Hypoxic and hypercapnic ventilatory responses during isoflurane sedation and anaesthesia in women

This study primarily examined the effect of three endtidal isoflurane concentrations (0.2, 1.0 and 1.4%) on the isocapnic hypoxic ventilatory response (HVR), as well as the hypercapnic ventilatory response (HCVR), in 18 women (ASA I) who were all in the follicular phase of their menstrual cycle. Capnography was used, together with pulseoximetry to indicate desired levels of hypoxia (SpO₂ 75–80%). This hypoxic challenge resulted, after 3–4 min, in a stable ventilation, and ventilation measurements were then taken during a 90 s period. The HCVR provocation (inhalation of 4.5% CO₂ in air) and measurements were conducted using a similar time frame as for HVR. Isoflurane 0.2% did not affect any ventilatory parameter. Isoflurane 1.0 and 1.4% dose-dependently increased endtidal CO₂ and respiratory rate, while tidal volumes decreased. Minute ventilation was not reduced. HVR, as well as HCVR, were both uninfluenced by isoflurane 0.2%. HVR was reduced by 60–70% at isoflurane 1.4% ( P <0.0l), and was parallelled by a similar depression of HCVR ( P <0.01). The HVR during anaesthesia was accomplished by a respiratory rate response, while the increase in tidal volume, seen in the awake state, was abolished. The HCVR during anaesthesia was, on the other hand, the result of a dose-dependently depressed tidal volume response, without any increase in respiratory rate. In conclusion, isoflurane 0.2% did not affect the ventilatory response to mild isocapnic hypoxia, nor to mild hypercapnic challenge. During anaesthesia with isoflurane (1.0 and 1.4%), there was a parallel reduction of HVR and HCVR.     

A Simple Technique for the Determination of the Ventilatory Response to Rising Arterial CO2 Tensions, Suitable for Patients with Neurological Disorders

Patients with neurological disorders may have a reduced ventilatory response to a rising PaCO₂. This is often unpredictable and may become apparent only when other complications, e.g. infections (pneumonia), occur or when the patient is subjected to general anaesthesia. This paper describes a simple method suitable for screening patients who may have an impaired capacity of eliminating CO₂ when stressed. Ventilatory changes were determined during the continuous recording of the CO₂ concentration in end-tidal air in 20 healthy subjects, who were breathing first air and then gas mixtures containing 21% O₂ and 2.5 or 5% CO₂. A prediction interval with 90 and 95% probability limits was constructed for healthy individuals. The normally expected change in minute ventilation per m² body surface area per change in PACO₂ (ΔV_E/m², l/min/ΔPACO₂) for this technique is also given.     

Effects of sevoflurane on intracranial pressure, cerebral blood flow and cerebral metabolism: A dose-response study in patients subjected to craniotomy for cerebral tumours

Background: Studies concerning the cerebrovascular effects of sevoflurane in patients with space-occupying lesions are few. This study was carried out as a dose-response study comparing the effects of increasing sevoflurane concentration (1.5% (0.7 MAC) to 2.5% (1.3 MAC)) on cerebral blood flow (CBF), intracranial pressure (ICP), cerebrovascular resistance (CVR), metabolic rate of oxygen (CMRO₂) and CO₂-reactivity in patients subjected to craniotomy for supratentorial brain tumours.
Methods: Anaesthesia was induced with propofol/fentanyl/atracurium and maintained with 1.5% sevoflurane in air/oxygen at normocapnia. Blood pressure was maintained constant by ephedrine. In group 1 (n=10), the patients received continuously 1.5% sevoflurane. Subdural ICP, CBF and CMRO₂ were measured twice at 30-min intervals. In group 2 (n=10), sevoflurane concentration was increased from 1.5% to 2.5% after CBF₁. CBF₂ was measured after 20 min during 2.5% sevoflurane. Finally, CO₂-reactivity was studied in both groups.
Results: In group 1, no time-dependent alterations in CBF, CVR, ICP and CMRO₂ were found. In group 2, an increase in sevoflurane from 1.5% to 2.5% resulted in an increase in CBF from 29 ± 10 to 34±12 ml 100g⁻¹ min⁻¹ and a decrease in CVR from 2.7±0.9 to 2.3±1.2 mmHg ml⁻¹ min 100g ( P <0.05), while ICP and CMRO₂ were unchanged. CO₂-reactivity was maintained at 1.5% and 2.5% sevoflurane.
Conclusion: Sevoflurane is a cerebral vasodilator in patients with cerebral tumours. Sevoflurane increases CBF and decreases CVR in a dose-dependent manner. CO₂-reactivity is preserved during 1.5% and 2.5% sevoflurane.     

