Carol L. Lake

The Decrease of the Minimum Alveolar Anesthetic Concentration Produced by Sufentanil in Rats

The anesthetic potency of sufentanil was established by determining its effect on the minimal alveolar anesthetic concentration (MAC) of halothane. Each of eight selected doses of sufentanil was administered to a group of four to five mechanically ventilated rats anesthetized with halothane. Sufentanil was administered as a constant infusion preceded by an intravenous bolus dose that was three times that of the infusion rate per minute. The tail-clamp technique was used to establish control MAC and the MAC of halothane with sufentanil. Increasing sufentanil dosages were nonlinearly related to reductions in the MAC of halothane. A sigmoidal dose-response curve was described. An abrupt, steep response follows the initial upward deflection of the curve with an additional 62% MAC reduction occurring between doses of 1·10−5 mg·kg−1·min−1 and 1·10−4 mg·kg−1·min−1. Essentially complete anesthesia was seen at the latter dosage. No significant adverse side effects were seen with sufentanil at doses up to 1·10−2 mg·kg−1·min−1.

Influence of magnesium ion on human ventricular defibrillation after aortocoronary bypass surgery

The administration of magnesium ion (Mg++) has been reported to defibrillate the ventricles and to decrease the incidence of arrhythmias after cardiopulmonary bypass. In a prospective study of 76 randomly selected patients undergoing coronary artery bypass grafting, patients received either no Mg++, 0.25 mEq/kg of Mg++ during cardiopulmonary bypass with the aorta clamped, or 0.375 mEq/kg of Mg++ before cardiopulmonary bypass. Spontaneous resumption of a cardiac rhythm or spontaneous defibrillation during reperfusion was not significantly affected by Mg++ administration. However, the number of shocks to initial and to sustained defibrillation and the energy required for the last direct-current shock was greatest in patients who received Mg++ before bypass and in those whose plasma Mg++ was greater than 2.26 mg/dl. Thus, the administration of Mg++ may have adverse effects on the heart if intraoperative plasma Mg++ exceeds 2.26 mg/dl.

Cardiovascular Effects of Nalbuphine in Patients with Coronary or Valvular Heart Disease

Although the hemodynamic changes produced by small doses of nalbuphine given to patients with cardiac disease are minimal, the cardiovascular effects of large doses which have been used as supplements for general anesthesia have not been investigated. Cardiovascular variables were measured after incremental doses of nalbuphine, up to 2 or 3 mg/kg in fourteen patients with coronary artery disease with normal left ventricular function and in seven patients with mitral valve disease. No significant changes in cardiac index, stroke work index, mean arterial pressure, pulmonary diastolic or wedge pressure, heart rate, or central venous pressure occurred in the preoperative period. However, nalbuphine alone did not produce surgical anesthesia and the addition of diazepam, nitrous oxide, or halothane was required in all patients. The addition of halothane coupled with surgical stimulation significantly decreased cardiac and stroke indices, increased mean arterial and pulmonary wedge pressures, and increased systemic vascular resistance in patients with coronary artery disease. In patients with mitral valve disease, following surgical incision, there were small but significant decreases in cardiac index and left ventricular stroke work index, and increases in systemic vascular resistance. Despite its lack of deleterious hemodynamic effects, the place of nalbuphine in the armamentarium of the anesthesiologist must be limited to use as a premedicant, as an adjunct to balanced anesthesia, or for postoperative pain relief.

Myocardial function during halothane and enflurane anesthesia in patients with coronary artery disease

Halothane and enflurane are known myocardial depressants in healthy individuals. Whether these two agents produce the same degree of myocardial depression in patients with coronary artery disease has not been studied. Informed consent was obtained from 16 adults with ischemic heart disease undergoing coronary artery bypass grafting. Patients with significant ventricular dysfunction were excluded from the study. Control measurements were made while the patient breathed 100% oxygen. The patients were divided into two groups, anesthetized with either halothane or enflurane, and repeat measurements made at 1/2 and 3/4 MAC for each agent. The last series of measurements (3/4 MAC) was made approximately 1 hour after the induction of anesthesia but before intubation, surgical skin preparation or surgical incision. Our data indicate that at 1/2 and 3/4 MAC for halothane, mean arterial blood pressure (MAP) decreased from 92 ± 2 torr to 73 ± 3 torr and 67 ± 2 torr, respectively (p < 0.05). Pulmonary capillary wedge pressure (PCWP) increased from 6.2 ± 0.7 torr to 9.1 ± 1.6 torr and 9.4 ± 1.7 torr at 1/2 and 3/4 MAC halothane (p < 0.05). Cardiac index decreased from the control values of 2.67 ± 0.08 L/min/m2 to 2.19 ± 0.06 L/min/m2 for 1/2 MAC and to 2.24 ± 0.08 L/min/m2 at 3/4 MAC halothane (p < 0.05). Assisted ventilation was maintained throughout and arterial Pco2 was unchanged from control. Enflurane likewise resulted in a decrease in MAP from 99 ± 6 torr to 75 ± 4 torr at 1/2 MAC and 68 ± 5 torr at 3/4 MAC (p < 0.05). PCWP did not increase. In contrast, however, cardiac index was unchanged from control value of 2.65 ± 0.16 L/min/m2 at both 1/2 and 3/4 MAC. Arterial Pco2 was unchanged from the awake control value. Our data indicate that while both halothane and enflurane decrease mean arterial blood pressure, the mechanisms responsible differ. The primary afterload-reducing effect of enflurane may be beneficial to some patients with ischemic heart disease whereas other patients may benefit from the greater myocardial depression seen with halothane.

