Within-breath arterial Po-2 oscillations in an experimental model of acuterespiratory distress syndrome

Tidal ventilation causes within-breath oscillations in alveolar oxygen conc entration, with an amplitude which depends on the prevailing ventilator set tings. These alveolar oxygen oscillations are transmitted to arterial oxyge n tension, Pa-O2, but with an amplitude which now depends upon the magnitud e of venous admixture or true shunt, (Q) over dot(S)/(Q) over dot(T). We in vestigated the effect of positive end-expiratory pressure (PEEP) on the amp litude of the Pa-O2 oscillations, using an atelectasis model of shunt. Bloo d Pa-O2 was measured on-line with an intravascular Pa-O2 sensor, which had a 2-4 s response time (10-90%). The magnitude of the time-varying Pa-O2 osc illation was titrated against applied PEEP while tidal volume, respiratory rate and inspired oxygen concentration were kept constant. The amplitude of the Pa-O2 oscillation, Delta Pa-O2, and the mean P-O2 value varied with th e level of PEEP applied. At zero PEEP, both the amplitude and the mean were at their lowest values. As PEEP was increased to 1.5 kPa, both Delta Pa-O2 and the mean Pa-O2 increased to a maximum. Thereafter, the mean Pa-O2 incr eased but Delta Pa-O2 decreased. Clear oscillations of Pa-O2 were seen even at the lowest mean Pa-O2, 9.5 kPa. Conventional respiratory models of veno us admixture predict that these Pao, oscillations will be reduced by the st eep part of the oxyhaemoglobin dissociation curve if a constant pulmonary s hunt exists throughout the whole respiratory cycle. The facts that the Pa-O 2 oscillations occurred at all mean Pa-O2 values and that their amplitude i ncreased with increasing PEEP suggest that (Q) over dot(S)/(Q) over dot(T), in the atelectasis model, varies between end-expiration and end-inspiratio n, having a much lower value during inspiration than during expiration.