Matthew Miller1, Natalie Kruit2, Charlotte Heldreich3, Sandra Ware4, Karel Habig5, Cliff Reid5, Brian Burns5. 1. Aeromedical and Retrieval Service, Ambulance Service, New South Wales, Sydney, Australia; Kent Surry Sussex Air Ambulance, Marden, Kent, United Kingdom. Electronic address: mattdotmiller@gmail.com. 2. Department of Anaesthesia, Westmead Hospital, Sydney, Australia. 3. Department of Anaesthesia, Austin Hospital, Melbourne, Australia. 4. Aeromedical and Retrieval Service, Ambulance Service, New South Wales, Sydney, Australia; School of Molecular Bioscience, University of Sydney, New South Wales, Australia. 5. Aeromedical and Retrieval Service, Ambulance Service, New South Wales, Sydney, Australia; Sydney Medical School, Sydney University, New South Wales, Australia.
Abstract
STUDY OBJECTIVE: Ketamine is considered a stable induction agent for rapid sequence induction; however, hypotension rates up to 24% are reported. The shock index (shock index=pulse rate/systolic blood pressure [SBP]) may identify patients at risk of adverse hemodynamic change. We investigate whether SBP and pulse rate response to ketamine induction differ when patients are classified as being at risk of shock by their shock index. METHODS: We conducted a prospective observational study of electronically collected vital sign data from patients undergoing rapid sequence induction with ketamine. Patients were grouped into low shock index (shock index <0.9) or high shock index (shock index ≥0.9) preinduction. Pulse rate and SBP were compared between 3 minutes preinduction and for 3 measurements postinduction (3-minute intervals) by repeated-measures ANOVA. Proportions of patients developing hypotension or hypertension are also reported. RESULTS: One hundred twelve patients were enrolled (81 low shock index, 31 high shock index). Low shock index patients had increased SBP after induction (16 mm Hg; 95% confidence interval [CI] 11 to 21 mm Hg), whereas high shock index patients did not (2 mm Hg; 95% CI -4 to 7 mm Hg). Pulse rate in low shock index patients increased after induction (20 beats/min; 95% CI 16 to 25 beats/min) and remained elevated, whereas in high shock index patients a difference occurred at the second postinduction measurement only (15 beats/min; 95% CI 11 to 18 beats/min). More high shock index patients became hypotensive (26%; 95% CI 12% to 45%) than low shock index ones (2%; 95% CI 0% to 9%), whereas more low shock index patients became hypertensive (40%; 95% CI 29% to 51%) than high shock index ones (13%; 95% CI 4% to 30%). CONCLUSION: After ketamine induction, high shock index patients exhibited blunted hypertensive responses and more frequent hypotension, whereas low shock index patients had sustained increases in pulse rate and SBP.
STUDY OBJECTIVE:Ketamine is considered a stable induction agent for rapid sequence induction; however, hypotension rates up to 24% are reported. The shock index (shock index=pulse rate/systolic blood pressure [SBP]) may identify patients at risk of adverse hemodynamic change. We investigate whether SBP and pulse rate response to ketamine induction differ when patients are classified as being at risk of shock by their shock index. METHODS: We conducted a prospective observational study of electronically collected vital sign data from patients undergoing rapid sequence induction with ketamine. Patients were grouped into low shock index (shock index <0.9) or high shock index (shock index ≥0.9) preinduction. Pulse rate and SBP were compared between 3 minutes preinduction and for 3 measurements postinduction (3-minute intervals) by repeated-measures ANOVA. Proportions of patients developing hypotension or hypertension are also reported. RESULTS: One hundred twelve patients were enrolled (81 low shock index, 31 high shock index). Low shock index patients had increased SBP after induction (16 mm Hg; 95% confidence interval [CI] 11 to 21 mm Hg), whereas high shock index patients did not (2 mm Hg; 95% CI -4 to 7 mm Hg). Pulse rate in low shock index patients increased after induction (20 beats/min; 95% CI 16 to 25 beats/min) and remained elevated, whereas in high shock index patients a difference occurred at the second postinduction measurement only (15 beats/min; 95% CI 11 to 18 beats/min). More high shock index patients became hypotensive (26%; 95% CI 12% to 45%) than low shock index ones (2%; 95% CI 0% to 9%), whereas more low shock index patients became hypertensive (40%; 95% CI 29% to 51%) than high shock index ones (13%; 95% CI 4% to 30%). CONCLUSION: After ketamine induction, high shock index patients exhibited blunted hypertensive responses and more frequent hypotension, whereas low shock index patients had sustained increases in pulse rate and SBP.
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