Nitrous oxide: cardiovascular effects in infants and small children during halothane and isoflurane anesthesia

Two-dimensional and pulsed Doppler echocardiography were used to measure cardiovascular function in 31 unmedicated infants and small children. In 15 patients, the cardiovascular effects of equipotent levels of halothane were compared with and without N2O. In 16 patients, the cardiovascular effects of isoflurane with and without N2O were compared. Prior to anesthesia induction, cardiovascular measurements of heart rate (HR), mean blood pressure (MBP), and two-dimensional and pulsed Doppler echocardiography were recorded. The echocardiographic measurements were used to determine cardiac output (CO), stroke volume (SV), ejection fraction (EF), and left ventricular end-diastolic and end-systolic volume (LVEDV and LVESV). Twenty minutes after mask inhalation induction with halothane or isoflurane with N2O and O2 (3:2 liters/min), cardiovascular measurements were repeated with end-expired halothane or isoflurane maintained at 0.9 MAC. A third set of cardiovascular data was collected 10 minutes after the discontinuation of N2O, with inspired isoflurane or halothane levels in O2 (5 liters/min) increased to maintain 1.5 MAC end-expired levels. Ventilation was controlled throughout the study period and the study was completed before intubation and the start of elective surgery. Heart rate and MBP decreased to similar degrees below awake levels in both patient groups during N2O with halothane or isoflurane. When N2O was discontinued and end-expired levels of halothane or isoflurane increased, MBP remained at levels observed during N2O-O2 with halothane or isoflurane. Heart rate increased during isoflurane in O2. Cardiac output decreased significantly and similarly below awake levels during both halothane of isoflurane with and without N2O.     

The effect of nitrous oxide on cortical cerebral blood flow during anesthesia with halothane and isoflurane, with and without morphine, in the rabbit

The effect of nitrous oxide on cortical cerebral blood flow (CBF) was examined during a varying background anesthetic state in the New Zealand White rabbit. Seventy percent nitrous oxide resulted in significant and similar increases in CBF during anesthesia with both 0.5 MAC of halothane (44 +/- 14 to 63 +/- 17 ml.100 g-1.min-1) (mean +/- SD) and anesthesia with isoflurane (34 +/- 9 to 41 +/- 11 ml.100 g-1.min-1). During anesthesia with 1.0 MAC halothane or isoflurane, N2O also increased CBF, but the increments (halothane, 73 +/- 34 to 111 +/- 54 ml.100 g-1 min-1; isoflurane 34 +/- 13 to 69 +/- 34 ml.100 g-1.min-1) were significantly greater than those observed at 0.5 MAC. When 0.5 MAC halothane or isoflurane was supplemented with morphine (10 mg/kg followed by an infusion of 2 mg.kg-1.min-1), the CBF effect of N2O was not significantly different from that observed with 0.5 MAC alone. It was concluded that, in the rabbit, the effects of N2O on cortical CBF vary with the background anesthetic state and that the increase in CBF caused by N2O becomes greater as the end-tidal concentration of halothane or isoflurane increases from 0.5 to 1.0 MAC. Morphine, when added to 0.5 MAC of halothane or isoflurane, does not alter the effect of 70% N2O on cortical CBF.     

Cardiovascular responses to acute loading with nifedipine alone and nifedipine plus propranolol during inhalation anesthesia in monkeys

