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Cardiovascular and Pulmonary, Responses Following Etomidate Induction of Anesthesia in Patients with Demonstrated Cardiac Disease John M

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Cardiovascular and Pulmonary, Responses Following Etomidate Induction of Anesthesia in Patients with Demonstrated Cardiac Disease John M ANESTH ANALG 51340-41.1979 Cardiovascular and Pulmonary, Responses following Etomidate Induction of Anesthesia in Patients with Demonstrated Cardiac Disease John M. Gooding, DO, Jen-Tsoh Weng, MD, PhD, Robert A. Smith, RRT, Gary T. Berninger, RRT, and Robert R. Kirby, MD GOODING, J. M., WENG, J.-T., SMITH, R. A., BERNINGER, G. T., AND KIRBY, R. R.: Cardiovascular and pulmonary responses following etomidate induction of anesthesia in patients with demon- strated cardiac disease. Anesth Analg 58:40-41, 1979. Cardiovascular and pulmonary effects following the administration of 0.3 mg/kg of etomidate were studied in patients with documented cardiac disease. The only significant change was a slight elevation (2 torr) in arterial carbon dioxide tension. Key Words: ANESTHETICS, Intravenous: etomidate; INDUCTION, Anesthetic: etomldate. N intravenous drug that produces rapid onset of mean age 55 f 9 years), A.S.A. classes I11 and IV, A hypnosis without adverse effects on the respi- were studied. (Approval for the study was given by ratory and cardiovascular systems would be appreci- the Use of Human Subjects Committee at Tulane ated by anesthesiologists. Such a drug would fill an University School of Medicine. Informed consent was existing gap in our current armanentarium of anes- obtained from each subject.) All had existing cardiac thetic induction agents. Previous reports have sug- disease documented by prior catheterization. Two gested that etomidate, a new rapid acting nonbarbi- patients were scheduled for peripheral vascular sur- turate hypnotic, lacks significant adverse cardiovas- gery, eight for valvular heart surgery, and 12 for cular and respiratory effects.'-' However, these stud- coronary artery bypass grafting. Premedication con- ies did not include patients with preexisting cardio- sisted of 5 mg of droperidoll hour prior to anesthetic vascular disease. induction in every patient. Balloon flotation, therm- In order to assess the cardiovascular and respiratory istor-tipped, pulmonary artery catheters as well as effects of etomidate in high risk patients we under- radial artery catheters were inserted percutaneously. took such a study in surgical patients with demon- Control measurements of heart rate (HR), mean ar- strated cardiac disease. terial pressure (AP),central venouSpressure (CVP), mean pulmonary artery pressure (PAP), pulmonary Materials and Methods artery occlusion pressure (PAOP), cardiac output (CO), and arterial and mixed venous blood gas ten- Twenty-two patients (18 men and four women, sions were obtained. Etomidate was then injected intravenously in a dose of 0.3 mg/kg in 60 seconds. Received from the Department of Anesthesiology, Tulane Uni- Oxygen was administered preceding and during the versity School of Medicine, 1430 Tulane Avenue, New Orleans, Louisiana 70112. Accepted for publication September 26, 1978. induction period. The above measurements were re- Address reprint requests to John M. Gooding, DO. peated between 1 and 3 minutes following etomidate ANESTHESIA AND ANALGESIA 40 Vol58. No 1, Jan-Feb 1979 GOODING ET AL TABLE on injection with the new, less acidic (pH 5.0) solu- Effect of Etomidate on Cardiac and Pulmonary Variables (n tion" that was used in our patients. The stability of - 22). cardiovascular function suggests a lack of significant Before etomi- effects on either the peripheral and pulmonary vas- After etomidate date cular beds or on the myocardium itself. Absence of HR 69f 12 70 f 9 appreciable changes in arterial blood gases confirms Ap (torr) 91 f18 88 f 21 previous finding^.