OXYGEN AND AIR: Further Studies in Mice with Oxygen and Air as the Anaesthetic Vehicles with Halothane

A further study has been made to test the sensitivity of miceto halothane anaesthesia when the anaesthetic vehicle was 100per cent oxygen or air. This study showed that the mice anaesthetizedwith halothane in 100 per cent oxygen for 120 minutes toleratedsignificantly higher concentrations of halothane than thoseanaesthetized with halothane in air.     

SURVIVAL OF BLED DOGS AFTER HALOTHANE AND ETHER ANAESTHESIA

Sixty spontaneously-breathing atropinized dogs anaesthetizedwith 79 per cent ethylene/21 per cent oxygen were bled to amean aortic blood pressure of 40 mm Hg for 90 minutes, and theirsurvival observed during and after an additional 30 minutesof halothane or di-ethyl ether anaesthesia followed by bloodreplacement. Blood volumes were reduced approximately 40 percent by an average haemorrhage of 46.3 ml/kg. It is concludedthat: (a) Survival experiments did not demonstrate a deleteriouseffect of 1.5 per cent halothane due to its hypotensive actionin oligaemia when compared with lighter planes of ether anaesthesia,(b) Maintenance of a normal minute volume will not suffice foradequate oxygenation of the arterial blood during anaesthesiawith either agent after haemorrhage with air as carrier gas.(c) Enrichment of the inspired oxygen to 30 per cent ensuresadequate arterial oxygenation when pulmonary ventilation isreduced by 1.5 per cent halothane after haemorrhage of thisseverity, and a survival rate insignificantly different fromthat resulting when 100 per cent oxygen is used as carrier gas. ^*Present address: University College Hospital, London.     

SOME ACTIONS OF HALOTHANE AND ETHER IN BLED DOGS

A method is described of bleeding dogs under anaesthesia withethylene (79 per cent) and oxygen (21 per cent) to an arbitrarylevel of hypotension. Arterial blood oxygen saturations remainednormal while the hyperventilation of the animals in responseto haemorrhage was unimpaired. In dogs rendered hypotensiveby 30-50 per cent reductions of their circulating blood volume,halothane caused a fall, and di-ethyl ether a rise in the arterialblood pressure, heart rate and respiratory minute volume. Venouspressure fell further on administration of halothane. Acuteexperiments in dogs bled to a mean blood pressure of 50 mm Hgdid not distinguish a lethal effect of halothane due to itshypotensive action. Increasing the severity of the bleedingprocedure demonstrated the lethal effect of impairing the hyperventilationwith halothane in air which caused marked arterial desaturation.Survival experiments might demonstrate a deleterious effectof halothane due to its hypotensive action in severe haemorrhagewhen compared with ether anaesthesia. Preliminary survival experimentsare reported. ^*Present address: University College Hospital, London, W.C.I.     

EFFECT OF HALOTHANE ANAESTHESIA AND HYPOTHERMIA ON SURVIVAL OF DOGS SUBJECTED TO ACUTE UNTREATED HAEMORRHAGE

The effect of halothane anaesthesia on the survival of bledanimals was investigated in seventy-one dogs divided into threegroups. In all dogs 40 ml/kg of arterial blood was taken out,this being followed 1 hour later by an additional haemorrhageof 10 ml/kg. Shed blood was not re-transfused and substitutionfor it was not carried out. Halothane anaesthesia alone andcombined with cooling was applied after the first haemorrhage.The greatest survival rate (66.6 per cent) was found in thecontrol (unanaesthetized) group, and the least (22.8 per cent)in dogs bled under halothane anaesthesia. The survival ratewas insignificantly lower (59.1 per cent) in dogs cooled underhalothane than in the control group. It is concluded that theadverse effect of halothane anaesthesia was counterbalancedby hypothermia.     

THE EFFECTS OF VARIOUS OXYGEN CONCENTRATIONS IN THE ANAESTHETIC VEHICLE ON INDUCTION TIMES AND SURVIVAL TIMES WITH HALOTHANE ANAESTHESIA

Studies were made to test the effects in mice exposed to halothaneof various percentages of oxygen in the anaesthetic vehiclewere on induction and survival times. Over all, increaing oxygenconcentrations in the vechicle were associated with longer inductiontimes with 4 per cent and 10 per cent halothane and with longersurvival times with 10 per cent halothane. It is not possiblefrom the results to define accurately the respective roles whichhaemoglobin, oxygen saturation, and the carriage of oxygen insolution in the plasma, play in prolonging induction and survivaltimes.     