The cardiovascular effects of the administration of nifedipine and nifedipine combined with propranolol were examined in 15 monkeys during 0.75 and 1.25 MAC of anesthesia with isoflurane, enflurane, or halothane. Hemodynamic variables measured included heart rate (HR), mean arterial pressure (MAP), left ventricular end-diastolic pressure (LVEDP), maximum rate of increase of the Left ventricular pressure (max LV dP/dt), and thermodilution cardiac output (CO). The infusion of nifedipine at a rate adequate to produce therapeutic blood levels during 0.75 MAC with each anesthetic decreased MAP and SVR, but had no effect on cardiac index (CI), max LV dP/dt, or HR. Increasing the anesthetic concentration from 0.75 to 1.25 MAC during nifedipine administration decreased HR and MAP in all groups and decreased CI with halothane and enflurane, but not with isoflurane. Addition of propranolol by infusion in amounts adequate to produce 75% beta-adrenergic blockade caused a further depression of CI, max LV dP/dt, HR, and MAP. However, the hemodynamic depression was significantly greater with halothane and enflurane than with isoflurane. Intravenous administration of calcium chloride (10 mg/kg) after calcium channel and beta-adrenergic blockade only partially reversed the hemodynamic depression that occurred with all three anesthetics. It was concluded that acute loading with nifedipine with and without propranolol exerts a greater cardiovascular depressant effect during enflurane or halothane anesthesia than during isoflurane anesthesia. The myocardial depressant effects of nifedipine and propranolol myocardial depressant effects of nifedipine and propranolol may be synergistic with the depressant effects of potent inhalation anesthetics.     

Comparative hemodynamic depression of halothane versus isoflurane in neonates and infants: an echocardiographic study.

The purpose of this study was to measure and compare the relationship of cardiovascular depression and dose during equal potent levels of halothane and isoflurane anesthesia in neonates (n = 19) (16.7 +/- 6.9 days) and infants (n = 54) (6.1 +/- 3.1 mo). Seventy-three children had heart rate, arterial blood pressure, and pulsed Doppler pulmonary blood flow velocity as well as two-dimensional echocardiographic assessments of left ventricular area and length recorded just before anesthesia induction. Anesthesia was induced by inhalation of increasing inspired concentrations of halothane or isoflurane in oxygen using a pediatric circle system and mask. During controlled ventilation, halothane and isoflurane concentrations were adjusted to maintain 1.0 MAC and then 1.5 MAC (corrected for age), and echocardiographic and hemodynamic measurements were repeated. A final cardiovascular measurement was recorded after intravenous administration of 0.02 mg/kg of atropine. All measurements were completed before tracheal intubation and the start of elective surgery. In neonates, 1.0 MAC concentrations of halothane and isoflurane decreased cardiac output (74% +/- 16%), stroke volume (75% +/- 15%), and ejection fraction (76% +/- 15%) similarly from awake levels. Decreases in cardiac output, stroke volume, and ejection fraction with halothane and isoflurane were significantly larger at 1.5 MAC (approximately 35% decreases from awake values) than at 1.0 MAC. Heart rate decreased significantly during 1.5 MAC halothane anesthesia (94% +/- 4%) but remained unchanged during isoflurane anesthesia. In infants, 1.0 MAC halothane and isoflurane decreased cardiac output (83% +/- 12%), stroke volume (78% +/- 12%), and ejection fraction (74% +/- 12%) when compared with awake measures.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pulsed Doppler and two-dimensional echocardiography: comparison of halothane and isoflurane on cardiac function in infants and small children