Control of Carbon Dioxide in Modified Mapleson A and D (Hafnia) Anaesthetic Systems. An Experimental Model

The effects of varying ventilations (V_e) and fresh gas flows (FGF) on end-expiratory CO₂ (F eco ₂) levels were investigated in an experimental model lung, employing the Hafnia modification of the Mapleson A and D anaesthetic systems during CO₂-absorption and CO₂-wash-out (rebreathing). Identical results were found in both systems: F eco ₂ was constant and independent of FGF with CO₂-absorption and constant V_e, whereas rebreathing resulted in increasing F eco ₂ levels as FGF was decreased. As control of F eco ₂ in the rebreathing systems by regulating FGF could only take place within F eco ₂ levels higher than that determined by V_e at complete CO₂-absorption, e. g. for the Hafnia A and D rebreathing systems, control of FGF necessitates relative hyperventilation. F eco ₂ with constant FGF decreased with increasing V_e during CO₂-absorption, as well as during rebreathing, although this decrease was less in the rebreathing systems. Thus a decrease in F eco ₂ with rising V_e can be avoided and hypocapnia prevented. The results agree with those obtained in clinical studies.     

DEPRESSION OF HYPOXIC VENTILATORY RESPONSE BY HALOTHANE, ENFLURANE AND ISOFLURANE IN DOGS

The ventilatory responses to isocapnic hypoxia and hypercapniawere studied in six dogs each with a tracheostomy, awake andduring anaesthesia with halothane, enflurane and isoflurane(1–2.5 MAC). Isocapnic hypoxic ventilatory response (HVR)was expressed as the parameter A, such that the greater thevalue of A, the greater the hypoxic response. In the anaesthetizeddogs HVR (A) was reduced significantly from the awake valueof 2010±172 (mean+SEM) to 630±173 by 1 MAC halothane,495± 105 by 1 MAC enflurane and 952±157 by 1 MACisoflurane (P<0.05). All three anaesthetic agents producedsignificant depression of HVR at 1 MAC, but enflurane was moredepressant than isoflurane. At 1.5 MAC all three anaestheticsproduced equal and significant depression of HVR at equianalgesicconcentrations. Further increases in anaesthetic concentrationcaused no increase in depression. Hypercapnic drive, as measuredby the slope of the VE/PA_co2 response curve, was reduced significantlyfrom 9.75 litre min^–1 kPa^–1 ± 2.4 in awakedogs to 0.83 ± 0.56 after 1 MAC halothane, 0.68 ±0.53after 1 MAC enflurane and 1.58 ±0.75 after 1 MAC isoflurane.In addition, hypercapnia-induced augmentation of the hypoxicdrive was abolished by 1 MAC halothane or enflurane and diminishedmarkedly by 1 MAC isoflurane. It may be clinically significantthat hypoxia and hypercapnia during anaesthesia with these agentsdid not produce optimal stimulation of ventilation.     