Changes in myocardial oxygen consumption,efficiency and haemodynamics when systemic pressure is increased during morphine and added halothane anaesthesia in dogs

Depression of left ventricular function by the combination of halothane anaesthesia and increased ventricular afterload may undesirably reduce stroke volume and increase myocardial oxygen consumption by increasing ventricular wall stress. To investigate this possibility we studied six dogs instrumented to measure systemic and left ventricular pressures, ascending aortic and left anterior descending coronary artery flows and external left ventricular diameters. We sampled arterial and coronary sinus blood gases and oxygen contents. During morphine anaesthesia (4mg·kg^-1 intravenously with hourly supplements of 0.1 mg·kg^-1) and during added halothane anaesthesia (1.5 per cent end tidal) we measured systemic pressure, heart rate, stroke volume, stroke work, cardiac output, left ventricular end diastolic pressure and diameter and myocardial oxygen consumption. After infusing phenylephrine (0.02 mg/ml) to increase systolic pressure to 23.28 kPa (175 torr) we repeated measurements in both groups. We found that added halothane depressed systemic pressures (52 per cent), stroke volume (30 per cent), and myocardial oxygen consumption (46 per cent) compared to morphine alone. When afterload was increased with phenylephrine, stroke volume (20 per cent), cardiac output (25 per cent) and myocardial efficiency (47 per cent) were further depressed during added halothane anaesthesia compared to control halothane anaesthesia. Left ventricular end diastolic diameter (5 per cent) and pressure (320 per cent) were significantly increased by added afterload, compared to the control added halothane state. Conversely, increased afterload produced few changes during morphine anaesthesia alone. However, at comparable systemic pressures, myocardial oxygen consumption was similar during both anaesthetic states. We conclude that during added halothane anaesthesia increased afterload decreases stroke volume and myocardial efficiency. Cardiac output is reduced without increased myocardial oxygen consumption compared to morphine anaesthesia at comparable afterload states. In patients with already compromised cardiac output, further depression of stroke volume by increased ventricular afterload during halothane anaesthesia may be deleterious.     

Arterial air embolism of venous origin in dogs: effect of nitrous oxide in combination with halothane and pentobarbitone

The effects of using nitrous oxide (N2O) with halothane or pentobarbitone anaesthesia on the filtration of venous air emboli (VAE) by the pulmonary circulation were studied in dogs. Dogs anaesthetized with either pentobarbitone, pentobarbitone/N2O, halothane, or halothane/N2O were embolized with venous air into the right atrium at 0.25 to 0.35 ml.kg-1.min-1 for 30 min. The animals were in a supine, head down position. A Doppler ultrasonic probe located over the suprarenal aorta detected arterial bubbles that escaped filtration by the lungs. No bubbles were detected at 0.25 ml.kg-1.min-1, but at 0.30 ml.kg-1.min-1 the incidence was 11 per cent (pentobarbitone), 0 per cent (pentobarbitone/N2O), 33 per cent (halothane), and 63 per cent (halothane/N2O) and at 0.35 ml.kg-1.min-1, 44 per cent (pentobarbitone), 14 per cent (pentobarbitone/N2O), and 56 per cent (halothane). Half of the dogs receiving VAE with halothane/N2O at 0.30 ml.kg-1.min-1 died within the first 10 min of the air infusion. Thus, no animals were studied at the next higher dose (0.35 ml.kg-1.min-1). The results suggest that the occurrence of VAE with nitrous oxide anaesthesia may result in greater haemodynamic consequence and increased likelihood for spillover of the venous bubbles into the arteries if used with halothane as compared to pentobarbitone.     

