A comparison of the myocardial metabolic and haemodynamic changes produced by propofol-sufentanil and enflurane-sufentanil anaesthesia for patients having coronary artery bypass graft surgery.

The purpose of this study was to compare propofol-sufentanil with enflurane-sufentanil anaesthesia for patients undergoing elective coronary artery bypass graft (CABG) surgery with respect to changes in (1) haemodynamic variables; (2) myocardial blood flow and metabolism; (3) serum cortisol, triglyceride, lipoprotein concentrations and liver function; and (4) recovery characteristics. Forty-seven patients with preserved ventricular function (ejection fraction greater than 40%, left ventricular end diastolic pressure less than or equal to 16 mmHg) were studied. Patients in Group A (n = 24) received sufentanil 0.2 microgram.kg-1 and propofol 1-2 mg.kg-1 for induction of anaesthesia which was maintained with a variable rate propofol (50-200 micrograms.kg-1.min-1) infusion and supplemental sufentanil (maximum total 5 micrograms.kg-1). Patients in Group B (n = 23) received sufentanil 5 micrograms.kg-1 for induction of anaesthesia which was maintained with enflurane and supplemental sufentanil (maximum total 7 micrograms.kg-1). Haemodynamic and myocardial metabolic profiles were determined at the awake-sedated, post-induction, post-intubation, first skin incision, post-sternotomy, and pre-cardiopulmonary bypass intervals. Induction of anaesthesia produced a larger reduction in systolic blood pressure in Group A (156 +/- 22 to 104 +/- 20 mmHg vs 152 +/- 26 to 124 +/- 24 mmHg; P less than 0.05). No statistical differences were detected at any other time or in any other variable including myocardial lactate production (n = 13 events in each group), time to tracheal extubation and time to discharge from the ICU. We concluded that, apart from hypotension on induction of anaesthesia, propofol-sufentanil anaesthesia produced anaesthetic conditions equivalent to enflurane-sufentanil anaesthesia for CABG surgery.

An appreciation of the coronary circulation.

Coronary sinus catheter techniques for evaluation of coronary flow and myocardial metabolism have the drawback that a global sampling method is used to evaluate a regional disease (coronary artery disease). Studies on the coronary circulation are further limited by the fact that interventions acting on the coronary bed may simultaneously modify several of the principal determinants of coronary blood flow. Results are also influenced by differences among species, and whether the coronary vascular bed is normal or pathologically narrowed. Because coronary flow is intimately coupled to myocardial oxygen demand, interpretation of values as abnormal require simultaneous evaluation of some index of myocardial oxygen consumption. Under normal conditions, myocardial flow is predominantly in diastole, and is subject to compromise by factors that abbreviate diastole (e.g., tachyarrhythmias). Autoregulation maintains constant coronary blood flow over a range of perfusion pressures (60-130 mm Hg), and increased flow demands are normally met by coronary vasodilation (coronary flow reserve). In proximal coronary stenosis, this capacity for additional vasodilation may be significantly reduced, and flow to potentially ischemic beds beyond the stenosis may be maintained by collaterals. Pharmacologic coronary vasodilation in this situation can result in coronary steal. When perfusion pressure decreases below the autoregulatory range, or when coronary flow reserve is exhausted early, as in coronary stenosis, flow becomes dependent on mechanical factors including duration of diastole and the perfusion pressure. In these situations, monitoring heart rate and diastolic pressure would allow reasonable assessment of adequacy of coronary flow and myocardial perfusion.

Myocardial metabolism and hemodynamic responses with isoflurane anesthesia for coronary arterial surgery.

Isoflurane-oxygen was given for induction and maintenance of anesthesia to ten patients having coronary artery bypass grafts. All had preserved ventricular function without hypertension or other cardiac lesions; treatment with beta-blocking drugs was maintained until the operation in all patients. Cardiac output, arterial and central pressures, coronary sinus (CS) blood flow, arterial and CS oxygen, Hb, and lactate contents were measured before, six times during, and twice after anesthesia. On induction, systolic arterial pressure was purposely reduced 33% along with systemic resistance by increasing the concentration of isoflurane; cardiac index, heart rate, and coronary flow did not change. Coronary resistance decreased 23% and CS oxygen content increased 56%; but in three of ten patients myocardial lactate production took place, evidence of global ischemia. Induction of anesthesia was not smooth in three patients. Controlled hemodynamic depression could be maintained with isoflurane-oxygen, but the frequency of myocardial lactate production before and after perfusion was greater than with other general anesthetics. Isoflurane dilated portions of the coronary bed but, because anaerobic metabolism occurred concomitantly, the theory that redistribution of flow can take place resulting in ischemic areas of ventricle is supported.

