Joel A. Kaplan

Comparative hemodynamic effects of propofol and thiamylal sodium during anesthetic induction for myocardial revascularization

The safety and efficacy of propofol, a new intravenous anesthetic agent, have been demonstrated in healthy patients. Twenty-one patients, ASA III-IV, undergoing elective myocardial revascularization, were randomly chosen to receive either propofol, 2.5 mg/kg, or thiamylal, 4 mg/kg. for the induction of anesthesia. Hemodynamics were recorded at one and three minutes after drug administration during spontaneous respiration. After the addition of halothane and pancuronium with controlled ventilation, measurements were made immediately prior to and one minute after intubation. Five patients were dropped from the study, four due to airway problems and one due to severe hypotension following an induction dose of propofol. Statistics were done using data from the remaining 16 patients, eight in each group. Administration of propofol resulted in significant decreases in mean arterial pressure (MAP), systemic vascular resistance (SVR), and left ventricular stroke work index (LVSWI); as well as an increase in heart rate (HR). These changes were further accentuated by the addition of halothane and pancuronium prior to intubation. Patients in the thiamylal group experienced no significant hemodynamic changes until halothane and pancuronium were added and controlled ventilation was instituted. With these additions, the thiamylal group showed significant decreases in MAP and LVSWI immediately prior to intubation. Both groups experienced significant increases in HR following intubation, but no evidence of myocardial ischemia was seen in either group. All other parameters returned toward control values. Propofol appeared to be safe and effective for the induction of anesthesia in this group of patients, although its hemodynamic effects were greater than those of thiamylal.

Dupont critical care lecture: Role of ultrashort-acting β-blockers in the perioperative period☆

beta-blockade can result in extreme bradycardia, significant conduction problems, bronchospasm, or left ventricular dysfunction. For this reason, the use of long-acting beta-blockers is of limited value in the perioperative period. Esmolol, due to its ultrashort action and cardioselective properties, has been shown to be safe and effective for use in treatment of tachycardia and hypertension. Doses of up to 300 microg/kg/min for up to seven hours have been used with a return to baseline parameters within 30 minutes of discontinuation of the infusion. It can also be safely used in treatment of the asthmatic patient with tachycardia or hypertension with no clinically significant increases in airway resistance. Studies using esmolol during general anesthesia have also demonstrated that it appears to have no significant interaction with various anesthetic agents.

Comparative hemodynamic effects of labetalol and hydralazine in the treatment of postoperative hypertension

The antihypertensive efficacy and safety of IV labetalol were evaluated and compared with the efficacy and safety of IV hydralazine in the treatment of postoperative hypertension. Twenty patients undergoing major noncardiac surgery were entered into the study. Patients were randomized and treated for postoperative hypertension with either labetalol (n = 10) or hydralazine (n = 10). Labetalol and hydralazine both produced significant reductions in arterial blood pressure (p less than 0.001) within 10 minutes, which lasted at least 2 hours. In addition, labetalol produced a significant reduction in the heart rate and rate-pressure product without creating any adverse effects. In contrast, hydralazine produced significant sinus tachycardia requiring IV propranolol in three patients, two of whom developed transient ST segment depression. These results indicate that labetalol is safe and effective for the control of postoperative hypertension, especially in those patients who are least able to tolerate tachycardia.

The effects of metabolic acidosis and alkalosis on the response to sympathomimetic drugs in dogs

Sympathomimetic drugs are commonly used in many circumstances to increase cardiac output, blood pressure, and myocardial contractility. However, factors such as acidosis or alkalosis are known to influence the action of these drugs. This study looked at the response to the administration of epinephrine, norepinephrine, dopamine, dobutamine, isoproterenol, and glucagon at normal pH and under acidotic (pH 7.2 +/- 0.01) and alkalotic (pH 7.59 +/- 0.01) conditions in 17 dogs. Acidosis was produced with an infusion of hydrochloric acid and alkalosis by infusion of sodium bicarbonate. The infusions were given over one hour followed by a 15- to 30-minute stabilization period. With the administration of each sympathomimetic drug at each pH level, hemodynamic parameters and measurements of myocardia; contractility were recorded. Epinephrine increased cardiac output at normal pH, but decreased cardiac output under conditions of both acidosis and alkalosis; the net change from values at pH 7.40 was nearly 3 L/min. The only other drug to demonstrate this reversal of cardiac output, though to a lesser degree, was dopamine, 10 microg/kg/min, and only in the alkalotic state. Dobutamine was the only drug that decreased contractility under acidotic conditions, while all other drugs caused an increase. In sum, epinephrine was the only drug markedly affected by metabolic acidosis and alkalosis. Isoproterenols hemodynamic effects were altered the least by changes in acid-base balance. Alkalosis had an equally adverse effect on the cardiovascular system as compared with acidosis.