The combination of two-dimensional and pulsed Doppler echocardiography was used to measure determinants of cardiac function in 20 ASA physical status I infants and small children (9 days-32 months of age) during equipotent halothane (n = 10) or isoflurane (n = 10) anesthesia in oxygen. Five sets of cardiovascular data were recorded in each patient. In the awake, unmedicated state prior to induction, at three different anesthetic levels, 0.75, 1.0, and 1.25 MAC (corrected for age) and a final measurement repeated at 1.25 MAC after the intravenous infusion of 15 ml X kg-1 of Lactated Ringers solution. The study was completed prior to intubation and surgery. Results are expressed as mean +/- SEM. Isoflurane and halothane decreased mean blood pressure from the awake level (isoflurane 76.6 +/- 2.3 to 60.6 +/- 3.1 mm, halothane 72.2 +/- 3.9 to 60.6 +/- 3.1 mm at 1.25 MAC). Isoflurane increased heart rate at all anesthetic levels (128.7 +/- 4.2 to 142.5 +/- 6.0 beats/min at 0.75 MAC). Halothane decreased heart rate at 1.25 MAC (124.6 +/- 4.6 to 119.4 +/- 3.5 beats/min). Isoflurane and halothane decreased cardiac index at 1.25 MAC. Stroke volume index decreased at 1.0 and 1.25 MAC with both isoflurane (36.9 +/- 3.8 to 30.2 +/- 3.5 ml/m2) and halothane (32.7 +/- 2.5 to 28.9 +/- 2.5 ml/m2). Ejection fractions also decreased significantly at 1.0 and 1.25 MAC in both groups of patients (22 +/- 6% at 1.25 MAC halothane and 28 +/- 8% at 1.25 MAC isoflurane).(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiovascular effects of acute changes in extracellular ionized calcium concentration induced by citrate and CaCl2 infusions in chronically instrumented dogs, conscious and during enflurane, halothane, and isoflurane anesthesia

To study the cardiovascular effects of low blood ionized calcium ion concentrations [Ca2+] induced by citrate infusion followed by high [Ca2+], induced by CaCl2 infusion awake and during enflurane (2.5% ET), halothane (1.2% ET), and isoflurane (1.6% ET) anesthesia, dogs were chronically instrumented to measure heart rate, aortic, left atrial, and left ventricular (LV) blood pressures, and cardiac output. In conscious dogs low [Ca2+] (decreased 0.35 mM); increased heart rate (HR) and mean aortic pressure (MAP) and decreased stroke volume (SV) and LV dP/dtmax. Low [Ca2+] increased HR during all three anesthetics and decreased LV dP/dtmax except during isoflurane anesthesia. Low [Ca2+] produced more hemodynamic depression during enflurane anesthesia than during anesthesia with halothane or isoflurane increasing left atrial pressure and decreasing MAP and SV. The differences seen were partially related to decreased systemic vascular resistance during halothane and isoflurane anesthesia. In conscious dogs following high [Ca2+] (increased 0.37 mM); only MAP and LV dP/dtmax increased. LVdP/dtmax was also increased by high [Ca2+] during all three anesthetics without a change in MAP. Cardiac output increased during halothane and isoflurane anesthesia but was unchanged during enflurane. It would appear that the hemodynamic sensitivity for the effects of changing [Ca2+] was enflurane greater than halothane greater than isoflurane greater than awake. The results suggest that the effects of changes in [Ca2+] induced by citrate and CaCl2 infusion are modified by the three volatile anesthetics.     

Isoflurane, halothane, and regional cerebral blood flow at various levels of PaCO2 in rabbits

The effects of halothane and isoflurane on regional cerebral blood flow (CBF) were studied in 18 New Zealand White rabbits anesthetized with nitrous oxide (N2O) and morphine sulfate (MS) at three different levels of PaCO2. CBF was measured using the hydrogen clearance technique. Monitored variables were intracranial pressure (ICP), central venous pressure, heart rate, mean arterial pressure, electroencephalogram, arterial blood gases, end-tidal (ET) volatile anesthetic, and ET CO2. Addition of 1 MAC halothane to the N2O/MS background anesthetic caused flow to increase significantly in all three regions studied (cortex, dorsal hippocampus, white matter) at all three levels of PaCO2 (low: 20-25 mmHg; normal: 35-40 mmHg; high: 50-55 mmHg). Addition of 1 MAC isoflurane to the background anesthetic caused CBF to decrease significantly in all regions during hypocapnia. During normocapnia, CBF was unchanged with the addition of 1 MAC isoflurane in all regions and during hypercapnia, CBF increased significantly only in the dorsal hippocampus following addition of 1 MAC isoflurane to the MS/N2O background anesthetic. Volatile anesthetic administration was associated with significant, although small, increases in ICP at all PaCO2 levels. We conclude that 1 MAC concentrations of halothane and isoflurane have opposite effects on CBF when added to a N2O/MS anesthetic during hypocapnia and that the effects of isoflurane on regional CBF are dependent on PaCO2 in rabbits under the anesthetic conditions of this experiment.     

