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Hypotension was induced with halothane and labetalol, an alpha and beta adrenergic blocking agent, in nine children undergoing operation for postductal coarctation of the aorta. The mean arterial pressure decreased by an average of 30% following labetalol, and in six patients the initial halothane concentration (1%) had to be reduced during this period. The heart rate decreased by an average of 8% after labetalol. Profound beta-blockade did not occur, and operating conditions were considered satisfactory. The usefulness of labetalol in the postoperative period is suggested.     

Hypotensive anaesthesia for microsurgery of the middle ear. A comparison between isoflurane and halothane

Fifty patients undergoing microsurgery of the ear were anaesthetised using thiopentone, nitrous oxide, oxygen and either halothane or isoflurane, via a low flow circle system with carbon dioxide absorption. Systolic blood pressure was reduced to approximately 70 mmHg by the additional use of increments of labetalol; the patients breathed spontaneously. The degree of haemostasis was assessed by the surgeon who was unaware which volatile agent was being used to supplement anaesthesia. Isoflurane, although it is a potent vasodilator produced operating conditions which were indistinguishable from halothane. Isoflurane is thus a safe and reliable alternative to halothane as a volatile agent used to supplement anaesthesia when using induced hypotension for middle ear surgery.     

Response of the heart to acute hypertension during halothane, enflurane, and isoflurane anesthesia

In the open chest dog model, the response of the left ventricle exposed to acute mechanical hypertension was evaluated while the animals were receiving various concentrations of halothane, enflurane, and isoflurane. Myocardial contractility was quantified by the end-systolic pressure-length relation (ESPL). When the mean aortic pressure was increased by 40% above the control value for a given concentration of inhalation agent, the end-diastolic volume increased and thereby maintained stroke work. However, as the end-tidal concentrations of the anesthetics increased, this compensatory mechanism became progressively more ineffective as a result of myocardial depression caused by the anesthetics. No evidence could be found of an improvement in myocardial contractility as the aortic pressure was increased. Mild depression of myocardial contractility could be demonstrated for 1.1 MAC halothane, 0.6 MAC enflurane, and 1.0 MAC isoflurane. Severe depression of contractility occurred at 2.3 MAC halothane, 1.2 MAC enflurane, and 1.5 MAC isoflurane.     

Influence of desflurane,isoflurane and halothane on regional tissue perfusion in dogs

The actions of desflurane, isoflurane and halothane on regional tissue perfusion were studied using radioactive microspheres in dogs chronically instrumented for measurement of arterial and left ventricular pressure, global (left ventricular dP/dtmax) and regional (percent segment shortening) contractile function, and diastolic coronary blood flow velocity. Systemic and coronary haemodynamics and regional tissue perfusion were measured in the conscious state and during anaesthesia with equihypotensive concentrations of desflurane, isoflurane, and halothane. All three volatile anaesthetics (P < 0.05) increased heart rate and decreased mean arterial pressure, left ventricular systolic pressure, and left ventricular dP/dtmax Myocardial perfusion was unchanged in subendocardial midmyocardial, and subepicardial regions by the administration of either dose of desflurane. No redistribution of intramyocardial blood flow (endo/epi ratio) was observed during desflurane anaesthesia. Although regional myocardial perfusion was reduced (P < 0.05) in a dose-related fashion by halothane and by isoflurane at high concentrations, redistribution of intramyocardial blood flow was not observed during halothane or isoflurane anaesthesia. All three volatile anaesthetics reduced blood flow to the renal cortex, but only desflurane produced a decrease in renal cortical vascular resistance. Hepatic blood flow decreased in response to halothane but not desflurane or isoflurane. Concomitant decreases in hepatic resistance were observed during administration of desflurane and isoflurane. Dose-related decreases in intestinal and skeletal muscle blood flow were observed during halothane and isoflurane but not desflurane anaesthesia. The results suggest that desflurane maintains myocardial, hepatic, intestinal, and skeletal muscle blood flow while halothane and isoflurane decrease regional tissue perfusion in these vascular beds to varying degrees during systemic hypotension in the chronically instrumented dog.     

