[Effect of halothane on ventilation and arterial blood gases in rats with and without diaphragmatic paralysis]. / Effets de l'halothane sur la ventilation et les gaz du sang arteriel chez le rat avec ou sans paralysie diaphragmatique.

Some patients with diaphragmatic paralysis or dysfunction maintain ventilation by use of other muscles. Anaesthesia, in modifying the performance of these muscles, presents a potential risk to such patients. To evaluate this risk, the effects of halothane on ventilation and arterial blood gases were studied on a model of bilateral diaphragmatic paralysis, the phrenectomized rat. The study was performed on 43 rats. Success of phrenectomy was confirmed at laparotomy, which did not result in blood gas changes. Laparotomy was performed in 23 rats and a carotid artery was catheterized. In 11 control rats, phrenic nerves were exposed but not sectioned, and in 12 other rats, the phrenic nerves were sectioned. Ventilation was measured by plethysmography in awake rats before and after surgery and in the same rats anaesthetized with halothane 1.1%. In the 23 rats, a decrease in weight and core temperature was observed after operation and this was more marked in phrenectomized than in control rats. In the 11 control rats, ventilation increased postoperatively without change in blood gases. In these rats, halothane caused a decrease in minute ventilation and PaO2 and an increase in PaCO2. Phrenectomy in awake rats led to an increase in minute ventilation, hypoxaemia and hypercapnia. In these rats, halothane led to death in three and a decrease in minute ventilation, with hypercapnia and hypoxaemia in the nine other rats. Blood gas changes were greater than in anaesthetized controls. In the intact rat, halothane leads to blood gas changes comparable to those observed in other species and humans. The present study confirms the effects of halothane on respiratory muscles other than the diaphragm and demonstrates the severe respiratory risk of anaesthesia in patients whose ventilation is maintained by these muscles.

[The effects of halothane on the changes in PaCO2, acid-base equilibrium and ventilation induced by hypoxia in the rat]. / Effets de l'halothane sur les modifications de la PaCO2, de l'équilibre acido-basique et de la ventilation provoquées par l'hypoxie chez le rat.

The effects of progressive hypoxia, obtained by decreasing FIO2 from 0.21 to 0.12, on arterial blood gases and acid-base balance were studied in 13 awake rats and 13 rats anaesthetized with halothane (inspired concentration 1.1%). The effects on ventilation of the decrease in FIO2 from 0.21 to 0.12 were studied in eight rats, awake and then anaesthetized. Halothane causes a decrease in PaO2 and an increase in PaCO2; it abolishes the ventilatory response to hypoxia. The effects of hypoxia on PaCO2 were identical in awake and in anaesthetized rats. In the awake rats, PaO2 decreased from 90.3 +/- 5.9 mmHg to 42.3 +/- 3.6 mmHg, and PaCO2 decreased from 36.7 +/- 3.3 mmHg to 28.1 +/- 1.8 mmHg. In the anaesthetized rats, PaO2 decreased from 78.8 +/- 6.2 mmHg to 34.8 +/- 4.2 mmHg, and PaCO2 decreased from 40.7 +/- 2.8 mmHg to 31.9 +/- 3.7 mmHg. The decrease in PaCO2 during acute hypoxia in the anaesthetized rat could be explained by a decrease in CO2 production, secondary to a decrease in oxygen consumption due to the metabolic and circulatory effects of halothane and hypoxia.

[Circulatory arrest after splanchnic neurolysis with phenol in unresectable cancer of the pancreas]. / Arrêt circulatoire après neurolyse splanchnique au phénol pour cancer du pancréas non reséquable.

One of the treatments for pain in patients with unresectable pancreatic cancer is chemical splanchnicectomy by phenol. We report two cases of severe cardiac arrhythmia followed by circulatory arrest, during intraoperative chemical splanchnicectomy. The cardiac toxicity of phenol is known in plastic surgery (face peeling). The reasons for this toxicity are not well known. We recommend that phenol be replaced by alcohol during chemical splanchnicectomy, because of its safety.

[The effect of halothane on blood gases and arterial acid-base equilibrium in intact rats and in chemo-denervated rats]. / Effets de l'halothane sur les gaz du sang et l'équilibre acido-basique artériels chez le rat intact et chez le rat chémodénervé.