Myocardial metabolism and hemodynamic responses with fentanyl-enflurane anesthesia for coronary arterial surgery.

Ten patients for coronary vein grafting had induction of anesthesia with fentanyl (30 micrograms/kg), followed by enflurane-oxygen sufficient to decrease systolic blood pressure by 27% before intubation. Enflurane was continued in concentrations to maintain blood pressure below that with patients awake. All patients had preserved ventricular function and effective beta-blockade. Studies of hemodynamic functions and myocardial blood flow and oxygenation were done before induction, six times during anesthesia, and twice postoperatively. The blood pressure decrease on induction and before bypass was due to reduced cardiac index without decreased heart rate or systemic resistance. Stroke work index decreased 47% on induction and remained below awake level throughout. Coronary sinus blood flow decreased 26% after intubation and remained so before bypass. Without change in coronary resistance, coronary sinus oxygen content increased 30% on induction and stayed elevated before bypass. Normal lactate extraction continued after induction and increased before bypass; mean extraction decreased after bypass, with one or two hearts producing lactate in the first 24 postoperative hr. Fentanyl-enflurane-oxygen maintained a steady mild hemodynamic depression during the operation and soon afterward, which preserved myocardial oxygenation.

Effects of intubation on coronary blood flow and myocardial oxygenation.

Effects on haemodynamics and myocardial oxygenation of endotracheal intubation were examined in 17 patients after halothane induction and 12 after 1 mg X kg-1 of IV morphine. Six patients having each anaesthetic were pretreated with IV propranolol (0.1 mg X kg-1) 45 minutes earlier. Arterial and intracardiac pressures, cardiac output and total coronary sinus blood flow (CSBF), both by thermodilution, were determined plus arterial-coronary differences of oxygen, haemoglobin and lactate. Blood pressure (BP), heart rate and CSBF were recorded continuously during intubation. The subjects were candidates for coronary bypass grafts, but had good ventricular function (mean ejection fraction 0.68 +/- 0.13 SD). From their reduced levels after induction, BP, cardiac index and systemic vascular resistance increased to awake levels following intubation. Mean CSBF in nonbetablocked patients increased to awake level along with BP. More myocardial oxygen was extracted and consumed after intubation, but lactate extraction continued: these data are evidence of adequate oxygen supply. Induction with either halothane or morphine effectively prevented the hypertensive response to intubation. Acute beta blockade led to less increase in heart rate from intubation.

The effects of nitrous oxide on myocardial metabolism and hemodynamics during fentanyl or enflurane anesthesia in patients with coronary disease.

Twenty patients about to have coronary artery bypass grafts were studied before and after 15 min of 50% nitrous oxide added to either fentanyl (75 micrograms/kg) or enflurane (0.5%) anesthesia. Arterial and central pressures and cardiac output were measured, plus coronary sinus blood flow and arterio-coronary sinus differences in oxygen, hemoglobin, and lactate contents. Fentanyl-N2O and enflurane-N2O both decreased systemic resistance, heart rate, cardiac output, and hence arterial pressure. Stroke work decreased significantly with little or no change in wedge pressure: ventricular function was impaired. Coronary flow and myocardial O2 consumption decreased with fentanyl-N2O. Oxygen extraction increased with enflurane-N2O, as did lactate contents of coronary sinus blood. Hemodynamic depression occurred from the combined effects of nitrous oxide and fentanyl or enflurane. The beta-blocked myocardia of nonstimulated coronary patients were becoming ischemic globally on 50% oxygen, after significant hypotension. From this and other evidence, we conclude that nitrous oxide may not be benign in patients with coronary arterial disease.

Myocardial metabolism and haemodynamic responses with enflurane anaesthesia for coronary artery surgery.

