Circulatory and Metabolic Effects of Oxygen in Myocardial Infarction

Kenmure, A. C. F.; Murdoch, W. R.; Beattie, A. D.; Marshall, Janice M.; Cameron, Allan

doi:10.1136/bmj.4.5627.360

Cited by 86 publications

(45 citation statements)

References 17 publications

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“…Hypoxemia is commonly observed in patients with pulmonary disease, patients in shock, after a myocardial infarction (2), and in normal persons at high altitude. Observations in animals indicate that hypoxia may interfere with adrenergic responses.…”

Section: Introductionmentioning

confidence: 99%

Effect of acute hypoxia on vascular responsiveness in man

Heistad¹,

Wheeler²

1970

J. Clin. Invest.

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A B S T R A C T An effect of hypoxemia on vascular responsiveness and blood pressure regulation has not been demonstrated in man. The response of forearm resistance vessels to several vasoconstrictor stimuli was compared during normoxia and acute hypoxia. Forearm vasoconstrictor responses to lower body negative pressure and to the application of ice to the forehead, which are neurogenic stimuli, were decreased during acute hypoxia. Lower body negative pressure caused a decrease in mean arterial pressure during hypoxia, but not during normoxia. Because norepinephrine is the neurotransmitter released during reflex vasoconstriction, we considered the possibility that decreased responsiveness to norepinephrine might be one mechanism for diminished responses to lower body negative pressure and ice on the forehead during hypoxia. Hypoxia decreased the response of forearm resistance vessels to infusions of norepinephrine and angiotensin into the brachial artery. In addition, the effectiveness of intravenous infusions of norepinephrine in elevating mean arterial pressure was decreased during hypoxia. Since exposure to acute hypoxia stimulates hyperventilation and hypocapnia, experiments were done to determine the contribution of hypocapnia during hypoxia to the decreased vasoconstriction. The results indicate that hypocapnia may diminish the vascular response to some stimuli, but the reduction in oxygen appears to be the primary mechanism for decreased vasoconstrictor responses during acute hypoxia.This work was presented in part at

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Section: Introductionmentioning

confidence: 99%

Effect of acute hypoxia on vascular responsiveness in man

Heistad¹,

Wheeler²

1970

J. Clin. Invest.

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“…[64][65][66] Foster et al found that as P aO 2 increased, so did arterial pressure and systemic vascular resistance. 67 Kenmure et al 68 and Thomas et al 69 found an increase in blood pressure and decrease in cardiac output when patients suffering from a myocardial infarction breathed F IO 2 of 0.4. McNulty et al, using a Doppler flow wire, showed in 18 subjects that coronary vascular resistance increased by 41% and coronary blood flow decreased by 29% when the subjects breathed F IO 2 of 1.0 for 15 min.…”

Section: Myocardial Infarctionmentioning

confidence: 98%

Evidence for Oxygen Use in the Hospitalized Patient: Is More Really the Enemy of Good?

Blakeman

2013

Respir Care

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SummaryOxygen in arguably one of the most frequently utilized drugs in modern healthcare, but is often administered to patients at caregivers' discretion with scant evidence as to its efficacy or safety. Although oxygen is administered for varied medical conditions in the hospital setting, published literature supports the use of oxygen to reverse hypoxemia, for trauma victims with traumatic brain injury and hemorrhagic shock, for resuscitation during cardiac arrest, and for carbon monoxide poisoning. Oxygen should be titrated to target an S pO 2 of 94 -98%, except with carbon monoxide poisoning (100% oxygen), ARDS (88 -95%), those at risk for hypercapnia (S pO 2 88 -92%), and premature infants (S pO 2 88 -94%). Evidence for use with other conditions for which oxygen is administered relies on anecdotal experiences, case reports, or small, underpowered studies. Definitive conclusions for oxygen use in these conditions where efficacy and/or safety are uncertain will require large randomized controlled clinical trials.

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“…Dr. Kenmure and I discussed the subject of oxygen supplementation and hyperbaric oxygen in acute myocardial infarction patients, and he made the point that high-flow oxygen supplementation as well as hyperbaric oxygen could be potentially detrimental in animal models of acute myocardial infarction, as well as in humans. 2,3,4 He and his colleagues have published several articles on this subject.…”

Section: My View Of the Issuementioning

confidence: 99%