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Does perioperative myocardial ischemia lead to postoperative myocardial infarction? By Stephen Slogoff and Arthur S. Keats. Anesthesiology 1985; 62:107-14. Reprinted with permission. To determine if a relationship exists between perioperative myocardial ischemia (ST segment depression greater than or equal to 0.1 mV) and postoperative myocardial infarction (PMI), nonparticipating observers recorded all electrocardiographic, hemodynamic, and other events between arrival of patients in the operating room and onset of cardiopulmonary bypass during 1,023 elective coronary artery bypass operations (CABG). The roles of preoperative patient characteristics, quality of the operation limited by disease as rated by the surgeon and duration of ischemic cardiac arrest as risk factors for PMI also were quantified. Electrocardiographic ischemia occurred in 36.9% of all patients, with almost half the episodes occurring before induction of anesthesia. PMI was almost three times as frequent in patients with ischemia (6.9% vs. 2.5%) and was independent of when ischemia occurred. Ischemia was related significantly to tachycardia but not hypertension nor hypotension and was frequent in the absence of any hemodynamic abnormalities. The anesthesiologist whose patients had the highest rate of tachycardia and ischemia had the highest rate of PMI. Although neither single nor multiple preoperative patient characteristics related to PMI, suboptimal quality of operation and prolonged ischemic cardiac arrest increased the likelihood of PMI independent of the occurrence of myocardial ischemia. The authors conclude that perioperative myocardial ischemia is common in patients undergoing CABG, occurs randomly as well as in response to hemodynamic abnormalities, and is one of three independent risk factors the authors identified as related to PMI. PMI is unrelated to preoperative patient characteristics such as ejection fraction and left main coronary artery disease, and its frequency will relate primarily to perioperative management rather than patient selection.

The role of perfusion pressure and flow during cardiopulmonary bypass with moderate hypothermia and hemodilution in the development of new postoperative renal or clinically apparent cerebral dysfunction was examined in 504 adults. Cardiopulmonary bypass flow was targeted at greater than 40 mL.kg-1.min-1 and pressure at greater than 50 mm Hg. Flows and pressures less than target occurred in 21.6% and 97.1% of patients, respectively. Fifteen patients (3.0%) suffered new renal and 13 (2.6%) new central nervous system dysfunction. Low pressure or flow during cardiopulmonary bypass, expressed in absolute values or in intensity-duration units, were not predictors of either adverse outcome. Multivariate analysis identified use of postoperative intraaortic balloon counterpulsation (p less than 10(-6], excessive blood loss in the ICU (p less than 10(-4], need for vasopressors before cardiopulmonary bypass (p less than 10(-4], postoperative myocardial infarction (p less than 10(-3], emergency reoperation (p less than 0.002), excessive postoperative transfusion (p less than 0.02), and chronic renal disease (p less than 0.03) as independent predictors of postoperative renal dysfunction. Independent predictors of postoperative central nervous system dysfunction were cardiopulmonary resuscitation in the intensive care unit (p less than 10(-6], intracardiac thrombus or valve calcification (p less than 0.02), and chronic renal disease (p less than 0.03). Age greater than 65 years (40.7% of patients) did not predict either outcome. We conclude that failure of the native circulation during periods other than cardiopulmonary bypass rather than the flows and pressures considered here is the major cause of renal and clinically apparent central nervous system dysfunction after cardiac operations.

The activated coagulation time (ACT) is widely used to monitor adequacy of anticoagulation during cardiopulmonary bypass despite absence of data establishing an ACT below which adverse outcomes occur. For anticoagulation before cardiopulmonary bypass, we administered a single dose of heparin (300 U/kg) to 193 patients and measured ACT and heparin levels at intervals after administration. No additional heparin was administered to any patient. Clot formation in the cardiopulmonary bypass circuit and excessive postoperative chest tube drainage were considered outcomes indicating inadequate anticoagulation. Cardiopulmonary bypass averaged 59 +/- 23 minutes (range, 30 to 138 minutes). Activated coagulation time values at every sampling period were normally distributed. In 51 patients (26.4%) ACT values were less than 400 seconds, including 4 less than 300 seconds, at some sampling time after heparinization. Patients with low ACT values did not bleed more postoperatively than those with high ACT values, nor was bleeding related to heparin level. No clots were found in any perfusion circuit. We conclude that a minimum ACT value for adequacy of heparinization is not yet defined but that it is less than 400 seconds.

