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

SummaryBackground: 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, ventila-

Excessive exercise ventilation in moderate left heart dysfunction. Influence of postural changes in central haemodynamics and blood gases

“…1), but no reduction of the hyperpnoea. This is in line with the effects of acute medical treatment in similar patients during supine exercise ( Jørgensen et al ., 1997 , 1999), indicting that the excessive ventilatory response is unrelated to acute pulmonary congestion.…”

“…The relationships between high V˙ / V˙ O 2 and low P v O 2 during lying and sitting exercise in the LHD patients ( Fig. 2) fit in with recent suggestions that the excessive ventilation is caused by a combination of signals from hypoxia‐induced disturbances in peripheral tissues, particularly in the working muscles ( Barlow et al ., 1994 ; Clark & Coats, 1994; Clark et al ., 1995 ; Sullivan & Hawthorne, 1995; Harrington & Coats, 1997; Jørgensen et al ., 1997 ; 1999), and augmented muscle ergo‐reflex and peripheral and central chemoreceptor activity ( Chua et al ., 1996 ; Piepoli et al ., 1996 ; 1999). However, the low exercise P v O 2 in the LHD patients reflects a poor CO response.…”

“…However, the low exercise P v O 2 in the LHD patients reflects a poor CO response. Thus, the data also fit in with studies demonstrating a close association between excessive ventilation and failing cardiac output ( Franciosa et al ., 1984 ; Jørgensen et al ., 1997 ), suggesting that the excessive ventilation is partly linked with changes in the integrated central control of circulation and ventilation ( Eldridge et al ., 1985 ; Daly, 1986). The exercise heart rate and systemic vascular resistance data indicate that the influence on the exercise ventilation of the neurohormonal systems activated by change of position and peripheral hypoxia most probably have been of minor importance.…”

“…Recent studies have emphasized the importance of stimuli from metabolic disturbances and structural changes in the exercising muscles ( Barlow et al ., 1994 ; Clark & Coats, 1994; Clark et al ., 1995 ; Sullivan & Hawthorne, 1995; Wilson, 1995; Piepoli et al ., 1996 ) and augmented ergoreflex and central and peripheral chemoreceptor activity ( Andreas et al ., 1996 ; Chua et al ., 1996 ; Piepoli et al ., 1999 ). Studies during acute medication, which prevents rise in PAWP, but leaves exercise ventilation ( V˙ ) unaltered high ( Fink et al ., 1986 ; Jørgensen et al ., 1997 ; 1999) and exercise mixed venous O 2 tension (P v O 2 ) and cardiac output (CO) unaltered low ( Jørgensen et al ., 1997 ; 1999), even after several hours, seem to support the latter, non‐pulmonary mechanisms.…”

Delayed respiratory response to exercise of short duration in patients with severe intermittent claudication due to bilateral atherosclerotic vascular disease: normalization after aorto‐bifemoral bypass operation

“…Several studies have demonstrated a close association between exertional hyperpnoea and cardiac dysfunction ( Clark & Coats, 1994; Sullivan & Hawthorne, 1995; Jørgensen et al ., 1997 ; Jørgensen et al ., 1999 ). Accordingly, the fact that part of the excessive ventilatory response to exercise observed pre‐operatively persisted after elimination of the peripheral vascular insufficiency, was probably because the patients showed distinct evidence of left heart disease, with marked left ventricular dysfunction during moderate exercise.…”