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R and S wave in lead V1 are due to

Reading File
Finding Sources
Searching PubMed

"Electrocardiography"[MeSH Terms] AND "V1"

The r wave in V1 is caused by depolarization of the interventricular septum. The S wave is caused by depolarization of the free walls of the left ventricle (the dominant, thicker mass).
Sequence of activation
  1. Septum (r wave). Septal depolarization begins on the left side and spreads to the right. This moves toward V1, so V1 records a small positive deflection. Harrison's describes this as the small "septal" r wave in V1 (Harrison's Principles of Internal Medicine 22E, QRS Complex).
  2. Left ventricular free wall (S wave). The impulse then spreads through the much larger left ventricular mass, which moves away from the right-sided lead V1. V1 therefore records a large negative deflection, the S wave. Goldman-Cecil says the same: initial septal activation inscribes an r wave, and later activation away from V1 records a dominant S wave (Goldman-Cecil Medicine, Electrocardiographic Leads).
In V6 the same events appear in reverse. The initial septal activation moves away from V6, giving a small septal q wave. The activation of the left ventricular free wall then moves toward V6, giving a tall R wave.
A normal V1 therefore shows a small r followed by a deep S (an rS complex). The transition to R-dominant usually occurs around V3 or V4 (Goldman-Cecil Medicine, Approach to Interpreting the Electrocardiogram).
Why it matters: A dominant R wave in V1 is abnormal. Causes include right ventricular hypertrophy, right bundle branch block, posterior MI, and WPW with a left-sided pathway.
I also ran a PubMed search for recent systematic reviews and meta-analyses. None of the results changes this basic electrophysiology.

Dominant R and Small S wave in V1 in RVH is due to what

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Reading File
A dominant R wave with a small S wave in V1 in RVH is due to increased right ventricular muscle mass, which overpowers the normally dominant left ventricular forces.
Mechanism
  • Normally the left ventricle is much thicker than the right. Its free wall activation moves away from V1 and produces the deep S wave.
  • In RVH from a sustained, severe pressure load, the right ventricle hypertrophies and generates larger electrical forces. These forces are directed anteriorly and rightward, toward V1.
  • The right ventricular free wall is the last part of the ventricles to be activated. With hypertrophy, this late rightward and anterior vector is large enough to outweigh the left ventricular vector. V1 therefore records a tall R wave (R ≥ S, or an R/S ratio above 1) and only a small S wave.
  • The shift in the mean QRS vector toward the right and anterior explains the associated right axis deviation. The R wave in V1 may be replaced by a qR pattern.
  • Hypertrophy with pressure overload also causes secondary repolarization changes. These are ST depression and T-wave inversion in the right to mid-precordial leads (the "strain" pattern).
Harrison's states that RVH from a sustained, severe pressure load (for example pulmonic stenosis or pulmonary hypertension) is characterized by a relatively tall R wave in V1 (R ≥ S), usually with right axis deviation. It also notes that a qR pattern in V1 or V3R may occur (Harrison's Principles of Internal Medicine 22E, Cardiac Enlargement and Hypertrophy). Barash's Clinical Anesthesia gives an R/S ratio greater than 1 in V1 as the RVH criterion. Goldman-Cecil gives the Sokolow-Lyon criterion for RVH as R in V1 plus S in V3 or V6 of at least 1.05 mV.
Other causes of a dominant R in V1
  • Right bundle branch block
  • Posterior MI
  • WPW syndrome with a left-sided pathway
  • Normal variant with early R wave progression
I did not run a new PubMed search for this follow-up. The first answer's search found nothing that changes basic ECG electrophysiology.

What causes RVH in COPD

Finding Sources
Searching PubMed

"Pulmonary Disease, Chronic Obstructive"[MeSH Terms] AND "Hypertension, Pulmonary"[MeSH Terms]

RVH in COPD is cor pulmonale. The right ventricle hypertrophies because chronic lung disease raises pulmonary artery pressure, so it must work against a sustained pressure load.
Causes of the raised pulmonary vascular resistance
  1. Chronic alveolar hypoxia with hypoxic pulmonary vasoconstriction (the main mechanism). In hypoventilated or poorly perfused lung units, low alveolar oxygen constricts the small pulmonary arterioles. This is a reflex that reduces V/Q mismatch. When it is extensive and sustained, pulmonary artery pressure rises and, if severe and prolonged, cor pulmonale follows (Fishman's Pulmonary Diseases and Disorders, Arterial Hypoxemia).
  2. Pulmonary vascular remodeling. Chronic hypoxia leads to intimal hyperplasia, smooth muscle hypertrophy and fibrosis of the small pulmonary arteries (Rosen's Emergency Medicine, Anatomy/Physiology/Pathophysiology).
  3. Loss of the pulmonary capillary bed. Emphysematous destruction of lung parenchyma reduces the total cross-sectional area of the vascular bed. The same section of Rosen's lists this together with hypoxic vasoconstriction.
  4. Hypercapnia and acidosis. Respiratory acidosis during exacerbations adds to pulmonary vasoconstriction.
  5. Polycythemia. Chronic hypoxia increases red cell mass, which raises blood viscosity and the work of the right ventricle.
  6. Hyperinflation. Raised intrathoracic and alveolar pressures compress alveolar capillaries and increase right ventricular afterload.
  7. Endothelial dysfunction. I am adding this from general knowledge, not from the retrieved textbook passages. Reduced nitric oxide and prostacyclin and increased endothelin contribute to the vasoconstriction and remodeling.
Result: pulmonary hypertension, then right ventricular pressure overload, then RVH and dilatation. Right heart failure follows if this continues. The ECG shows the pattern we discussed: a tall R in V1, right axis deviation, and P pulmonale.
Clinical points
  • Long-term oxygen therapy is indicated when PaO2 is 55 mmHg or less at rest, or 60 mmHg or less with evidence of cor pulmonale or polycythemia (Swanson's Family Medicine Review, Treatment). It reduces hypoxic vasoconstriction and improves survival.
  • High altitude worsens hypoxic vasoconstriction, so COPD patients there face an increased risk of cor pulmonale (Rosen's Emergency Medicine, Respiratory Illnesses).
Recent evidence: A 2025 SEPAR systematic review and position paper covers diagnosis of pulmonary hypertension in lung disease. A 2025 systematic review examined PAH-approved drugs in COPD-associated pulmonary hypertension. Neither changes the mechanism above. They concern diagnosis and treatment, and I did not read their full text.
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