Halothane decreases the ventilatory response to hypoxia and the activity of peripheral arterial chemoreceptors, resulting in "chemical chemodenervation." In order to evaluate the role of this halothane-induced "chemical denervation" in acid-base and arterial blood gas changes, these values were measured in intact and chemodenervated rats, awake and under anaesthesia. Since the depth of anaesthesia could be modified by the anatomical chemodenervation, the ED50 of inspired halothane was determined in six rats before and after anatomical chemodenervation. To prevent haemodynamic changes due to halothane and/or anatomical chemodenervation from interfering with the results, systemic arterial blood pressure and heart rate were measured in six intact rats, awake and then anaesthetized, and in the same rats after chemodenervation, awake and then anaesthetized. In nine intact rats and in 19 chemodenervated rats, arterial pH, arterial bicarbonate concentration, and arterial blood gases (PaO2 and PaCO2) were measured before and after administration of halothane. Anatomical chemodenervation modified neither the inspired ED50 (1.1%), nor the mean arterial blood pressure or heart rate. The haemodynamic effects of halothane were comparable in intact and in chemodenervated rats. Changes in arterial blood gases and acid-base balance due to halothane in intact rats and due to chemodenervation in awake rats were not different, but there was a decrease in PaO2 and pHa, and an increase in PaCO2. In chemodenervated rats, halothane caused a further decrease in PaO2 and a further increase in PaCO2. The fact that halothane and anatomical chemodenervation have similar effects on arterial blood gases and acid-base balance favours a "chemical chemodenervating" action of halothane. However, the additional effects of halothane in the anatomically chemodenervated animal show that the action of halothane on blood gases and acid-base balance is the result of multiple sites of impact on the respiratory system.

[Serious heart rate disorders following perioperative splanchnic nerve phenol nerve block]. / Troubles du rythme cardiaque graves après phénolisation splanchnique peropératoire.

The cardiac toxicity of phenol is known. A variety of cardiac arrhythmias has been noted, particularly after application to the skin, more rarely when used for neurolysis. We report a case of severe cardiac arrhythmia followed by circulatory arrest in a patient with pancreatic cancer which occurred a few minutes after injecting 30 ml phenol 6.66% to produce splanchnic neurolysis. Due to the cardiotoxicity of phenol, recommendations are made for the prevention of cardiac arrhythmias. When high doses of phenol are used on the skin, e.g., face peeling, applications should be over small areas with division of the phenol to each area a sufficient iv fluid load should be given, forcing diuresis with furosemide may be given, and lidocaine hydrochloride used as a prophylactic antiarrhythmic agent. In these cases, as for neurolysis (low doses of phenol), ECG monitoring is mandatory. For neurolysis, alcohol could with advantage replace phenol.

[Respiratory effects of moderate hypothermia (36 degrees C-28 degrees C) in dogs under halothane anesthesia]. / Effets ventilatoires d'une hypothermie modérée (36 degrees C-28 degrees C) chez le chien anesthésie à l'halothane.

Changes in systemic haemodynamic variables (mean arterial pressure, MAP; heart rate, HR; cardiac output, Qc), in oxygen consumption, VO2, and in ventilation (minute ventilation, V; respiratory frequency, f; tidal volume, VT; and arterial blood gases) with particular attention to respiratory times (duration of inspiration, TI; duration of expiration, TE; duration of the breathing cycle, TTOT), to respiratory timing (TI/TTOT) and respiratory drive (VT/TI) were studied during moderate progressive hypothermia (36 degrees C to 28 degrees C) during stable halothane anaesthesia (MAC = 1.5) in six dogs. MAP, HR and Qc decreased; V and f decreased, the decrease in f being correlated with that in temperature (r = 0.66; P < 0.01). Tidal volume did not change. The PaO2 and pHa decreased while PaCO2 increased slightly. The decrease in ventilation was related to changes in respiratory times (TI and TE) which increased (TE more than TI) and in respiratory drive (VT/TI which decreased due to the increase in TI). The relation between VT/TI and TI/TTOT changes was not constant during cooling. Changes in respiratory times and drive could be due to the effect of cold on medullar respiratory control.

[The measurement of pH and gases in the blood using microanalysis: the effect of storage at 4 degrees C for an hour. A study in the rat]. / Mesure du pH et des gaz du sang sur des micro-echantillons: effets de la conservation à 4 degrees C pendant une heure. Etude chez le rat.

