Quality of recovery after general anesthesia with isoflurane or halothane

The quality of recovery and the time required for it were compared in two groups of 20 patients after general anaesthesia with isoflurane or halothane for elective head and neck surgery. The groups were comparable with regard to age, sex ratio, ASA physical status, type of surgery and duration of anaesthesia. After premedication with diazepam and atropine, a standard induction technique was used (thiopentone, succinylcholine), avoiding opiates and sedatives. Maintenance was assured with a mixture of 30% oxygen, 70% nitrous oxide and isoflurane or halothane. The time between the end of administration of anaesthetic drugs and eye opening was 7.15 +/- 2.9 min in the isoflurane group, and 11.0 +/- 4.7 min in the halothane group (p less than 0.01). The differences between the times for the return of spatial and temporal orientation and of mental arithmetic were not significant, though they were clinically clearly perceptible. The patients were less sleepy, livelier and less agitated in the isoflurane group in the first hour of recovery. Recovery was more rapid after general anaesthesia with isoflurane, and of better clinical quality.     

Endocrine stress response in halothane, enflurane and isoflurane anesthesia in surgical interventions

The endocrine stress response under inhalation anesthesia with halothane, enflurane, and isoflurane was investigated in 30 patients during and after orthopedic surgery (Table 2). Plasma levels of adrenaline and noradrenaline (by HPLC/ECD), ADH, ACTH, and cortisol (by RIA), glucose, lactate, and free glycerol were determined before induction of anesthesia, 10 min after intubation, 10 min before the end of the operation, and 5 and 30 min after extubation. Statistical evaluation was undertaken by analysis of variance with repeated measures on one factor. P values of less than 0.05 were considered significant. There were no significant differences in the concentrations of plasma catecholamines (Table 4, Figs. 1 and 2), ADH, ACTH (Table 5, Figs. 3 and 4), or cortisol before and during surgery between the groups. ADH was lower in the halothane group 5 and 30 min after extubation (P = 0.05), which might be due to the prolonged elimination of halothane after anesthesia. Blood pressure, heart rate (Table 3), and plasma concentrations of glucose, lactate, and free glycerol (Table 6) were comparable in all groups. It is concluded that for clinical practice halothane, enflurane, and isoflurane are comparable in their influence on the surgical stress response.     

Atracurium with halothane and isoflurane in pediatric anesthesia

The study was carried out to assess the effects of atracurium neuromuscular blockade in children anaesthetized with N2O:O2: halothane vs N2O:O2: isoflurane. Thirty-two ASA I-II children, age 1-13 yr, undergoing elective surgery, were divided into two groups according to age and the mode of anaesthesia induction. Anaesthesia was induced in the younger children (group 1: 1-6 yr) with nitrous oxide and inspired halothane or isoflurane in oxygen via a face mask. Intravenous thiopental (6-7 mg/kg-1) was used to induce anaesthesia in older children (group 2: 7-13 yr). Each group of patients was randomly allocated to two groups each receiving halothane (group A: n = 8) or isoflurane (group I: n = 8). Halothane 0.8% end-tidal and isoflurane 1% end-tidal as anaesthesia maintenance. A bolus dose of atracurium 0.35 mg/kg-1 was administered. Premedication consisted of oral flunitrazepam (0.04 mg/kg-1) and bellafoline (0.02 mg/kg-1). Heart rate (by electrocardiography), arterial pressure (by auscultation) were monitored. Then end-expired carbon dioxide concentration was maintained at 30-40 mmHg. Neuromuscular transmission was evaluated by response to indirect stimulation (TOF) of the ulnar nerve at the wrist via surface electrodes. Conditions for endotracheal intubation were excellent in 25 of the children, good in 6 and poor in 1. The intubation was carried out within 112 s (group 1A), 130 s (group 1 I), 112 s (group 2A) and 135 s (group 2 I) following the administration of atracurium. The maximum twitch depression was recorded in the isoflurane groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Psychological eff-cts of halothane and isoflurane anesthesia.

Psychological effects of halothane (16 subjects) and isoflurane (24 subjects) anesthesia on healthy young men were assessed prior to and 2,3,4,6,8, and 30 days after anesthesia. The results with each agent were compared with each other and with the results for 41 unanesthetized controls. Both agents altered psychological function. Changes in function were greatest 2 days after anesthesia; function had returned to near preanesthesia values 8 days after anesthesia. Only slight symptom and mood effects and no intellectual effect attributable to anesthesia remained 30 days after anesthesia. Halothane produced greater negative effects on moodds and symptoms and tended to produce greater negative effects on intellectural function than did isoflurane. The differences between the two anesthetics are consistent with differences in their solubilities and metabolism.     

