G. Bernardin et al., Influence of alveolar ventilation changes on calculated gastric intramucosal pH and gastric-arterial PCO2 difference, INTEN CAR M, 25(3), 1999, pp. 269-273
Objective: To evaluate the influence of changes in alveolar ventilation on
the following tonometry-derived variables: gastric intramucosal CO2 tension
(PtCO2), gastric arterial CO, tension difference (PgapCO2), gastric intram
ucosal pH and arterial pH-pHi difference (pH(gap)).
Design: Clinical prospective study.
Setting: A medical intensive care unit in a university hospital.
Patients: Ten critically ill, mechanically ventilated patients requiring he
modynamic monitoring with pulmonary artery catheter.
Interventions: Gastric tonometer placement. A progressive increase in tidal
volume (V-T) from 7 to 10 ml/kg followed by an abrupt return to baseline V
-T level.
Measurements and main results: Tonometer saline PtCO2 and hemodynamic data
were collected hourly at various V-T levels: H0 and H0' (baseline V-T = 7 m
l/kg), H1 (V-T = 8 ml/kg), H2 (V-T = 9 ml/kg) H3 (V-T = 10 ml/kg), H4 (base
line V-T). During the "hyperventilation phase" (H0-H3), pHi (p < 0.01) and
pH(gap) (p < 0.05) increased but PgapCO2 remained unchanged. Cardiac output
(CO) was not affected by ventilatory change. During the "hypoventilation p
hase" (H3-H4), pHi fell from 7.27 +/- 0.11 to 7.23 +/- 0.09 (p < 0.01) and
PgapCO2 decreased from 16 +/- 5 mmHg to 13 +/- 4 mmHg (p < 0.05). V-T reduc
tion was associated with a significant cardiac output elevation (p < 0.05).
Conclusions: PaCO2 and PtCO2 are similarly influenced by the changes in alv
eolar ventilation. Unlike pHi, the PgapCO2 is not affected by ventilation v
ariations unless CO changes are associated.