Circulatory effects of labetalol during halothane anaesthesia

Labetalol is a drug possessing both alpha and beta adrenergic receptor blocking properties. Its possible use in induced hypotension during halothane anaesthesia has been investigated. It causes a satisfactory decrease in arterial pressure unaccompanied by tachycardia. The circulatory effects of the drug during halothane anaesthesia, both with spontaneous and controlled respiration, have been measured and compared with those of halothane alone. In patients anaesthetised with 1% halothane, labetalol, with both spontaneous and controlled ventilation, was associated with a reduction in MAP from 71.5 mmHg to 54.0 mmHg (P less than 0.001) and 66.8 mmHg to 50.4 mmHg (P less than 0.001) respectively. This reduction was associated with decreases in Qt of 18% and 12% respectively. In the presence of labetalol, with 3% halothane and spontaneous respiration, the depressant effects of the anaesthetic on the heart became rapidly apparent: Qt was reduced by a further 28%. In patients not receiving labetalol, the depressant effects of 3% halothane were frequently countered by the positive inotropic effects of hypercarbia.     

Labetalol-induced hyperkalemia in renal transplant recipients

BACKGROUND: Labetalol is a commonly used agent for perioperative hypertension in renal transplant recipients. A previous report suggested that labetalol may cause life-threatening hyperkalemia after renal transplantation. METHODS: We performed a retrospective review of 103 consecutive renal transplants to determine whether labetalol was an independent predictor of hyperkalemia treatment. Thirty-eight patients (36.9%) received labetalol, and 65 patients (63.1%) had no labetalol medication. RESULTS: Of the 103 patients, 24 (23.3%) required treatment for hyperkalemia. Thirteen (34.2%) of the patients who had labetolol medication and 11 (16.9%) of the patients who did not receive labetalol were treated for hyperkalemia (p = 0.045). Factors considered for a logistic regression model included: the use of labetalol, cold ischemia time, diabetes, and dialysis method; intake of tacrolimus, beta blockers, angiotensin-converting enzyme inhibitors, or other antihypertensives prior to admission; the mannitol dose given intraoperatively, and the 24-hour urine output postoperatively. Intravenous labetalol (odds ratio OR = 4.52, confidence interval CI = 1.33-15.28; p = 0.02), 24- hour urine output (OR = 4.4, CI = 0.97-20.1: p = 0.47), increasing cold ischemia time (OR = 1.09, CI = 1.01-1.17; p = 0.02), and continuous ambulatory peritoneal dialysis (OR = 0.17, CI = 0.29-0.98; p = 0.036) were independent predictors. CONCLUSION: Labetalol appears to increase the risk of hyperkalemia in patients after renal transplantation.     

Sevoflurane Depresses Myocardial Contractility Less than Halothane during Induction of Anesthesia in Children

Background: Cardiovascular stability is an important prerequisite for any new volatile anesthetic. We compared echocardiographically derived indices of myocardial contractility during inhalation induction with sevoflurane and halothane in children.

Methods: Twenty children were randomized to receive either halothane or sevoflurane for inhalation induction of anesthesia. No preoperative medications were given. Myocardial contractility was evaluated at baseline and at sevoflurane and halothane end-tidal concentrations of 1.0 minimum alveolar concentration (MAC) and 1.5 MAC.

Results: There were no differences between groups in patient age, sex, physical status, weight, or height. Equilibration times and MAC multiples of sevoflurane and halothane were comparable. Vital signs remained stable throughout the study. Left ventricular end-systolic meridional wall stress increased with halothane but remained unchanged with sevoflurane. Systemic vascular resistance decreased from baseline to 1 MAC and 1.5 MAC with sevoflurane. Halothane depressed contractility as assessed by the stress-velocity index and stress-shortening index, whereas contractility remained within normal limits with sevoflurane. Total minute stress and normalized total mechanical energy expenditure, measures of myocardial oxygen consumption, did not change with either agent.     

No evidence for blood flow redistribution with isoflurane or halothane during acute coronary artery occlusion in fentanyl-anesthetized dogs

