Abnormal Cerebrovascular Responses to CO2 in Sleep Apnea Patients
Author(s) -
Jack A. Loeppky,
Fernando G. Miranda,
Marlowe W. Eldridge
Publication year - 1984
Publication title -
sleep
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.222
H-Index - 207
eISSN - 1550-9109
pISSN - 0161-8105
DOI - 10.1093/sleep/7.2.97
Subject(s) - hyperventilation , medicine , anesthesia , pco2 , apnea , hypoxia (environmental) , hypercapnia , respiratory system , cerebral blood flow , vascular resistance , cardiology , respiration , hypocapnia , ventilation (architecture) , hemodynamics , chemistry , anatomy , oxygen , mechanical engineering , organic chemistry , engineering
The responses of common carotid blood flow (CCF), pressure (BP), and resistance (R) to variations in respiratory gases were compared during waking periods in 10 sleep apnea patients (SA) and 10 healthy controls (N) of similar age. Respiratory gases were altered by 3-min CO2 rebreathing (RB), 3-min hyperventilation (HV), and 4-min hypoxia (HYP) procedures. CCF was measured continuously by a 5-MHz pulsed Doppler duplex scanner and R was calculated using brachial BP. During RB, which increased end-tidal PCO2 (PACO2) by 15 mm Hg, SA had a lower CCF and greater BP response and therefore a significantly different (positive) change in R compared with N. The ventilatory responses to CO2 were not significantly different. With HV the PACO2 fell by 13 mm Hg in both groups and CCF fell more markedly in SA than N with the same change in BP; therefore, R was increased significantly more in SA. The HYP results did not demonstrate a difference between groups. These results suggest that abnormal cerebrovascular responses to PACO2, initiated either by unusual vasoactive properties of cerebral resistance vessels or peculiar venous outlow patterns, may initiate or potentiate periodic breathing in SA by prolonging lung-to-brain circulation time.
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