^ Total intrapulmonary shunt was CVP (torr) 6;t5 7f4 not altered and suggests a role for etomidate in an- PAP (torr) 20 f 5 20 f 5 esthetizing patients with respiratory insufficiency PAOP (torr) 14 f 5 15f5 CI (L-min-'. m2-') 2.6 f 0.7 2.7 f 0.6 and/or preexisting intrapulmonary shunting. P~Q(torr) 290 f 68 292 f 70 Cardiovascular stability in our study of high risk Pacq (torr) 41 f4 43 f 5t cardiac patients corroborates previous findings in C (a - Y)02 (mi %) 4.6 f 1 4.7 f 1 noncardiac patients. Alterations in arterial blood gas dap/d, (%I 21 f 0.05 21 f 0.05 tensions or total intrapulmonary shunt did not occur. Values are means f SD. See text for abbreviations. In patients at risk because of heart disease it would t p < 0.05. appear that etomidate would provide a greater margin of safety during the induction of anesthesia than the injection. Using the above data and body surface area, ultrashort-acting barbiturates which produce vascular cardiac index (CI), arteriovenous oxygen content dif- dilation, adversely affect cardiac output, and depress ference (C(a-+)OZ), and total intrapulmonary shunt respiration. (QnP/Qt)were calculated. ResuI t s REFERENCES 1. Kettler D, Sonntag H, Donath U, et al: Hemodynamics, my- Due to rapid onset and brief duration of action of ocardial mechanics, oxygen requirements and oxygen con- etomidate (at a dose of 0.3 mg/kg, sleep is produced sumption of the human heart during etomidate induction into in a single arm-brain circulation time and inactive anaesthesia. Anaesthesist 23:116-121.1974 2. Doenicke A, Gabanyi D, Lemce H, et al: Circulatory dynamics metabolites peak by 7 minutes6'?, it was elected to and myocardial function following three short-acting IV hyp- obtain data between 1 and 3 minutes following injec- notics: etomidate, propanidid, methohexital. Anaesthesist 23: 108-115, 1974 tion. A slight elevation of arterial carbon dioxide 3. Rifat K, Gamulin 2, Cemperle M: Etomidate: effects cardio- tension (Faco,) was the only change of statistical vasculaires du nouvel agent anaesthesique intraveineux. Can significance (Table); however, this change was not Anaesth Soc J 23492-504, 1976 4. Gooding J,Corssen G: Effect of etomidate on the cardiovascular clinically remarkable. Some patients tended to de- system. Anesth Analg 56:717-719,1977 velop upper airway obstruction indicated by episodes 5. Hempelmann G,Seitz W, Piepenbrock S: Kombination von of snoring. No other consistent effects on respiration Etomidate und Fentanyl. Anaesthesist 26:231-238,1977 6. Gooding J, Corssen G: Etomidate: an ultrashort-acting nonbar- were noted. biturate agent for anesthesia induction. Anesth Analg 55: 286-289, 1976 Discussion 7. Fragen RJ, Caldwell N, Brunner EA: Clinical use of etomidate for anesthesia induction: a preliminary report. Anesth Analg Hemodynamic stability was observed following the 55:730- 733, 1976 8. Morgan M, Lumley J, Whitwam JG: Respiratory effects of administration of 0.3 mg/kg of etomidate in patients etomidate. Br J Anaesth 49:233-236,1977 at risk because of cardiac disease. The slight elevation 9. Morgan M, Lumley J, Whitwam J: Etomidate a new water- in heart rate reported in previous studies of noncar- soluble nonbarbiturate intravenous induction agent. Lancet 955-956, 1975 diac patients', 3, ' did not occur in our patients. This 10. Hendry JGB,Miller BM, Lees NW: Etomidate in a new solvent: may be due to the reduced incidence of venous pain a clinical evaluation. Anaesthesia 32:996-999.1977 ANESTHESIA AND ANALGESIA Vol58. No 1, Jan-Feb 1979 41 .
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