The present study examines the postulate that isoflurane, in contrast to halothane, causes redistribution of blood flow away from an ischemic myocardial region through vasodilation of adjacent normally perfused myocardium. The study was performed in open-chest dogs anesthetized with fentanyl; ischemia was induced by occlusion of the left anterior descending coronary artery. At 0.6% alveolar concentration, isoflurane increased transmural blood flow to 125% of control values (P less than 0.05) in the normal region without concomitant changes in blood flow to the ischemic region or in the endocardial/epicardial flow ratio in the ischemic region. The evidence excludes either transmural steal or regional redistribution phenomena. Myocardial blood flow variables returned to control values at 1.8% isoflurane, and no blood flow redistribution effects were evident. In contrast, whereas halothane 0.4% caused no significant effect on myocardial blood flows, an alveolar concentration of 1.2% decreased transmural blood flow to normally perfused left ventricle to 70% of control (P less than 0.05). Regional myocardial oxygen consumption in the normal and ischemic areas decreased at higher alveolar concentrations and was unchanged at the lower concentrations for both agents. Myocardial lactate production from the ischemic region was unchanged with either agent, suggesting that, in terms of metabolic changes, neither agent worsened ischemia during sustained occlusion of the left anterior descending coronary artery. The present data show no evidence for worsening of myocardial ischemia with either isoflurane or halothane. Isoflurane causes a relatively greater increase in perfusion compared to myocardial oxygen consumption of normally perfused myocardium; nevertheless, sufficient coronary vascular reserve remains in the native collateral circulation so that myocardial metabolic supply-and-demand relationships during ischemia are not further compromised.     

Cardiovascular effects of and interaction between calcium blocking drugs and anesthetics in chronically instrumented dogs. I. Verapamil and halothane

In order to assess the interaction between halothane and verapamil on the cardiovascular system, mongrel dogs were instrumented so that the following measurements could be made awake and under the influence of the drugs: aortic, left ventricular, and left atrial blood pressures; myocardial segment length shortening; heart rate and rhythm; and coronary, carotid, and renal blood flows. The effect of two infusion doses of verapamil (3 micrograms X kg-1 X min-1 and 6 micrograms X kg-1 X min-1 after 200 micrograms X kg-1 bolus) were examined awake. On a different day in the same dogs, two concentrations of halothane (1.2-low and 2.4-high % end-tidal) and the effect of the two infusion doses of verapamil during low and high halothane were studied. Thirty minutes of either infusion dose of verapamil produced only heart rate and electrocardiographic P-R interval increases in conscious dogs. Halothane produced dose-related decreases in mean aortic pressure, left ventricular maximum rate of tension development (dP/dt), and segment length shortening and increases in heart rate and left atrial pressure. Carotid blood flow was increased by low halothane concentrations and returned to control with high halothane concentrations. There were no significant changes in coronary or renal blood flow produced by halothane. Verapamil infusion during low halothane concentration produced minimal effects. However, both the 3 and 6 micrograms X kg-1 X min-1 verapamil doses further depressed hearts already depressed by the high concentrations of halothane and decreased renal and carotid blood flows.(ABSTRACT TRUNCATED AT 250 WORDS)     

Deliberate hypotension induced by labetalol with halothane, enflurane or isoflurane for middle-ear surgery

The feasibility of using labetalol, an alpha- and beta-adrenergic blocking agent, as a hypotensive agent in combination with inhalation anaesthetics (halothane, enflurane or isoflurane) was studied in 23 adult patients undergoing middle-ear surgery. The mean arterial pressure was decreased from 86 +/- 5 (s.e. mean) mmHg to 52 +/- 1 mmHg (11.5 +/- 0.7 to 6.9 +/- 0.1 kPa) for 98 +/- 10 min in the halothane (H) group, from 79 +/- 5 to 53 +/- 1 mmHg (10.5 +/- 0.7 to 7.1 +/- 0.1 kPa) for 129 +/- 11 min in the enflurane (E) group, and from 80 +/- 4 to 49 +/- 1 mmHg (10.7 +/- 0.5 to 6.5 +/- 0.1 kPa) for 135 +/- 15 min in the isoflurane (I) group. The mean H concentration during hypotension in the inspiratory gas was 0.7 +/- 0.1 vol%, the mean E concentration 1.6 +/- 0.2 vol%, and the mean I concentration 1.0 +/- 0.1 vol%. In addition, the patients received fentanyl and d-tubocurarine. The initial dose of labetalol for lowering blood pressure was similar, 0.52-0.59 mg/kg, in all the groups. During hypotension, the heart rate was stable without tachy- or bradycardia. The operating conditions regarding bleeding were estimated in a double-blind manner, and did not differ significantly between the groups. During hypotension, the serum creatinine concentration rose significantly in all groups from the values before hypotension and returned postoperatively to the initial level in the other groups, except the isoflurane group. After hypotension there was no rebound phenomenon in either blood pressure or heart rate. These results indicate that labetalol induces easily adjustable hypotension without compensatory tachycardia and rebound hypertension.     

