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“AIRWAY CLOSURE” IN ALLOXAN INDUCED PULMONARY OEDEMA AND RAISED LEFT ATRIAL PRESSURE
PROCEEDINGS OF THE ANAESTHETIC RESEARCH SOCIETY THE EFFECTS OF HALOTHANE ANAESTHESIA ON OXYGEN CONSUMPTION AND RESPIRATION IN MAN M. H. AL-ABRAK, C. E. BRISCOE, AND J. P. PAYNE
Paramagnetic O2 analyser Uras ni lnlra-red CO2 analyser Hook & Tucker Halotnano meter Circle system = Boyle mark ID COjabsorbcr
FIG. 1. Schematic arrangement of the closed circle system and measuring equipment. The halothane concentration in the circuit was varied stepwise by adjusting the vaporizer setting and each level was maintained for at least 10 min. The halothane and oxygen concentrations in the circuit were recorded during these periods together with the patient's pulse, arterial pressure and nasopharyngeal temperature. The tidal and minute volumes and respiratory rate were obtained by analysing the respiratory trace. The oxygen consumption was taken as the flow rate of a specially calibrated accurate oxygen rotameter plus or minus the volume changes in the spirometer. Corrections were made for changes in carbon dioxide content in the circuit. The changes in the measurements of oxygen consumption and respiratory pattern were calculated as a percentage of the initial values obtained after anaesthesia was stabilized at the smallest practical halothane concentration for 30 min. In every patient a highly significant reduction (P<0.001) in oxygen uptake occurred as the halothane concentration was increased from 1 to 4%. The mean reduction in oxygen consumption over the concentration range for all patients was 44 ml/min which corresponded to a 19% reduction. Moreover each step increase of 1% in halothane concentration up to 4% showed a significant
reduction (P<0.01) in oxygen consumption when pairs of values from each patient were subjected to the Student i-test. The tidal and minute volumes steadily declined as the halothane concentration increased but the respiratory rate increased. These values returned to the initial figures as the halothane concentration was reduced.
"AIRWAY CLOSURE" IN ALLOXAN INDUCED PULMONARY OEDEMA AND RAISED LEFT ATRIAL PRESSURE J. G. JONES*, R. LEMEN, AND P. D. GRAF
Cardiovascular Research Institute, University of California, San Francisco. (*Present address: Division of Anaesthesia, Clinical Research Centre, Watford Road, Harrow.) The changes in resistance of small airways were investigated in anaesthetized dogs using the "closing volume" method. The lungs were inflated from a sub-atmospheric pressure of — 5 cm H.O to + 30 cm H2O with an oxygenfilled syringe. Following inflation readings were made of airway pressure, expired volume, flow and nitrogen concentration during a slow maximum expiration. The best results were obtained using a controlled flow of 0.2 l./sec produced using a needle valve and a vacuum source. In 6 dogs measurements of "closing volume" were made before and after an intravenous injection of alloxan (100-200 mg/kg). There was an increase in the "closing volume" from 27.7 + 6.2% of the vital capacity (VC) to 39.7+4.8% VC (P<0.05) within 30 min after alloxan. After 30 min "closing volume" began to decrease and there were diffuse radiological opacities in the lungs and froth in the airways. In 10 dogs more detailed studies were made during the early stages of pulmonary oedema (Staub stages I—II). Left atrial pressure (l.a.p.) was increased using a balloon-tipped catheter. Lung water (Qwl) was measured in vivo using tritiated water and 125 I-albumin. Qwl was also examined using postmortem compartmental analysis and histological examination of the lungs frozen in vivo in liquid nitrogen. There was a linear increase in "closing volume" with elevated l.a.p. up to 15 mm Hg. The "closing volume" returned to control values within 5 min of the l.a.p. being lowered to normal. After raising the l.a.p. sufficiently to increase "closing volume" there was no significant change in lung water and histology showed no evidence of oedema cuffs around small airways. The increase in "closing volume" associated with an increase in l.a.p. up to 15 mm Hg was mediated via the vagus nerves.
CARDIOVASCULAR INTERACTIONS OF HALOTHANE, HIGH-DOSE PROPRANOLOL AND HYPOXAEMIA IN THE DOG J. G. ROBERTS, P. FOEX, T. N. S. CLARKE, C. PRYS-ROBERTS, AND M. J. BENNETT
The Nuffield Department of Anaesthetics, University of Oxford A previous communication from this department (Roberts et al., 1973) reported that propranolol 0.3 mg/kg Lv. or practolol 2.0 mg/kg i.v. had no deleterious effect on the haemodynamic responses to haemorrhage of the anaesthetized dog with severe organic heart disease. In the present study we have observed, in chronically implanted dogs, the haemodynamic consequences of increasing inspired halothane concentrations in 5 untreated dogs and in 7 dogs pretreated with high-dose oral propranolol (20 mg/kg/day) for 3 weeks before study. The effect of
Downloaded from http://bja.oxfordjournals.org/ at University of Exeter on August 10, 2015
Research Department of Anaesthetics, Royal College of Surgeons of England, Lincoln's Inn Fields, London, and St. Peter's Hospitals, London The effects of varying the depth of halothane anaesthesia on oxygen consumption and the respiratory pattern in man were studied in 9 unpremeditated patients before surgery. Continuous monitoring of these variables was obtained by recording, on a Brush Clevite recorder, the movements of a Benedict-Roth spirometer substituted for the reservoir bag of a completely closed circle system (VIC) flushed with 100% oxygen. The nitrogen in the lungs and blood was washed out by breathing a mixture of oxygen and halothane from a Magill circuit for 15 min. The gases in the circuit were sampled through a fine nylon catheter passed into the endotracheal tube and analysed by a Uras infra-red carbon dioxide analyser, a paramagnetic oxygen analyser and a Hook and Tucker halothane meter before being returned to the circuit (fig. 1). The carbon dioxide trace was recorded continuously on the Brush recorder.
