Use this URL to cite or link to this record in EThOS: https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.475939
Title: Studies on canine myocardial blood flow related to anaesthesia : an examination of the effects of changes in blood gas tensions and blood pressure
Author: Vance, John Peden
ISNI:       0000 0001 3542 5525
Awarding Body: University of Glasgow
Current Institution: University of Glasgow
Date of Award: 1974
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Abstract:
The contents of this thesis describe experiments which attempt to determine the responses of blood flow and oxygen consumption in the myocardium along with those of systemic haemodynamic variables to certain of the physiological changes which are imposed by or encountered by anaesthetists in their daily work with patients. The experiments were carried out on closed-chest anaesthetised dogs and the responses to the following conditions have been examined: 1. hypocapnia, induced firstly by increasing minute ventilation of the lungs and secondly, by the withdrawal of carbon dioxide gas which had previously been added to the inspired gas mixture of the hyperventilated animal. 2. hypotension induced by three dose levels of halothane. 3. the combination of halothane-induced hypotension and hypocapnia. 4. hypercapnia induced by the addition of carbon dioxide gas to the inspired gases. 5. hypoxia induced by reduction of the inspired oxygen concentration. 6. hypotension induced by haemorrhage of two different grades of severity (moderate and severe). An experiments were carried out under light general anaesthesia which was usually induced with thiopentone and maintained with trichloroethylene. In 2 and 3 above (i.e. those experiments involving halothane) anaesthesia was induced with pentobarbitone. Catheters were positioned in the left coronary artery, the coronary sinus, the ascending aorta and the right atrium under radiographic control using an image intensifier. Myocardial blood flow was measured by estimating the rate of clearance of the radioactive isotope 133Xenon which was injected, in solution, into the coronary artery. Xenon clearance was estimated using a scintillation counter suspended externally over the praecordial area. The clearance was displayed as a curve from which the half time of the clearance was calculated and the half time, when substituted in an equation which was derived on the basis of the Pick principle, allowed the calculation of myocardial blood flow. Blood oxygen content was calculated from blood oxygen tension. Myocardial oxygen consumption was calculated as the product of the measured blood flow and the arterial-coronary sinus oxygen content difference. Hypocapnia of moderate degree (arterial carbon dioxide tension 25 mmHg) caused a significant reduction in myocardial blood flow with an associated increase in myocardial oxygen extraction so that oxygen consumption of the myocardium was unaltered. This degree of hypocapnia did not cause significant systemic haemodynamic changes nor were any metabolic changes observed in the myocardium. Hypotension induced with halothane caused a dose-related reduction in myocardial blood flow and oxygen consumption along with corresponding reductions in heart rate and cardiac output. The higher doses of halothane (1.0% and 1.5%) were associated with increases in myocardial vascular resistance. The decremental effects of halothane-induced hypotension and hypocapnia on myocardial blood flow were additive when the two conditions were produced simultaneously. During recovery from halothane-induced hypotension, arterial blood pressure gave a poor indication of returning myocardial function. Hypercapnia caused a marked but poorly sustained increase in myocardial blood flow along with a considerable but also poorly sustained reduction in myocardial oxygen consumption. Systemic haemodynamic changes were unremarkable. Similar changes occurred when metabolic acidosis was artificially produced by the infusion of lactic or hydrochloric acid. The responses to hypercapnia were unaffected by beta adrenergic blockade or partial parasympathetic blockade. Hypoxia did not cause changes in myocardial blood flow until the arterial oxygen tension fell to less than 35 mmHg when a brisk increase in flow occurred. Oxygen consumption was unaffected if hypoxia was sustained for less than 20 minutes. However oxygen consumption fell when hypoxia was sustained for longer periods. Hypoxia was associated with increased blood pressure, increased or decreased heart rate, frequent cardiac arrhythmias and, when sustained, with metabolic acidosis. The responses to hypoxia were not affected by beta adrenergic blockade or partial parasympathetic blockade. Haemorrhagic hypotension was associated with considerable reductions in myocardial blood flow. Severe haemorrhage was accompanied by a marked fall in myocardial vascular resistance and also by respiratory and metabolic acidosis. Myocardial oxygen consumption was reduced and oxygen extraction increased, the latter especially so during moderate haemorrhage.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (M.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.475939  DOI: Not available
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