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Ventilatory Instability in Patients With Congestive Heart Failure and Nocturnal Cheyne-Stokes Breathing
Author(s) -
Mansoor M. Ahmed,
Carl Serrette,
M. Kryger,
N. R. Anthonisen
Publication year - 1994
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/17.6.527
Subject(s) - ventilation (architecture) , hyperoxia , hyperventilation , medicine , heart failure , anesthesia , cardiology , periodic breathing , respiratory minute volume , hypoxia (environmental) , ejection fraction , respiratory system , lung , oxygen , chemistry , mechanical engineering , organic chemistry , engineering
Many of the factors that appear to cause Cheyne-Stokes Breathing (CSB) in sleeping patients with congestive heart failure (CHF) are present during wakefulness. We studied the stability of ventilatory pattern in nine awake CHF patients (left ventricular ejection fraction 9-48%) who demonstrated CSB only while asleep and compared results with 13 age-matched normals. The test involved brief (30-50-second) exposure to hypoxia (end-tidal PO2 = 55 Torr) followed by breathing pure oxygen. During hypoxia, ventilation increased about 40% above air breathing control in both groups, whereas end-tidal CO2 declined to 92% of control in both groups. During hyperoxia, however, breathing pattern differed between groups. In the normals, ventilation gradually declined to air-breathing levels and did not significantly undershoot. In the patients, ventilation dropped more rapidly to baseline and an overshoot was present with ventilation being 72% and air-breathing control at 45 seconds of hyperoxia. Circulatory delay was calculated from the time interval between alveolar hypoxia and in increase in ventilation, and when corrections for circulatory delay were applied to ventilation during hyperoxia the differences between groups increased in that the patients' ventilation was less than baseline immediately after the delay. In the normals, the gradual decline in hyperoxic ventilation probably represents the decay of short-term potentiation (STP) activated by hypoxic hyperventilation. Results in the patients were compatible with absence of such STP decay, but could also have been due to a reduction in ventilatory drive early in hyperoxia related to prolonged circulation times.(ABSTRACT TRUNCATED AT 250 WORDS)

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