Effects of dose and concentration of rectal methohexitone for induction of anaesthesia in children

To investigate the effect of dose and concentration of rectal methohexitone for induction of anaesthesia, 60 children (ASA physical status 1 or 2) undergoing outpatient surgery were studied. Each child was randomly assigned to receive one of three rectal solutions (each containing atropine 0.02 mg X kg-1): Group A - ten per cent methohexitone, 25 mg X kg-1 (n = 20); Group B - ten per cent methohexitone, 15 mg X kg-1 (n = 20); or Group C - one per cent methohexitone, 15 mg X kg-1 (n = 20). After induction of anaesthesia, or a maximum period of 20 minutes following rectal administration of methohexitone, halothane, nitrous oxide, and oxygen were administered by mask. The time to induction of anaesthesia, complications, postanaesthetic recovery scores, and recovery time did not differ significantly among the three groups. The incidence of failed inductions did not differ significantly between Group A (zero per cent) and Group C (ten per cent) but both were significantly less than Group B (45 per cent) (p less than 0.05). Heart rate increased significantly between 10 and 30 minutes after rectal administration of methohexitone and atropine. The authors conclude that ten per cent rectal methohexitone 25 mg X kg-1 and one per cent rectal methohexitone 15 mg X kg-1 are equally effective for induction of anaesthesia in children and both are significantly more effective than ten per cent methohexitone 15 mg X kg-1.     

Effects of haemorrhage on wound strength and fibroblast function

The impairment of healing in laparotomy wounds in rats with compensated oligaemia has been studied in two parallel investigations. Animals bled 1 ml/100 g body weight (bled) were compared with unbled animals undergoing the same operation (control). Firstly, wounds were assessed after 22 days for strength of skin and muscle layers (11 control: 9 bled). Both layers were significantly weaker in bled animals; by 36 per cent for skin (P less than 0.02) and by 22 per cent for muscle (P = 0.02). Secondly, wound fibroblast function was assessed after 10 days by quantitative histology and autoradiography (30 control: 31 bled). There were no significant differences between the two groups for fibroblast density, replication ([3H]thymidine), or general protein synthesis ([3H]leucine). Bled animals had less dense collagen packing by 21 per cent (P less than 0.01), but 33 per cent more incorporation of ([3H]proline) by fibroblasts (P less than 0.01) compared with control animals. The effect of compensated oligaemia on wound healing is more marked in skin than in muscle; it appears to be a specific increase in collagen turnover with the increase in reabsorption exceeding that in synthesis.     

CEREBRAL VASODILATATION BY HALOTHANE ANAESTHESIA IN MAN AND ITS POTENTIATION BY HYPOTENSION AND HYPERCAPNIA

In ten young normal adults the cerebral blood flow and oxygenuptake during normotensive and normocapnic halothane anaesthesia(1 per cent) were studied by means of the ⁸⁵Kr inhalation method.Compared with a similar group studied when awake, a significantincrease of 27 per cent in cerebral blood flow was found duringanaesthesia while the oxygen uptake was reduced by 26 per cent.After discussing previous conflicting reports, it is concludedthat halothane per se acts as a cerebral vasodilator. Ten patientsfrom the neurological service with and without cerebrovasculardisease were studied when awake and during hypotensive hypercapnichalothane anaesthesia (1 per cent). In five cases a third studywas made during either hypotension (three cases) or hypercapnia(two cases) alone. Cerebral blood flow was measured by the ¹³³Xeinjection method. The results suggested a potentiation of thecerebral vasodilatation of halothane by hypotension and/or hypercapniaeven in patients with cerebrovascular disease. The very highblood flows found during normotensive, moderately hypercapnichalothane anaesthesia indicated a sort of controlled cerebralhyperoxygenation, the application of which is discussed.     

HUMAN OXYGENATION BY AIR DURING ANAESTHESIA: THE RELATION OF VENTILATORY VOLUME AND ARTERIAL OXYGEN SATURATION

Ventilation and arterial oxygen saturation have been measuredin 18 patients during anaesthesia with ether or halothane carriedin air. All patients were ventilated artificially with a Jeffersonventilator at a frequency of 16 breaths per minute and variabletidal volume. Ventilation has been expressed as a percentageof Radford's standard, Nunn's standard and the patient's pre-operativeresting ventilation. 110 per cent of both Radford's and Nunn'sstandard ventilation and 98 per cent of the patient's own restingventilation were found to yield a mean arterial oxygen saturationof 95 per cent. Below this the mean saturation fell sharplywith decreasing ventilation. Cyanosis was never visible evenwith a saturation as low as 70 per cent, although desaturationwas evident in the colour of the arterial blood when sampled.     