The effects of one hour storage at 4 degrees C on micro blood gas samples (150 microliters) were studied for a wide range of values (pH: 7.11-7.58; PCO2: 26-97 mmHg; PO2: 31-503 mmHg) in 20 rats with indwelling carotid artery catheters. Blood gas values were modified by varying the composition of inspired gases: normoxia, hypocapnic hypoxia, hyperoxia, hypercapnia (in this case eight animals were anaesthetized with halothane 1.1%). One hundred and eight double micro-samples were taken. For each double sample, one was analysed immediately (H0) and compared with the second sample after one hr storage at 4 degrees C (H1). The Bland and Altman method was used for the statistical analysis of results. After one hr storage at 4 degrees C, the PCO2 was slightly higher than at H0 (mean difference +/- SD: +1.08 +/- 1.7 mmHg) and arterial pH was slightly lower (mean difference +/- SD: -0.016 upH +/- 0.011 upH). These results show that for these two variables, in the range studied, one hour storage at 4 degrees C had little effect. In contrast, for arterial PO2 the mean difference between all measurements between H1 and H0 was -17 +/- 25 mmHg. If results lower than 200 mmHg (56 double samples) are considered separately, the mean difference between values at H1 and H0 was only -0.98 +/- 5.3 mmHg. For PaO2 greater than 200 mmHg (52 double samples), the mean difference was -34 +/- 26.3 mmHg; this may be due to low reproducibility of measurements of elevated PO2 levels and to the effects of cellular metabolism.(ABSTRACT TRUNCATED AT 250 WORDS)

Ventilatory effects of almitrine bismesilate in dogs breathing normoxic, hyperoxic and hypoxic mixtures.

The ventilatory effects of 1 mg.kg-1 i.v. almitrine were studied in five dogs anaesthetized with halothane 2% under conditions of normoxia, hyperoxia and hypoxia. Ventilation (minute ventilation, respiratory frequency, tidal volume, duration of inspiration and expiration, ratio TI/Ttot and VT/TI), Pao2, Paco2, pHa, systemic arterial pressure and heart rate were measured in air before and following almitrine; in air, after inhalation of pure oxygen and after almitrine in hyperoxia; in air, during hypoxia with Fio2 progressively decreased from 0.21 to 0.12 and after almitrine in hypoxia (FIO2 = 0.12). Halothane decreased ventilatory response to hypoxia. Almitrine stimulated ventilation irrespective of the level of oxygenation and restored the ventilatory response to hypoxia. Hyperoxia did not suppress ventilatory action of almitrine whose action is probably partly central. Hypoxia and almitrine did not induce major systemic haemodynamic modification.

[Respiratory effects of almitrine on various levels of the fraction of inspired oxygen. A study in the anesthetized dog]. / Effets ventilatoires de l'almitrine à différents niveaux de FIO2. Etude chez le chien anesthésié.

The effects of intravenous almitrine under normoxic, hyperoxic, and hypoxic conditions were studied in 5 male beagle dogs (mean weight 15.2 +/- 5 kg) anaesthetized with thiopentone. Plasma concentrations of thiopentone were maintained constant at 27-29 mg.1(-1). Each animal underwent twice the three different experiments, with a lapse of a fortnight between each experiment: a) breathing room air, with intravenous administration of 1 mg.kg-1 almitrine over 30 s, b) breathing room air, then pure oxygen for 15 min, followed by an intravenous administration of 1 mg.kg-1 almitrine over 30 s with the dog still breathing pure oxygen, and c) breathing room air, then progressively less oxygen (FIO2 0.18, 0.16, 0.14, 0.12 for 5 min each), followed by an intravenous administration of 1 mg.kg-1 almitrine over 30 s with the dog still breathing a mixture with 12% oxygen. Tidal volume, respiratory rate, minute ventilation, inspiratory and expiratory duration, arterial pH, PaO2 and PaCO2 were measured respectively in room air, after 100% oxygen, in hypoxia (FIO2 = 0.12), before, 5 and 10 min after the injection of almitrine. Hyperoxia depressed ventilation (-21%), whilst hypoxia stimulated it (+126%), although significantly less than in the awake animal. Almitrine restored the respiratory response to hypoxia, but hyperoxia did not suppress respiratory stimulation due to the drug. It would therefore seem likely that almitrine acts on peripheral arterial chemoreceptors, but also on other structures. The results of this study suggest that almitrine may be useful in restoring the respiratory response to hypoxia during recovery from anaesthesia.

Effects of ketamine on isolated human bronchial preparations.