Microcirculatory response to halothane and isoflurane anesthesia.

Microcirculatory hemodynamics are often used to monitor tissue and organ survival. This study investigated the effect of halothane and isoflurane anesthesia on peripheral microcirculation using the cremaster muscle during intravital microscopy. Twenty-three Sprague-Dawley rats were studied in four groups. Two groups served as controls and did not undergo flap isolation but did receive halothane (N = 6) or isoflurane (N = 5). After induction with a single dose of intraperitoneal pentobarbital (40 mg per kilogram), rats were ventilated with either 2 minimum alveolar concentration (MAC) halothane or 2 MAC isoflurane. Esophageal temperature, electrocardiography, central venous pressure, mean arterial pressure, and blood gases were measured over 4 hours. In groups receiving surgery with either halothane (N = 6) or isoflurane (N = 6), the cremaster muscle was isolated on the neurovascular pedicle. Microcirculatory responses to both halothane and isoflurane anesthesia were evaluated by measuring red blood cell (RBC) velocity, vascular diameters in arterioles (A1, A2-1, A2-2, and A3) and the main venule (V1), functional capillary perfusion, and leukocytic endothelial interactions in postcapillary venules (rolling, adherent, and transmigrating leukocytes). Hemodynamic variables were compared among all four groups, and microcirculatory variables were compared between the two surgical groups. During isoflurane anesthesia in animals with flaps, significantly higher (p < 0.05) RBC velocities were recorded in arterioles A1 (24.4%), A2-2 (28.2%), and A3 (17.4%). Capillary perfusion was significantly higher in animals with flaps and halothane anesthesia (17.8%; p < 0.05). The number of rolling leukocytes (39.4%) was significantly higher during isoflurane anesthesia in animals with flaps (p < 0.05). Better flow hemodynamics in the peripheral microcirculation were seen during halothane anesthesia, and were confirmed by greater functional capillary perfusion and fewer activated leukocytes. In the isoflurane group, RBC velocity alone cannot serve as an indicator of microcirculatory function.     

The hemodynamic and cardiovascular effects of isoflurane and halothane anesthesia in children

The hemodynamic and cardiovascular effects of isoflurane and halothane anesthesia were studied in 15 unpremedicated ASA I children using measurements of heart rate, blood pressure and M-mode echocardiography (echo). The children (ages 2 to 7.3 yr) were randomly assigned to receive either isoflurane (N = 8) or halothane (N = 7) with oxygen. End-tidal carbon dioxide concentrations (range 30-44 mmHg) were monitored throughout the study in each child. The experimental protocol was completed prior to intubation and the initiation of surgery. Within each anesthetic group, preinduction (control) hemodynamic and echo measurements were compared with measurements obtained at two sequential equipotent end-tidal anesthetic concentrations (0.74% and 2.22% isoflurane; or 0.5% and 1.5% halothane). We also compared the data of the isoflurane group with that of the halothane group at each equipotent end-tidal anesthetic concentration. Preinduction hemodynamic (heart rate, blood pressure) and echo measurements (left ventricular dimensions and function) were similar between the two anesthetic groups. With isoflurane or halothane administration, blood pressure decreased significantly, while heart rate remained essentially unchanged. The observed alterations in heart rate and blood pressure were similar in both study groups at each equipotent end-tidal anesthetic concentration. In contrast, there were marked differences in the echo measurements of the two anesthetic groups. Halothane was associated with a significant dose-dependent decrease in echo-measured left-ventricular shortening fraction and mean velocity of circumferential fiber shortening. These echo measurements were not significantly altered by isoflurane at either end-tidal anesthetic concentration. These alterations suggest halothane is associated with significant myocardial depression in normal children, while myocardial function is well preserved during isoflurane anesthesia.     

