ECG criteria
- Low QRS voltage: typically <5 mm in each limb lead and/or <10 mm in each chest lead; this criterion is nonspecific and does not diagnose emphysema.
- Vertical (approximately +70…+90°) or indeterminate (northwest) QRS axis position due to descent and rotation of the heart; more pronounced deviation forms right axis deviation (>+90°), which is correctly designated separately.
- Poor R-wave progression in V1–V3 (an approximate nonspecific sign requiring verification of electrode placement and comparison with prior ECGs), sometimes a pseudo-infarct QS pattern in the right chest leads.
- The transition zone is often shifted to the left, toward V5–V6, as a result of delayed R-wave progression during clockwise rotation of the heart.
- P pulmonale: tall, peaked P wave, usually >2,5 mm in lead II, frequently also in III and aVF; reflects possible right atrial enlargement/overload, but is nonspecific and does not prove pulmonary hypertension.
- Marked electrical alternans is more characteristic of significant pericardial effusion, but its absence does not rule out effusion; this sign is not used to confirm emphysema.
- In chronic cor pulmonale, right axis deviation (>+90°), R/S predominance in V1, signs of right ventricular overload (strain), and P pulmonale are possible; the SI-QIII-TIII pattern is nonspecific and, if appearing acutely, requires evaluation for pulmonary embolism in light of the clinical picture.
What it looks like on ECG
A possible finding is diffusely decreased QRS amplitude: typically <5 mm in limb leads and/or <10 mm in chest leads. The cause is mechanical rather than electrical: the air "cushion" of the lungs increases the distance between the heart and electrodes and acts as an insulator. This criterion is general for low voltage of any etiology and does not confirm emphysema on its own.
The QRS axis is often vertical (approximately +70…+90°) or even indeterminate (northwest zone) because the lowered and clockwise-rotated diaphragm pulls the heart downward and posteriorly. More pronounced deviation (>+90°) is correctly interpreted as right axis deviation, which develops in some patients during the formation of cor pulmonale. In the chest leads, poor R-wave progression from V1 to V3 may occur, sometimes with QS-type complexes in V1–V2 — this can mimic a prior anterior myocardial infarction, although there are no reciprocal or dynamic ST-T changes. Such a pattern must always be correlated with correct electrode placement and previous tracings.
The transition zone (where R becomes larger than S) is often shifted to the left, toward V5–V6, reflecting delayed R-wave progression during clockwise heart rotation.
With concomitant pulmonary hypertension and the development of chronic cor pulmonale, P pulmonale may be added (most commonly assessed in lead II, also possible in III and aVF), along with signs of right ventricular overload (RV strain) — ST depression and negative T waves in V1–V3/V4, sometimes involving V5–V6 and inferior leads (severity depends on the degree of overload) — and right axis deviation.
| Sign | Leads | Criterion |
|---|---|---|
| Low voltage | limbs / chest | <5 mm / <10 mm |
| Poor R progression | V1–V3 | nonspecific, approximate |
| Vertical QRS axis | frontal plane | approximately +70…+90° |
| Right axis deviation (in cor pulmonale) | frontal plane | >+90° |
| P pulmonale | predominantly II, also III, aVF | P >2,5 mm |
Mechanism
Emphysema increases the volume of air in the lungs and the distance between the myocardium and chest electrodes. Air conducts electrical current poorly, so part of the heart's electrical potential is dissipated without reaching the body surface — hence the possible diffuse decrease in voltage. The low, flat position of the diaphragm and barrel-shaped chest displace and rotate the heart: the apex shifts downward and posteriorly, which can result in a vertical QRS axis and clockwise rotation with delayed R-wave progression in the right chest leads. With the development of chronic cor pulmonale against the background of pulmonary hypertension, signs of right ventricular hypertrophy/overload and right atrial enlargement may appear.