There is a great need to define serious morbidity and mortality attributable to anesthesia, including their incidences and etiologies

Benefits from the use of glucose-containing intravenous and priming solutions during coronary artery bypass operation have not been documented, but an increased risk of postoperative neurologic deficit by hyperglycemia has been suggested. To determine benefits, 107 patients undergoing coronary artery bypass operation were managed identically except that one group (n = 54) received 5% dextrose in lactated Ringer's solution (D5LR) as the sole intravenous and priming solution during operation and a second group (n = 53) received the same solution without glucose (LR). During cardiopulmonary bypass, the D5LR group required significantly less additional crystalloid to maintain safe oxygenator levels and flow (1.8 +/- 3.3 vs 15.8 +/- 20.9 mL.kg-1.h-1) and produced more urine (3.5 +/- 3.2 vs 1.2 +/- 1.4 mL.kg-1.h-1). By 24 h after operation, fluid balance in the LR group was approximately 2 L more positive than in the D5LR group. Five days after operation, the D5LR group weighed less than preoperatively (-0.8 +/- 2.6 kg), whereas the LR group gained weight (+1.0 +/- 2.8 kg). We conclude that use of glucose-containing solutions during coronary artery bypass operation benefits patients by decreasing perioperative fluid requirements and postoperative fluid retention. Because embolism is the cause of most postoperative neurologic deficits, any increased risk by hyperglycemia is small.

The respiratory depressant capacities of intravenous nalbuphine, a potent analgesic of the narcotic antagonist type, and of morphine were compared in 23 healthy subjects using displacement of CO2 response by a steady-state method as the index of respiratory depression. At equianalgesic doses of 10 mg/70 kg, respiratory depression by nalbuphine was equal to that by morphine. When increments of 10 mg/70 kg were given hourly the dose-effect curve for respiratory depression by nalbuphine was flatter than that of morphine, and maximum respiratory depression occurred after 30 mg/70 kg. In a separate study of 10 subjects nalbuphine was administered in 10 mg/70 kg increments to a total dose of 60 mg/70 kg; doses in excess of 30 mg/70 kg failed to increase respiratory depression beyond that induced by morphine 20 mg/70 kg. A ceiling effect for respiratory depression previously known to exist only for nalorphine was thereby demonstrated to apply to nalbuphine. The respiratory depression of nalbuphine was readily antagonized by naloxone 0.4 mg, nalorphine 10 mg, and levallorphan 1.0 mg. Subjective effects of nalbuphine were milder than those of morphine, and dysphoria suggestive of the psychotomimetic effects of narcotic antagonists was reported only 4 times in 24 subject exposures. The ceiling effect for respiratory depression by nalbuphine provides a unique safety factor among potent analgesics.

Incidence elevee d'ischemie en periode de preinduction et incidence elevee d'ischemie peroperatoire non en rapport avec l'hemodynamique

During surgical correction of cyanotic heart disease with associated polycythemia, sufficient reduction of hemoglobin and hematocrit values has proved effective in preventing postoperative coagulopathies. Three groups of surgical patients were studied: Group I--a control group consisting of 75 adults undergoing uncomplicated correction of acquired heart disease and requiring no blood or blood component transfusion; Group II--15 patients with tetralogy of Fallot whose intraoperative hemoglobin values remained above 10 gm/dl with conventional hemodilution techniques; and Group III--21 cyanotic surgical patients whose intraoperative hemoglobin values were lowered to less than 10 gm/dl with sufficient hemodilution. Group III was further broken down into a subgroup of six patients (Group IIIa) who underwent sequential laboratory determinations, as in Group I. In Group IIIa, postoperative coagulation function tests were only slightly more abnormal than in the nonpolycythemic control group (Group I). Patients in Group III (who had ample hemodilution) experienced 45% less bleeding and required 54% fewer blood components than those in Group II (who underwent conventional hemodilution).