OBSERVATIONS ON DENTAL ANAESTHESIA INTRODUCED WITH METHOHEXITONE II: MAINTENANCE AND RECOVERY

This paper summarizes observations made during maintenance ofand recovery from anaesthesia in 2,000 patients undergoing dentalextractions. The anaesthetic sequence (previously described)consisted of a single dose of methohexitone followed by nitrousoxide and oxygen with the addition of halothane as a supplementin 30 per cent of patients. In 97 per cent of men and 99 percent of women a still operating field was provided without interruption,and 90 per cent of patients remained completely immobile throughoutsurgery. During recovery 97 per cent of patients were Rombergsteady and considered fit to leave the surgery within 30 minutesof discontinuing anaesthesia. The incidence of postoperativeretching and vomiting was 3 per cent. These results are attributedto the relatively large doses of methohexitone combined withthe frequent use of halothane as a supplement for the more resistantindividuals and those undergoing prolonged surgery.     

Induction reflex actions with intravenous nalbuphine as an adjunct to isoflurane

Ninety unpremedicated patients undergoing mask anaesthesia were assigned to one of three groups according to the volatile anaesthetic and the acute intravenous premedication administered. Group I received saline placebo as premedication and halothane by inhalation. Group II received saline placebo and isoflurane by inhalation. Group III received nalbuphine 0.1 mg.kg-1 IV as premedication and isoflurance by inhalation. Mean time to loss of consciousness (71 sec) did not differ among groups. The dosage of thiopentone required to induce loss of consciousness was decreased by 15 per cent (from 3.9 to 3.3 mg.kg-1) by nalbuphine premedication (P less than 0.05), and time to induction of surgical anaesthesia using isoflurane was decreased by 15 per cent (P less than 0.05). The incidence of reflex actions (coughing, laryngospasm, breath holding, hiccoughs and movement) during induction was no different in the saline-premedicated halothane or isoflurane groups. Acute intravenous nalbuphine premedication decreased significantly the incidence of reflex actions during induction of isoflurane anaesthesia from 77 per cent to 37 per cent (P less than 0.02). Desaturation episodes (SaO2 less than 90 per cent) were more frequent with isoflurane inductions compared with halothane (55 per cent vs 17 per cent, P less than 0.01). Apnoeic episodes accounted for the majority of desaturations associated with nalbuphine premedication, while excitatory reflexes (coughing and laryngospasm) accounted for more desaturations with isoflurane alone.     

CIRCULATORY EFFECTS OF PENTAZOCINE AND PETHIDINE DURING GENERAL ANAESTHESIA WITH NITROUS OXIDE, OXYGEN AND HALOTHANE

Pentazocine 30 mg and pethidine 30 mg were given intravenouslyto two groups of patients receiving general anaesthesia withnitrous oxide, oxygen and halothane. The injections were repeatedafter 10 minutes. The effects on cardiac output, arterial bloodpressure, heart rate and central venous pressure were measured.Both drugs caused a transient fall (approximately 20 per cent)in cardiac output and a sustained rise in central venous pressure.     

Occupational exposure to sevoflurane, halothane and nitrous oxide during paediatric anaesthesia Waste gas exposure during paediatric anaesthesia

We report the findings of a study on exposure of operating room staff to sevoflurane, halothane and nitrous oxide during induction and maintenance of anaesthesia in children. Concentrations of anaesthetic agents in the operating theatre were measured directly by highly sensitive, photoacoustic infrared spectrometer during 20 anaesthetics. Samples were taken from the breathing zones of the anaesthetist and the circulating nurse. The operating theatre was of modern design with an air conditioning system providing 20 changes of air each hour. The threshold values of 100 ppm N₂O, 50 ppm isoflurane and 10 ppm halothane recommended by the United Kingdom Committee for Occupational Safety and Health (COSH) were exceeded in several cases for a short time during mask induction. After tracheal intubation, trace concentrations of sevoflurane, halothane and N₂O were mostly under the recommended levels and comparable to levels measured during adult anaesthesia.     

METHOXYFLURANE IN DENTAL ANAESTHESIA: A BLIND TRIAL

Anaesthesia with nitrous oxide and oxygen, alone or supplementedwith methoxyflurane or halothane, was administered for dentalextractions in 256 patients (204 children and 52 antenatal women).Anaesthesia was regarded as "good" in 69 per cent of patientswith methoxyflurane and 75 per cent with halothane, but only50 per cent with unsupplemented nitrous oxide and oxygen. Afurther trial was carried out in 144 children and 8 antenatalwomen, nitrous oxide and oxygen being supplemented in all caseswith methoxyflurane or halothane. There were 59 per cent "good"results with methoxyflurane and 76 per cent with halothane.Methoxyflurane was found to be considerably cheaper than halothane.The shortcomings of purely inhalational anaesthesia for dentalextractions was shown by the finding that in no series was thepercentage of "good" results as high as 80.     