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Paramagnetic O2 analyser Uras ni lnlra-red CO2 analyser Hook & Tucker Halotnano meter Circle system = Boyle mark ID COjabsorbcr
FIG. 1. Schematic arrangement of the closed circle system and measuring equipment. The halothane concentration in the circuit was varied stepwise by adjusting the vaporizer setting and each level was maintained for at least 10 min. The halothane and oxygen concentrations in the circuit were recorded during these periods together with the patient's pulse, arterial pressure and nasopharyngeal temperature. The tidal and minute volumes and respiratory rate were obtained by analysing the respiratory trace. The oxygen consumption was taken as the flow rate of a specially calibrated accurate oxygen rotameter plus or minus the volume changes in the spirometer. Corrections were made for changes in carbon dioxide content in the circuit. The changes in the measurements of oxygen consumption and respiratory pattern were calculated as a percentage of the initial values obtained after anaesthesia was stabilized at the smallest practical halothane concentration for 30 min. In every patient a highly significant reduction (P<0.001) in oxygen uptake occurred as the halothane concentration was increased from 1 to 4%. The mean reduction in oxygen consumption over the concentration range for all patients was 44 ml/min which corresponded to a 19% reduction. Moreover each step increase of 1% in halothane concentration up to 4% showed a significant
reduction (P<0.01) in oxygen consumption when pairs of values from each patient were subjected to the Student i-test. The tidal and minute volumes steadily declined as the halothane concentration increased but the respiratory rate increased. These values returned to the initial figures as the halothane concentration was reduced.
"AIRWAY CLOSURE" IN ALLOXAN INDUCED PULMONARY OEDEMA AND RAISED LEFT ATRIAL PRESSURE J. G. JONES*, R. LEMEN, AND P. D. GRAF
Cardiovascular Research Institute, University of California, San Francisco. (*Present address: Division of Anaesthesia, Clinical Research Centre, Watford Road, Harrow.) The changes in resistance of small airways were investigated in anaesthetized dogs using the "closing volume" method. The lungs were inflated from a sub-atmospheric pressure of — 5 cm H.O to + 30 cm H2O with an oxygenfilled syringe. Following inflation readings were made of airway pressure, expired volume, flow and nitrogen concentration during a slow maximum expiration. The best results were obtained using a controlled flow of 0.2 l./sec produced using a needle valve and a vacuum source. In 6 dogs measurements of "closing volume" were made before and after an intravenous injection of alloxan (100-200 mg/kg). There was an increase in the "closing volume" from 27.7 + 6.2% of the vital capacity (VC) to 39.7+4.8% VC (P<0.05) within 30 min after alloxan. After 30 min "closing volume" began to decrease and there were diffuse radiological opacities in the lungs and froth in the airways. In 10 dogs more detailed studies were made during the early stages of pulmonary oedema (Staub stages I—II). Left atrial pressure (l.a.p.) was increased using a balloon-tipped catheter. Lung water (Qwl) was measured in vivo using tritiated water and 125 I-albumin. Qwl was also examined using postmortem compartmental analysis and histological examination of the lungs frozen in vivo in liquid nitrogen. There was a linear increase in "closing volume" with elevated l.a.p. up to 15 mm Hg. The "closing volume" returned to control values within 5 min of the l.a.p. being lowered to normal. After raising the l.a.p. sufficiently to increase "closing volume" there was no significant change in lung water and histology showed no evidence of oedema cuffs around small airways. The increase in "closing volume" associated with an increase in l.a.p. up to 15 mm Hg was mediated via the vagus nerves.
CARDIOVASCULAR INTERACTIONS OF HALOTHANE, HIGH-DOSE PROPRANOLOL AND HYPOXAEMIA IN THE DOG J. G. ROBERTS, P. FOEX, T. N. S. CLARKE, C. PRYS-ROBERTS, AND M. J. BENNETT
The Nuffield Department of Anaesthetics, University of Oxford A previous communication from this department (Roberts et al., 1973) reported that propranolol 0.3 mg/kg Lv. or practolol 2.0 mg/kg i.v. had no deleterious effect on the haemodynamic responses to haemorrhage of the anaesthetized dog with severe organic heart disease. In the present study we have observed, in chronically implanted dogs, the haemodynamic consequences of increasing inspired halothane concentrations in 5 untreated dogs and in 7 dogs pretreated with high-dose oral propranolol (20 mg/kg/day) for 3 weeks before study. The effect of
Downloaded from http://bja.oxfordjournals.org/ at University of Exeter on August 10, 2015
Research Department of Anaesthetics, Royal College of Surgeons of England, Lincoln's Inn Fields, London, and St. Peter's Hospitals, London The effects of varying the depth of halothane anaesthesia on oxygen consumption and the respiratory pattern in man were studied in 9 unpremeditated patients before surgery. Continuous monitoring of these variables was obtained by recording, on a Brush Clevite recorder, the movements of a Benedict-Roth spirometer substituted for the reservoir bag of a completely closed circle system (VIC) flushed with 100% oxygen. The nitrogen in the lungs and blood was washed out by breathing a mixture of oxygen and halothane from a Magill circuit for 15 min. The gases in the circuit were sampled through a fine nylon catheter passed into the endotracheal tube and analysed by a Uras infra-red carbon dioxide analyser, a paramagnetic oxygen analyser and a Hook and Tucker halothane meter before being returned to the circuit (fig. 1). The carbon dioxide trace was recorded continuously on the Brush recorder.
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