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 GTN, exercise PAWP was 32.2 +/- 6.1 mmHg and V/V O2 was 33.8 +/- 7.7 l/l (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 l/l (124% of predicted) (p < 0.05). Exercise physiologic dead space (VD/VT) 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 VD/VT. 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.
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 GTN, exercise PAWP was 32.2 +/- 6.1 mmHg and V/V O2 was 33.8 +/- 7.7 l/l (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 l/l (124% of predicted) (p < 0.05). Exercise physiologic dead space (VD/VT) 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 VD/VT. 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.
Authors: A J Coats; S Adamopoulos; A Radaelli; A McCance; T E Meyer; L Bernardi; P L Solda; P Davey; O Ormerod; C Forfar Journal: Circulation Date: 1992-06 Impact factor: 29.690
Authors: G S Roubin; S D Anderson; W F Shen; C Y Choong; M Alwyn; S Hillery; P J Harris; D T Kelly Journal: J Am Coll Cardiol Date: 1990-04 Impact factor: 24.094