Constant End-tidal Concentration Research Articles

Effects of isoflurane anesthesia on cerebrovascular autoregulation in horses

To test a hypothesis predicting that isoflurane would interfere with cerebrovascular autoregulation in horses and to evaluate whether increased mean arterial blood pressure (MAP) would increase cerebral blood flow and intracranial pressure (ICP) during isoflurane anesthesia. 6 healthy adult horses. Horses were anesthetized with isoflurane at a constant end-tidal concentration sufficient to maintain MAP at 60 mm Hg. The facial, carotid, and dorsal metatarsal arteries were catheterized for blood sample collection and pressure measurements. A sub-arachnoid transducer was used to measure ICP Fluorescent microspheres were injected through a left ventricular catheter during MAP conditions of 60 mm Hg, and blood samples were collected. This process was repeated with different-colored microspheres at the same isoflurane concentration during MAP conditions of 80 and 100 mm Hg achieved with IV administration of dobutamine. Central nervous system tissue samples were obtained after euthanasia to quantify fluorescence and calculate blood flow. Increased MAP did not increase ICP or blood flow in any of the brain tissues examined. However, values for blood flow were low for all tested brain regions except the pons and cerebellum. Spinal cord blood flow was significantly decreased at the highest MAP. Results suggested that healthy horses autoregulate blood flow in the CNS at moderate to deep planes of isoflurane anesthesia. Nonetheless, relatively low blood flows in the brain and spinal cord of anesthetized horses may increase risks for hypoperfusion and neurologic injury.

Effect of morphine on the bispectral index during isoflurane anesthesia in dogs

ObjectiveTo assess the effect of morphine on the bispectral index (BIS) in dogs during isoflurane anesthesia maintained at a constant end–tidal concentration. Study designProspective, randomized, experimental trial. AnimalsEight adult Beagle dogs, weighing between 7.1 and 9.8 kg. MethodsAnesthesia was induced with isoflurane via a face mask. Dog's tracheas were intubated and anesthesia maintained with isoflurane at a constant end–tidal concentration (e′Iso) of 1.81% for a 30–minute equilibration period. Pulmonary ventilation was controlled to normocapnia. After equilibration, baseline values were recorded prior to intravenous administration of morphine sulfate (0.5 mg kg−1) (MT) or an equal volume of saline (CT). Measurements for heart rate, systolic, diastolic and mean arterial pressure (SAP, DAP and MAP) were recorded at 10, 20, 30, 45, 60, 75, 90, 105 and 120 minutes after treatment. Bispectral index was recorded every 10 seconds for 3 minutes for each time measurement. Venous blood samples were collected at baseline, 10, 20, 30, 45, 60 and 120 minutes for determination of morphine serum concentrations. Anesthesia was discontinued after the last measurement and dogs were allowed to recover. ResultsBaseline BIS for MT and CT at 1.81%e′Iso were 63 ± 10 and 58 ± 9, respectively. Bispectral index in MT was 4–8% lower at 20, 75, 90 and 105 minutes compared with CT. There were no differences in BIS between baseline and any subsequent measurement within either MT or CT. Heart rate, SAP, MAP, and DAP decreased after morphine administration. Conclusion and clinical relevanceIntravenous administration of 0.5 mg kg−1 morphine sulfate did not cause clinically significant changes in the BIS of unstimulated dogs during isoflurane anesthesia at an e′Iso of 1.81%.

The effects of caudal local anesthesia blockade on the Bispectral Index during general anesthesia in children

Peripheral deafferentation induced by epidural or spinal anesthesia reduces the degree of cortical arousal in adults. This study aimed at determining if caudal blockade decreases the level of arousal, as measured by Bispectral Index (BIS) in unstimulated children, and to determine if this effect differed between age groups. Hospital ethics committee approval and parental consent was obtained. Children (age between 24 months and 5 years) and infants (between 6 and 24 months of age) were recruited if they were scheduled for below umbilical surgery that would usually require caudal local anesthesia blockade. Before the procedure, subjects within each age group were randomized to either caudal group (1 ml.kg(-1) 0.25% bupivacaine), or control group (no caudal). In all groups, anesthesia was induced with sevoflurane and maintained at a constant endtidal concentration of 1.5% sevoflurane without N(2)O. Five minutes after induction a baseline BIS was recorded (BIS(1)). In the caudal groups, a caudal block was then performed while in the control groups no block was performed. Fifteen minutes later, the BIS was again recorded (BIS(2)). The change in BIS over this time period was the primary outcome (BIS(Delta)). After measurement, subjects in the control groups received a caudal block before the start of surgery. Twenty-nine infants and 18 children completed the study protocol. In children, BIS(Delta) was significantly different between the caudal group and control (-5.7 vs -0.7, P = 0.04). In infants, no significant difference was detected in BIS(Delta) between caudal and control groups. Caudal blockade decreased the degree of arousal, as measured by BIS, in unstimulated children aged 2-5 years. No change in arousal was detected in infants.

