Osama Abou Arab1, Marc Olivier Fischer2, Alexis Carpentier2, Christophe Beyls2, Pierre Huette3, Abdel Hchikat3, Amar Benammar2, Beatris Labont2, Yazine Mahjoub4, Stéphane Bar5, Pierre-Grégoire Guinot6, Emmanuel Lorne7. 1. Medical doctor, Department of Anaesthesiology and Critical Care Medicine, Amiens Picardy University Hospital, Amiens, 80054, France; MP3CV, EA7517, CURS, Jules Verne University of Picardie, 80054 Amiens, France. Electronic address: osama.abouarab@gmail.com. 2. Medical doctor, Department of Anaesthesiology and Critical Care Medicine, Amiens Picardy University Hospital, Amiens, 80054, France. 3. Medical doctor, Department of Anaesthesiology and Critical Care Medicine, CHU de Caen, Anaesthesiology. Caen University Hospital. Caen, 14000, France. 4. Professor, Department of Anaesthesiology and Critical Care Medicine, Dijon University Hospital, Dijon, 14033 France; SSPC (Simplification des Soins des Patients Complexes) - Clinical Research Unit, University of Picardie Jules Verne, 80054 Amiens Cedex 01, France. 5. Medical doctor, Department of Anaesthesiology and Critical Care Medicine, Amiens Picardy University Hospital, Amiens, 80054, France; SSPC (Simplification des Soins des Patients Complexes) - Clinical Research Unit, University of Picardie Jules Verne, 80054 Amiens Cedex 01, France. 6. Professor, Department of Anaesthesiology and Critical Care Medicine, Dijon University Hospital, Dijon, 14033 France. 7. Professor, Department of Anaesthesiology and Critical Care Medicine, Amiens Picardy University Hospital, Amiens, 80054, France; SSPC (Simplification des Soins des Patients Complexes) - Clinical Research Unit, University of Picardie Jules Verne, 80054 Amiens Cedex 01, France.
Abstract
INTRODUCTION: Anaesthesia frequently induces hypotension. Several recent studies have analysed arterial elastance (Ea) in order to describe clinical variations of mean arterial pressure (MAP). The objective of the study was to assess Ea to explain MAP variation following etomidate induction. METHODS: We conducted a prospective single-centre study. Inclusion criteria were patients undergoing elective cardiac surgery with invasive blood pressure monitoring. Ea was expressed as Pes/SV (Pes: end systolic pressure, SV: stroke volume). Cardiac index (CI), peripheral vascular resistance (PVR) and arterial compliance (C) was compared before and 2 minutes after etomidate induction. Arterial hypotension was defined as a decrease greater than 15% of the baseline MAP. RESULTS: Of the 45 patients included, 24 (53%) had a preserved MAP and 21 (47%) had an etomidate-induced hypotension. Ea was similar before induction and decreased in the decreased MAP group 2 minutes after induction (2.0 mmHg.ml-1 [1.7-2.4] vs 1.4 mmHg.ml-1 [0.9-1.9]; p = 0.001). Arterial compliance (C) increased in the decreased MAP group 2 minutes after induction (0.8 ml. mmHg-1 [0.6-1.0] vs 0.5 ml. mmHg-1 [0.4-0.6], p < 0.0001). No significant change in CI or PVR was observed between patients with or without etomidate-induced hypotension. CONCLUSION: Etomidate-induced hypotension was associated to a decrease in Ea. Ea variations can mainly be explained by induced changes in arterial compliance.
INTRODUCTION: Anaesthesia frequently induces hypotension. Several recent studies have analysed arterial elastance (Ea) in order to describe clinical variations of mean arterial pressure (MAP). The objective of the study was to assess Ea to explain MAP variation following etomidate induction. METHODS: We conducted a prospective single-centre study. Inclusion criteria were patients undergoing elective cardiac surgery with invasive blood pressure monitoring. Ea was expressed as Pes/SV (Pes: end systolic pressure, SV: stroke volume). Cardiac index (CI), peripheral vascular resistance (PVR) and arterial compliance (C) was compared before and 2 minutes after etomidate induction. Arterial hypotension was defined as a decrease greater than 15% of the baseline MAP. RESULTS: Of the 45 patients included, 24 (53%) had a preserved MAP and 21 (47%) had an etomidate-induced hypotension. Ea was similar before induction and decreased in the decreased MAP group 2 minutes after induction (2.0 mmHg.ml-1 [1.7-2.4] vs 1.4 mmHg.ml-1 [0.9-1.9]; p = 0.001). Arterial compliance (C) increased in the decreased MAP group 2 minutes after induction (0.8 ml. mmHg-1 [0.6-1.0] vs 0.5 ml. mmHg-1 [0.4-0.6], p < 0.0001). No significant change in CI or PVR was observed between patients with or without etomidate-induced hypotension. CONCLUSION:Etomidate-induced hypotension was associated to a decrease in Ea. Ea variations can mainly be explained by induced changes in arterial compliance.