Sufentanil Does Not Block Sympathetic Responses to Surgical Stimuli in Patients Having Coronary Artery Revascularization Surgery

The effects of a moderate dose of sufentanil (1 μg·kg−1 + 0.015 μg·kg−1 ·min−1) plus nitrous oxide (30% O2/70% N2O) anesthesia (group I; n = 8) and of high-dose sufentanil/O2 anesthesia (10 μg·kg−1 + 0.15 μg·kg−1·min−1) without N2O (group II; n = 8) on cardiovascular dynamics, myocardial blood flow, myocardial oxygen consumption, myocardial lactate balance, and hypo-xanthine release were studied in two groups of male patients scheduled for elective coronary artery bypass surgery. All patients were on maintenance doses of calcium channel blockers and nitrates with the last doses of medications given the morning of operation. All patients were premedicated with flunitrazepam (2 mg orally), piritramide (7.5 mg IM) and promethazine (25 mg IM). Measurements were performed before the induction of anesthesia with the patients premedicated but awake; 20 min after induction of anesthesia with sufentanil plus pancuronium 0.1 mg·kg−1 for muscle relaxation before surgery; and during sternotomy and sternal spread. Sufentanil at either dose decreased mean arterial pressure, as well as cardiac and stroke volume index while heart rate remained unchanged. Following the induction myocardial blood flow and myocardial oxygen consumption decreased 23% (79 ml·min−1 ·100 g−1 to 61 ml·min−1 ·100 g−1 and 28% (9.2 ml O2·min−1·100 g−1 to 6.6 ml O2·min−1·100 g−1) in group I and 14% (78 ml·min−1 100 g−1 to 67 ml·min−1 100 g−1 and 18% (8.7 ml O2·min−−1·100 g−1 to 7.1 ml O2·min−1·100 g−1) in group II. Myocardial ischemia was seen in one patient of group II (patient No. 4), as indicated by a hypoxanthine release into the coronary sinus, when after the induction MAP decreased from 93 to 67 mm Hg and heart rate increased from 56 to 71 min−1. During sternotomy 8 of 16 patients (56%) developed hypertension and 9 of 16 patients (56%) showed signs of myocardial ischemia, i.e., a lactate and for hypoxanthine release. Ischemia was related to hypertension in three patients but occurred in six patients without significant alterations in heart rate, PAP, PCWP, or arterial pressures. These data demonstrate that sufentanil, like fentanyl, produces incomplete anesthesia in patients with coronary heart disease and is not able to protect the myocardium adequately from autonomic sympathetic responses, even though sufentanil has the advantage of having more rapid onset of action than fentanyl.

[1]  P. McLaughlin,et al.  Effects of anaesthetic induction on myocardial function and metabolism: a comparison of fentanyl, sufentanil and alfentanil , 1988 .

[2]  D. Ansley,et al.  Hemodynamic variables and the incidence of prebypass ischemia during sufentanil/O2/pancuronium anesthesia in patients undergoing coronary artery surgery. , 1987, Journal of cardiothoracic anesthesia.

[3]  G. Heusch,et al.  Cardiac sympathetic nerve activity and progressive vasoconstriction distal to coronary stenoses: feed-back aggravation of myocardial ischemia. , 1985, Journal of the autonomic nervous system.

[4]  A. Keats,et al.  Does Perioperative Myocardial Ischemia Lead to Postoperative Myocardial Infarction? , 1985, Anesthesiology.

[5]  J. Bovill,et al.  Comparison of Fentanyl, Sufentanil, and Alfentanil Anesthesia in Patients Undergoing Valvular Heart Surgery , 1984, Anesthesia and analgesia.

[6]  J. Moss,et al.  Hemodynamics and histamine release during induction with sufentanil or fentanyl. , 1984, Anesthesiology.

[7]  W. Bellows,et al.  Noninvasive detection of periinduction ischemic ventricular dysfunction by cardiokymography in humans: preliminary experience. , 1984, Anesthesiology.

[8]  G. Heusch,et al.  The Effects of Cardiac Sympathetic Nerve Stimulation on Perfusion of Stenotic Coronary Arteries in the Dog , 1983, Circulation research.

[9]  E. Bassenge,et al.  Norepinephrine constricts the canine coronary bed via postsynaptic α2-adrenoceptors , 1982 .

[10]  H. Sonntag,et al.  Myocardial Blood Flow and Oxygen Consumption during High‐dose Fentanyl Anesthesia in Patients with Coronary Artery Disease , 1982, Anesthesiology.

[11]  P. Sebel,et al.  Cardiovascular Effects of Sufentanil Anesthesia , 1982, Anesthesia and analgesia.

[12]  J. Craver,et al.  Hemodynamic Changes during Fentanyl—Oxygen Anesthesia for Aortocoronary Bypass Operation , 1981, Anesthesiology.

[13]  W. Hood,et al.  Limitations of Lactate Production as an Index of Myocardial Ischemia , 1979, Circulation.

[14]  G. Kugler Myocardial Release of Lactate, Inosine and Hypoxanthine During Atrial Pacing and Exercise-Induced Angina , 1979, Circulation.

[15]  D. Waters,et al.  Myocardial ischemia: detection and quantitation. , 1978, Annals of internal medicine.

[16]  D. Tzivoni,et al.  Diagnostic Accuracy of Ambulatory ECG Monitoring in Ischemic Heart Disease , 1975, Circulation.

[17]  W. Daggett,et al.  Left Ventricular Performance and Pulmonary Circulation Following Addition of Nitrous Oxide to Morphine during Coronary‐artery Surgery , 1975, Anesthesiology.

[18]  G. Reed,et al.  Release of adenosine from human hearts during angina induced by rapid atrial pacing. , 1974, The Journal of clinical investigation.

[19]  R. Stoelting,et al.  Hemodynamic Effects of Morphine and Morphine–Nitrous Oxide in Valvular Heart Disease and Coronary-artery Disease , 1973, Anesthesiology.

[20]  R. Bing,et al.  Measurement of coronary blood flow in man. , 1960, Circulation.

[21]  P. Serruys,et al.  Hypoxanthine production by ischemic heart demonstrated by high pressure liquid chromatography of blood purine nucleosides and oxypurines. , 1981, Clinica chimica acta; international journal of clinical chemistry.

[22]  S. Holm A Simple Sequentially Rejective Multiple Test Procedure , 1979 .

[23]  C. Niemegeers,et al.  Sufentanil, a very potent and extremely safe intravenous morphine-like compound in mice, rats and dogs. , 1976, Arzneimittel-Forschung.