Response of lower esophageal contractility to changing concentrations of halothane or isoflurane: A multicenter study

A multiple-center study was performed to determine the relationship between lower esophageal contractility, clinical signs, and anesthetic concentration as expressed by minimum alveolar concentration (MAC). One hundred four American Society of Anesthesiologists Class I through III patients were exposed to isoflurane (with and without nitrous oxide) or halothane in concentrations of 0.5, 1.0, and 1.5 MAC. Heart rate and systolic blood pressure were continuously monitored. Both the amplitude and frequency of spontaneous and provoked lower esophageal contractions were measured in situ by using a 24-F probe equipped with provoking and measuring balloons. Combined results demonstrated statistically significant correlations (P<0.001) between lower esophageal contractility and MAC. Spontaneous lower esophageal contractions decreased from 1.10±0.12 (SEM) contractions per minute (0.5 MAC) to 0.42±0.05 (1 MAC) to 0.18±0.05 (1.5 MAC). Provoked lower esophageal contractility values decreased from 45±4 mm Hg (0.5 MAC) to 29±3 (1 MAC) to 19±2 (1.5 MAC). Heart rate changes did not correlate with MAC, and systolic blood pressure correlated in only one of three centers. Intracenter and intercenter analyses failed to demonstrate a significant relationship between lower esophageal contractility and heart rate or systolic blood pressure. No intracenter differences in either amplitude or frequency of lower esophageal contractions were observed, despite differences in volatile agents, induction techniques and agents, patient populations, and duration of anesthesia. Our studies indicate that lower esophageal contractility may be an indicator of anesthetic depth as reflected by MAC, but further studies are needed to quantify the effects of surgical stimulus, intravenous anesthetics, vasodilators, anticholinergics, calcium channel blockers, beta-adrenergic agonists, and the presence of a nasogastric tube.

Cardiovascular physiology: an overview

C ARDIAC PHYSIOLOGY will be discussed in a stepwise fashion. The events occurring during a single cardiac contraction will be described and the importance of stroke volume, as the mechanical product of such a contraction, and its determinants will be reviewed. The relationship between cardiac output and the peripheral circulation will also be analyzed by the use of ventricular function curves.

The Inodilators: An Expanding Role in the Perioperative Period

A NESTHESIOLOGISTS are seeing a changing patient population that is older and has more complex medical histories and multisystem diseases. Improvements in surgical techniques and medical management now allow high-risk cardiac patients to undergo procedures for which they would have been ineligible in the past. One of the major advances contributing to this change is the development of improved inotropic and vasodilator drugs. For many years, inotropes such as epinephrine have been used to improve contractility, but their use has been limited by side effects including increases in peripheral vascular resistance and myocardial oxygen demand. The addition of a vasodilator, such as nitroglycerin or nitroprusside, has allowed unloading of the right and left ventricles, resulting in further improvement in cardiac output (CO) and contractility. Though this combination therapy is useful, it is complicated and requires careful titration. A new category of drugs, the “inodilators,” has simplified the management of patients in severe heart failure or cardiogenic shock.’ Dopamine, dobutamine, and amrinone are mixed inotropicvasodilator drugs commonly used in the perioperative period.

Reversal of the adverse cardiovascular effects of intravenous diltiazem in anesthetized dogs

Intravenous diltiazem can be used to treat myocardial ischemia, hypertension, and supraventricular dysrhythmias, but significant adverse effects including atrioventricular block and hypotension have been reported. At the present time, there is controversy as to which drug is most effective in reversing these sequelae. This study was designed to assess the effectiveness of calcium chloride v epinephrine in reversing these side effects. The hemodynamic and electrophysiologic effects of diltiazem infusion were investigated in eight dogs anesthetized with fentanyl and nitrous oxide/oxygen. This study confirmed that diltiazem infusions in high concentrations produced predominantly atrioventricular conduction depression followed by profound hypotension. Epinephrine infusion proved to be most effective in attenuating and eliminating each of these deleterious side effects. In contrast, calcium chloride did not significantly increase heart rate or blood pressure or reverse atrioventricular block. In two instances calcium chloride produced further depression of atrioventricular conduction, leading to severe bradycardia and sinus arrest. Although calcium chloride increased left ventricular contractile force (LV dP/ dt) and cardiac index (CI), mean arterial pressure was not affected and SVR was further decreased. This study indicates that calcium chloride should not be given to reverse the side effects of diltiazem in the presence of atrioventricular conduction block or profound hypotension. Calcium chloride is indicated only when isolated myocardial depression is present and after the calcium channels have been reopened by epinephrine.

Cardiovascular effects of a nifedipine infusion during fentanyl-nitrous oxide anesthesia in dogs

The hemodynamic effects of a nifedipine infusion were investigated in eight dogs given fentanyl/pancuronium/nitrous oxide/oxygen anesthesia. Nifedipine (20 micrograms/kg) was given intravenously over two minutes immediately prior to each 30-minute infusion at 2 micrograms/kg/min, 4 micrograms/kg/min, and 6 micrograms/kg/min. The range of plasma nifedipine levels obtained was 52.1 to 113.7 ng/mL. The predominant hemodynamic effects were significant reductions in systemic vascular resistance (SVR) and mean aortic pressure (MAP), accompanied by a rise in cardiac index and heart rate (HR). Administration of calcium chloride (20 mg/kg) after the nifedipine infusion had no effect on SVR or MAP, but HR was significantly reduced. Serum epinephrine and norepinephrine levels increased after the infusion of nifedipine and suggested that fentanyl did not completely overcome the sympathetic response to the profound vasodilatation. The resulting tachycardia in combination with diastolic hypotension from nifedipine could have a detrimental effect on the myocardial oxygen balance.