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

Background: The mechanisms underlying the excessive ventilatory respon se to exercise in patients with cardiac failure are still not fully un derstood. Hypothesis: This study was undertaken to investigate the mec hanisms behind exercise hyperpnea in patients with exercise-induced le ft ventricular dysfunction. Methods: In 18 patients, aged 57-82 years, all with atherosclerotic lumbar aorta aneurysm and pulmonary artery w edge pressure (PAWP) > 25 mmHg during supine exercise, ventilation (V) , central hemodynamics, and arterial and venous blood gases were exami ned during supine rest and exercise, before and during infusion of gly ceryl trinitrate (GTN). Results: Before GTN, exercise PAWP was 32.2 +/ - 6.1 mmHg and V/V O-2 was 33.8 +/- 7.7 yl (130% of predicted). With G TN, exercise PAWP was markedly reduced to 15.3 +/- 3.8 mmHg (p < 0.001 ), whereas V/V O-2 was only marginally reduced to 32.3 +/- 3.0 yl (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 w as reduced from 5.20 +/- 0.31 to 5.10 +/- 0.24 kPa (p < 0.05). PvO(2) and cardiac output (CO), however, were unchanged, below normal. Conclu sion: The data show that exercise-induced hyperpnea was not substantia lly 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 per sistence of exercise hyperpnea and reduced PvO(2) after GTN is consist ent 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.