Causes
- Chronic obstructive pulmonary disease (COPD) with an emphysematous component
- Primary (bullous) emphysema, alpha-1 antitrypsin deficiency
- Pronounced hyperinflation of the lungs of any etiology (severe bronchial asthma with hyperinflation, bilateral pneumothorax)
- Senile emphysema as part of age-related changes in lung tissue
Differential diagnosis
- Pericardial effusion and tamponade: low voltage is also possible, sometimes with electrical alternans of QRS and clinical presentation of tamponade rather than chronic respiratory failure
- Hypothyroidism: low voltage + sinus bradycardia, without verticalization of the QRS axis and without a history of COPD
- Obesity: low voltage due to chest wall tissue volume, but without typical poor R progression and vertical axis
- Prior anterior myocardial infarction: QS in V1–V3 can mimic both; the absence of acute ST-T dynamics reduces the likelihood of acute infarction but does not rule out an old scar — history, comparison with previous ECGs, and echocardiography are needed
- Diffuse myocardial infiltration (amyloidosis): low voltage with normal or increased wall thickness on echocardiography, without a pulmonary history
Clinical significance and management
The ECG changes themselves are nonspecific and do not allow the diagnosis of emphysema without clinical and functional evaluation. Spirometry assesses the presence and degree of bronchial obstruction and overall lung function, but does not establish the anatomical diagnosis of emphysema; emphysema as a structural lesion is confirmed or characterized by imaging — usually chest CT — when clinically indicated, whereas radiography can only provide indirect signs. The final diagnosis is based on a combination of clinical, functional, and imaging data. The ECG finding usually does not require emergency intervention, but its clinical context must be evaluated: low voltage, pseudo-infarct QS complexes, or signs of right ventricular overload may also reflect potentially dangerous conditions (tamponade, pulmonary embolism, severe pulmonary hypertension) that require separate exclusion. It is important for the functional diagnostics physician not to interpret pseudo-infarct QS complexes in the right chest leads as a sign of prior infarction without clinical data, and not to miss the early development of chronic cor pulmonale (P pulmonale, signs of right ventricular overload) — in which case an echocardiographic study assessing pulmonary artery pressure is indicated.
Common interpretation errors
- Interpreting poor R progression and QS in V1–V3 as a prior infarction without considering the clinical picture, history, and previous ECGs
- Failing to associate low QRS voltage with pulmonary pathology, searching only for cardiac causes (pericarditis, hypothyroidism)
- Overlooking developing P pulmonale and signs of right ventricular overload — early markers of cor pulmonale
- Interpreting the SI-QIII-TIII pattern as specific for cor pulmonale without considering acute pulmonary embolism in the appropriate clinical setting
- Overestimating a vertical QRS axis as pathology without remembering its frequency in thin patients and in emphysema
1. Which of the following findings is considered specific and sufficient for diagnosing pulmonary emphysema on an ECG?
All of the listed changes occur inconsistently in emphysema and are nonspecific; the diagnosis is based on clinical, functional, and imaging data.
2. Which QRS axis position is typical for pulmonary emphysema?
Descent and rotation of the heart in emphysema most commonly result in a vertical (approximately +70…+90°) or northwest (indeterminate) axis.
3. How is the pseudo-infarct QS pattern in V1–V3 best evaluated when emphysema is suspected?
The absence of acute ST-T changes lowers the probability of acute myocardial infarction, but does not rule out an old scar; therefore, checking the recording technique, comparing with previous ECGs, and clinical data are required.
Frequently asked questions
Is pulmonary emphysema on ECG dangerous?
The ECG changes themselves usually do not require emergency measures. Their significance is a possible indirect sign of chronic pulmonary disease, which itself can lead to complications such as pulmonary hypertension and chronic cor pulmonale; final evaluation requires clinical data and functional tests.
How to distinguish low voltage in emphysema from pericardial effusion?
There are no specific ECG differences: emphysema is more frequently characterized by a vertical electrical axis of the heart (EAH), poor R-wave progression, and a pulmonary history, whereas cardiac tamponade may present with electrical alternans, sinus tachycardia, and clinical signs of acute heart failure or shock. The absence of alternans does not rule out effusion, so clinical presentation and echocardiography are crucial.
Why might QRS have low voltage in emphysema?
Excess air in the lungs increases the distance between the heart and the electrodes and attenuates part of the electrical signal, which is why the amplitude of waves on the surface ECG can decrease diffusely across all leads. This sign is non-specific and is not present in all patients with emphysema.
Can QS waves in V1–V3 in emphysema be mistakenly interpreted as a myocardial infarction?
Yes, clockwise rotation of the heart and displacement of the transition zone to the left can produce a pseudoinfarction pattern in the right chest leads. The absence of acute ST-T dynamics reduces the likelihood of acute myocardial infarction, but does not rule out a prior (old) myocardial infarction — checking electrode placement, comparison with previous ECGs, clinical presentation, and echocardiography are needed.
What other ECG changes appear in long-standing emphysema?
With progression to chronic cor pulmonale, P pulmonale may appear (predominantly in lead II, as well as in III and aVF), along with signs of right ventricular overload in the right chest and sometimes inferior leads, as well as rightward axis deviation. The SI-QIII-TIII pattern in this context is non-specific and is not a typical sign of chronic cor pulmonale.
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Related terms
More in the section "Pericardium, Lungs, Brain and Others"
Sources
- Goldberger's Clinical Electrocardiography, latest edition
- Surawicz B., Knilans T. Chou's Electrocardiography in Clinical Practice
- Orlov V.N. Guide to Electrocardiography
- AHA/ACCF/HRS Recommendations for the Standardization of the Electrocardiogram, 2009
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.