Indices of myocardial oxygenation during coronary-artery revascularization in man with morphine versus halothane anesthesia.

A prospective study in 12 adult male patients undergoing coronary-artery revascularization was conducted to compare the effects of a morphine versus a halothane anesthetic technique on several indices of myocardial oxygen supply and demand. Indices reflecting myocardial contractility, preload, afterload, and heart rate were measured. Undesirable increases in systemic and pulmonary capillary wedge pressure were minimized using sodium nitroprusside as needed. In the period after sternotomy but before revascularization, patients anesthetized with morphine (mean 2.1 mg/kg) had significant (P < .05) increases in rate-pressure product, tension-time index, blood pressure, and heart rate, as well as relative myocardial ischemia, evidenced by significant ST-segment depression in the V3 lead of the EKG and a decreased diastolic pressure-time index/tension-time index compared with patients anesthetized with halothane (mean .75 per cent inspired). Few difficulties associated with myocardial depression were seen in patients anesthetized with halothane. Halothane, at least in a well-monitored environment, is safe for use in patients without severe ventricular dysfunction undergoing coronary-artery revascularization.

Anesthesia and pericardial disease.

Compressive pericardial disease, which may occur as pericardial tamponade or constrictive pericarditis, is often a subclinical disease. Severe myocardial compression is distinctly uncommon, but its exact incidence is unknown. Despite improved diagnostic tools, prolonged longevity in many diseases, and increased use of cardiac catheterization, heart surgery, renal dialysis, and antibiotics, all of which may contribute to an increase in the incidence of pericardial disease, surgery is required in only a minority of patients who have chronic pain or severe hernodynamic impairment. Thus, the anesthetic literature contains only a few brief reports (1-6) on the perioperative care of patients with pericardial disease. However, the care of these critically ill patients demands extensive knowledge of the physiologic alterations in pericardial disease and the effects of anesthetics and other pharmacologic agents upon them. This review considers not only the anesthetic management, but also the diagnosis and pathophysiology of pericardial disease.

Reduction in halothane MAC: comparison of morphine and alfentanil.

The anesthetic potency and effectiveness of alfentanil and morphine were established by determining the effects of increasing drug doses on the alveolar anesthetic requirement of halothane to maintain a constant anesthetic (MAC) level. Six selected doses of alfentanil and four of morphine were administered to groups of mechanically ventilated rats anesthetized with halothane. Alfentanil was given as a loading dose followed by an intravenous infusion of 0.01–100 μg. kg −1.min −1, and morphine was administered as a subcutaneous dose of 4–20 mg/kg. The reduction in halothane requirement after morphine was biphasic, with a rapid linear increase occurring up to an 8 mg/kg subcutaneous dose, followed by a further, slower reduction in halothane requirement after doses of 8–20 mg/kg. At a 20 mg/kg dose, the halothane MAC was reduced approximately 84%. With alfentanil, a curvilinear reduction in halothane MAC occurred up to an alfentanil dose of 15μg. kg −1.min −1, where a 48% reduction was found. Larger doses produced severe truncal, chest wall, and abdominal rigidity, precluding adequate ventilation and the determination of MAC

Cardiovascular Anatomy and Physiology

Modern cardiac anesthesia probably began with the successful anesthetic procedure for mitral commissurotomy performed by Dr. Kenneth Keown on June 10, 1948 (34). The first use of cardiopulmonary bypass occurred on May 6, 1953, paving the way for more complex surgery and thus more complicated anesthetic management for cardiac patients. The need for a distinct subspecialty of cardiac anesthesia was recognized in the early 1970s, an event that has contributed immeasurably to successful cardiac surgery. The modern cardiac anesthesiologist must be conversant with the anatomy, physiology, and pathology of the cardiovascular system.

Lidocaine enhances intraoperative ventricular defibrillation.

The efficacy of lidocaine during myocardial reperfusion in coronary artery bypass surgery was evaluated in 20 patients randomly assigned to a control group (n = 10) or to receive lidocaine, 1 mg/kg intravenously 5 min before aortic unclamping and cardiac reperfusion, followed by infusion at 40 μg·kg−1 ·min−1 (n = 10). We recorded ECG leads II and V5 continuously, and number, energy, and current of direct current (DC) shocks starting at 1 joule. The number of low energy DC shocks to sustained defibrillation (5.5 ± 2.0 vs 3.5 ± 2.0, mean ± SD, P < 0.05) decreased significantly with lidocaine infusion. The energy (11.0 ± 6.3 vs 5.6 ± 3.9 joules, P < 0.05) and current (12.7 ± 4.2 vs 8.9 ± 4.7 amperes, not significant) likewise decreased with lidocaine infusion. Energy and current for the first successful shock, although lower in the lidocaine group, were not statistically significantly lower than in the control group. Initial reperfusion rhythm was not influenced by lidocaine. Plasma electrolyte levels, arterial blood gas tensions, myocardial temperature, and surgical technique—factors known to influence defibrillation—were similar in all patients. Administration of lidocaine during myocardial reperfusion allows defibrillation with fewer DC shocks of lower energy and current.

Arch Vessel Injury during Pulmonary Artery Catheter Placement

We have observed seven instances of unintentional cannulation of major arteries with 8F sheaths during preparation for open-heart operation. When the sheath was removed and the operation delayed, there were no complications; in the two instances in which the open-heart operation was performed immediately after arterial cannulation, there was 1 death due to hemorrhage and 1 false aneurysm of the carotid artery. Elective open-heart operations should be delayed if unintentional cannulation of a major artery occurs.