Ten patients were studied before, during and after enflurane anaesthesia for coronary vein grafting. All had good ventricular function and nine were receiving effective beta blockade. Cardiac output and vascular pressures were measured, plus coronary sinus blood flow (CBF), myocardial oxygen consumption (MVO2) and lactate extraction (MLE). Enflurane induction (10 minutes, mean 1.72 per cent end tidal) reduced blood pressure (MAP), due to decreased cardiac index (CI), with no change in heart rate or systemic resistance. Intubation returned MAP and CI to control level but the heart rate increased. Subsequently, enflurane kept MAP, CI and stroke work below the awake level. CBF decreased on induction, rose again on intubation and remained normal before bypass. MVO2 fell on induction from an increase in CS oxygen content, which remained elevated. Normal MLE continued in every patient. There was no evidence of myocardial ischaemia in patients on beta blockade, when haemodynamics were maintained at or below those of the sedated, awake state.

Rate-pressure product correlates poorly with myocardial oxygen consumption during anaesthesia in coronary patients.

In 26 patients having coronary grafts, haemodynamics, coronary sinus blood flow and the arterio-coronary sinus difference of oxygen content were determined, awake and at four intervals during morphine-oxygen or halothane--oxygen anaesthesia. Rate-pressure product (RPP), triple product (TP) and myocardial oxygen consumption (MVO2) were calculated. The correlation of the two indirect indices to MVO2 were tested by repeated measures and regression analyses. No significant correlations were seen at four of five study times, when outlying data points were appropriately excluded. A pitfall of using more than one data point from each patient in the linear regression analysis is pointed out. In addition to the lack of correlation of RPP to MVO2, RPP was an imprecise predictor of myocardial lactate production and of postoperative infarction.

Myocardial and systemic effects of nitroglycerin, given awake and during anaesthesia in coronary patients.

The haemodynamic and myocardial energy-metabolic effects of intravenous nitroglycerin (NTG) were investigated in seven male patients about to undergo coronary artery bypass grafting. Effects of one mg of NTG given at a rate of 100 micrograms . min-1 to sedated, awake hypertensive patients, were compared to effects of the same dose of NTG in the same patients, after sternotomy. Coronary sinus flow was measured by a thermodilution catheter and myocardial oxygen consumption (MVO2) was calculated using the arterio-coronary sinus difference of oxygen content. With the patients awake, cardiac index and stroke volume and work indices fell during NTG administration. There was only a small fall in arterial pressure as heart rate and systemic resistance increased. Pulmonary capillary wedge pressure decreased but not MVO2. With NTG administration during anaesthesia, arterial pressure fell significantly to normal, as systemic resistance decreased, without a change in heart rate or cardiac index. Calculated MVO2 decreased as the arterial-coronary venous difference of oxygen content increased. Both oxygen and lactate balance of the myocardium were maintained. NTG given during anaesthesia was more effective in reducing blood pressure and MVO2 than when given to awake patients.

Nitrous oxide added to halothane reduces coronary flow and myocardial oxygen consumption in patients with coronary disease.

The haemodynamic and myocardial metabolic effects of adding 50 per cent nitrous oxide to 0.5 per cent halothane were studied in 13 patients, before the surgical incision for coronary artery vein grafts. Cardiac output and coronary sinus blood flow were determined by thermodilution, along with haemodynamic measurements. Measurements 15 minutes after addition of nitrous oxide revealed a significant decrease in heart rate, arterial pressure, cardiac index, coronary sinus blood flow and myocardial oxygen consumption. There was a significant increase in coronary sinus lactate content, and a significant decrease, from 27 to 11 per cent, in myocardial lactate extraction. We conclude that these circulatory changes were likely to be due to a depression of ventricular function by the nitrous oxide. The myocardia of these patients with severe coronary disease were becoming globally ischaemic while they were receiving 50 per cent oxygen, in the presence of hypotension. Nitrous oxide should be turned off when hypotension occurs in coronary patients.

Myocardial metabolism and hemodynamic responses to halothane or morphine anesthesia for coronary artery surgery.