Effect of Naloxone Reversal on CO2 Output, Oxygen Uptake and Cardiac Index During Recovery from Fentanyl-Supplemented Anaesthesia

For reversal of contingent residual narcotic depression after fentanyl administration during balanced anaesthesia, the effect of 0.08 mg of naloxone on CO₂ output, O₂ uptake and cardiac index was studied immediately after extubation. This dose maintained normocapnia (5.7 kPa) during early recovery, while in the control group slight hypercapnia was present (6.0 kPa). No significant differences, however, could be detected between the groups in CO₂ output, O₂ uptake or cardiac index. When 0.16 mg of naloxone was given to six other patients 10 min after the anaesthesia, when spontaneous respiration had stabilized on the same level as in the control group, significant increases in respiratory minute volume and rate and CO₂ output were recorded as compared with the respective prenaloxone levels. O₂ uptake increased with simultaneous improvement of Pa_O2 and the cardiac index also increased significantly. A slight but highly significant increase in CO₂ output was detected after 0.16 mg of naloxone in six patients during anaesthesia and volume-controlled IPPV. A significant increase in Pa_cO2 was also measured. These findings indicate that if naloxone is used postoperatively, a significant metabolic increase may take place due to increased muscular work, restlessness and shivering. Ventilation and cardiac output were adequate for demand under present conditions using 2 μg/kg of naloxone, but careful titration of naloxone is recommended in order to avoid harmful metabolic changes.     

Use of the Combitube for airway maintenance during percutaneous dilatational tracheostomy

The Combitube airway allows short-term ventilation during cardiopulmonary resuscitation and can be useful in the management of the difficult airway. In a prospective observational study we assessed its use during percutaneous dilatational tracheostomy (PDT). Twenty-one intensive care patients scheduled for elective PDT had their tracheal tube replaced by a Combitube airway retaining the same ventilator settings. Arterial blood gases, airway pressures, SpO₂ and end-tidal CO₂ were measured as were the transmural pressures exerted by the Combitube cuffs. Combitube placement was successful in 20 of 21 patients although adequate ventilation was possible in only 17 (85%). There was no significant change in P a O ₂, S p O ₂, end-tidal CO₂, P a CO ₂ or mean airway pressure during Combitube ventilation. A high mean (SD) transmural pressure of 14.7 (5) kPa was exerted by the distal cuff. The Combitube provided a satisfactory alternative airway to the tracheal tube during performance of PDT in 85% of our patients. Potential problems associated with its use in intensive care patients are outlined.     

Clinical application of differential ventilation with selective positive end-expiratory pressure in adult respiratory distress syndrome

Differential ventilation in the lateral position with positive end-expiratory pressure (PEEP) selectively applied to the dependent lung (DVSP) has been shown to reduce venous admixture and improve oxygenation without compromizing cardiac output in short term studies of patients with acute respiratory failure. We have applied this ventilation technique as a long-term treatment in severe adult respiratory distress syndrome (ARDS) in an open clinical trial. Eleven patients with ARDS of varying aetiology were treated with DVSP for a total of 34 days.
Median duration of conventional ventilatory therapy before start of DVSP was 5 days (1 to 18 days), inspiratory oxygen fraction (F₁***₂) was 0.61 ±0.16 (mean±s.d.), resulting in a mean arterial oxygen tension (Pao₂) of 7.1±2.1 kPa (Pao₂/F₁o₂= 11 ± 4 kPa). A gradual improvement in gas exchange was seen during the first 24 h of DVSP such that Pao₂ increased to 8.4±1.4 with a decreased F₁o₂ (0.52±0.14) resulting in an increased Pao₂/F₁o₂ (16±5 kPa). Five out of the eleven patients survived. No major complication was noted using DVSP as a method. We found a steady improvement in gas exchange over the first 24 hours in most patients. However, mortality rate was no lower than expected. Drawbacks with DVSP were increased demand on staff and difficulties with adequate endo-bronchial suctioning.     