Noxious stimulation during orthopaedic surgery results in EEG ‘arousal’ or ‘paradoxical arousal’ reaction in isoflurane-anaesthetised sheep

The effects of surgical stimuli on haemodynamic and electroencephalographic (EEG) variables were determined in 25 adult ewes undergoing an experimental orthopaedic procedure in isoflurane anaesthesia. Data were recorded after 15 min of constant end-tidal concentration of approximately 2.2% isoflurane (SS: steady state=baseline), during skin disinfection (DIS), incision (INC), drilling of the first hole through the tibia (DRI) and insertion of a threaded pin (PIN) for external fixation. Stimulation resulted in a significant increase in systolic and mean arterial pressure above SS at INC, DRI and PIN. Haemodynamic changes were accompanied by either significant increases or decreases in EEG median frequency (MF) and 80% spectral edge frequency (SEF80) above or below SS at all four stimulation time points suggesting ‘arousal’ or ‘paradoxical arousal’ reaction, respectively. We conclude, that either type of EEG activation pattern could be elicited dependent on stimulation intensity and level of anaesthetic depth.

Circulatory and respiratory responses of spontaneously breathing, laterally recumbent horses to 12 hours of halothane anesthesia

Summary Cardiovascular and respiratory changes that accompany markedly long periods (12 hours) of halothane anesthesia were characterized. Eight spontaneously breathing horses were studied while they were positioned in left lateral recumbency and anesthetized only with halothane in oxygen maintained at a constant end-tidal concentration of 1.06% (equivalent to 1.2 times the minimal alveolar concentration for horses). Results of circulatory and respiratory measurements during the first 5 hours of constant conditions were similar to those previously reported from this laboratory (ie, a time-related significant increase in systemic arterial blood pressure, cardiac output, stroke volume, left ventricular work, pcv, plasma total solids concentration, and little change in respiratory system function). Beyond 5 hours of anesthesia, arterial blood pressure did not further increase, but remained above baseline. Cardiac output continued to increase, because heart rate significantly (P < 0.05) increased. Peak inspiratory gas flow increased significantly (P < 0.05) in later stages of anesthesia. There was a significant decrease in inspiratory time beginning at 4 hours. Although PaO2 and PaCO2 did not significantly change during the 12 hours of study, increased significantly (P < 0.05) and progressively with time, beginning 6 hours after the beginning of constant conditions. Metabolic acidosis increased with time (significantly [P < 0.05] starting at 9 hours), despite supplemental iv administered NaHCO3, Plasma concentrations of eicosanoids: 6-ketoprostaglandin F1α (pgf1α a stable metabolite of pgi1), pgf2α, pge, and thromboxane (TxB2, a stable metabolite of TxA2) were measured in 5 of the 8 horses before and during anesthesia. Significant changes from preanesthetic values were not detected. Dynamic thoracic wall and lung compliances decreased with time.

Dynamic baroreflex sensitivity in anesthetized horses, maintained at 1.25 to 1.3 minimal alveolar concentration of halothane

SUMMARY Dynamic baroreflex sensitivity for increasing arterial pressure (dbsi) was used to quantitatively assess the effects of anesthesia on the heart rate/arterial pressure relationship during rapid (≤ 2 minutes) pressure changes in the horse. Anesthesia was induced with iv administration of xylazine and ketamine and maintained with halothane at a constant end-tidal concentration of 1.1 to 1.2% (1.25 to 1.3 minimal alveolar concentration). Systolic arterial pressure (sap) was increased a minimum of 30 mm of Hg in response to an iv bolus injection of phenylephrine HCl. Linear regression was used to determine the slope of the r-r interval/sap relationship. During dynamic increases in sap, a significant correlation between r-r interval and sap was observed in 8 of 8 halothane-anesthetized horses. Correlation coefficients between r-r interval and sap were > 0.80 in 5 of 8 horses. Mean (± sd) dbsi was 4.8 ± 3.4 ms/mm of Hg in anesthetized horses. A significant correlation between r-r interval and sap was observed in only 3 of 6 awake horses during dynamic increases in sap. Lack of correlation between r-r interval and sap in 3 of 6 awake horses indicated that rapidly increasing sap with an iv phenylephrine bolus is a poor method to evaluate baroreceptor-mediated heart rate changes in awake horses. Reflex slowing of heart rate in response to a rising arterial pressure appeared to have been overridden by the effects of excitement. Mean (± sd) dbsi (3 horses) was 7.3 ± 3.3 ms/mm of Hg in awake horses.

