Objective: Vectorcardiography (VCG) QRS loop area is thought to reflect hemodynamic abnormalities in cardiac lesions. The aim of the present study was to evaluate the response of VCG QRS loop area and intrapulmonary flow (PF) to acute hypoxia in patients with chronic bronchitis (CB) and pulmonary arterial hypertension (PAH). Methods: One-hundred and eleven patients (mean age 45.0±1.0 years) with chronic bronchitis (CB) and 43 comparable healthy subjects were included into the study. Diagnosis of CB was based on clinical, radiological, spirography and oximetry investigations. Cardiac catheterization, 2-dimensional and Doppler echocardiography, VCG by Mcfee-Parungao (VCG) and electrocardiography were used to establish PAH and right ventricular hypertrophy (RVH). Pulmonary flow was studied using impedance plethysmography (IP). Vectorcardiography, IP and Doppler echocardiography were also performed to assess the changes in QRS loop area, PF and mean pulmonary artery pressure (PAPm) in response to acute hypoxia (inhalation of hypoxic mixture 16% O2 for 5-10 minutes) in 21 patients with CB and 7 healthy subjects. Results: At baseline, patients with CB were characterized by pulmonary ventilation disturbances of mixed and obstructive types. Among patients who underwent acute hypoxia test PAPm was increased in 10 patients (29.2±2.1 mmHg) (Group 1), while in the latter 11 patients the PAPm was within normal values (16.5+1.8 mmHg) (Group 2). The IP showed reduction of PF and increase in pulmonary vascular resistance. Patients with CB react to the acute hypoxic test by increase in PAPm by 32% (absolute increase up to 22.5±0.7 mm Hg) in group 2 and by 38.9% (absolute increase up to 39.7±2.1 mmHg) in patients of group 1. There was a displacement of PF on IP to the upper and middle zones of lungs during acute hypoxia: PF in the upper and middle zones of the right lung increased by 35.6% and 32.5% in patients of group 2; while in patients of group 1 the PF increased by 33.5% and 4.8% at the same zones. On VCG QRS loop area was enhanced significantly in horizontal plane by 68% (p<0.05), but more significant changes were recorded in the anterior direction (by 75%, p<0.02) during acute hypoxia. Conclusion: Thus, in patients with early stages of PAH, changes in PF and QRS loop area during acute hypoxia may reflect the compensatory redistribution of pulmonary flow in response to hypoxia.