The anticonvulsant effects of volatile anesthetics on lidocaine-induced seizures in cats

Large concentrations of sevoflurane and isoflurane, but not halothane, induce spikes in the electroencephalogram. To elucidate whether these proconvulsant effects affect lidocaine-induced seizures, we compared the effects of sevoflurane, isoflurane, and halothane in cats. Fifty animals were allocated to 1 of 10 groups: 70% nitrous oxide (N2O), 0.6 minimum alveolar anesthetic concentration (MAC) + 70% N2O, 1.5 MAC + 70% N2O, and 1.5 MAC of each volatile agent in oxygen. Lidocaine 4 mg x kg(-1) x min(-1) was infused IV under mechanical ventilation with muscle relaxation. Electroencephalogram in the cortex, amygdala, and hippocampus and multiunit activities in the midbrain reticular formation (R-MUA) were recorded. Lidocaine induced spikes first from the amygdala or hippocampus in the 70% N2O and halothane groups and from the cortex in the sevoflurane and isoflurane groups. Lidocaine induced seizures in all cats in the 70% N2O and 0.6 MAC + N2O groups. Seizure occurrence was reduced in the 1.5 MAC + N2O group (P < 0.05 versus 70% N2O). The onset of seizure was delayed in the 0.6 MAC + N2O and 1.5 MAC groups for sevoflurane and isoflurane, but not for halothane, compared with the 70% N2O group (P < 0.05). Lidocaine increased R-MUA with seizure by 130%+/-56% in the 70% N2O group. The increase of R-MUA with seizure was more suppressed in the volatile anesthetic groups than in the 70% N2O group (P < 0.05). In the present study, sevoflurane and isoflurane attenuated seizure when the blood lidocaine concentration was accidentally increased. IMPLICATIONS: Increasingly, epidural blockade is combined with general anesthesia to achieve stress-free anesthesia and continuous pain relief in the postoperative period. In the present study, sevoflurane and isoflurane attenuated seizure when the blood lidocaine concentration was accidentally increased.     

Additive contribution of nitrous oxide to halothane MAC in infants and children

Fifty-one infants and small children (14.7 +/- 7.2 mo) were studied to determine the MAC of halothane in O2 (n = 11) and in the presence of three different nitrous oxide (N2O) concentrations (25% [n = 13], 50% [n = 13], and 75% [n = 14]). In the three N2O groups, after randomly assigning patients to an N2O group, anesthesia was induced with halothane and N2O using a pediatric circle system. After endotracheal intubation, halothane and N2O end-expired concentrations were adjusted to predetermined concentrations. The initial halothane concentrations in each group were based on the assumption that each percent N2O reduced halothane concentrations by 0.01 vol % (assumed halothane MAC = 1.0 vol %). Based on the response of the preceding subject in each group, halothane concentrations were increased or decreased depending on whether the response was to move or not to move, respectively, in response to the surgical incision. The mean duration of constant end-tidal concentrations before skin incision was 10 min. End-tidal gases were sampled and measured from a separate distal sampling port of an endotracheal tube during controlled ventilation (Perkin-Elmer Mass Spectrometer). The MAC value for halothane in O2 was 0.94 +/- 0.08 vol % (mean +/- SD). The MAC values of halothane in the presence of 25%, 50%, and 75% N2O were 0.78 +/- 0.12 vol %, 0.44 +/- 0.10 vol %, and 0.29 +/- 0.06 vol %, respectively. All concentrations of N2O significantly reduced the MAC of halothane. A regression analysis through all four data points yielded a linear relationship (r2 = 0.87) with a predicted MAC for N2O of 105 vol %. Unlike halothane and isoflurane, the predicted MAC of N2O in infants and children is similar to that reported by others in adults. Similar to the results of clinical studies in adults, the contribution of N2O to halothane MAC in children is additive.     