Blood/gas solubility coefficient and blood concentration of enflurane during normothermic and hypothermic cardiopulmonary bypass

The blood/gas solubility coefficient and blood concentration of enflurane were measured at intervals in 10 patients undergoing coronary artery revascularization with cardiopulmonary bypass (CPB) and moderate hypothermia. A constant end-tidal concentration of enflurane was maintained throughout the study. Blood/gas solubility coefficient was determined at 37°C, which when combined with an initial single-step equilibration of the blood sample with air, permitted the accurate measurement of blood concentration. Blood/gas solubility coefficient and blood concentration both decreased significantly with the onset of CPB. During the period of hypothermia, blood/gas solubility as measured at 37°C showed little change; however, there was a progressive, marked increase in blood concentration with a mean increase of 80% prior to rewarming. Therefore, the level of anesthesia provided by enflurane may lighten with the onset of CPB, and a deeper level will accompany any decrease in blood temperature. On rewarming, blood concentration levels rapidly returned to levels similar to those measured before cooling. The increased uptake and accumulation of volatile anesthetic agent that occurred as a result of the period of hypothermic CPB was rapidly cleared. The rapidity with which blood concentration responded to the changes occurring during CPB make it unlikely that there was any significant increase in myocardial depression in response to the raised blood concentration secondary to the hypothermia.

Effect of clenbuterol on arterial oxygen tension in the anaesthetised horse

In horses in dorsal recumbency, spontaneously breathing oxygen, with halothane at a constant end-tidal concentration, the arterial oxygen tension (PO2) increased from 9.9 +/- 0.3 SEM kPa to 21.7 +/- 4.0 kPa with 0.8 micrograms kg-1 clenbuterol and to 29.1 +/- 3.8 kPa with 2.4 micrograms kg-1 clenbuterol. In horses initially in dorsal recumbency then turned to sternal recumbency the PaO2 rose to 54.0 +/- 3.0 kPa, but this rise was unaffected by clenbuterol administration. The response in dorsal recumbency was consistent with clenbuterol counteracting the factor postulated to direct the pulmonary blood flow caudodorsally, but the response to clenbuterol in sternal recumbency was not. Although these results do not unequivocally characterise the postulated factor, the effect of the clenbuterol itself is of interest because of its potential as a treatment for the low PaO2 often observed in anaesthetised horses.

Improvement in arterial oxygen tension with change in posture in anaesthetised horses

Observations were made on horses spontaneously breathing oxygen, with halothane at a constant end tidal concentration. The horses were positioned in dorsal recumbency for the first 45 minutes of each anaesthetic episode during which the arterial oxygen tension (PaO2) was found to peak and then decline. The remaining 60 minutes of each anaesthesia was used to test the effect of various manoeuvres on PaO2. The PaO2 of horses decreased further both when remaining in dorsal recumbency and when repositioned in right or left recumbency. In contrast, placing the horses in sternal recumbency for these remaining 60 minutes caused the PaO2 to rise rapidly providing evidence for redistribution of ventilation. Replacing some inspired oxygen with less absorbable nitrogen did not improve PaO2 in dorsal recumbency. Thus there was no evidence that the low PaO2 of dorsal recumbency was associated with alveoli that had collapsed because of gas absorption.

SERVO-CONTROLLED CLOSED-CIRCUIT ANAESTHESIA: A method for the automatic control of anaesthesia produced by a volatile agent in oxygen

A method of closed-circuit anaesthesia has been developed in which the end-tidal concentration of the volatile anaesthetic agent used is controlled automatically using a closed-loop servo system. End-tidal anaesthetic concentrations, measured by the Engstrom EMMA, were maintained in the closed circuit by direct liquid injection. The system was tested in the laboratory and in clinical use (12 subjects). Accurate estimation of anaesthetic uptake was readily obtained and results for the uptake of halothane agreed closely with those of previous workers. The major sources of error in the method were the result of zero offset in the Engstrom EMMA which in turn was caused by humidity and the intrinsic characteristic of the simple proportional controller used. These errors were easily correctable, and end-tidal halothane concentration could be controlled to within 0.1%. Mean halothane vapour uptake at a constant end-tidal concentration of 0.8% was 114 ml min-1 at 1 min, 36 ml min-1 at 5 min, 29 ml min-1 at 10 min and between 22 and 18 ml min-1 at 20-35 min.