TY - JOUR
T1 - Myocardial metabolic and hemodynamic changes during propofol anesthesia for cardiac surgery in patients with reduced ventricular function
AU - Hall, R. I.
AU - Murphy, J. T.
AU - Landymore, R.
AU - Pollak, P. T.
AU - Doak, G.
AU - Murray, M.
PY - 1993
Y1 - 1993
N2 - This study examined the hypothesis that the use of propofol for induction and maintenance of anesthesia in patients with reduced ejection fraction (<0.5) undergoing coronary artery revascularization would not be associated with a greater degree or incidence of myocardial ischemia as compared to patients receiving a moderate dose sufentanil-enflurane anesthetic technique. Two groups of patients were assigned randomly to receive one of two propofol anesthetic regimes. Group A (n = 21) received propofol 1-2 mg/kg as the induction drug and sufentanil 0.03 μg · kg-1 · min-1 (fixed rate) plus propofol 50-200 μg · kg-1 · min-1 (variable rate) infusions for maintenance of anesthesia. Group B (n = 21) received sufentanil 5 μg/kg for induction and propofol 50-200 μg · kg-1 · min-1 (variable rate) infusion for maintenance of anesthesia. For comparison, a third group (Group C, n = 18) was studied subsequently. This group received sufentanil 5 μg/kg for induction of anesthesia which was maintained with enflurane. Adverse hemodynamic changes (hypertension, tachycardia) were managed by additional propofol (Groups A and B), sufentanil (Group C), or vasopressors (hypotension). Hemodynamic and myocardial metabolic profiles were measured when awake and sedated and at postinduction, postintubation, postincision, poststernotomy, and precardiopulmonary bypass times. Ischemia was assessed by measuring myocardial lactate production. The incidence of myocardial lactate production was reduced in Group B as compared to Group C (Group A, 45/126; Group B, 23/126; Group C, 58/107; P < 0.05). Myocardial lactate flux declined in all groups as surgery progressed; but apart from the reduction in flux (indicative of increased ischemia) noted in Group C versus Group B postinduction, no between-group differences were detected. No between-group differences were noted in hemodynamics, inotropic requirements to separate from cardiopulmonary bypass, complications, (e.g., myocardial infarction, cerebrovascular accident, death), or changes in laboratory variables (e.g., cortisol, high- and low density lipoproteins) pre- versus postoperative. Recovery from anesthesia was prolonged in Group B versus Group A but not versus Group C. We conclude that use of propofol in patients with reduced ejection fractions undergoing coronary artery revascularization provides satisfactory anesthetic control of hemodynamics and was not associated with an increased incidence or degree of myocardial ischemia.
AB - This study examined the hypothesis that the use of propofol for induction and maintenance of anesthesia in patients with reduced ejection fraction (<0.5) undergoing coronary artery revascularization would not be associated with a greater degree or incidence of myocardial ischemia as compared to patients receiving a moderate dose sufentanil-enflurane anesthetic technique. Two groups of patients were assigned randomly to receive one of two propofol anesthetic regimes. Group A (n = 21) received propofol 1-2 mg/kg as the induction drug and sufentanil 0.03 μg · kg-1 · min-1 (fixed rate) plus propofol 50-200 μg · kg-1 · min-1 (variable rate) infusions for maintenance of anesthesia. Group B (n = 21) received sufentanil 5 μg/kg for induction and propofol 50-200 μg · kg-1 · min-1 (variable rate) infusion for maintenance of anesthesia. For comparison, a third group (Group C, n = 18) was studied subsequently. This group received sufentanil 5 μg/kg for induction of anesthesia which was maintained with enflurane. Adverse hemodynamic changes (hypertension, tachycardia) were managed by additional propofol (Groups A and B), sufentanil (Group C), or vasopressors (hypotension). Hemodynamic and myocardial metabolic profiles were measured when awake and sedated and at postinduction, postintubation, postincision, poststernotomy, and precardiopulmonary bypass times. Ischemia was assessed by measuring myocardial lactate production. The incidence of myocardial lactate production was reduced in Group B as compared to Group C (Group A, 45/126; Group B, 23/126; Group C, 58/107; P < 0.05). Myocardial lactate flux declined in all groups as surgery progressed; but apart from the reduction in flux (indicative of increased ischemia) noted in Group C versus Group B postinduction, no between-group differences were detected. No between-group differences were noted in hemodynamics, inotropic requirements to separate from cardiopulmonary bypass, complications, (e.g., myocardial infarction, cerebrovascular accident, death), or changes in laboratory variables (e.g., cortisol, high- and low density lipoproteins) pre- versus postoperative. Recovery from anesthesia was prolonged in Group B versus Group A but not versus Group C. We conclude that use of propofol in patients with reduced ejection fractions undergoing coronary artery revascularization provides satisfactory anesthetic control of hemodynamics and was not associated with an increased incidence or degree of myocardial ischemia.
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U2 - 10.1213/00000539-199310000-00005
DO - 10.1213/00000539-199310000-00005
M3 - Article
C2 - 8214649
AN - SCOPUS:0027426381
SN - 0003-2999
VL - 77
SP - 680
EP - 689
JO - Anesthesia and Analgesia
JF - Anesthesia and Analgesia
IS - 4
ER -