Hepatic circulation during surgical stress and anesthesia with halothane, isoflurane, or fentanyl

Hepatic blood flow and the oxygen supply/uptake relation were studied in 19 miniature pigs using labeled microspheres. Changes in hepatic arterial blood flow and portal blood flow, as well as total hepatic blood flow during halothane anesthesia were more closely associated with changes in mean arterial pressure (MAP) and cardiac output than during anesthesia with isoflurane or fentanyl. Halothane or isoflurane administered in concentrations that decreased MAP by approximately 30% were accompanied by decreases in hepatic oxygen delivery (DO2th) averaging 46% during halothane and 31% during isoflurane anesthesia and parallel decreases in hepatic blood flow. In concentrations that decreased MAP by 50%, halothane and isoflurane decreased DO2th 61 and 37%, respectively. DO2th was maintained (statistically insignificant, 23% increase) during both doses of fentanyl administered (20 micrograms/kg followed by 0.17 microgram . kg-1 . min-1, and 50 micrograms/kg followed by 0.42 microgram . kg-1 . min-1). Hepatic oxygen uptake increased 50% during fentanyl and was maintained at baseline levels during both doses of halothane and isoflurane anesthesia. Oxygen content in hepatic venous blood was maintained at baseline levels during fentanyl and isoflurane administration and was decreased by both concentrations of halothane anesthesia. The hepatic oxygen supply demand ratio was maintained at baseline levels after both doses of fentanyl and during isoflurane administered in a concentration that decreased blood pressure 30%; the ratio decreased during isoflurane administered in a concentration decreasing blood pressure by 50% and during both doses of halothane anesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparative study of the behavior of isoflurane and halothane in pediatric anesthesia]

This study involves 60 patients below the age of 14 years who were subjected to short duration surgical procedures under inhalation anesthesia with halothane and isoflurane at equivalent CAM in 50% protoxide. The objectives of the study were: a) to establish which of the two inhalational agents produced the more rapid anesthetic induction; b) to determine which exerted the more marked potentiation of the neuromuscular blockade induced by succinylcholine, and c) to compare the anesthetic quality during the induction and recovery periods of both halogenated agents. Induction was more rapid after halothane (mean induction time of 2.91 +/- 0.97 min) than after isoflurane (mean induction time of 6.24 +/- 2.88 min; p less than 0.001). Potentiation of succinylcholine induced neuromuscular blockade was greater after isoflurane than after halothane: the mean time of apnea was 4.56 +/- 1.82 min for isoflurane and 3.41 +/- 1.63 min for halothane (p less than 0.05). Undesirable effects were larger in patients treated with isoflurane than in patients anesthetized with halothane (mean score: 12.60 +/- 3.53 points vs 14.41 +/- 2.33 points; p less than 0.001). The analysis of anesthetic quality during the recovery period gave a mean punctuation of 16.62 +/- 2.21 to patients treated with halothane, whereas patients anesthetized with isoflurane showed a lower score of 14.25 +/- 1.99 points (p less than 0.001). The higher scores corresponded to the most well tolerated anesthetic induction and recovery. The highest attainable score in this study was 18.     

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)     

Hepatic oxygen supply during halothane or isoflurane anesthesia in guinea pigs

The present study was designed to determine changes in hepatic oxygen supply in guinea pigs during halothane or isoflurane anesthesia. Twenty-seven guinea pigs were randomly divided into three equal groups: control (no anesthesia) group, and animals anesthetized with halothane or isoflurane to decrease mean arterial pressure (MAP) by 50%. Hepatic arterial blood flow (HABF) and portal blood flow (PBF), as well as arterial and portal venous blood oxygen content, were determined in awake animals (stage I, baseline values), and during anesthesia (stage II). HABF was found to be extremely low (0.04 ml.min-1.g-1) during both stages of observation in the control (no anesthesia) group, as well as during stage I (awake) in animals treated with halothane or isoflurane. Equal degrees of arterial hypotension during halothane and isoflurane anesthesia were accompanied by decreased HABF during halothane (37%), but no significant change in HABF during isoflurane anesthesia. PBF decreased significantly in both experimental groups; however, the decrease was more prominent during halothane than during isoflurane anesthesia (57% vs. 23%). The observed hepatic circulatory changes led to a 65% decrease in hepatic oxygen delivery during halothane, but only a 34% decrease during isoflurane anesthesia. The present study does not exclude the possibility that liver damage in the guinea pig model is related to the reductive metabolism of halothane or any other mechanism. However, the extremely low HABF and a prominent reduction in both HABF and PBF during halothane anesthesia may be responsible for hepatic damage observed in the guinea pig model.     

