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Recent referrals to our intensive care unit have led us to question the indication for morphine in acute pulmonary oedema. Acute pulmonary oedema is a common, life-threatening emergency. Appropriate prompt therapy can provide rapid improvements in symptoms by reducing pre-load and after-load, or increasing myocardial contractility. Oxygen, loop diuretics, and nitrates are well-established therapeutic options. Most textbooks of acute medicine1,2 also recommend that intravenous morphine (or diamorphine in the UK) is given to “cause systemic vasodilatation and sedate the patient”,2 despite the absence of evidence supporting its efficacy. Treatment with morphine may be associated with respiratory depression in an already hypoxic patient, potentially exacerbating cardiac insufficiency. Respiratory failure secondary to opiates in pulmonary oedema has previously been reported elsewhere.3
In vivo experiments have confirmed that intravenous morphine results in significant peripheral vasodilatation and reduction in systemic vascular resistance.4 Further studies reveal that these effects are mediated via histamine receptors rather than opiate receptors however,5 and directly correlate with the rise in plasma histamine concentrations associated with morphine administration.6
In view of the potential iatrogenic morbidity and non-specific pharmacological action of morphine in acute pulmonary oedema, we question the recommendation of its use. There are more potent vasodilators available without the side-effects of respiratory depression. We suggest that it is only used in acute pulmonary oedema, with caution, when analgesia is required in association with acute myocardial infarction. The use of titrated intravenous diuretics and nitrates to promote vasodilatation is preferable.
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