The bronchodilator effects of ketamine were examined in human bronchial preparations contracted maximally with histamine, acetylcholine, barium chloride or potassium chloride. Antagonism between ketamine and either histamine or acetylcholine was examined also. Ketamine caused bronchial relaxation irrespective of the constricting agent, and exerted a partial and non-competitive antagonism to histamine and acetylcholine. Propranolol and indomethacin did not inhibit the effect of ketamine, excluding the involvement of beta activation and of prostaglandins.

Ventilatory effects of oxygen in the dog under thiopentone anaesthesia.

The ventilatory effects of prolonged oxygen administration were examined in seven dogs during thiopentone anaesthesia. Ventilation, tidal volume (VT), ventilatory rate (f), minute ventilation (VE), inspiratory time (TI), expiratory time (TE), period (Ttot), TI/Ttot and mean inspiratory flow (VT/TI) were measured during the inhalation of room air, after 30 min of oxygen inhalation, and finally after a return to breathing room air. Arterial blood-gas tensions were measured before and after 5, 10, 20 and 30 min of oxygen administration and 15 min after return to breathing room air. Oxygen administration produced an immediate, significant and persistent decrease in ventilation, principally from a decrease in ventilatory rate and changes in ventilatory times. This was in contrast to what occurred in awake animals. Modifications in ventilatory mechanics or suppression of an hypoxic stimulus to ventilation were probably not involved. Anaesthesia may modify centrally mediated ventilatory responses to hyperoxia.

Effects of increasing enflurane concentrations on intraocular pressure.

The effects of enflurane at various concentrations on intraocular pressure (IOP) were studied. In 15 healthy patients, intubated and mechanically ventilated, IOP was measured the day before surgery, after premedication and during anaesthesia, after administration of 0.5%, 1.0% or 1.5% enflurane. Enflurane in combination with general anaesthesia and controlled ventilation (PCO2 4.7-5.3 kPa) caused a significant decrease in IOP. The decrease was more marked (44%) with 1% enflurane than with 0.5% enflurane (21%). The change in IOP was comparable with 1.0% and 1.5% enflurane; however, systolic arterial pressure decreased more with enflurane 1.5%. Increasing the inspired concentration of enflurane from 1% to 1.5% did not appear to be associated with any further decrease in IOP.

The effects of cremophor EL in the anaesthetized dog.

The effects of cremophor EL were studied in 13 anaesthetized, paralyzed and ventilated dogs. Twenty per cent cremophor EL in a dose of 4.3 +/- 0.92 ml was infused at a rate of 30 ml X hr-1. In seven dogs, thoracopulmonary compliance, heart rate, systemic arterial pressure (SAP), pulmonary pressures (PAP, PCWP, RAP), cardiac output (CO) and platelet and white cell counts, were measured before the injection of cremophor EL, at the end of infusion and 5, 10, 30 and 150 minutes after the end of infusion. In six dogs, SAP, CO, and blood volume were measured before the injection of cremophor EL, at the end of infusion and 10, 30, 90 and 150 minutes after the end of infusion. Plasma histamine and catecholamines were assayed before the injection of cremophor EL and 2, 5, 10, 30, 90 and 150 minutes after starting the infusion. Cremophor EL induced a marked, sustained and significant decrease in SAP at the end of infusion and at 5, 10 and 30 minutes after the completion of the infusion (-68, -71, -70 and -43 per cent respectively), in PCWP, RAP and CO (-78 per cent at the end of infusion, -32 per cent 150 minutes after the end of infusion). Heart rate and systemic vascular resistance did not vary significantly. Pulmonary vascular resistance increased at the end of infusion, five and ten minutes after the end of infusion (+734, +548 and +439 per cent respectively). Plasma volume decreased 10 and 30 minutes after the end of infusion (-28 and -30.5 per cent respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

[Evaluation of a protocol for selective ordering of preoperative tests in healthy subjects]. / Evaluation d'un protocole de prescription sélective des examens paracliniques préopératoires chez des sujets sains.

A protocol for selective ordering of 12 preoperative tests was prospectively evaluated during one year in a teaching hospital. 1600 consecutive healthy patients had an average of 2.4 tests each, but 270 of them had none. Usefulness of tests was assessed by taking into account not simply their abnormality yield, but also their impact on patient care during the whole hospital stay in the anaesthetist view. The possible value of tests omitted was assessed by anaesthetists at the end of hospital stay. As a consequence of test results, surgery was delayed in one patient, and a treatment was started or the anaesthetic management adapted in 16.7% of tests performed (279/3905) were found to be useful and 0.1% of tests not carried out (21/15295) would have been potentially useful. No complication inducing sequelae or death could be linked to tests not carried out. This study showed that routine preoperative investigations in healthy patients could be avoided without any adverse effects on patient care.

