VENTILATORY POSTSTIMULUS POTENTIATION IN PATIENTS WITH BRAIN-DAMAGE

In normal humans when a brief hypoxic ventilatory stimulus is terminat ed abruptly by breathing 100% O-2, ventilation during hyperoxia gradua lly 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 hig her center inputs. STP decay may be important in preventing periodic b reathing 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 tracheostomize d patients with severe brain damage (Glasgow score 9.9 +/- 0.6) were s tudied. Breathing stability was estimated by at least 6 h of capnograp hy and from these records apnea index (Al, episodes/hour) and cyclic c hanges of end-tidal CO2 (c-PET(CO2), cycles/hour) were derived. TTP ac tivation was examined by brief exposure to hypoxia (45 s, end-tidal O- 2 = 50 mm Hg) followed by hyperoxia. Forty-four hypoxic-hyperoxic runs were analyzed and compared with 19 normoxic-hyperoxic trials. At the end of hypoxia ventilation (V-I) increased 39.5 +/- 5.8% and PET(CO2) decreased 2.7 +/- 0.6 mm Hg to 91.5 +/- 2.2% of baseline value. When h ypoxia was terminated abruptly by hyperoxia V-I dropped immediately to 63.2 +/- 7.2% of baseline, remaining for 35 s significantly lower tha n the corresponding values acquired during hyperoxia after normoxia. A fter hypoxia, apneas occurred in 19 of 44 hyperoxic runs. There was a negative relationship between nadir hyperoxic ventilation after hypoxi a and both Al and c-PET(CO2). Our results indicate that patients with brain damage, contrary to normal humans, hypoventilate after brief hyp oxia, and the degree of hypoventilation is related to breathing instab ility. We concluded that V-L in patients with brain damage and unstabl e breathing is largely dependent on chemical stimuli, perhaps because of abnormally rapid STP decay, which may contribute to periodic breath ing.