Microcirculatory alterations induced by sedation in intensive care patients. Effects of midazolam alone and in association with sufentanil.

INTRODUCTION

Sedation is widely used in intensive care unit (ICU) patients to limit the risk of pulmonary barotrauma and to decrease oxygen needs. However, adverse effects of cc5128sedation have not been fully evaluated; in particular, effects of benzodiazepine and opiates on microcirculation have not been extensively studied. The aim of this study was to evaluate the microcirculatory effects of a sedation protocol commonly prescribed in the ICU.

METHODS

Ten non-septic patients under controlled ventilation requiring sedation for therapeutic purposes were enrolled in a prospective observational study conducted in an ICU of a university hospital. Sedation was conducted in two successive steps: first, each patient received midazolam (0.1 mg/kg per hour after a bolus of 0.05 mg/kg, then adapted to reach a Ramsay score of between 3 and 5). Second, after one hour, sufentanil was added (0.1 microg/kg per hour after a bolus of 0.1 microg/kg). Arterial pressure, heart rate, cardiac output determined by transthoracic impedance, transcutaneous oxygen (tcPO2) and carbon dioxide (tcPCO2) pressures, and microcirculatory blood flow determined by laser Doppler flowmetry at rest and during a reactive hyperaemia challenge were measured before sedation (NS period), one hour after midazolam infusion (H period), and one hour after midazolam-sufentanil infusion (HS period).

RESULTS

Arterial pressure decreased in both sedation periods, but heart rate, cardiac output, tcPO2, and tcPCO2 remained unchanged. In both sedation periods, microcirculatory changes occurred with an increase in cutaneous blood flow at rest (H period: 207 +/- 25 perfusion units [PU] and HS period: 205 +/- 25 PU versus NS period: 150 +/- 22 PU, p < 0.05), decreased response to ischaemia (variation of blood flow to peak: H period: 97 +/- 16 PU and HS period: 73 +/- 9 PU versus NS period: 141 +/- 14 PU, p < 0.05), and attenuation of vasomotion.

CONCLUSION

Sedation with midazolam or a combination of midazolam and sufentanil induces a deterioration of vasomotion and microvascular response to ischaemia, raising the question of whether this effect may further alter tissue perfusion when already compromised, as in septic patients.