Differential effects of isoflurane/nitrous oxide on posterior tibial somatosensory evoked responses of cortical and subcortical origin

Posterior tibial somatosensory evoked responses (SSERs) were recorded during administration of isoflurane and nitrous oxide. Responses arising from cortical and subcortical neural generators were examined to compare their relative resistance to anesthetic-related degradation. Recordings were performed in ten adults during anesthesia with 0.5 MAC isoflurane/60% N2O, 1.0 MAC isoflurane/60% N2O, and 1.5 MAC isoflurane/60% N2O. Thereafter, N2O was omitted and recordings were repeated during anesthesia with 1.5 and 1.0 MAC isoflurane/O2. Isoflurane resulted in a significant (P less than 0.001) dose-related decrease in the amplitude of cortical waveforms. The amplitude loss was substantial; e.g., for the first cortical waveform, amplitude decreased from 1.21 +/- 0.67 microV during 0.5 MAC isoflurane/N2O to 0.28 +/- 0.29 microV during 1.5 MAC/N2O. Elimination of N2O resulted in an increase in amplitude of approximately 100% (P less than 0.04). By contrast, the amplitude of the subcortical response as recorded in vertex to linked mastoid and vertex to upper cervical spine derivations was not significantly altered by changing concentrations of isoflurane or N2O. The results suggest that subcortical SSERs may be preferable to those of cortical origin for spinal cord monitoring in situations where isoflurane and nitrous oxide, especially in varying concentrations, are the primary anesthetic agents.     

The stress reaction in the recovery phase from halothane and isoflurane anesthesia

This study was undertaken to investigate the influences of halothane and isoflurane as well as different extubation techniques on the endocrine stress response during recovery from general anesthesia. Forty patients scheduled for herniorrhaphy and cholecystectomy were randomly allocated to 4 groups: 20 received halothane and 20 received isoflurane anesthesia. Within the halothane and isoflurane groups, 10 patients each were extubated during anesthesia (1/2 MAC) and a further 10 had awake extubation. Premedication, induction of anesthesia, and intraoperative anesthetic management were standardized in all groups. Plasma levels of endocrine stress parameters as well as mean arterial pressure (MAP), heart rate (HR), and arterial oxygen saturation (SaO2) were measured at nine time points up to 60 min after extubation. Biometric data and duration of operation and anesthesia were comparable in all groups. In the recovery period, epinephrine levels were higher in the isoflurane groups than in the halothane groups (P = 0.02). With respect to time course, earlier and more marked increases of epinephrine, norepinephrine, and antidiuretic hormone (ADH) levels were observed in the isoflurane groups compared to the halothane groups (P less than 0.01), representing the more rapid elimination of isoflurane. The sympathoadrenergic stress response was more pronounced in patients with extubation during anesthesia than in those with awake extubation: epinephrine levels were slightly higher and group levels of norepinephrine were significantly increased (P = 0.02). No influence of the extubation techniques was observed on ADH, ACTH, and cortisol levels or on MAP, HR, or SaO2. In summary, extubation during anesthesia did not reduce the endocrine stress response. It is concluded that awake extubation should be preferred unless the operation or the patient's condition requires extubation during anesthesia.     