The Combined Effects of Antihypertensive Drugs and Anaesthetics (Halothane and Ketamine) on the Isolated Heart

The effects of three concentrations of halothane or ketamine were investigated on isolated rabbit hearts, which were perfused with hydralazine, clonidine, propranolol or methyldopa. In hearts not subjected to the influence of an anaesthetic, clonidine was the only drug stimulating myocardial function. In those perfused with halothane or ketamine alone, both anaesthetics exerted a negative chronotropic and inotropic action in a dose-related manner. Ketamine markedly increased the coronary flow. Clonidine distinctly reduced the myocardial depression caused by halothane or ketamine. Hydralazine had no marked effects with either of these anaesthetics, except that it sensitized the hearts to the arrhythmic action of a high concentration of halothane. Propranolol, when combined with halothane, aggravated myocardial depression and decreased coronary flow. With ketamine, propranolol caused no other harmful interactions, apart from inhibiting the increase in coronary flow caused by this anaesthetic. Methyldopa intensified the myocardial depression induced by halothane, but tended to diminish that caused by ketamine. The results suggest that clonidine has a stimulatory cardiac action when combined with either of these anaesthetics. Disadvantageous interactions may exist between methyldopa or propranolol and halothane.     

Comparative coronary vascular reactivity and hemodynamics during halothane and isoflurane anesthesia in swine

To assess the dose-response effects of isoflurane and halothane anesthesia on hemodynamics and coronary artery reactivity, the authors studied myocardial hyperemic responses following brief single artery flow arrests in 21 open chest, isocapnic swine in which arterial blood pressures and cardiac outputs were recorded. A specially designed Doppler probe was used to measure the peak and time course of coronary blood flow velocity in the left anterior descending coronary artery (LAD) after 15-s LAD occlusions. The ratio of peak velocity of blood flow to resting velocity (coronary reserve), relative repayment of flow debt, and duration of hyperemic responses were studied. Surgery was performed at MAC end-tidal concentrations ([Et]isoflurane = 1.45%. [Et]halothane = 1.25%) of isoflurane (n = 7) or halothane (n = 7), and recordings were made after 15-min steady state [Et]agent at 0.5, 1, 1.25, 1.5, 1.75, 2 MAC, and further 0.5 MAC increments until the demise of each animal. To compare coronary reactivity at similar coronary pressures, an aortic snare was used to elevate arterial pressures in a third group of halothane anesthesized pigs (n = 7) to those in the previously studied isoflurane group at each MAC level. There were three major differences between halothane and isoflurane. First, cardiac depression (reduction in arterial pressure, cardiac output, and stroke volume) was less with isoflurane compared with halothane anesthesia. Second, with halothane anesthesia, there was a marked decrease in coronary reactivity independent of coronary perfusion pressures with marked, dose-dependent reductions in both coronary reserve and relative flow repayment. During isoflurane anesthesia, coronary reactivity and coronary reserve was well preserved within physiologic limits up to 1.75 MAC [Et]. Third, halothane anesthesized pigs died in cardiac collapse at much lower agent concentrations than with isoflurane (no animals survived 1.75 MAC halothane, whereas all animals survived 2.5 MAC isoflurane). Therefore, pigs anesthesized with isoflurane had greater coronary reserve, better preserved cardiac function, and greater tolerance to increasing agent concentration than pigs anesthesized with halothane.     

Comparison of the effects of halothane on skinned myocardial fibers from newborn and adult rabbit. I. Effects on contractile proteins

The effect of halothane on maximal and submaximal Ca2+-activated tension development of the contractile proteins of newborn and adult cardiac muscle from rabbits was determined. Right ventricular muscle was removed from newborn and adult rabbits, and the sarcolemma was disrupted (skinned) by homogenization. Fiber bundles were dissected from the homogenate and mounted on tension transducers. Fiber bundles were alternately immersed in relaxing solution [( Ca2+] less than 10(-9) M) and contracting solutions (various [Ca2+] from 10(-5.6) to 10(-3.8) M), which were saturated with 100% N2 alone or with three concentrations of halothane-N2 mixture. In the absence of halothane, newborn skinned myocardial fibers were slightly more sensitive to submaximal Ca2+ concentrations than were adult myocardial fibers. [Ca2+] required for 50% maximum tension were 10(-5.43) M and 10(-5.31) M, respectively (P less than 0.05). Halothane (1-3%) decreased the maximal Ca2+-activated tension (at [Ca2+] = 10(-3.8) M) similarly in adult and newborn myocardial fibers in a dose-dependent fashion. Tension was reduced by 5.9% for each 1% increase in halothane concentration. Halothane also decreased the sensitivity of adult myocardial skinned fibers to submaximal Ca2+ concentrations (10(-5.6) M to 10(-5.0) M) by shifting the Ca2+-tension response curve to the right. Only 3% halothane decreased the sensitivity of newborn myocardial skinned fibers to Ca2+. The authors conclude that halothane causes less depression of Ca2+ activation of the contractile proteins in newborn than adult rabbit myocardium and that this effect of halothane cannot account for greater negative inotropy of halothane in the newborn.     