Delayed elevation of plasma endothelin-1 during unilateral alveolar hypoxia without systemic hypoxemia in humans

Background: The mechanisms by which acute alveolar hypoxia induces pulmonary vasoconstriction remain unclear. We investigated whether endothelin-1 (ET-1) could be detected in plasma during pulmonary alveolar hypoxia without systemic hypoxemia (one-lung hypoxia) and whether the levels could be related to hemodynamic status in humans.
Methods: Thirteen adult patients with primary lung carcinoma were studied prior to surgery. Anesthesia was induced with fentanyl, diazepam, and pancuronium iv. Differential lung ventilation was performed for 40 min. The right lung was ventilated with a mixture of 6% O₂, 5% CO₂ and 89% N₂ and the left lung ventilated with 100% O₂. Blood gas values, hemodynamic parameters, and plasma ET-1 levels were measured.
Results: Mean pulmonary artery pressure increased from 13.±3.5 to 17.·3.2mm Hg ( P <0.01) after 20 min of one-lung hypoxia. The plasma ET-1 levels in arterial blood and wedged right pulmonary arterial blood increased from 1.69M.61 to 2.13 ±0.48 μg/ml ( P <0.01) and from 1.75±.47 to 2.26±.40 μg/ ml ( P <0.001), respectively, after 40 min of one-lung hypoxia.
Conclusions: We concluded that ET-1 may play a supporting, but not a primary, role in human hypoxic pulmonary vasoconstriction.     

Responses of respiratory drive and breathing pattern to inspiratory loading during nitrous oxide and isoflurane sedation

Background: Increased inspiratory resistance in combination with mild gas narcosis is common during recovery after a general anesthesia, but there are only few previous studies on inspiratory loading during subanesthetic gas narcosis.
Methods: Responses of respiratory drive (central inspiratory activity P_0.1) and ventilatory pattern to an inspiratory threshold load of –6 cm H₂O were studied in 16 healthy subjects during mild subanesthetic gas narcosis. One group (n=9) was exposed to 13, 26 and 39% nitrous oxide (N₂O) and air control (Group N). Another group (n=7) was exposed to 0.1, 0.2 and 0.3% isoflurane and air control (Group I). Measurements were done after 1 min adaptation to the load.
Results: Nitrous oxide and isoflurane had no effect on respiratory drive and V_T either during unloaded breathing or during inspiratory threshold loading. Across all gas concentrations (including 0% control), inspiratory threshold loading resulted in significant P_0.1 increases, amounting to 62% in group N and 38% in group I. At the same time V_T decreased by 11 and 12%, respectively. A significantly increased end-expired CO₂ and decreased minute volume compared to air control was found during isoflurane inhalation but could be ascribed to normalization of the hyperventilation in the control situation.
Conclusions: It is concluded that the steady-state ventilatory responses to loading, consisting of increased P_0.1 and decreased V_T, are maintained during inhalation of subanesthetic doses of N₂O (0.13–0.38 MAC) and isoflurane (0.09–0.26 MAC).     

Permissive hypercapnia in ARDS and its effect on tissue oxygenation

Many experimental studies have shown that mechanical ventilation with high tidal volumes (V₁) or with a low end-expiratory volume allowing repeated end-expiratory collapse, can result in acute parenchymal lung injury and probably an inflammatory response. Low volume ventilation with permissive hypercapnia has been used in an attempt to avoid such injury in ARDS.
Such management can affect oxygenation in many complex ways. The right-shift of the haemoglobin-oxygen dissociation curve during acute respiratory acidosis may increase venous oxygen tension (PvO₂) which could allow increased O₂ uptake in ischaemic tissues. Acidosis may reduce intrapulmonary shunt (Q_s/Q_t) by potentiating hypoxic pulmonary vasoconstriction, and there may also be direct and autonomically mediated effects of hypercapnia both on the lung vasculature and on the airways. Cardiac output usually increases as a consequence of hypercapnia and perhaps as a result of reduced intrathoracic pressure, further increasing Pv0₂ and CvO₂, but the increase in cardiac output (CO) may tend to increase Q_s/Q_t as flow increases preferentially in unventilated lung. The reduction of mean airway pressure may directly increase Q_s/Q_t. Hypercapnia may affect the distribution of systemic blood flow both within organs and between organs.
Limited clinical studies suggest that tissue oxygenation is usually unchanged or improved during permissive hypercapnia with increased CO₂ reduced arterio-venous O₂ content difference and reduced blood lactate concentration. However, acute hypercapnia per se can reduce lactate production. Further studies are required of this complex issue.     

