OBJECTIVE: To evaluate the influence of changes in alveolar ventilation on the following tonometry-derived variables: gastric intramucosal CO2 tension (PtCO2), gastric arterial CO2 tension difference (PgapCO2), gastric intramucosal pH (pHi) and arterial pH-pHi difference (pHgap). DESIGN: Clinical prospective study. SETTING: A medical intensive care unit in a university hospital. PATIENTS: Ten critically ill, mechanically ventilated patients requiring hemodynamic 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 ml/kg), H1 (V(T) = 8 ml/kg), H2 (V(T) = 9 ml/kg), H3 (V(T) = 10 ml/kg), H4 (baseline V(T)). During the "hyperventilation phase" (H0-H3), pHi (p<0.01) and pHgap (p<0.05) increased but PgapCO2 remained unchanged. Cardiac output (CO) was not affected by ventilatory change. During the "hypoventilation phase" (H3-H4), pHi fell from 7.27+/-0.11 to 7.23+/-0.09 (p<0.01) and PgapCO2 decreased from 16+/-5 mm Hg to 13+/-4 mm Hg (p<0.05). V(T) reduction was associated with a significant cardiac output elevation (p<0.05). CONCLUSIONS: PaCO2 and PtCO2 are similarly influenced by the changes in alveolar ventilation. Unlike pHi, the PgapCO2 is not affected by ventilation variations unless CO changes are associated.
OBJECTIVE: To evaluate the influence of changes in alveolar ventilation on the following tonometry-derived variables: gastric intramucosal CO2 tension (PtCO2), gastric arterial CO2 tension difference (PgapCO2), gastric intramucosal pH (pHi) and arterial pH-pHi difference (pHgap). DESIGN: Clinical prospective study. SETTING: A medical intensive care unit in a university hospital. PATIENTS: Ten critically ill, mechanically ventilated patients requiring hemodynamic 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 ml/kg), H1 (V(T) = 8 ml/kg), H2 (V(T) = 9 ml/kg), H3 (V(T) = 10 ml/kg), H4 (baseline V(T)). During the "hyperventilation phase" (H0-H3), pHi (p<0.01) and pHgap (p<0.05) increased but PgapCO2 remained unchanged. Cardiac output (CO) was not affected by ventilatory change. During the "hypoventilation phase" (H3-H4), pHi fell from 7.27+/-0.11 to 7.23+/-0.09 (p<0.01) and PgapCO2 decreased from 16+/-5 mm Hg to 13+/-4 mm Hg (p<0.05). V(T) reduction was associated with a significant cardiac output elevation (p<0.05). CONCLUSIONS:PaCO2 and PtCO2 are similarly influenced by the changes in alveolar ventilation. Unlike pHi, the PgapCO2 is not affected by ventilation variations unless CO changes are associated.