Open AccessRelationship between exercise hyperpnea, hemodynamics, and blood gases before and during glyceryl trinitrate infusion in patients with exercise‐induced elevation of pulmonary artery wedge pressure
Author(s) -
Jørgensen Lars H.,
Thaulow Erik,
Refsum Harald E.
Publication year - 1997
Publication title -
clinical cardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.263
H-Index - 72
eISSN - 1932-8737
pISSN - 0160-9289
DOI - 10.1002/clc.4960200912
Subject(s) - medicine , hyperpnea , supine position , cardiology , pulmonary wedge pressure , cardiac output , anesthesia , hemodynamics , physical exercise , pulmonary artery , respiratory minute volume , ventilation (architecture) , respiratory system , mechanical engineering , engineering
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 O 2 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 O 2 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 PaCO 2 was 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. 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 PaCO 2 in the presence of high V D /V T . The persistence of exercise hyperpnea and reduced PvO 2 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.