meet the formal low-voltage criterion.
| Sign | Leads | Criterion |
|---|---|---|
| P pulmonale | II (may be present in III, aVF) | P ≥2.5 mm, peaked, without widening |
| SI-SII-SIII | I, II, III | S in each, without a standardized amplitude threshold |
| Low voltage | all limb and/or all chest leads | <5 mm / <10 mm respectively |
| Poor R progression | V1–V6 | R does not grow, transition zone shifted toward V5–V6 |
When pulmonary hypertension and chronic cor pulmonale develop, some patients may acquire additional signs of right ventricular overload (increased R in V1, incomplete or complete right bundle branch block), but confirming right ventricular hypertrophy or strain requires a combination of findings and echocardiography rather than isolated findings.
Mechanism
Lung hyperinflation increases the distance between the heart and the chest wall and depresses the diaphragm, causing the heart to assume a more vertical position and rotate clockwise — hence the vertical/right axis, SI-SII-SIII, and poor R progression. In some patients with severe COPD, chronic alveolar hypoxia and pulmonary vascular remodeling lead to pulmonary hypertension and right ventricular strain, which may secondarily be accompanied by right atrial enlargement (P pulmonale). These processes do not develop in everyone, and P pulmonale does not prove the presence or severity of pulmonary hypertension. Low QRS voltage is attributed to increased distance to the electrodes, changes in heart position, and attenuation of the recorded electrical field in hyperinflated lung tissue.
Causes
- Chronic obstructive pulmonary disease with emphysema
- Severe bronchial asthma with emphysematous changes
- Bronchiectasis
- Cystic fibrosis
- Chronic pulmonary hypertension of any genesis leading to chronic cor pulmonale
- Severe kyphoscoliosis and other restrictive chest wall diseases (similar axis and voltage changes)
Differential diagnosis
- P mitrale (left atrial enlargement): P wave is broad (≥120 ms), notched in I, II, aVL, V5–V6 — versus the narrow, peaked P pulmonale.
- Hyperkalemia: P wave may decrease or disappear rather than increase, accompanied by QRS widening and tall T waves — a different clinical picture.
- PE (pulmonary embolism): may also present with SI-QIII-TIII and right axis deviation, but sinus tachycardia, right bundle branch block, and acutely developed changes are typical, rather than chronic low voltage; isolated findings without clinical context neither confirm nor rule out PE.
- Pericardial effusion: significant effusion may cause low QRS voltage and electrical alternans, but their absence does not exclude effusion, and the presence of P pulmonale or SI-SII-SIII does not exclude concomitant effusion; ECG cannot reliably differentiate low voltage due to emphysema from effusion — echocardiography is needed.
- Normal variant: isolated low voltage, vertical axis, or SI-SII-SIII pattern in slender individuals without a pulmonary history — clinical correlation and, if in doubt, echocardiography are required.
Clinical significance and management
An ECG can provide indirect, nonspecific signs of emphysema or chronic right heart strain, but it does not reliably assess COPD severity or pulmonary artery pressure; functional tests, imaging, and echocardiography are required for this. The presence of P pulmonale and signs of right ventricular strain in a patient with known COPD is an indication to assess the risk of chronic cor pulmonale and refer for echocardiography: it assesses the probability of pulmonary hypertension and right ventricular size and function, while direct confirmation and pressure measurement are performed via right heart catheterization when indicated. Multifocal atrial tachycardia and frequent atrial arrhythmias in such patients are often provoked by hypoxia and exacerbation of the underlying disease; treatment is based on managing the provoking condition, oxygen therapy as indicated, and correcting potassium and magnesium levels, while medical rate control for persistent symptomatic tachycardia is considered individually, taking into account COPD, ventricular function, and contraindications. In acute symptoms (dyspnea, chest pain, syncope) or high clinical probability of PE, it should be evaluated via a diagnostic algorithm; isolated ECG findings (right axis deviation, SI-SII-SIII) without the appropriate clinical context neither confirm nor rule out PE.