Somatosensory evoked potentials during isoflurane anaesthesia

Short latency somatosensory evoked potentials (SEPs) to median nerve stimulation during isoflurane anaesthesia were recorded in 12 elective–surgery patients. The effect of isoflurane on the shape, amplitude and latency of SEPs was evaluated. SEPs were recorded at awake, 1 MAC, 1.5 MAC, at electroencephalogram (EEG) burst suppression and at continuous suppression levels. Finally, SEPs were recorded when anaesthesia was lightened back to 1 MAC. The peak latency and amplitude of the first cortical N₂₀ wave were measured. The latencies increased with increasing isoflurane concentrations. At high concentrations only an almost monophasic N₂₀ wave was recorded, reduced in shape and amplitude. No specific changes could be correlated with the burst suppression or suppression patterns. This suggests that EEG and SEP generators are differently affected with increasing isoflurane concentration. The results indicate that SEPs can also be recorded in drug–induced EEG suppression.     

Effects of esmolol on haemodynamic response to CO2 pneumoperitoneum for laparoscopic surgery

Background : Carbon dioxide (CO₂) pneumoperitoneum for laparoscopic surgery increases arterial pressures, systemic vascular resistance and heart rate and decreases urine output.
Methods : In this double-blind randomized study esmolol, an ultrashort-acting β1-adrenoceptor antagonist was compared with physiological saline (control) in 28 patients undergoing laparoscopic surgery in standardized 1 MAC isoflurane anaesthesia. Alfentanil infusion was used to prevent the increase of mean arterial pressure more than 25% from baseline.
Results : Esmolol effectively prevented the pressor response to induction and maintenance of CO₂ pneumoperitoneum. Significantly ( P <0.001) less alfentanil was needed in the esmolol group than in the control group. Urine output was higher ( P <0.05) and plasma renin activity ( P <0.01) and urine N-acetyl-β-D-glucosaminidase levels lower in the esmolol group when compared with the control group.
Conclusions : Esmolol blunts the pressor response to induction and maintenance of pneumoperitoneum and may protect against renal ischaemia during pneumoperitoneum.     

Reliability of CO2 measurements from the airway by a pharyngeal catheter in unintubated, spontaneously breathing subjects

Although several short communications have appeared describing attempts to record the concentrations of carbon dioxide (CO₂) from the unintubated airway by a catheter placed in the nose, so far only few reports have documented the reliability of the method. To evaluate the reliability of CO₂ measurements by a catheter in the open, unintubated airway during spontaneous respiration, a 12 CH PVC catheter was forwarded through the nostril to the hypopharynx and connected to a capnograph in nine healthy volunteers. Another capnograph was connected to a tightly fitting face mask and simultaneous CO₂ recordings were attained from the two parts of the airway during normoventilation, hyperventilation and rebreathing. A corresponding blood sample was drawn from the radial artery for blood gas analysis. The configurations of the capnograms recorded from the pharyngeal catheter were similar to those recorded from the face mask. The results were analysed by a multifactor analysis of variance. The carbon dioxide tension ( p CO₂) was significantly influenced by degree of ventilation ( P <0.0001), subject ( P <0.0001), measurement site ( P =0.030) and interaction subject-ventilation ( P =0.015). In spite of the significant influence of the measurement site, the difference between end tidal carbon dioxide tension ( P CO₂(ET)) and carbon dioxide tension in arterial blood ( P CO₂(a)) was small. The mean differences between paired measurements ( p CO₂(ET)- p CO₂(a)) were -0.10 kPa±0.41 kPa (mean±SD) for the catheter and -0.20 kPa ±0.43 kPa for the face mask. The study demonstrates that reliable recordings of CO₂ concentrations during spontaneous respiration can be obtained by a thin catheter positioned in the hypopharynx.     

