Relationship between exercise hyperpnea, hemodynamics, and blood gases before and during glyceryl trinitrate infusion in patients with exercise- induced elevation of pulmonary artery wedge pressure

Abstract

Background: The mechanisms underlying the excessive ventilatory response to exercise in patients with cardiac failure are still not fully understood. Hypothesis: This study was undertaken to investigate the mechanisms behind exercise hyperpnea in patients with exercise-induced left ventricular dysfunction. Methods: In 18 patients, aged 57-82 years, all with atherosclerotic lumbar aorta aneurysm and pulmonary artery wedge pressure (PAWP) > 25 mmHg during supine exercise, ventilation (V), central hemodynamics, and arterial and venous blood gases were examined during supine rest and exercise, before and during infusion of glyceryl trinitrate (GTN). Results: Before GRIN, exercise PAWP was 32.2 ± 6.1 mmHg and V/V O2 was 33.8 ± 7.7 1/1 (130% of predicted). With GTN, exercise PAWP was markedly reduced to 15.3 ± 3.8 mmHg (p < 0.001), whereas V/V O2 was only marginally reduced to 32.3 ± 3.0 1/1 (124% of predicted) (p<0.05). Exercise physiologic dead space (V(D)/V(T)) declined from 0.31 ± 0.16 to 0.26 ± 0.17 (p<0.05), while PaCO2 was reduced from 5.20 ± 0.31 to 5.10 ± 0.24 kPa (p < 0.05). PvO2 and cardiac output (CO), however, were unchanged, below normal. Conclusion: The data show that exercise-induced hyperpnea was not substantially reduced by rapid normalization of PAWP and could not be related to preservation of normal PaCO2 in the presence of high V(D)/V(T). The persistence of exercise hyperpnea and reduced PvO2 after GTN is consistent with augmented ventilatory stimuli from hypoxia-induced metabolic abnormalities in the skeletal muscles, or/and persistently reduced CO, due to changes in the integrated superior command of ventilation and circulation.