Pulmonary venous admixture before, during, and after halothane: oxygen anesthesia in man.

Marshall, Bryan E.; Cohen, Peter J.; Klingenmaier, C. H.; Aukberg, Stanley J.

doi:10.1152/jappl.1969.27.5.653

Cited by 31 publications

(5 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…With the exception of the changes in the deadspace/tidal volume ratio (VD/VT), the other effects we have observed were more or less predictable from our previous knowledge of the behaviour of normotensive patients during anaesthesia (Prys-Roberts et al, 1968). The reduction of oxygen uptake during all three stages during anaesthesia was in accord with a number of recent studies in a wide range of patients, anaesthetized with a variety of volatile anaesthetic agents (Theye and Tuohy, 1964;Prys-Roberts et al, 1968;Cullen, Eger and Gregory, 1969;Marshall et al, 1969;Price et al, 1969;Eger et al, 1970). Less predictable, and of less moment were the changes in carbon dioxide elimination.…”

Section: Pulmonary Gas Exchangessupporting

confidence: 80%

Studies of Anaesthesia in Relation to Hypertension

Prys‐Roberts

Foëx

Greene

et al. 1972

British Journal of Anaesthesia

View full text Add to dashboard Cite

The cardiovascular responses, ventilation and pulmonary gas exchanges of 8 treated and 6 untreated hypertensive patients were studied during artificial ventilation under nitrous oxide/oxygen/relaxant anaesthesia, with and without halothane (1%). Mean arterial pressure (m.a.p.) fell to 69% and 62% of the awake values in the treated and untreated patients respectively during hypocapnia (mean Pa CO2 23 mm Hg) induced by IPPV under nitrous oxide anaesthesia. When halothane (1%) was added under the same conditions of IPPV, m.a.p. fell to 60% and 53% of the awake values respectively, as a result of reduced cardiac output (50% and 53% respectively of awake values), whereas systemic vascular resistance was raised above the awake values in all patients. Electrocardiographic evidence of myocardial ischaemia was observed during these periods of arterial hypotension in 50% of the treated patients and in all the untreated patients. Increased alveolar-arterial Po, differences during IPPV were due to desaturation of mixed venous blood associated with raised arteriovenous oxygen content differences. Pulmonary venous admixture did not change significantly during the course of anaesthesia with IPPV, and recovery. VD/VT increased during spontaneous ventilation following induction of anaesthesia, but decreased significantly below awake values during IPPV, returning to control values in the postoperative period.

show abstract

Section: Pulmonary Gas Exchangessupporting

confidence: 80%

Studies of Anaesthesia in Relation to Hypertension

Prys‐Roberts

Foëx

Greene

et al. 1972

British Journal of Anaesthesia

View full text Add to dashboard Cite

show abstract

“…Arterial hypoxemia, characterized by an increased alveolo-arterial oxygen tension difference, is frequently observed during general anesthesia. Although this condition is welldocumented (STARK & SMITH 1960, BERGMAN 1963, NUNN 1964, NUNN et al 1965, MARSHALL 1966, MARSHALL et al 1969, PRICE et al 1969, the pathophysiologic mechanisms involved are still incompletely understood. Most investigators have studied changes in ventilation mechanics during anesthesia, while the pharmacologic effects of anesthetics on the pulmonary circulation have attracted much less attention.…”

Section: Receivrd 17 May Accepted For Publication I4 June 1976mentioning

confidence: 99%

Hypoxia‐induced Vasoconstriction in Isolated Perfused Lungs exposed to Injectable or Inhalation Anesthetics

Bjertnæs¹

1977

Acta Anaesthesiol Scand

106

View full text Add to dashboard Cite

Investigations during the last two decades have revealed a tendency to inpaired pulmonary gas exchange in patients during general anesthesia. In the awake state, arterial hypoxemia is counteracted by a mechanism which tends to normalize the ventilation/perfusion ratio of the lungs by way of a hypoxia-induced vasoconstriction in poorly ventilated areas. This results in a redistribution of perfusion to more adequately ventilated lung regions. Recent observations suggest, however, that this beneficial mechanism is blunted by some commonly used inhalation anesthetics. In the present study the effect of inhalation anesthetics and injectable anesthetics on the vasoconstrictor response to acute alveolar hypoxia have been compared in isolated blood-perfused rat lungs. The experiments showed that the response was unaffected by N2O and injectable anesthetics, while a reversible, dose-dependent damping effect was demonstrated for the volatile inhalation anesthetics, ether, halothane and methoxyflurance. The effect could be demonstrated at blood concentrations comparable to those used in clinical anesthesia, and it was not due to a general paralysis of the vascular smooth muscle. The findings might, at least in part, explain the occurrence of arterial hypoxemia during general inhalation anesthesia.

show abstract

“…There have been many reports of an increase in the alveolar-to-arterial oxygen tension difference (A-a Po 2 ) after the induction of general anaesthesia in man (Campbell, Nunn and Peckett, 1958;Marshall, 1966;Marshall and Grange, 1966;Prys-Roberts, Kelman and Greenbaum, 1967;Marshall et al, 1969;Bergman, 1970;Foex, Meloche and Prys-Roberts, 1971).…”

mentioning

confidence: 99%

The Effect of Inhalational Anaesthetics on Hypoxic Pulmonary Vasoconstriction and Pulmonary Vascular Resistance in the Perfused Lungs of the Dog and Cat

Sykes¹,

Loh²,

Seed³

et al. 1972

British Journal of Anaesthesia

View full text Add to dashboard Cite

Alveolar hypoxia produced an increase in pulmonary vascular resistance in isolated cat and dog lungs or lobes perfused at constant flow. This response was abolished for varying periods of time by the administration of high concentrations of inhalational anaesthetic agents. In these preparations 5 per cent halothane caused pulmonary vasodilatation whereas 15 per cent ether, 1.5 per cent trichloroethylene and 79 per cent nitrous oxide caused vasoconstriction. Two per cent methoxyflurane did not cause a significant change in pulmonary vascular resistance. It is postulated that the abolition of the pulmonary vasoconstrictor response to hypoxia may increase the proportion of blood flowing through shunts or areas of lung with a low ventilation/perfusion ratio and so may contribute to a decrease in arterial oxygen tension during anaesthesia. The pulmonary vasodilatation or vasoconstriction produced by inhalational agents may augment this effect.

show abstract

Pulmonary venous admixture before, during, and after halothane: oxygen anesthesia in man.

Cited by 31 publications

References 0 publications

Studies of Anaesthesia in Relation to Hypertension

Studies of Anaesthesia in Relation to Hypertension

Hypoxia‐induced Vasoconstriction in Isolated Perfused Lungs exposed to Injectable or Inhalation Anesthetics

The Effect of Inhalational Anaesthetics on Hypoxic Pulmonary Vasoconstriction and Pulmonary Vascular Resistance in the Perfused Lungs of the Dog and Cat

Contact Info

Product

Resources

About