Common interpretation errors
- Mistaking P pulmonale for P mitrale and vice versa — rely on P-wave amplitude (height) versus width (duration)
- Interpreting low voltage as an independent diagnosis without considering the context (emphysema, obesity, effusion, hypothyroidism) and without verifying that the criterion is met in all leads of the group
- Confusing SI-SII-SIII with the acute SI-QIII-TIII syndrome in pulmonary embolism — look at the clinical presentation and dynamics
- Attributing poor R-wave progression exclusively to prior anterior myocardial infarction without ruling out incorrect electrode placement, COPD, and cardiac rotation
- Considering R/S>1 in V1 or incomplete right bundle branch block as sufficient evidence of right ventricular hypertrophy without clinical evaluation and echocardiography
- Forgetting that ECG changes lag behind the severity of pulmonary hypertension and do not replace echocardiography
P pulmonale — a "peak" in II, III, aVF: tall and pointed, like a mountain peak
1. Which criterion corresponds to P pulmonale?
P pulmonale is a tall, peaked P wave without increased duration, reflecting right atrial overload; the criterion is most applicable in lead II.
2. Which precordial lead pattern is characteristic of COPD due to clockwise cardiac rotation?
Clockwise cardiac rotation shifts the transition zone to the left, which is why the R wave is slow to progress in the right and mid-precordial leads.
3. Which statement regarding ECG signs of COPD is correct?
The standardized low voltage criterion requires QRS amplitude <5 mm in all six limb leads and/or <10 mm in all precordial leads; the other statements are incorrect because ECG signs in COPD are inconstant and non-specific.
Frequently asked questions
How does P pulmonale differ from P mitrale on an ECG?
P pulmonale is tall (≥2.5 mm) and peaked, but not widened, visible in II (possible in III, aVF). P mitrale is wide (≥120 ms) and notched, visible in I, II, aVL, V5–V6. The former is associated with right atrial overload, the latter with left atrial overload.
Does COPD always cause ECG changes?
No, the ECG has low sensitivity for COPD: typical signs appear with marked emphysema or established cor pulmonale, while in early stages the ECG may be normal. Many signs, including P pulmonale, are often absent even in severe disease.
Are ECG changes dangerous in COPD?
ECG signs are non-specific, but in the presence of dyspnea, chest pain, syncope, hypotension, tachycardia, or new ECG changes, acute conditions must be ruled out (including pulmonary embolism, cardiac tamponade, severe hypoxemia). The signs themselves do not allow for risk assessment without clinical context.
How to distinguish low voltage in COPD from pericardial effusion?
In COPD, low voltage is more often combined with P pulmonale, vertical or right axis deviation, and an SI-SII-SIII pattern, whereas with effusion, electrical alternans may occur with a large volume of fluid. These signs are not always present and do not reliably differentiate the causes — echocardiography is needed.
What additional diagnostics are needed when cor pulmonale is suspected on an ECG?
Echocardiography to assess the probability of pulmonary hypertension, right ventricular size and function (if necessary, right heart catheterization for direct pressure measurement), as well as pulmonary function tests and chest X-ray or CT.
ECG Course
Interpretation from basics to myocardial infarction — learn to read any ECG using a systematic algorithm.
- Video lessons and theory for every topic
- Simulator case studies under every lesson
- Unlimited ECG simulator practice
- Study guide: "All ECGs in 25 minutes"
ECG Strip Simulator
ECG, radiology, histology, pathomorphology, pharmacology — thousands of flashcards with detailed explanations.
- Real ECG strips, not textbook drawings
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Related terms
More in the section "Pericardium, Lungs, Brain and Others"
Sources
- Goldberger A. Clinical Electrocardiography: A Simplified Approach
- Surawicz B., Knilans T. Chou's Electrocardiography in Clinical Practice
- Orlov V.N. Guide to Electrocardiography
- Hampton J. The ECG Made Easy
Educational material for medical students and physicians. Does not replace clinical guidelines and physical examination; the ECG must always be interpreted in conjunction with the clinical picture.