Effects of induced hypotension on arterial blood–gases under spontaneous breathing

The effects of deliberate hypotension on both Pao₂ and Paco₂ were investigated under isoflurane anaesthesia with spontaneous breathing from a laryngeal mask. Lumbar epidural block was introduced; anaesthesia was induced with thiamylal (4 mg kg^-1) and maintained with 0.5% isoflurane in nitrous oxide (4 1 min^-1) and oxygen (2 1 min^-1) under spontaneous breathing. After that nitroglycerin, trimetaphan or prostaglandin E₁ were used to induce a hypotension of 70% of control. All three drugs significantly decreased Pao₂, from 19.9 ± 3.3, 19.2 ±2.7, and 19.6 ± 3.1 kPa to 14.6 ± 1.9, 16.6 ± 2.2, and 16.2 ± 2.4kPa (mean ± s.d.), respectively; none of them increased Paco₂. In spite of the sparing of functional residual capacity under spontaneous breathing, the levels of reduction of Pao₂ were the same as levels reported in paralyzed and mechanically ventilated subjects. In conclusion, under deliberate hypotension Pao₂ decreases to a considerable degree, even under spontaneous breathing, presumably not because of alveolar hypoventilation, but because of the suppression of hypoxic pulmonary vasoconstriction by the drugs used in this study.     

Intrathoracic and pulmonary blood volume during CO2-pneumoperitoneum in humans

Background : Induction of CO₂-pneumoperitoneum may have significant effects on systemic and pulmonary haemodynamics. We hypothesized, that intrathoracic (ITBV) and pulmonary blood volume (PBV) are affected during intra-abdominal CO₂-insufflation, which may be pronounced by positional changes of the patient.
Methods : Sixteen anaesthetized patients were studied before, during and after CO₂-pneumoperitoneum for laparoscopic cholecystectomy. A dye indicator technique was used to assess ITBV and PBV. In addition, gas exchange and haemodynamics were recorded.
Results : In the supine position, induction of CO₂-pneumoperitoneum had no effects on ITBV, PBV and cardiac output. Mean systemic arterial pressure increased from 10.9±1.5 kPa (82±11 mmHg) to 12.7±1.5 kPa (95±11 mmHg, P<0.01). In the reverse Trendelenburg position ITBV decreased from 19.8±5.1 ml . kg^-1 to 16.7±3.7 ml . kg¹ ( P <0.05) during CO₂-insufflation, but increased to control values after 20 min. PBV decreased from 4.2±1.2 ml . kg^-1 to 3.4±1.1 ml . kg^-1 (P<0.05) and remained decreased during CO₂-pneumoperitoneum. Calculated venous admixture was unchanged throughout the study. Deflation of CO₂-pneumoperitoneum increased ITBV (22.4±5.2 ml . kg^-1, P<0.05) and cardiac output above control values.
Conclusions : In anaesthetized-paralyzed patients in the reverse Trendelenburg position intra-abdominal CO₂-insufflation is associated with significant alterations of ITBV and PBV. The release of CO₂-pneumoperitoneum is associated with a re-distribution of blood into the thorax.     

Continuous positive airway pressure by mask in patients after coronary surgery

Thirty patients who underwent coronary artery bypass grafting were randomized to receive 30% oxygen by mask either with an ambient airway pressure or with 7.4 mmHg (1 kPa) continuous positive airway pressure (CPAP) for 8 h after extubation. Arterial blood oxygen tension (Pao₂) decreased remarkably in the control group after extubation (from 19.2± 5.3 kPa to 12.4 ± 2.7 kPa) but less in the CPAP group (from 16.4 ± 3.3 kPa to 14.0 ± 2.1 kPa). On the second postoperative morning Pao₂ was equally low in both groups (control: 8.4 ± 1.5 kPa, CPAP: 8.9 ± 1.9 kPa). Atelectatic areas were seen with similar frequency in both groups, 17% (whole material) on the first and 50% on the second postoperative morning. Atelectasis was more common in patients with internal thoracic artery grafting and/or pleural drainage. In conclusion, CPAP therapy was well tolerated, and minimized the decrease in Pao₂ after extubation, but could not prevent the poor oxygenation or the late development of atelectatic areas on the second postoperative day.     