Electro-acupuncture modification of halothane anaesthesia in the dog

The effects of electro-acupuncture on minimum alveolar anaesthetic concentration (MAC) was studied during halothane anaesthesia in the dog. Following induction of anaesthesia, MAC was determined in duplicate. Ten dogs then received electro-acupuncture bilaterally at San Yin Chiao for 30 minutes. MAC was determined in duplicate while electro-acupuncture was continued. Electro-acupuncture significantly lowered MAC from 1.2 percent to 1.0 per cent (p< 0.01). A crossover experimental design was used in an additional eleven dogs. Here MAC was lowered from 1.17 per cent to 1.04 per cent (p < 0.05). Electro-acupuncture produces a small but statistically significant reduction in halothane MAC.     

Negative pressure in the middle ear in children after nitrous oxide anaesthesia

A study was conducted to measure the pressure in the middle ear in healthy children, following nitrous oxide anaesthesia. Premedication with chloral hydrate and scopolamine orally was similar in all patients and awake patients received thiopentone 4-5 mg X kg-1 for induction of anaesthesia. All received nitrous oxide (66 per cent) in oxygen and halothane or isoflurane as required. Exposure to nitrous oxide varied from 17-100 minutes, mean 47 minutes. All patients developed negative pressure in one or both ears in the first day following anaesthesia. This is a higher incidence than previously reported and may be explained by the inability of children to equilibrate negative middle ear pressure via the eustachian tube.     

DREAMING ASSOCIATED WITH ANAESTHESIA: THE INFLUENCE OF MORPHINE PREMEDICATION AND TWO VOLATILE ADJUVANTS

An investigation is described into the problems of dreamingand recall under anaesthesia. One hundred and twenty patientswere divided into four equal groups. Group 1 were anaesthetizedusing thiopentone for induction and nitrous oxide for the maintenanceof anaesthesia, muscle relaxation being provided by tubocurarineand no premedicant or volatile anaesthetic agent being used.The three other groups received modifications of this technique:group 2 received pre-anaesthetic medication with morphine (1mg/stone body weight (6.3 kg) 30–60 min before operation);group 3 received small concentrations (0.5–0.3 per cent)of halothane as an adjuvant, and group 4 small concentrations(0.3–0.1 per cent) of methoxyflurane. The incidence ofdreaming in association with anaesthesia was high in the caseof group 1 (57 per cent) but significantly less in group 2 (23per cent; P<0.02), group 3 (0 per cent; P<0.001), andgroup 4 (23 per cent; P<0.02). There was no unequivocal evidenceof awareness of the surgical procedure, but there were a numberof dreams which appeared to be connected with the site of theoperation. The significance of this is discussed.     

Haemodynamic and plasma vasopressin responses with high-dose fentanyl anaesthesia during aorto-coronary bypass operations

Twelve male patients were given high dose fentanyl (75-100 microgram.kg-1) anaesthesia with oxygen during elective aorto-coronary bypass operations, and their haemodynamic and vasopressin responses were determined during induction, sternotomy, cardiopulmonary bypass, post-bypass and recovery periods. For comparison, a group of 12 male patients were anaesthetized with morphine, halothane 0.5 per cent, nitrous oxide and oxygen, and were similarly studied. Significant alterations in haemodynamics included increased mean arterial pressure after sternotomy in the fentanyl group, increased heart rate in both groups, increased systemic vascular resistance after sternotomy only in the halothane group, and decreased left ventricular stroke work index in both groups following induction, bypass, and during the recovery periods. Plasma vasopressin levels increased significantly in both groups during the bypass period, but returned to baseline levels following bypass. Serum sodium and osmolality did not change significantly, and urinary sodium and potassium excretion rose with the progress of the operation in both groups. A positive correlation was found between mean arterial pressure and vasopressin only in the halothane group. Systemic vascular resistance was correlated to vasopressin levels in both groups. Vasopressin response in both groups was similar, with significant but relatively low increases in levels during cardiopulmonary bypass. Fentanyl-oxygen anaesthesia did not provide haemodynamic stability in eight of 12 patients.