To examine the role of primary anesthetic agent on outcome of coronary artery bypass grafting operations, 1,012 patients were prospectively randomized to receive enflurane (257), halothane (253), isoflurane (248), or sufentanil (254). Except for administration of the primary anesthetic, anesthesia management was standardized for all patients. The randomized groups did not differ in demographic characteristics, extent of coronary artery disease, chronic antianginal therapy, hemodynamic characteristics including new myocardial ischemia at arrival to the operating room, and surgical characteristics that might influence the rate of postoperative myocardial infarction or death. From anesthetic induction to start of cardiopulmonary bypass, new ST segment depression appeared in 310 (30.4%) patients and was not different among primary anesthetic groups (28.0-33.5%). Similarly, the incidence of postoperative myocardial infarction (3.6-4.7%) and death (1.2-2.4%) was not different. Although intraoperative hypotension was twice as common in patients receiving any volatile anesthetic and hypertension twice as common with sufentanil, tachycardia (greater than or equal to 110 bpm) was not related to any primary anesthetic (4.3-9.1%) and was the only hemodynamic abnormality significantly related to intraoperative ischemia. The strongest predictor of intraoperative ischemia was ischemia on arrival to the operating room. The authors postulate that approximately 90% of new myocardial ischemia observed during anesthesia is the manifestation of silent ischemia observed in patients before operation and only 10% is related to anesthetic management. They conclude that, despite differences in the hemodynamic consequences of the primary anesthetics studied, none of the primary anesthetics influenced outcome and the primary role of the anesthesiologist in management of these patients is control of heart rate.

Dezocine in equianalgesic intravenous doses depressed respiratory response to CO2 breathing of six healthy subjects to approximately the same degree as morphine but with a more rapid onset and higher peak depression. The depression was dose related up to 30 mg/70 kg but was not increased by an additional 10 mg/70 kg dose. Its duration of effect was approximately the same as that of morphine. Respiratory depression by dezocine was promptly and almost completely antagonized by 0.4 mg naloxone, but antagonism lasted less than 1 hr. Healthy subjects found dezocine less pleasant than morphine and after large doses reported sensations suggestive of psychotomimetic effects. A ceiling effect for respiratory depression has now been demonstrated for three agonist-antagonist analgesics: nalorphine, nalbuphine, and dezocine. It is not yet clear to what extent this is a general characteristic of agonist-antagonist analgesics.

Respiratory depression induced by tilidine was compared with that of morphine in a crossover study in 6 healthy subjects. Increments of tilidine, 150 mg/70 kg, and morphine, 10 mg/70 kg, were given intravenously and displacement of each subject's CO2 response curve was measured after each dose increment. Both tilidine and morphine caused dose-related displacement of the CO2 response curves to the right. Approximately 80 to 120 mg of tilidine can be expected to induce the respiratory depression of morphine, 10 mg, when given intravenously. Subjective effects after tilidine were qualitatively similar to those of morphine but were of longer duration with nausea and vomiting more frequent. The respiratory depression of both drugs was effectively antagonized by naloxone.

Alteration of coagulation status and certain clinical chemistry laboratory determinations of 75 adult patients undergoing cardiopulmonary bypass procedures for acquired heart disease was studied during and after surgery. None of the patients was given transfusions of blood or blood components. With hemodilution, the mean hematocrit value dropped from 38% to 28% during the procedure. Fibrin degradation products and euglobulin lysis time were transiently abnormal. Factor V diminished somewhat during the procedure, whereas factors VIII and IX increased after surgery. Clottable fibrinogen values decreased slightly, but increased to an abnormally high value at 24 and 48 hours. Mean value of platelet counts decreased from 194,000 to 144,000/microliter immediately after surgery. Knowledge of expected deviation of coagulation factors and certain clinical chemistry tests following open heart surgery is helpful in evaluating the status of the postoperative patient.

