A Casati1, I Salvo, G Torri, E Calderini. 1. Department of Anaesthesia and Intensive Care, IRCCS H S. Raffaele, University of Milan.
Abstract
METHODS: One hundred and five ASA I-II patients, scheduled for elective surgical procedures were studied in order to evaluate the effect of different surgical postures on physiological pulmonary dead space (VDphys/ VT) and arterial to end-tidal carbon dioxide gradient [P(a-Et)CO2]. Patients were divided into four groups according to their position on the operating table: supine position (acting as control group, n = 33), 20 degree Trendelenburg position (n = 24), lateral position (n = 24) and prone position with convex saddle frame (n = 24). Physiologic dead space was measured using Enghoff modification of Bohr equation. Arterial CO2 partial pressure was measured by blood gas analysis and end tidal CO2 was measured by means of an infrared CO2 analyser. All measurements were performed 20 minutes after general anaesthesia induction, with patients mechanically ventilated by a constant inspiratory flow (TV = 8 ml kg-1, RR = 10-14, EIP = 10%) in order to reach a steady state end tidal CO2 ranging between 32 and 36 mmHg; afterwards surgery started. RESULTS: Arterial blood pressure showed a mean decrease of about 5-10% compared to baseline values, but no significant differences in arterial pressure decrease were found between the four groups. A significant VDphys/VT increase in postures other than supine was observed, unless it was statistically significant in lateral and prone position only; while P(a-Et)CO2 was higher in all postures compared to supine. Changes of intrapulmonary gas and blood distribution due to patients' posture are probably responsible for the observed physiologic dead space and CO2 gradient differences. CONCLUSIONS: In conclusion, the clinical practice of predicting PaCO2 from EtCO2 must be tempered by recognition of the potential magnitude of P(a-Et)CO2 gradient, which is higher than normal during general anaesthesia and further increased when positioning the patient other than supine.
METHODS: One hundred and five ASA I-II patients, scheduled for elective surgical procedures were studied in order to evaluate the effect of different surgical postures on physiological pulmonary dead space (VDphys/ VT) and arterial to end-tidal carbon dioxide gradient [P(a-Et)CO2]. Patients were divided into four groups according to their position on the operating table: supine position (acting as control group, n = 33), 20 degree Trendelenburg position (n = 24), lateral position (n = 24) and prone position with convex saddle frame (n = 24). Physiologic dead space was measured using Enghoff modification of Bohr equation. Arterial CO2 partial pressure was measured by blood gas analysis and end tidal CO2 was measured by means of an infrared CO2 analyser. All measurements were performed 20 minutes after general anaesthesia induction, with patients mechanically ventilated by a constant inspiratory flow (TV = 8 ml kg-1, RR = 10-14, EIP = 10%) in order to reach a steady state end tidal CO2 ranging between 32 and 36 mmHg; afterwards surgery started. RESULTS: Arterial blood pressure showed a mean decrease of about 5-10% compared to baseline values, but no significant differences in arterial pressure decrease were found between the four groups. A significant VDphys/VT increase in postures other than supine was observed, unless it was statistically significant in lateral and prone position only; while P(a-Et)CO2 was higher in all postures compared to supine. Changes of intrapulmonary gas and blood distribution due to patients' posture are probably responsible for the observed physiologic dead space and CO2 gradient differences. CONCLUSIONS: In conclusion, the clinical practice of predicting PaCO2 from EtCO2 must be tempered by recognition of the potential magnitude of P(a-Et)CO2 gradient, which is higher than normal during general anaesthesia and further increased when positioning the patient other than supine.
Authors: Daniel P Davis; Robyn Heister; Jennifer C Poste; David B Hoyt; Mel Ochs; James V Dunford Journal: Neurocrit Care Date: 2005 Impact factor: 3.210