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A Test of the Ventilatory Response to Hypoxia and Hypercapnia for Clinical Use
Author(s) -
Hensley M. J.,
Read D. J. C.
Publication year - 1977
Publication title -
australian and new zealand journal of medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.596
H-Index - 70
eISSN - 1445-5994
pISSN - 0004-8291
DOI - 10.1111/j.1445-5994.1977.tb04396.x
Subject(s) - hypercapnia , hypoxia (environmental) , medicine , pco2 , anesthesia , respiration , ventilation (architecture) , oxygen , chemistry , acidosis , mechanical engineering , organic chemistry , engineering , anatomy
Summary:A test of the ventilatory response to hypoxia and hypercapnia for clinical use . M. J. Hensley and D. J. C. Read, Aust. N.Z. J. Med ., 1977, 7 , pp. 362–367. A new technique is described for testing the ventilatory response to hypoxia and to hypercapnia The test consists of interposing 15–20 seconds of hypoxia in 3–4 minutes of rebreathing 7% CO 2 ; the hypoxia is induced by taking three to five breaths from a bag containing N 2 , and CO 2 at an identical level. When required, hypoxic tests can be performed at several different PCO 2 levels to define the interaction of hypoxic and hypercapnic stimuli In eight healthy subjects, 29 hypoxic tests were performed, at an average PCO 2 of 58 mm Hg (range 53–64). The correlation between ventilatory increments and 0 2 ‐desaturation was significant in 27 of the 29 tests (r = 0.81‐0.99). At the minimum 0 2 ‐saturation (average 85%; range 75–91%) there was a statistically significant ventilatory response to hypoxia in all 29 tests (average +60%; range +14 to +141%). At 90% O 2 ‐saturation, the average increment of ventilation was +48% This method has important theoretical and practical advantages for clinical studies: (i) the test involves only 15–20 seconds of hypoxia; (ii) since the hypoxic drive to breathing is greatly enhanced by hypercapnia only a mild degree of hypoxaemia is necessary to obtain a clearly defined response; (iii) the augmented ventilation, produced by rebreathing, allows N 2 to be rapidly introduced into the lungs without the need for voluntarily imposed deep breathing; (iv) the elevated PCO 2 increases cerebral blood flow and minimises brain tissue hypoxia. (v) Since rebreathing 7% CO 2 greatly reduces mixed venous‐arterial and cerebral tissue‐arterial PCO 2 differences, the cerebral tissue PCO 2 and CO 2 stimulus are virtually unaffected by both ventilatory and cerebral blood flow responses in this test