We reviewed the perioperative courses of 110 children of members of the Jehovah's Witness faith who underwent 112 operations for complete repair of congenital heart disease with cardiopulmonary bypass. Operations were performed over a 20 year period, ending June, 1983. The children ranged in age from 6 months to 12 years and weighed 5.2 to 42.3 kg. Thirty-nine (34.8%) of the patients weighed less than 15 kg, 36 (32.1%) were polycythemic preoperatively, and 26 (23%) had previous thoracic operations. All operations were performed during normothermic cardiopulmonary bypass with a glucose crystalloid prime. No patient received any blood or blood products during hospitalization. Perioperative mortality was 5.4%. Only one of the deaths could be attributed to blood loss. Complications occurred in 10 patients, and none of these could be attributed to failure to transfuse. The results demonstrate that cardiac operations can be safely performed in children denied transfusion and suggest that hemodilution techniques might be used more extensively in children undergoing cardiac operations.

SUMMARY Arterial blood gases were studied at several periods during complete surgical correction of tetralogy of Fallot in 35 patients. Administration of 100 per cent oxygen during spontaneous respiration increased PaO2 in all patients. Administration of oxygen by positive pressure increased PaO2 over that of spontaneous respiration. In contrast to patients with isolated ventricular septal defect, a marked decrease in PaO2 was observed when the pleural spaces were open, despite full expansion of both lungs and continued positive pressure respiration with oxygen. It was postulated that the loss of normal negative intra-pleural pressure combined with positive pressure ventilation increased pulmonary vascular resistance sufficiently to increase right-to-left shunt. Intravenous phenylephrine altered this response in 2 of 6 patients. Some clinical implications of these observations are discussed.

An attempt has been made to collect the large amount of new information which has become available in the past ten years concerning postoperative pain, its characteristics, its use for research, and its treatment. With a better understanding of the postoperative patient, it is hoped that an improved treatment of this common and neglected painful state will result. Part of this improvement awaits the discovery of an ideal analgesic drug, and this challenge remains. The rest of the improvement awaits the intelligent use of available drugs, good nursing care, and a consideration of the psychologic needs of the patients.

Several investigators have shown that some narcotic antagonists are potent analgesics in man, and suggested that a clinically useful nonaddicting potent analgesic could he found among the narcotic antagonists. Since these compounds are respiratory depressants as well, concern has been expressed that the use of narcotic antagonists as analgesics would be handicapped by the lack of an antagonist to its toxic effects, especially respiratory depression. This study was undertaken to demonstrate that a nonspecific analeptic could antagonize the respiratory depression induced by a narcotic antagonist. The respiratory depressant effects of pentazocine, a weak narcotic antagonist which is a potent nanaddicting analgesic in man, was used as the test object. Methylphenidate (30 mg. per 70 Kg. intravenously) significantly antagonized the respiratory depression of pentazocine (40 mg. per 70 Kg. intramuscularly) compared to a placebo in a complete crossover study of six healthy subjects. Antagonism was incomplete at 30 minutes but almost complete at 75 minutes after methylphenidate.

During cardiopulmonary bypass for open-heart operations utilizing anoxic cardiac arrest, the heart and lungs are excluded from the circulation and the remaining vascular bed is perfused at a fairly constant flow. Under these circumstances actions of vasoactive drugs on the peripheral systemic circul

The possibility that venous blood could be withdrawn through a radial artery cannula when venous pressure is high was examined in 30 patients during cardiopulmonary bypass for coronary artery bypass operation. Progressive desaturation of radial artery blood occurred when venous pressure was equal to arterial pressure. Desaturation not only increased with duration of venous obstruction but also occurred immediately if the arterial tree was emptied after occlusion. We believe that these observations result from the transcapillary aspiration of deep venous blood and may produce a potential source of error in measuring arterial oxygen tension during cardiopulmonary resuscitation, cardiac tamponade, and profound right heart failure, as well as cardiopulmonary bypass.