Myocardial epinephrine sensitization with subanesthetic concentrations of halothane in dogs

The authors investigated myocardial epinephrine sensitization by subanesthetic concentrations of halothane. The dose-response relationship for the action of halothane was examined with etomidate plus varying subanesthetic concentrations of halothane in dogs. The arrhythmogenic threshold of epinephrine was decreased in a dose-dependent manner at end-tidal concentrations of halothane between 0.1 and 0.3%. At end-tidal halothane is greater than 0.3%, and no further reduction of arrhythmogenic threshold of epinephrine occurred. The plasma concentrations of epinephrine producing four or more premature ventricular contractions in 15 s were 201.3 +/- 34.3, 98.1 +/- 13.9, 60.3 +/- 8.63, 57.9 +/- 12.8, 54.5 +/- 8.61, and 53.9 +/- 4.86 ng/ml (mean +/- SEM), at 0, 0.1, 0.3, 0.5, 1.0, and 1.5% of halothane at end-tidal concentrations, respectively. The results suggest that in the presence of etomidate, halothane produces myocardial sensitization to epinephrine at subanesthetic concentrations as low as 0.1%. Increasing halothane to 0.3% produces a further reduction in the arrhythmogenic dose of epinephrine.     

Beta-adrenergic blocking drugs and renal function

A baboon model was used to investigate the effects of atenolol, nadolol, sotalol and labetalol on renal function. The glomerular filtration rate (GFR) and renal blood flow (RBF) were measured, using radionuclides and a gamma camera, before and after 1 week's oral administration of these drugs. All the drugs caused an increase in the GFR, but this reached statistical significance only in the cases of sotalol (P less than 0,025) and labetalol (0,05 less than P less than 0,10). The RBF was not significantly changed, although it decreased in all cases.     

Comparison of the in vitro myocardial depressant effects of isoflurane and halothane anesthesia

The myocardial depressant effects of isoflurane and halothane were compared using feline right ventricular papillary muscles bathed in Krebs-bicarbonate solution. In experiment 1 muscles were stimulated by field electrodes (0.2 Hz) to obtain control measurements of developed tension (dt) and maximal rate of tension development (dF/dt) prior to exposing the papillary muscles to four concentrations of either isoflurane (4.0%, 2.0%, 1.0%, 0.5%) or halothane (2.0%, 1.0%, 0.5%, 0.25%). Repeat measurements of dt and dF/dt were recorded after 20 min at each concentration. Isoflurane and halothane both caused dose-dependent depression of dt and dF/dt, but at 0.5%, 1.0%, and 2.0%, halothane was significantly more depressant than isoflurane (P less than 0.01 for dt and dF/dt). Quadratic equations were fitted to the dose-response data by least squares analysis (R2 greater than .985 for both anesthetics), and the isoflurane and halothane concentrations that decreased dt to 90%, 70%, 50%, and 30% of control were determined to compare the relative myocardial depressant potency of isoflurane and halothane by linear regression analysis. This potency relationship is described by the equation: isoflurane concentration = -0.005 + 1.445 (halothane concentration). In experiment 2 papillary muscle responses at two similar cardiodepressant concentrations of isoflurane (1.25% and 2.0%) or halothane (0.80% and 1.35%) were compared at stimulus frequencies of 0.05, 0.1, 0.2, 0.4, 0.8, 1.0, and 2.0 Hz. The concentrations of isoflurane and halothane were selected from the data obtained in experiment 1 and represent the anesthetic concentrations that diminish muscle function to approximately 70% and 50% of control.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison of the effects of sevoflurane and halothane on the quality of anaesthesia and serum glutathione transferase alpha and fluoride in paediatric patients