Ventilatory response of the conscious or anesthetized cat to oxygen breathing.

In conscious intact cats, oxygen breathing for up to 1 h does not modify ventilation, and the ventilatory response to CO2 in hyperoxia is not consistently decreased. However, oxygen breathing induces sustained hyperventilation in conscious cats after carotid body denervation. In anesthetized cats, oxygen breathing provokes a hypoventilation which is transient under light anesthesia but more sustained under deeper levels of anesthesia. At all levels of anesthesia, the ventilatory response to CO2 is decreased in hyperoxia as compared with normoxia. These results suggest that: the effects of hyperoxia include a central stimulating component, seen only in conscious animals, which offsets the decreased ventilatory drive from peripheral chemoreceptors; this central component is sensitive to anesthesia, thus allowing an explanation for the permanent decrease in ventilation and decrease in ventilatory response to CO2 observed when oxygen is given during deep anesthesia; and anesthesia may help to purposefully unmask factors involved in the control of breathing, but it markedly alters the normal functioning of the respiratory network.

Ventilatory recovery from hypothermia in anesthetized cats.

Ventilation and breathing pattern were recorded in a group of seven anesthetized cats during rewarming from 24 to 38 degrees C of esophageal temperature. It was found that at 24 degrees C, ventilation was very much depressed accounting for an alveolar hypoventilation resulting in hypoxia and hypercapnia. During rewarming, ventilation increased steadily; this was caused by sequential changes in central inspiratory activity (VT/Ti) and Ti/Tt ratio reflecting breath timing. Changes in VT/Ti have been initially attributed to an improvement in chemoresponsiveness and subsequently, to an involvement of supra-pontine thermoregulatory control areas during rewarming. Marked changes in breath timing, especially observed between 28 and 34 degrees C, have been attributed to a direct effect of rewarming upon the brain stem respiratory network. It has the result, that during hypothermia, several components of the respiratory control system are differently affected causing marked changes in breathing pattern and ventilation. They are accompanied by modifications in arterial blood pressure and heart rate.

Evaluation of a protocol for selective ordering of preoperative tests.

A protocol for selective ordering of 12 preoperative tests, according to clinical status and type of surgery, was prospectively tested for one year in a teaching hospital. 3866 consecutive surgical patients had an average of about 4 tests each. The possible value of tests that were omitted was assessed in the light of events during and after operation. According to predetermined criteria, 0.4% of non-ordered tests would have been potentially useful; but in the opinion of the anaesthetists, only 0.2% would actually have been useful. The protocol therefore had little adverse effect on patient care and was acceptable to clinicians.

Ventilatory effects of oxygen-enriched mixtures in the dog under althesin anaesthesia.

In six dogs anaesthetized with Althesin, minute ventilation, respiratory rate, tidal volume, PaO2 and PaCO2 were measured while breathing air (F/O2 = 0.21), and then after correction of hypoxaemia (F/O2 = 0.35), and again while breathing 100% oxygen (F/O2 = 1.00). The administration of 35% oxygen corrected the hypoxaemia (PaO2 = 8.98 +/- 0.76 kPa in air; PaO2 = 16.39 +/- 1.59 kPa with 35% oxygen), but produced a significant and sustained depression of ventilation. The administration of 100% oxygen induced a further significant and sustained decrease in ventilation. It is concluded that hypoxaemia is not necessary for the ventilatory depressant action of oxygen in the anaesthetized dog and that, under Althesin anaesthesia, peripheral arterial chemoreceptors are active up to high PaO2 values.

Epidural morphine strongly depresses nociceptive flexion reflexes in patients with postoperative pain.

The comparative effects of low doses (0.03-0.04 mg/kg) of epidural morphine on a nociceptive flexion reflex of the lower limb and on postoperative pain in volunteer patients were studied after orthopedic surgery on one knee. According to the stimulation parameters, it was found that 40-50 min after the injection, morphine produced an increase of 87% and 83% of the reflex threshold and of the threshold of maximal reflex response, respectively, as well as a 80-90% depression of the nociceptive responses when elicited by a constant level of stimulation. Onset of pain relief occurred by the 25th min and increased to a maximum stable level 40-50 min after the injection. These data support the hypothesis that the main site of the pain-relieving effect of epidural morphine is located directly at a spinal level.