title: Cardiovascular response to acute airway obstruction and hypoxia.
abstract: We wished to evaluate the role of hypoxia in the production of cardiovascular manifestations of acute airway obstruction. We monitored blood pressure, electrocardiogram, and radionuclide ejection fraction in 14 healthy volunteers on exposure to four experimental conditions: expiratory resistive loading while breathing room air (RAL), expiratory resistive loading while hypoxic (HL), hypoxia alone (H), and expiratory resistive loading while voluntarily hyperventilating in a pattern similar to HL trials (VL). Mean respiratory-related oscillation in systolic blood pressure (pulsus paradoxus) increased significantly under each experimental condition compared with those at baseline (2 +/- 2.3 mm Hg): for RAL, 21 +/- 8.4 mm Hg; for HL, 34 +/- 16.3 mm Hg; for H, 10 +/- 5.4 mm Hg; for VL 26 +/- 13.4 mm Hg. Pulsus paradoxus was significantly greater under conditions of moderate hypoxia (saturation, 80%) than of mild hypoxia (saturation, 90%). Electrocardiographic changes were more marked under HL and H conditions than under RAL and VL conditions. HL induced changes in blood pressure and frontal QRS axis that were qualitatively similar to those seen in naturally occurring asthma. Radionuclide ejection fraction showed no dramatic change with any experimental condition. We conclude that hypoxia magnifies the cardiovascular changes induced by acute expiratory resistive loads and may contribute to the degree of pulsus paradoxus seen in severe asthma.
authors.affiliation: Division of Respiratory Medicine, Toronto Western Hospital, Ontario, Canada.
authors.forename: K R
authors.initials: KR
authors.lastname: Chapman
authors.forename: A D
authors.initials: AD
authors.lastname: D'Urzo
authors.forename: M N
authors.initials: MN
authors.lastname: Druck
authors.forename: A S
authors.initials: AS
authors.lastname: Rebuck
mesh_terms: D000208:Acute Disease; D000328:Adult; D000402:Airway Obstruction / Q000503:physiopathology*; D000403:Airway Resistance; D002319:Cardiovascular System / Q000503:physiopathology*; D005260:Female; D006801:Humans; D006985:Hyperventilation / Q000503:physiopathology; D000860:Hypoxia / Q000503:physiopathology*; D012119:Respiration