Postoperative analgesia by nicomorphine intramuscularly versus high thoracic epidural administration: Effects on ventilatory and airway occlusion pressure responses to CO2

In this study the effects of nicomorphine, administered either intramuscularly or by high thoracic epidural route, on the ventilatory and airway occlusion pressure response to CO₂ were investigated and compared. Twenty-four patients scheduled for thoracic surgery were allocated randomly to postoperative pain relief by i.m. nicomorphine or by high thoracic epidural nicomorphine. The ventilatory response to 5% carbon dioxide was measured in all patients: first 1 day before operation, secondly on the first day after surgery immediately before nicomorphine administration and finally after the administration, at the moment when no further rise in end-tidal Pco₂ (P_etco₂) was measured. Respiratory response was assessed in two ways, by measuring minute ventilation (Ve) and mouth occlusion pressure (p_0.1). There was a significant depression in ventilatory response to CO₂ in the intramuscular group ( P = 0.03) due to nicomorphine as assessed by the slope of V_e vs P_etCO₂ No significant depression was found in the epidural group, irrespective of measurement of V_E, or P_0.1. No significant shift of apnoeie threshold-P_ETco₂ was observed in either group.     

Respiratory Depressant Action of Tilidine during N2O+O2, Anaesthesia

The respiratory depressant actions of pethidine and tilidine during anaesthesia were compared in 18 surgical patients anaesthetized with N₂O + O₂ after thiopental induction. Five minutes after thiopental, 0.5 mg/kg pethidine or 1.5 mg/kg tilidine were each given intravenously to six patients, the remaining six patients serving as controls.
Minute ventilation, respiratory rate, end-tidal CO₂ and Pco₂ from arterialized venous blood were measured up to 30 min. Pethidine caused the following maximal changes: 0–0.98±0.24 (s.e. mean) 1/min, rate -.5.5 ± 0.7/min, C0_2ET+0.7±0.1 vol % and Pco₂ + 5.7±1.1 mm Hg. These changes occurred within 10 xnin of the injection.
In terms of the above parameters, tilidine caused at least as pronounced a respiratory depression as pethidine. The peak effect of tilidine, however, could not be measured with certainty, since the respiratory depression first became apparent 15 min after the injection, and then increased throughout the study period. The long onset time of tilidine explains our previous failure to demonstrate tilidine-induced respiratory depression.     

Spontaneous breathing with the use of a laryngeal mask airway in children: comparison of sevoflurane and isoflurane

We compared respiratory parameters during anaesthesia with sevoflurane and isoflurane through a laryngeal mask airway (LMA). Children were anaesthetized with O₂ and air with 2.3% (1MAC) sevoflurane ( n =20) or 1.5% (1MAC) isoflurane ( n =20). After insertion of LMA, patients were allowed to breathe spontaneously and respiratory rate (RR) and P ECO2 were measured (presurgery state). After the measurement, anaesthetic concentration was increased to 1.3 MAC (3.0% sevoflurane or 2.0% isoflurane) and surgical stimulation was added. Fifteen min after incision, the measurements were again performed (during surgery). In the sevoflurane group, mean RR and P ECO2 were 32 breaths.min⁻¹, and 6.0 kPa (45 mmHg) respectively, before surgery, and 35 breaths.min⁻¹ and 7.0 kPa (52 mmHg) during surgery. In the isoflurane group, mean RR and P ECO2 were 32 breaths.min⁻¹ and 6.1 kPa (46 mmHg) respectively, before surgery, and 37 breaths.min⁻¹ and 6.7 kPa (52 mmHg) during surgery. There were no statistical differences between the two anaesthetic groups. Clinical respiratory and cardiovascular parameters during spontaneous breathing with LMA in children are similar during sevoflurane and isoflurane anaesthesia.