Eighteen patients having coronary artery bypass grafts were randomly anesthetized with morphine (1 mg/kg) or halothane and oxygen. Central and peripheral pressures were measured serially, plus cardiac output and total coronary sinus blood flow, both by thermodilution catheters, starting before induction of anesthesia and continuing until completion of sternotomy. No significant differences in hemodynamic responses were seen between the two anesthetic techniques during induction: blood pressure and peripheral vascular resistance decreased significantly, but not cardiac output or coronary flow. Myocardial oxygen consumption decreased significantly with induction as oxygen content of coronary sinus blood increased, indicating preservation of oxygen balance. Heart rate and blood pressure increased after sternotomy in the patients given morphine, with the myocardium producing lactate in two of six patients and with nitroprusside being required in four patients to decrease arterial pressure. Halothane-oxygen anesthesia effectively controlled autonomic responses to sternotomy, although one of 12 patients had myocardial lactate production at that time. Neither rate-pressure product or ST segment changes were useful predictors of the ratio between myocardial oxygen consumption and supply. Myocardial oxygen balance can be maintained in coronary patients before cardiopulmonary bypass if pulse rate and blood pressure are kept at less than awake levels.

Dobutamine and cardiac oxygen balance in patients following myocardial revascularization.

Dobutamine is frequently used in the early postoperative period following myocardial revascularization to improve cardiac output. Seven postoperative adult patients with low output syndrome were studied before and during intravenous dobutamine (mean +/- SD: 5.1 +/- 2.5 micrograms/kg/min) infusion. The metabolic effects were evaluated and related to hemodynamic changes. Cardiac index increased 40% (p less than 0.05) with an increase in heart rate (p less than 0.05) and decreases in systemic vascular resistance and right atrial pressure (p less than 0.05). No significant changes occurred in arterial or pulmonary capillary wedge pressures or in stroke volume index. Dobutamine produced a 29% increased in myocardial oxygen consumption which, in these revascularized patients, was accompanied by a 35% increase in coronary blood flow. No significant alteration was observed in coronary sinus oxygen content or in global myocardial lactate extraction. Thus, despite the increased metabolic cost of dobutamine, global myocardial ischemia was not observed.

Intravenous nitroglycerin and myocardial metabolism during anesthesia in patients undergoing myocardial revascularization.

Although intravenous nitroglycerin has been used to control the hypertensive response during sternotomy in patients undergoing myocardial revascularization, the effects of the drug on myocardial oxygen supply and demand have not been anesthetized for coronary artery bypass, were studied before and after administration of intravenous nitroglycerin (mean dose 12 microgram/kg in 6 minutes). Evaluation of myocardial metabolism showed an increase in coronary sinus oxygen content (p less than 0.05) and a reduction in myocardial oxygen consumption (p less than 0.05). Although mean myocardial lactate extraction and coronary sinus blood flow were not significantly altered in the group as a whole, variations in individual patient responses were observed and are discussed. These direct observations of global myocardial metabolism observed in this study group are similar to the conclusions reached by other investigators using indirect indices of myocardial oxygen supply and demand.

Effects of calcium on the coronary and systemic circulation in patients after coronary surgery.

Nine patients were studied three hours after aorto-coronary bypass. Before anaesthesia a radial arterial cannula was inserted and a thermodilution catheter placed into the pulmonary artery by fluoroscopy. A special thermodilution catheter was manipulated into the coronary sinus. Haemodynamic measurements were made plus cardiac output and coronary sinus blood flow. Content of oxygen and lactate in arterial and coronary sinus blood was determined. Series of measurements were done before and after 1 gm of CaCl2 given intravenously over 15 minutes. Calcium increased cardiac index and arterial pressure but not systemic vascular resistance. Total coronary sinus blood flow did not change, nor did myocardial oxygen consumption or coronary sinus oxygen content. Content of lactate in arterial and coronary sinus blood was unaltered and lactate extraction by the heart continued, in eight of nine patients. The improved haemodynamics were accomplished without inordinate risk to global ventricular energy metabolism.

Effects of digoxin on myocardial oxygen supply and demand in patients following coronary artery bypass surgery.

Although digoxin is used frequently in patients in the prophylaxis of postoperative supraventricular tachyarrhythmias, the effects of the drug on myocardial oxygen supply and demand after coronary bypass have not been described. Seven adult patients with good ventricular function who underwent myocardial revascularization were studied before and three hours after digoxin (0.5 mg, iv). There were no significant changes observed in any measured systemic hemodynamic variable. Evaluation of global myocardial metabolism showed an increase in myocardial oxygen consumption (P less than 0.05) which was compensated satisfactorily, as no significant alteration was noted in the coronary sinus oxygen content, or in the lactate gradient across the myocardium. Since the authors studied the effects of only one dose of digoxin, the effects of full digitalization in these patients remains to be defined.