Circulatory Influences of Artificial Ventilation During Nitrous Oxide Anaesthesia in Man

Prys‐Roberts, C.; Kelman, G. R.; Greenbaum, R.; Robinson, R. H.; Crawford, Edward W.

doi:10.1097/00132586-196806000-00005

Cited by 6 publications

(7 citation statements)

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“…In fact, a complex situation arises once respiratory depression occurs. Apart from the direct effects of the drug upon the myocardium and the peripheral circulation, the rising carbon dioxide tension will have effects of its own, tending to raise both cardiac output and arterial blood pressure (Theye, Milde and Michenfelder, 1966;Prys-Roberts et al, 1967). Moreover, as less halothane is being inhaled, the effects of this drug cannot be assumed to be stable throughout the observation period.…”

Section: Discussionmentioning

confidence: 99%

Circulatory Effects of Pentazocine and Pethidine During General Anaesthesia With Nitrous Oxide, Oxygen and Halothane

Stephen

Davie

Scott

1970

British Journal of Anaesthesia

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Pentazocine 30 mg and pethidine 30 mg were given intravenously to two groups of patients receiving general anaesthesia with nitrous oxide, oxygen and halothane. The injections were repeated after 10 minutes. The effects on cardiac output, arterial blood pressure, 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.

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Section: Discussionmentioning

confidence: 99%

Circulatory Effects of Pentazocine and Pethidine During General Anaesthesia With Nitrous Oxide, Oxygen and Halothane

Stephen

Davie

Scott

1970

British Journal of Anaesthesia

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“…For the anaesthetized state we assumed an alveolar ventilation of 4 l/min, being the ventilation required for the maintenance of Pco, of 40 torr with the reduced level of carbon dioxide output observed during anaesthesia (Nunn & Hill, 1960). Cardiac output was also assumed to be 4 l/min, being the mean value found under comparable conditions by Prys-Roberts et al (1967).…”

Section: Discussionmentioning

confidence: 99%

Influence of Anaesthesia on the Regional Distribution of Perfusion and Ventilation in the Lung

Hulands¹,

Greene²,

Iliff³

et al. 1970

Clinical Science

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1. Distribution of lung volume, pulmonary ventilation and perfusion were studied in supine patients before and during anaesthesia with paralysis and artificial ventilation. Inspired gas and pulmonary blood flow were measured with 33xenon and the chest was scanned with vertically moving counters at a lung volume of 1 litre above functional residual capacity.2. Ventilationlunit lung volume was slightly greater and perfusionlunit lung volume substantially greater during anaesthesia in the dependent parts of the lungs. The spread of ventilation/perfusion ratios in supine conscious patients was small in comparison with that reported in upright conscious patients. During anaesthesia and artificial ventilation, the inequality of ventilation to perfusion was marginally increased in three of the four patients.3. Ventilationlperfusion inequality alone was insufficient to explain the alveolararterial Po, difference usually observed during anaesthesia.In the conscious patient the alveolar and arterial Po, normally differ by only a few torr. A substantial increase has been consistently found to follow the induction of anaesthesia and the normal difference is not regained until some hours after the end of anaesthesia and surgery (Nunn & Payne, 1962;Nunn, Bergman & Coleman, 1965). The change remains unexplained. Although there is usually some increase in the measured venous admixture, it is uncertain to what extent this might be explained by an increase in the normal gravitational spread of ventilationlperfusion (P/Q) ratios found in the conscious patient (west, 1965); we are not aware of any previous reports of measurement of the regional distribution of ventilation and pulmonary blood flow during anaesthesia. In this study, we have measured the effect of anaesthesia with paralysis and artificial ventilation on the distribution of ventilation and pulmonary blood flow using 133xenon, modified from the method of Ball et al. (1962).

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“…Mean arterial pressure rose by a mean value of 12 per cent from 89 to 99 mm Hg, and total peripheral resistance fell by a mean of 14 per cent. Assuming that the differences between these series are due to differences in the anaesthetic techniques employed, the explanation depends on the use of artificial ventilation, changes in arterial carbon dioxide tension (Prys-Roberts et al, 1967) and the sympathetic blocking effect of halothane (Price and Price, 1966).…”

Section: Discussionmentioning

confidence: 99%

Circulatory Effects of Atropine in Patients Anaesthetized With Gallamine Triethiodide and Nitrous Oxide

Farman

Kennedy

1969

British Journal of Anaesthesia

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Circulatory responses to the intravenous injection of accelerating doses of atropine sulphate were studied in ten patients anaesthetized with nitrous oxide, oxygen and gallamine triethiodide and ventilated artificially. Small but significant increases in heart rate and cardiac output were accompanied by lowering of total peripheral resistance and circulation time. Arterial pressures, stroke volumes and stroke work were unchanged. Initial heart rates and pressures were high, due to the use of gallamine, and it is suggested that the control levels of cardiac output were also high. This would account for the smaller changes seen compared with earlier reports of the effect of atropine in patients artificially ventilated using tubocurarine and in those spontaneously breathing nitrous oxide, oxygen and halothane.

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Circulatory Influences of Artificial Ventilation During Nitrous Oxide Anaesthesia in Man

Cited by 6 publications

References 0 publications

Circulatory Effects of Pentazocine and Pethidine During General Anaesthesia With Nitrous Oxide, Oxygen and Halothane

Circulatory Effects of Pentazocine and Pethidine During General Anaesthesia With Nitrous Oxide, Oxygen and Halothane

Influence of Anaesthesia on the Regional Distribution of Perfusion and Ventilation in the Lung

Circulatory Effects of Atropine in Patients Anaesthetized With Gallamine Triethiodide and Nitrous Oxide

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