1986
DOI: 10.1378/chest.89.1.39
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Augmented Ventilatory Response to Exercise in Pulmonary Hypertension

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Cited by 54 publications
(30 citation statements)
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“…In contrast to Theodore et al [1986], we have observed a high degree of hyperpnea during the test as demon strated by the statistically different slopes of the line for minute ventilation over expira tory carbon dioxide production. Notwith standing the fact that both groups of patients (CABG and transplanted) had a ventilation in excess compared to normal subjects, in relation probably with the consequences of extracorporeal circulation (restrictive lung deficit) [Braun et al, 1978;Rea et al, 1978], heart recipients had a much higher degree of hyperpnea than the CABG patients.…”
Section: Discussioncontrasting
confidence: 80%
“…In contrast to Theodore et al [1986], we have observed a high degree of hyperpnea during the test as demon strated by the statistically different slopes of the line for minute ventilation over expira tory carbon dioxide production. Notwith standing the fact that both groups of patients (CABG and transplanted) had a ventilation in excess compared to normal subjects, in relation probably with the consequences of extracorporeal circulation (restrictive lung deficit) [Braun et al, 1978;Rea et al, 1978], heart recipients had a much higher degree of hyperpnea than the CABG patients.…”
Section: Discussioncontrasting
confidence: 80%
“…V′E-V′CO 2 slope was reduced significantly after surgical (thromboendarterectomy and lung transplant) intervention and the decreases were strongly related to the reduction in PVR post-surgery [87,88]. V′E-V′CO 2 indices respond to pharmacological interventions: with phosphodiesterase-5 inhibitors [89], endothelin receptor antagonists [67] and prostanoids [90][91][92] in idiopathic PAH; with bosentan and sildenafil in adult patients with Eisenmenger syndrome [93]; and with beraprost in patients with thromboembolic pulmonary hypertension [94].…”
Section: Clinically Meaningful Differencementioning
confidence: 99%
“…The main underlying mechanisms are sympathetic overexcitation and increased chemosensitivity with hyperventilation-associated increased physiological dead space. Moreover, there is an inadequate increase in cardiac output during exercise, leading to a low mixed-venous and arterial oxygen saturation and early lactic acidosis that raises ventilatory requirements even further due to excessive CO 2 production (39,65,77). These mechanisms lead to arterial oxygen desaturation during exercise as a cardinal feature of PH with, consequently, reduced oxygen delivery to the muscles, the brain, and other organs, resulting in impaired exercise performance (28,37).…”
Section: Effect Of Hyperoxia On Exercise Performance In Patients With Phmentioning
confidence: 99%