Intraocular pressure and hemodynamic changes following tracheal intubation in children

STUDY OBJECTIVE: To determine the optimal time in which to make intraocular pressure (IOP) measurements in children following tracheal intubation. DESIGN: Randomized, controlled trial. SETTING: Operating rooms of a tertiary-care children's hospital. PATIENTS: Thirteen healthy children undergoing elective strabismus correction surgery under halothane and nitrous oxide (N2O) endotracheal anesthesia. INTERVENTIONS: Following induction of anesthesia, patients were randomly assigned to receive stable end-tidal halothane concentrations of 0.5% or 1.0% in 66% N2O. MEASUREMENTS AND MAIN RESULTS: Baseline (preintubation) IOP, heart rate (HR), and mean arterial pressure (MAP) were recorded after 10 minutes of steady-state end-tidal concentrations. These measurements were repeated at 1-minute intervals following tracheal intubation, which was facilitated with atracurium. HR and MAP changes were found to be good predictors of IOP changes. IOP returned to baseline (preintubation) values when HR and MAP returned to preintubation levels. However, IOP measurements under anesthesia may not reflect awake values. CONCLUSIONS: We recommend that IOP be measured only after HR and MAP have returned to preintubation levels in children who have undergone tracheal intubation during halothane and N2O anesthesia.     

Plasma cortisol in experimental anesthesia with halothane, enflurane, isoflurane and nitrous oxide

The influence of anesthesia on plasma cortisol has most often been studied in connection with routine operations. To investigate the specific effects of modern inhalation anesthetics more accurately, we examined the specific effects of four inhalation anesthetics on human plasma cortisol during volunteer studies on the influence of anesthetics on the electroencephalogramm. METHODS. A group of 17 (10 m, 7 f) young healthy volunteers who had not received any premedication and were not intubated were studied after informed consent had been obtained. In the first series of experiments the concentration of halothane, enflurane, isoflurane or N2O was increased to MAC (minimal alveolar concentration) 0.5 for a 15-min steady-state period. Blood samples were taken 5 min prior to induction (I), 35 min after induction, on steady-state MAC 0.5 (II), and 15 (III) and 35 (IV) min after the end of anesthesia. In a second series, with 5 subjects, the concentration of halothane, enflurane or isoflurane was first increased to a steady state of MAC 1.0. After reduction to MAC 0.5 steady-state, anesthesia was supplemented with 53% N2O to give a steady state of MAC 1.0 again. Blood samples were taken 5 min prior to induction (I), after the attainment of steady-state MAC 1.0 (II), 35 min later at MAC 0.5 (III), 40 min later at MAC 1.0 with volatile anesthetic/N2O (IV), and 15 (V) and 35 (VI) min after the end of anesthesia. RESULTS. MAC 0.5 N2O produced a marked rise in mean plasma cortisol, from 64.2 micrograms/l to 164.5 micrograms/l.(ABSTRACT TRUNCATED AT 250 WORDS)     

Duration of preoperative fast correlates with arterial blood pressure response to halothane in infants

In this study, we sought to determine whether the duration of preoperative fasting affects the decrease in blood pressure observed in infants and children during halothane anesthesia. Two-hundred-fifty pediatric patients were divided into 5 age groups: term neonates (n = 50), 1-6 mo (n = 50), 6-24 mo (n = 50), 2-6 yr (n = 50), and 6-12 yr (n = 50). After anesthetic induction with halothane, end-tidal halothane was maintained at 2 minimum alveolar anesthetic concentration (MAC) for 10 min to allow myocardial uptake. Patients were grouped by duration of preoperative fast (0-4 h, 4-8 h, 8-12 h, and >12 h). Changes in heart rate and systolic (SAP) and mean (MAP) arterial blood pressure from preinduction to 2 MAC were compared among fasting groups within each age group. In the 1- to 6-mo age group, the changes in SAP and MAP were significantly greater in infants fasting 8-12 h than in those fasting 0-4 h (SAP, -51 mm Hg versus -31 mm Hg, respectively; MAP, -48 mm Hg versus -32 mm Hg; P < 0.05). No statistically significant differences were noted in the older age groups. The results of this study demonstrate that prolonged preoperative fasting is associated with a greater decrease in blood pressure in infants. This exacerbation of the already significant hemodynamic depression observed in infants during halothane anesthesia underscores the importance of adherence to published fasting guidelines. IMPLICATIONS: We studied changes in blood pressure during halothane anesthesia in infants and children and found that blood pressure decreased to a greater extent in infants who fasted for longer than 8 h before surgery. This exacerbation of the already significant hemodynamic depression observed in infants during halothane anesthesia underscores the importance of adherence to published fasting guidelines.     

