Chronic Cor Pulmonale on ECG

What it looks like on ECG

The picture consists of signs of right atrial and right ventricular overload, often modified by concomitant emphysema. The diagnostic value of individual signs is limited; they must be evaluated comprehensively and in conjunction with the clinical presentation.

P wave. In II, III, aVF — tall, peaked P pulmonale (≥ 2.5 mm) reflecting right atrial overload. In V1, the P wave is often normally biphasic (positive phase followed by negative); an increase in its initial positive phase (usually > 1.5 mm) may support right atrial abnormality, but the biphasic nature of P in V1 itself is nonspecific and lacks diagnostic value. The primary criterion for P pulmonale is P amplitude in the inferior leads.

Axis and QRS. Rightward axis deviation is typical, often pronounced (> +110°). The S1S2S3 pattern is described (S wave in all three standard leads), but it is nonspecific and occurs in healthy individuals with a vertical heart position. In the right precordial leads (V1), a qR, R, or Rs complex with R/S > 1 may form, supporting the diagnosis of RVH in the presence of other signs. Additionally, rsR' in V1–V2 with a wide S in I and V6 and QRS 110–119 ms represents incomplete right bundle branch block; it is a frequent finding in COPD, but by itself does not prove RVH and can be a normal variant.

Transition zone and voltage. In concomitant pulmonary emphysema, a reduction in QRS voltage (especially in limb leads) and poor/delayed R-wave progression with a later transition zone are possible due to increased distance between the heart and electrodes, increased lung lucency, and clockwise rotation of the heart. Low voltage is assessed by standard thresholds (QRS < 5 mm in all limb leads and/or < 10 mm in all precordial leads); it does not need to be present in all leads simultaneously, and the position of the transition zone is variable.

ST segment and T wave. In V1–V3, occasionally in inferior leads — negative or biphasic T, minor ST depression as a sign of right ventricular strain, especially worsening during exacerbations or acute increases in pulmonary hypertension.

Mechanism

Chronic pulmonary diseases (COPD, fibrosis, chronic PE, kyphoscoliosis, neuromuscular disorders with hypoventilation) lead to a sustained increase in pulmonary artery pressure. The right ventricle works against increased resistance, leading to hypertrophy and subsequent dilatation. The mass and electrical activity of the right heart increase, and the depolarization vector shifts rightward and anteriorly — hence the axis deviation, tall R in V1, and ST depression/negative T as signs of strain. At the same time, lung hyperinflation (emphysema) depresses the diaphragm, increases the air cushion between the heart and electrodes, and rotates the heart — which can produce low voltage, verticalization of the axis, and shift of the transition zone, potentially both enhancing and masking "true" signs of right ventricular hypertrophy.

Causes

• COPD and pulmonary emphysema (most common cause)
• Chronic thromboembolic pulmonary hypertension
• Interstitial lung diseases, pulmonary fibrosis
• Kyphoscoliosis and other chest wall deformities
• Neuromuscular diseases with chronic alveolar hypoventilation
• Obstructive sleep apnea syndrome (severe forms)
• Primary (idiopathic) and other forms of pulmonary arterial hypertension
• Cystic fibrosis, bronchiectasis

Differential diagnosis

• Right ventricular hypertrophy of other etiology (congenital heart disease, pulmonary stenosis) — ECG picture is similar, differentiated by history and echocardiography; cor pulmonale usually has signs of chronic pulmonary pathology.
• Acute PE — acute and chronic RV overload cannot be reliably distinguished by ECG. The S1Q3T3 pattern described in acute PE is nonspecific and optional; it can also occur in chronic RV overload. Sinus tachycardia, bundle branch block, and other nonspecific changes are also possible. When PE is suspected, clinical probability assessment is required along with, depending on it, D-dimer, CT pulmonary angiography, or other algorithmic methods, rather than interpreting a single ECG.
• Anterior myocardial infarction — T-wave inversion and ST depression in V1–V3/4 can mimic RV strain. ST elevation in these leads should not be attributed to chronic cor pulmonale without ruling out ACS: manage ST elevation according to the ACS algorithm. The absence of pathological Q also does not rule out infarction, including NSTEMI — ECG dynamics, clinical picture, and serial high-sensitivity troponins are required.
• Dextrocardia and incorrect electrode placement — also cause axis deviation and precordial lead changes. Dextrocardia is characterized by negative P, QRS, and T waves in lead I, a positive complex in aVR, and reversed or abnormal R-wave progression in precordial leads; dextrocardia may be combined with congenital heart disease and true right heart overload, so P pulmonale and RVH signs may be present. Electrode placement errors are checked by repeat recording with correct positioning.
• Incomplete right bundle branch block as a normal variant — isolated rsR' in V1 without P pulmonale and without axis deviation in healthy individuals should not be interpreted as cor pulmonale.

Clinical significance and management

ECG signs of chronic cor pulmonale appear late, when RV hypertrophy and strain are already pronounced — the sensitivity of the method is limited. The diagnosis of pulmonary hypertension and cor pulmonale is established clinically and via echocardiography/right heart catheterization; the ECG plays an auxiliary role, helping to suspect the condition, assess the dynamics of right heart strain, and detect associated arrhythmias (frequently atrial tachyarrhythmias, including multifocal atrial tachycardia and atrial fibrillation, typical for decompensation in COPD). The physician should: correlate findings with clinical presentation (dyspnea, cyanosis, edema, spirometry data), refer for echocardiography to assess the probability of pulmonary hypertension, RV dimensions and function, confirm the diagnosis by right heart catheterization when indicated, identify and treat the underlying lung disease, and monitor for the development of right ventricular decompensation and atrial arrhythmias over time.

Common interpretation errors

• Interpret isolated incomplete right bundle branch block as a sufficient sign of cor pulmonale without assessing P pulmonale and the axis.
• Confuse low voltage in emphysema with pericardial effusion or hypothyroidism without considering the clinical picture.
• Mistake negative T waves in V1–V3 for ischemia without serial ECGs, clinical correlation, and troponins; or erroneously attribute ST elevation in these leads to RV strain instead of ruling out ACS.
• Fail to consider that S1S2S3 can occur in healthy individuals with a vertical heart position.
• Ignore atrial arrhythmias (MAT, AF) that frequently accompany cor pulmonale decompensation and require separate rhythm evaluation.

Frequently asked questions

Related terms

More in the section "Pericardium, Lungs, Brain and Others"

Entire section

Sources

• Goldberger A. Clinical Electrocardiography: A Simplified Approach
• Surawicz B., Knilans T. Chou's Electrocardiography in Clinical Practice
• Orlov V.N. Guide to Electrocardiography
• AHA/ACCF/HRS Recommendations for Standardization of ECG, 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.