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Cardiovascular responses and the need for intervention with vasoactive agents were measured prospectively in a randomized study of 50 adult patients receiving sufentanil (n = 20), fentanyl (n = 20), or morphine (n = 10) anesthesia for cardiac surgery. Measurements were recorded and compared during induction and prebypass at intervals during which airway or surgically induced stress responses were likely to be greatest. Randomized, double-blinded doses of opioids were administered slowly and titrated according to clinical responses (hemodynamics) and the electroencephalogram. Mean doses were as follows: from induction until time of incision, sufentanil, 9.1 microg/kg; fentanyl, 58 microg/kg; and morphine, 2.5 mg/kg; and total dose for surgery; sufentanil, 18.9 microg/kg; fentanyl, 95.4 microg/kg; and morphine, 4.4 mg/kg. Equi-anesthetic depth in patients receiving sufentanil or fentanyl was confirmed by continuous electroencephalographic monitoring. Patients anesthetized with sufentanil and fentanyl showed marked cardiovascular stability and rarely responded to stimuli. Systolic arterial pressure, mean arterial pressure, heart rate, cardiac index, systemic vascular resistance index, pulmonary vascular resistance index, stroke volume index, and stroke work index values were similar in the two groups. Patients receiving morphine experienced large changes in several variables. Pharmacologic intervention was made when systolic arterial pressure deviated more than 30% from pre-event values and was uncontrolled by additional opioids. Interventions were necessary more often in patients receiving morphine (nine of ten) or fentanyl (12 of 20) than in patients receiving sufentanil (six of 20), P < 0.05. Results from this study suggest that morphine is a relatively unsatisfactory anesthetic, while sufentanil and fentanyl, at equi-anesthetic depths, provide stable and satisfactory hemodynamics.

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There are numerous mechanisms of hypoxemia and hypercapnia during the perioperative period. Mechanisms of hypoxemia include oxygen delivery problems, decreased FAC-CC relationship, hypoventilation, decreased cardiac output, increased oxygen consumption, decreased hypoxic pulmonary vasoconstriction, and increased nonalveolar right-to-left shunting. Mechanisms of hypocapnia include increased carbon dioxide production, increased alveolar dead space, and increased external dead spaces. Pulmonary diseases often involve multiple mechanisms to produce hypoxemia and hypercapnia.

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Blood anesthetic concentration and clinical indicators related to anesthetic management during surface-induced deep hypothermia were determined in seven adult mongrel dogs. The azeotrope of halothane and diethyl ether was assayed by gas chromatography. Blood concentration of halothane ranged from a pre-cooling control of 0.74 vol % to 0.11 vol % at 20 degrees C rewarming; ether ranged from 0.06 vol % at 20 degrees C rewarming to 0.22 vol % at 35 degrees C rewarming. Administration of anesthetic was reduced during cooling because of the spontaneous decrease in mean arterial pressure and heart rate. After elective circulatory arrest was induced, anesthetic was not required until after cardiac resuscitation at about 22 degrees C rewarming. Initial clinical signs indicating a need to increase administration of anesthetic included spontaneous respiration and an increase in mean arterial pressure. Blood azeotrope concentration was significantly lower during rewarming than at comparable temperatures during cooling. We conclude that blood concentration of halothane and ether changes as a function of body temperature and that anesthetic demand may be diminished following total circulatory arrest.

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In an effort to describe the immediate course of pulmonary hypertension following mitral valve replacement, we reviewed preoperative and postoperative data from 62 patients who underwent mitral valve replacement. Patients were divided based on the absence (Group I) or presence (Group II) of severe preoperative pulmonary hypertension, defined as a mean pulmonary artery pressure greater than or equal to 40 mm Hg. Group II patients were subdivided based on the absence (Group IIa) or presence ( Group IIb) of markedly elevated preoperative pulmonary vascular resistance indices, defined as a greater than or equal to 700 dynes . sec . cm-5 . m2. Pulmonary artery wedge pressures fell promptly following mitral valve replacement in all groups, but the course of other hemodynamic parameters varied among groups. Cardiac index increased significantly among Group I and IIb patients but not among Group IIa patients. Group I patients did not have significant changes in mean pulmonary artery pressure and pulmonary vascular resistance index. Group IIa patients had substantial reductions in mean pulmonary artery pressure while pulmonary vascular resistance index remained near 400 dynes . sec . cm-5 . m2. Group IIb patients had substantial reductions in mean pulmonary artery pressure while pulmonary vascular resistance index fell significantly to about 400 dynes . sec . cm-5 . m2. Primary valvular lesion and pharmacologic support were insignificant variables. Data from these hemodynamic groups suggest that at least three mechanisms contribute to the pulmonary hypertension seen in mitral valve disease: passive transmission of elevated left atrial pressures, reactive pulmonary arteriolar vasoconstriction, and morphologic changes in the pulmonary vasculature. The first two mechanisms appear to be rapidly reversed following mitral valve replacement. While others have described the regression of pulmonary hypertension several months following mitral valve operations, data presented here suggest that changes in pulmonary artery pressures and pulmonary vascular resistance index may occur much earlier.

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