John Holmes, author of the article, comments:
The mode of action of frusemide in the treatment of acute left ventricular failure is probably preload reduction. Clinical improvement is seen well in advance of its diuretic effect.7 In this respect, frusemide is acting very similarly to nitrates. However, as mentioned in the article, there are potential adverse effects of frusemide in vascularly depleted patients and elevation of plasma renin and noradrenaline levels can exacerbate afterload, increase myocardial oxygen demand and thereby aggravate coronary ischaemia.8 These potential effects make nitrates preferable as a first-line treatment, especially as, unlike frusemide, they have a more rapid onset of action and can be administered by intravenous infusion titrated to effect.7,8
My article discussed the use of emergency drugs in a general practice setting. I am therefore bemused that Drs Camuglia and Walters should criticise the established management of acute pulmonary oedema in Australian emergency departments. There is a world of difference between general practice and the management capabilities and choices available in a critical care environment. In the latter, the primary use of nitrates and non-invasive ventilation strategies in acute pulmonary oedema has been well established worldwide for over a decade.8,9 Non-invasive ventilation in particular has been shown to reduce the need for intubation in severe acute pulmonary oedema.10,11 Frusemide still has a role in selected cases, predominantly left-sided failure and the absence of intravascular depletion. However, the level of evidence is variously reported as II to III.
Irrespective of this, my article does not advocate removal of frusemide from the doctor’s bag. However, while boluses of frusemide may be useful in a life-threatening situation outside of hospital, such treatment may be neither optimal nor appropriate in an environment where other and better therapeutic interventions are available.