We have compared sevoflurane and halothane anaesthesia in paediatricpatients with reference to induction and recovery. We also assessedhepato-cellular integrity by measurement of serum gluta-thionetransferase alpha (GSTA) concentration and sevoflurane metabolismby serum fluoride concentration. Fifty unpremedicated 5–12-yr-oldchildren were allocated randomly to induction of anaesthesiavia a face mask with 66% nitrous oxide in oxygen and sevoflurane(up to 7%) or halothane (up to 3.5%). Anaesthesia was maintainedfor 1.8 h at 1–1.2 MAC of the volatile agent. Childrenreceiving sevoflurane had significantly faster induction andrecovery variables than those receiving halothane. There wasa small postanaesthetic increase in GSTA in both groups, suggestingthat halothane and sevoflurane may disturb hepato-cellular integrity.Serum concentrations of fluoride were significantly greaterafter sevoflurane than after halothane anaesthesia. There wereno clinical signs or symptoms of hepatic or renal disturbance.Children tolerated sevoflurane better than halothane, whichmay have been because of the non-pungency of sevoflurane andthe rapid psycho-motor recovery after anaesthesia.     

Myocardial ischemia in untreated hypertensive patients: effect of a single small oral dose of a beta-adrenergic blocking agent

In a non-double-blind, prospective, randomized study, the intra-operative electrocardiograms of 128 mildly hypertensive surgical patients were examined in order to determine the incidence of myocardial ischemia during anesthesia. No patient had been receiving chronic antihypertensive therapy prior to the study, but a single small oral dose of a beta-adrenergic blocking agent (labetalol, atenolol, or oxprenolol) was given to 89 of them along with premedication. Forty-four per cent of the untreated control patients and 61% of the patients pretreated with a beta-adrenergic blocking agent had normal preoperative electrocardiograms and no risk factors for coronary artery disease other than hypertension (this difference between groups was not statistically significant). During tracheal intubation and/or emergence from anesthesia, a brief, self-limited episode of myocardial ischemia was detected in 11 of 39 untreated control patients, and in two of 89 patients pretreated with a beta-adrenergic blocking agent (P less than 0.001). Tachycardia always accompanied the ischemic events, but a conspicuous increase in blood pressure did not. The authors conclude that mild hypertension, when untreated prior to the induction of anesthesia, is associated with a high incidence of myocardial ischemia; and that a single small oral dose of a beta-adrenergic blocking agent, given with pre-medication, can significantly reduce that risk.     

ISOFLURANE DOES NOT INCREASE THE INCIDENCE OF INTRAOPERATIVE MYOCARDIAL ISCHAEMIA COMPARED WITH HALOTHANE DURING VASCULAR SURGERY

We have studied the incidence of new intra-operative myocardialischaemia (IMI), myocardial infarction (Ml) and cardiac death(CD) in 500 consecutive patients undergoing elective major non-cardiacvascular surgery. Patients were allocated randomly to receiveeither halothane (n = 226) or isoflurane (n = 274) as principalanaesthetic agent. Using real-time ST segment trend analysis(leads V5 and II) IMI (halothane 39%, isoflurane 38%), MI (halothane1.3%, isoflurane 1.5%) and CD (halothane 0.4%, isoflurane 0.7%)did not differ significantly between the two groups. Twenty-threeper cent of IMI episodes were related to haemodynamic disturbances,but unrelated to the type of surgery: 148 supra-aortic (IMI= 39%), 244 abdominal aortic (IMI = 41%) and 108 lower extremityrevascularizations (IMI = 33%). We conclude that the choiceof volatile anaesthetic agent does not influence cardiac morbidityor mortality in this type of patient     

Myocardial metabolism and oxygenation in man awake and during halothane anesthesia.

Cardiac catheters were placed in seven healthy conscious patients so that aortic and left ventricular pressures (and the derivative), cardiac output (thermodilution) and myocardial blood flow (argon washin) could be measured. Blood was drawn for measurement of arterial blood-gas and arterial and coronary venous oxygen, glucose, lactate, pyruvate and fatty acid values. After induction of anesthesia by inhalation of halothane, the measurements were made during administration of low (0.70%) and high (1.54%) end-tidal halothane concentrations. Myocardial function decreased in a dose-related fashion without a change in heart rate. Myocardial blood flow and oxygen consumption were depressed in a similar manner. Myocardial oxygen extraction decreased and lactate did not change, suggesting that myocardial oxygenation was adequate. The heart rate-systolic blood pressure product correlated poorly with myocardial oxygen consumption. Systolic blood and the contractile performance index dP/dt/IP were better correlated with myocardial oxygen consumption, but the value of the coefficient was still low. Without significant changes in heart rate, systolic blood pressure is the best correlate of myocardial oxygen consumption in healthy man during the myocardial depression produced by halothane.