Interaction between cold and hypoxia on pulmonary circulation in COPD.

Abstract

This study was designed to investigate the interaction of mild and localized cold exposure and hypoxia on pulmonary hemodynamics in chronic obstructive pulmonary disease (COPD). Nineteen patients with COPD were studied at sea level and seven at an altitude of 2,640 m. For all patients, pulmonary hemodynamic measurements were performed 10 min after insertion of a catheter in a femoral vein and following 10 min of cold exposure. Cold exposure was restricted to the forehead, and subjects breathed air at ambient temperature. Flow and temperature of air (1.5 L.s(-1), 5 degrees C) to the forehead were chosen to cool down the forehead skin to approximately 20 degrees C without discomfort for the subject. For the seven patients studied at high altitude, the same measurements were also performed after 5 min of oxygen supplementation with and without cold exposure. At sea level, an increase in pulmonary vascular resistance (PVR) during cold exposure was inversely related to the initial PaO2. In six severe hypoxic subjects (PaO2 < 50 mm Hg), PVR increased by 24%. At high altitude, PVR was significantly increased by 15%. After O2 supplementation, cold exposure did not induce an increase in PVR. We concluded that mild and localized cold exposure to the forehead only induced an increase in PVR in COPD patients with severe hypoxia. Moreover, in cold exposure responders, O2 supplementation negated the effect of cold exposure on pulmonary hemodynamics.

Blood pressure and plasma catecholamines in acute and prolonged hypoxia: effects of local hypothermia

“…The reduced fluid content would be ϳ0.3 liters (25). This agrees with earlier results showing an increased pulmonary reactivity to cold in longer lasting hypoxia (2,3).…”

“…In the pulmonary circulation, acute hypoxia in-duces in most species, including humans, an immediate arteriolar constriction, leading to elevated pulmonary BP (6). An increased pulmonary vascular responsiveness to adrenergic stimuli such as local cooling has been found in hypoxemic subjects (2). In normoxia a cold pressor test produces an exaggerated systemic pressor response in hypertension-prone subjects compared with normotensive individuals (20).…”

“…In healthy high-altitude (3,700 m) residents, a pronounced response to local facial cooling has been reported, because pulmonary vascular resistance increased by 23% (at a mean arterial PO 2 of 53 Torr) (3). Bedu et al (2) found a 15% increase in pulmonary vascular resistance in seven subjects with chronic obstructive pulmonary disease (COPD) and reduced arterial oxygen content at 2,650-m altitude as a response to 10 min of facial cooling. At sea level, six subjects with COPD and reduced arterial oxygen pressure (arterial PO 2 Ͻ50 Torr) had a pronounced increase in pulmonary vascular resistance (24%) and mean pulmonary pressure (8%) after facial cooling, whereas 13 subjects with COPD and higher oxygen pressures showed no changes.…”

Travel to high altitude with pre-existing lung disease

“…At altitude, alveolar hypoxia triggers HPV and further increases in Ppa, which may promote oedema formation or increase right heart strain. Cold exposure at high elevations may also contribute to increased pulmonary vascular resistance, although this effect can be blocked with supplemental oxygen administration [95]. Although no studies have examined the impact of hypobaric hypoxia on patients with COPD and pulmonary hypertension, it is reasonable to conclude that the risk of HAPE and acute right heart failure at high altitude will be greater than in patients without secondary pulmonary hypertension.…”

Time-dependent changes in pulmonary vascular responses to acute hypoxia during and after cold exposure in rats

“…In healthy high-altitude residents, cold exposure of the face increases pulmonary vascular resistance (PVR) (Douguet et al 1987). In addition, in patients with chronic obstructive pulmonary disease, cold exposure increases PVR and the increase in PVR is related inversely to the initial partial oxygen tension (Bedu et al 1996) and, oxygen supplementation negates the eVect of cold-induced pulmonary hypertension. These Wndings suggest an interaction between cold and hypoxia and/or an altered pulmonary vascular reactivity to cold during chronic hypoxia.…”