Ventilatory and Pulmonary Vascular Responses to Acute Hypoxia Are Nonuniform in Healthy Man

Abstract

The present study was undertaken to examine the pulmonary vascular and ventilatory responses to acute hypoxia in healthy individuals. Pulmonary hemodynamics and minute ventilation (V_E) were serially measured during inhalation of 13% O₂ for 15 min. There was a wide variability in the pulmonary vascular response to acute hypoxia, and a significant negative correlation between the initial increase in V_E after the start of hypoxia (ΔV_E) and the percent increase in mean pulmonary arterial pressure (r = -0.646; p < 0.01). The fall in arterial oxygen tension significantly decreased in response to an increase in ΔV_E. These results support the view that a blunted ventilatory response to acute hypoxic stimulation enhances alveolar hypoxia, thereby favoring the constriction of pulmonary vasculature. Thus, our results suggest that the ventilatory response to acute hypoxia plays a significant role in the pulmonary vascular response to acute hypoxia.

High Altitude Pulmonary Edema

“…The radiographic appearance of HAPE is more homogeneous and diffuse in advanced cases and during recovery [13][14][15], Moreover, in patient suffering from two episodes of HAPE. the similarity of radiograph ic appearance between the two episodes was at random, suggesting that structural abnormalities do not account for edema location [14] [43] and reducing the number of recruitable vessels. Further more, microneurography in HAPE subjects demonstrates increased muscle sympathetic activity during hypoxia at low altitude and prior to HAPE at high altitude [44], In accordance with these findings, increased plasma and/or urinary levels of norepinephrine compared to controls were found to precede [45] Fig.…”

Pulmonary Heart Disease: The Heart‐Lung Interaction and its Impact on Patient Phenotypes

“…Studies in healthy human volunteers and patients with COPD have shown that pulmonary hypertension in response to acute hypoxia represents an aggregate effect of both a modest increase in the cardiac output (CO) and increased pulmonary vascular resistance (PVR). [7–9] The variability in the HPV response is likely multifactorial, but seems to relate in part to the degree of muscularization of the pulmonary arteries at baseline, modulating effects of blood pH, and possibly genetic predisposition. [10] Acute correction of hypoxia with supplemental oxygen exerts the opposite hemodynamic effects, with the fall in pulmonary artery pressure typically occurring due to reductions in heart rate, stroke volume, and PVR; as with HPV, changes in mean pulmonary artery pressure (mPAP) to oxygen are variable.…”

“…This serves to lessen the amplifying effect of a falling pH on HPV. [ 7 , 14 ] Thus, patients with both hypoxia and hypercapnia (i.e., obesity hypoventilation) are at greater risk of developing PH in response to hypoxia; this may explain why patients with sleep‐disordered breathing generally require both daytime hypoxia and hypercapnia to develop significant daytime pulmonary hypertension. [ 15 ] We will discuss important extracardiac physiological effects of hypercapnia below.…”