Cerebral blood flow and oxygen consumption during isoflurane and halothane anesthesia in man

In 13 patients, the effects on cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) of isoflurane and halothane administered in a clinically relevant situation were studied. Measurements were performed during fentanyl/nitrous oxide (65%) anesthesia together with moderate hyperventilation (PaCO2 approx 4.5 kPa), and repeated after addition of 0.65 MAC of isoflurane (n = 6) or halothane (n = 7). CBF was measured after intravenous administration of 133xenon and CMRO2 was calculated from the arterial venous differences of oxygen content (AVDO2) determined in arterial and jugular venous bulb blood. CBF and CMRO2 (means +/- s.e. mean) determined prior to administration of volatile agents were 28 +/- 5 ml x 100(-1) x min-1 and 2.0 +/- 0.3 ml x 100 g-1 x min-1, respectively, in the isoflurane group. In the halothane group, CBF was 25 +/- 0.4 ml x 100 g-1 x min-1 and CMRO2 was 2.0 +/- 0.4 ml x 100 g-1 x ml-1. There were no significant intergroup differences. Isoflurane did not change CBF, whereas halothane produced an increase of 36% (P less than 0.05) compared to values obtained during fentanyl/N2O anesthesia. In addition, isoflurane caused a further decrease in CMRO2 of 12% (P less than 0.01) as compared to a 20% increase (P less than 0.05) with halothane. The cerebral metabolic depression caused by the short-acting anesthetic induction agents would be expected to decrease with time, and could partly explain the observed increase in CMRO2 produced by halothane. The study suggests that the cerebrovascular and metabolic properties of isoflurane differ from those of halothane, also in man.     

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.     

Distribution of cerebral blood flow during halothane versus isoflurane anesthesia in rats

The effects of halothane versus isoflurane on distribution of cerebral blood flow (CBF) were compared using 14C-iodoantipyrine autoradiography. Sprague-Dawley rats were exposed to 1 MAC of either halothane (n = 8) or isoflurane (n = 7) in 33% O2/balance nitrogen for 55 min prior to determination of CBF. Normoxia, normothermia, and normocapnia were maintained throughout the experiment and arterial pressures (MAP) were held within the range of 90-100 mmHg by infusion of blood. Coronal autoradiographic brain images were then digitized and optical density values converted to CBF with the use of 14C autoradiographic standards and arterial radioactivity data. Hemispheric, neocortical, subcortical, and selected local anatomical regions were defined on a cathode ray screen display by cursor outline. Mean CBF for each region was determined at each of eight standardized coronal brain sections, and area weighted average values for the whole brain were also calculated. Hemispheric CBF was identical in the two anesthetic groups: halothane = 150 +/- 16 ml.100 gm-1.min-1; isoflurane = 147 +/- 19 ml.100 gm-1.min-1. However, neocortical CBF was greater in halothane anesthetized animals (halothane = 185 +/- 16 ml.100 gm-1.min-1; isoflurane = 154 +/- 19 ml.100 gm-1.min-1, P = .004). The authors conclude that halothane and isoflurane exert regionally selective effects on CBF with halothane appearing to have a more pronounced effect on the neocortex. Previously reported discrepancies concerning the relative effects of these two agents on CBF may be due to inherent differences in the tissue regions measured by the different techniques.     

Atracurium infusion requirements in children during halothane, isoflurane, and narcotic anesthesia

We were interested in determining the dose-response relationship of atracurium in children (2-10 yr) during nitrous oxide-isoflurane anesthesia (1%) and the atracurium infusion rate required to maintain about 95% neuromuscular blockade during nitrous oxide-halothane (0.8%), nitrous oxide-isoflurane (1%), or nitrous oxide-narcotic anesthesia. Neuromuscular blockade was monitored by recording the electromyographic activity of the adductor pollicis muscle resulting from supramaximal stimulation at the ulnar nerve at 2 Hz for 2 sec at 10-sec intervals. To estimate dose-response relationships, three groups of five children received 80, 100, 150 micrograms/kg atracurium, respectively. During isoflurane anesthesia, the neuromuscular block produced by 80 micrograms/kg was 23.6% +/- 6.5 (mean +/- SEM), by 100 micrograms/kg was 45% +/- 7.2, and by 150 micrograms/kg was 64% +/- 8.7. The ED50 and ED95 (estimated from linear regression plots of log dose vs probit of effect) were 120 micrograms/kg and 280 micrograms/kg, respectively. At equipotent concentrations, halothane and isoflurane augment atracurium neuromuscular block to the same extent, compared to narcotic anesthesia. Atracurium steady-state infusion requirements averaged 6.3 +/- 0.6 micrograms . kg-1 . min-1 during halothane or isoflurane anesthesia; the requirements during balanced anesthesia were 9.3 +/- 0.8 micrograms . kg-1 . min-1 (P less than 0.05). There was no evidence of cumulation during prolonged atracurium infusion.