Equi-MAC concentrations of halothane and isoflurane do not produce similar bispectral index values

Minimum alveolar concentration (MAC) has been traditionally used to measure the potency of an inhalational anesthetic agent. Recently, bispectral index (BIS) derived from the frontal cortical electroencephalogram has been used frequently for quantifying the hypnotic component of anesthesia. The present study was designed to examine the BIS values produced by equi-MAC concentrations of halothane and isoflurane. In 34 patients undergoing spinal surgery, BIS and spectral edge frequency (SEF95) were recorded at 3 different concentrations of halothane and isoflurane--namely 0.5, 0.75, and 1.0 MAC. The measurements were made both during wash-in and wash-out phases of the anesthetic agent. Eighteen patients received halothane and 16 received isoflurane. Heart rate, mean arterial pressure, oxygen saturation, and end tidal carbon dioxide pressure values were not different between the 2 groups at various MAC concentrations of the anesthetic agents. BIS and SEF95 values decreased significantly with increasing concentrations of both the anesthetic agents (P<0.001). At any given MAC concentration of the anesthetic, BIS and SEF(95) values were significantly lower under isoflurane compared with halothane anesthesia both during wash-in and wash-out phases (P<0.001). For a given anesthetic agent, BIS values were comparable at equi-MAC concentrations during wash-in and wash-out phases. In conclusion, BIS values are significantly lower under isoflurane compared with halothane anesthesia at similar MAC concentrations. For a given anesthetic agent and a given MAC concentration, the BIS values are similar during wash-in and wash-out phases of anesthesia.     

Halothane concentrations required to block the cardiovascular responses to incision (MAC CVR) in infants and children

The purpose of this study was to determine the halothane concentration in N₂O required to block the cardiovascular responses to skin incision (MAC CVR) in infants and children. We studied 64 unpremedicated ASA 1 infants and children (one month to seven years). In each infant or child, anaesthesia was induced slowly with halothane and N₂O, and an endotracheal tube was placed. The MAC CVR was assessed, after a steady state end-tidal halothane concentration had been established for ten minutes, by the “up and down technique” of Dixon. Positive responses were defined as an increase in MAP or HR > 10%. The MAC CVR50 values of halothane with 60% N₂O were 1.16 ± 0.23% at 1–6 mo, 1.17 ± 0.18% at 7–12 mo, 0.95 ± 0.26% at 1–3 yr, and 1.12 ± 0.16% at 4–7 yr. The value at 1–3 years children was less than those in the other age groups (P < 0.05). The changes of MAP were correlated with changes of both HR and pupillary diameter. These results indicate that the values of MAC CVR50 of halothane in infants and children are higher than those required to block motor responses (MAC). The halothane requirement to block cardiovascular responses is lowest in the children aged one to three years.     

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.     

Hemo- and cardiodynamic action of halothane or isoflurane following peroral long-term pretreatment with nifedipine. An animal experimental study

