Cardiovascular and respiratory responses to severe hypoxaemia under anaesthesia

Gray, I. G.; Nisbet, H. I. A.; Olley, Peter M.; Welsh, B.E.; Johnston, A. E.; Volgyesi, G. A.

doi:10.1007/bf03026261

Cited by 5 publications

(1 citation statement)

References 21 publications

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“…In the intact dogs under inhalation anaesthesia, the effects of hypoxaemia were, in general, similar to those described in other studies (Cullen and Eger, 1970;Gray et al, 1973). During hypoxaemia increases in heart rate, cardiac output and haemoglobin concentration maintained oxygen delivery to the tissues.…”

Section: Discussionsupporting

confidence: 85%

The Effect of Splenectomy on Circulatory Adjustments to Hypoxaemia in the Anaesthetized Dog

Ffoulkes-Crabbe

Creighton

Volgyesi

et al. 1976

British Journal of Anaesthesia

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Six intact and seven splenectomized dogs were subjected to a similar degree of hypoxaemia while under light anaesthesia and artificial ventilation. In the intact animals, heart rate, cardiac output, myocardial contractility and oxygen consumption were increased as a result of hypoxaemia; oxygen transport was not affected. In the splenectomized animals the changes in cardiac output and myocardial contractility were small, and oxygen availability was decreased.

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Section: Discussionsupporting

confidence: 85%

The Effect of Splenectomy on Circulatory Adjustments to Hypoxaemia in the Anaesthetized Dog

Ffoulkes-Crabbe

Creighton

Volgyesi

et al. 1976

British Journal of Anaesthesia

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Cardiovascular signs of acute hypoxaemia and hypercarbia during enflurane and halothane anaesthesia in man

Manninen

Knill

1979

Canad. Anaesth. Soc. J.

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HYPOXIA AND HYPERCARBIA are always potential complications of anaesthesia. How can they be recognized quickly? Signs frequently sought in the anaesthetized patient are changes in heart rate and rhythm and blood pressure. In awake man, acute hypoxaemia accelerates heart rate obviously, while increasing blood pressure only slightlyJ'2; acute hypercarbia augments both) ,4 The cardiovascular responses to steady states of hypercarbia during anaesthesia have been previously described s,6 and are well known; however, there is no information on the human response to hypoxia during anaesthesia.We have studied changes in heart rate and blood pressure brought about by brief periods of controlled hypoxaemia (Po~ approximately 6.0 kPa [45 torr]) in human subjects awake and when anaesthetized with enflurane or halothane. We have also recorded their responses to a mild carbon dioxide stimulus (Pco2 increment of 1.3 kPa [ 10 torr]). Our results indicate that during anaesthesia with these drugs, neither blood pressure nor heart rate is a reliable indicator of acute moderate hypoxaemia or of mild hypercarbia. METHODSWe studied 13 young healthy subjects. Their mean age, weight and height (-I-S.D.) were respectively 22 _ 5 years, 66 --. 14 kg and 170 4-9 centimetres. All were patients scheduled for elective dental surgical procedures, usually multiple odontectomy. Each was informed of the protocol and risks involved and signed a written consent form which had been approved by the University Human Research Committee. We Canad. Anaesth. Soc. J., vol. 26, no. 4, July 1979 studied each subject twice, first while anaesthetized with either enflu rane (n = 8) or halothane (n == 5) and subsequently while conscious.Anaesthesia studies were conducted during a 45-minute period of anaesthesia before the operation. The subjects were not premedicated. We induced anaesthesia with thiopentone 3 to 5 rag" kg -I and, after producing neuromuscular paralysis with succinylcholine I mg. kg -~ we intubated the trachea with an 8 or 9 mm cuffed tube. The subject inhaled a mixture of oxygen and either enflurane or halothane from a nonrebreathing circuit for a period of at least 30 minutes. The concentration of inspired vapour was set to achieve a steady end-tidal concentration equivalent to I.l MAC. Intravenous fluid (5 per cent dextrose in 0,2 percent saline) was infused in amounts up to one litre to maintain systolic blood pressure above 70 per cent of the awake vatue. Nasopharyngeal temperature was monitored and remained above 36 degrees Celsius in all subjects. When the end-tidal vapour concentration had been steady for ten minutes, we induced periods of hypoxaemia and hypercarbia individually and recorded heart rate and blood pressure responses.We conducted conscious studies in a quiet laboratory approximately one week after the operation. Each subject sat in a comfortable chair breathing through a mouthpiece with a nose-clip in place. We induced hypoxaemia and hypercarbia by the same methods employed during anaesthesia and recorded the responses fo...

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