Am. J. Respir. Crit. Care Med., Vol 152, No. 5, Nov 1995, 1627-1632.
Ventilatory post-stimulus potentiation in patients with brain damage
D Georgopoulos, I Mitrouska, K Koletsos, K Markopoulou, D Riggos, D Patakas and NR Anthonisen
General Hospital G. Papanicolaou, Department of Pulmonary and Critical Care Medicine, University of Thessaloniki, Exoxi, Greece.
In normal humans when a brief hypoxic ventilatory stimulus is terminated
abruptly by breathing 100% O2, ventilation during hyperoxia gradually
declines to baseline prehypoxic levels without an undershoot. This has been
interpreted as evidence of decay of short-term potentiation (STP), a
mechanism located in the brainstem and not dependent upon higher center
inputs. STP decay may be important in preventing periodic breathing by
damping ventilatory responses to cyclic stimuli. Patients with brain damage
commonly have periodic breathing that may be caused partly by impairment of
STP activation. To test this 12 tracheostomized patients with severe brain
damage (Glasgow score 9.9 +/- 0.6) were studied. Breathing stability was
estimated by at least 6 h of capnography and from these records apnea index
(AI, episodes/hour) and cyclic changes of end-tidal CO2 (c-PETCO2,
cycles/hour) were derived. STP activation was examined by brief exposure to
hypoxia (45 s, end-tidal O2 = 50 mm Hg) followed by hyperoxia. Forty-four
hypoxic-hyperoxic runs were analyzed and compared with 19
normoxic-hyperoxic trials. At the end of the hypoxia ventilation (VI)
increased 39.5 +/- 5.8% and PETCO2 decreased 2.7 +/- 0.6 mm Hg to 91.5 +/-
2.2% of baseline value. When hypoxia was terminated abruptly by hyperoxia
VI dropped immediately to 63.2 +/- 7.2% of baseline, remaining for 35 s
significantly lower than the corresponding values acquired during hyperoxia
after normoxia. After hypoxia, apneas occurred in 19 of 44 hyperoxic runs.
There was a negative relationship between nadir hyperoxic ventilation after
hypoxia and both AI and c-PETCO2.(ABSTRACT TRUNCATED AT 250 WORDS)