This study investigated the influence of chronic oral nifedipine on the hemodynamic effects of halothane or isoflurane anesthesia in dogs. Under general anesthesia with fentanyl 0.3 microgram/kg/min i.v. and 3:1 N2O/O2 inhalation mixture a left thoracotomy was performed and two needle force probes were placed in the left ventricular wall to measure myocardial force of contraction. In the halothane group (n = 12) a Hall-effect sensor was placed on the anterior surface of the left ventricle, which in combination with a magnet on the posterior surface allowed measurements of left ventricular diameter. In the isoflurane group (n = 15) a Widney gauge was placed around the left ventricle to measure left ventricular circumference changes. The dogs were also monitored with left ventricular tip manometers, pulmonary arterial thermodilution catheters, and femoral arterial and venous catheters. Prior to surgery, in the halothane group 6 dogs were pretreated with nifedipine 6 mg/kg p.o. for 10 days; the other 6 served as controls. In the isoflurane group, 8 dogs were pretreated with nifedipine in the same way and 7 served as controls. Three hours after instrumentation baseline hemodynamic measurements were performed and repeated 15 min after adding 1 MAC and then 2 MAC halothane or isoflurane. Oral pretreatment with nifedipine caused vasodilation with a significant decrease in systemic vascular resistance (SVR) and mean arterial pressure (MAP); heart rate (HR) and dp/dt max were unchanged in comparison to the control group. The cardiac output (CO) increased. Halothane (1 MAC/2 MAC) had a dose-related circulatory depressant effect. This occurred to the same extent in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effects of sevoflurane, halothane, enflurane, and isoflurane on hepatic blood flow and oxygenation in chronically instrumented greyhound dogs.

Inhalational anesthetics produce differential effects on hepatic blood flow and oxygenation that may impact hepatocellular function and drug clearance. In this investigation, the effects of sevoflurane on hepatic blood flow and oxygenation were compared with those of enflurane, halothane, and isoflurane in ten chronically instrumented greyhound dogs. Each dog randomly received enflurane, halothane, isoflurane, and sevoflurane, each at 1.0, 1.5, and 2.0 MAC concentrations. Mean arterial blood pressure and cardiac output decreased in a dose-dependent fashion during all four anesthetics studied. Heart rate increased compared to control during enflurane, isoflurane, and sevoflurane anesthesia and did not change during halothane anesthesia. Hepatic arterial blood flow and portal venous blood flow were measured by chronically implanted electromagnetic flow probes. Hepatic O2 delivery and consumption were calculated after hepatic arterial, portal venous, and hepatic venous blood gas analysis. Hepatic arterial blood flow was maintained with sevoflurane and isoflurane. Halothane and enflurane reduced hepatic arterial blood flow during all anesthetic levels compared to control (P less than 0.05), with marked reductions occurring with 1.5 and 2.0 MAC halothane concomitant with an increase in hepatic arterial vascular resistance. Portal venous blood flow was reduced with isoflurane and sevoflurane at 1.5 and 2.0 MAC. A somewhat greater reduction in portal venous blood flow occurred during 2.0 MAC sevoflurane (P less than 0.05 compared to control and 1.0 MAC values for sevoflurane). Enflurane reduced portal venous blood flow at 1.0, 1.5, and 2.0 MAC compared to control. Halothane produced the greatest reduction in portal venous blood flow (P less than 0.05 compared to sevoflurane).(ABSTRACT TRUNCATED AT 250 WORDS)     

Values of the bispectral index do not parallel the hemodynamic response to the rapid increase in isoflurane concentration

PURPOSE: To investigate the changes in hemodynamic variables and bispectral index (BIS) in response to a rapid increase in isoflurane or sevoflurane concentration. METHOD: Thirty adult patients were anesthetized with either isoflurane (isoflurane group) or sevoflurane (sevoflurane group). Two minutes after induction of anesthesia with thiamylal, the inspired concentrations of isoflurane and sevoflurane were rapidly increased from 0.5 minimum alveolar anaesthetic concentration (MAC) to 3 MAC and maintained for five minutes. Heart rate (HR), mean arterial pressure (MAP), and BIS were measured every minute. RESULTS: An increase in the anesthetic concentration caused increases in HR and MAP in the isoflurane group and a decrease in MAP in the sevoflurane group. Consequently, HR and MAP in the isoflurane group were significantly higher than those in the sevoflurane group. After inhalation of high concentrations, BIS significantly and progressively decreased in both groups. CONCLUSION: BIS values decrease after a step increase in volatile agent concentration, whether or not a hyperdynamic action occurs.