Evaluation of hypotension following induction of general anaesthesia due to thiopentone, propofol and etomidate using perfusion index



general anaesthesia, induction, perfusion index, hypotension, blood pressure, echocardiogram, myocardial depression, ejection fraction


Background: Whether peripheral vasodilation or decrease in cardiac output causes the reduction in blood pressure (BP) following induction of anaesthesia, is not clearly understood. Therefore, an attempt was made to elucidate the mechanism of hypotension in terms of change in perfusion index (PI) and cardiac output.

Methods: With institutional ethics committee permission and consent, 66 patients were assigned equally to three groups. Each group received a titrated dose of a different induction agent, namely thiopentone (5 mg/kg), propofol (2 mg/kg) or etomidate (0.3 mg/kg). PI, heart rate (HR), and systolic, diastolic and mean arterial pressure were recorded at baseline and then every minute until 10 minutes post intubation. Echocardiography parameters (i.e. ejection fraction (EF), contractility and left ventricular end diastolic volume (LVEDV)) were measured at baseline, three minutes post induction and five minutes post intubation. Statistical analysis included one-way analysis of variance (ANOVA), Bonferroni test or Kruskal Wallis/Mann Whitney-U test.

Results: The EF and contractility remained stable after induction with all three induction agents. However, LVEDV and hence stroke volume increased significantly with etomidate (p = 0.011). There was gradual and continued increase in PI and reduction in the BP from the time of induction, which was minimal with etomidate and maximum with propofol. A marginal increase in HR was seen with thiopentone, while others caused a steady fall.

Conclusion: Vasodilation and reduced HR were responsible for the hypotension following induction of anaesthesia by intravenous agents. The effect was maximal with propofol with no evidence of myocardial depression. Etomidate lead to increase in stroke volume which explains its cardiovascular stability.

Author Biographies

A Kalluri, K S Hegde Medical Academy

Department of Anaesthesiology and Critical Care, K S Hegde Medical Academy, India

SG Mehandale, K S Hegde Medical Academy

Department of Anaesthesiology and Critical Care, K S Hegde Medical Academy, India


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