The Editorial Executive Committee welcomes letters, which should be less than 250 words. Before a decision to publish is made, letters which refer to a published article may be sent to the author for a response. Any letter may be sent to an expert for comment. When letters are published, they are usually accompanied in the same issue by their responses or comments. The Committee screens out discourteous, inaccurate or libellous statements. The letters are sub-edited before publication. Authors are required to declare any conflicts of interest. The Committee's decision on publication is final.

Letter to the Editor

Editor, – The recent article by John Holmes about the doctor’s bag (Aust Prescr 2012;35:7-9) recommended that frusemide be relegated to a second- or third-line treatment in patients with acute heart failure. This recommendation is concerning and is counter to international evidence-based guidelines. Both the European Society of Cardiology1 and the American Heart Association/American College of Cardiology guidelines 2 recommend the use of intravenous loop diuretics in acute heart failure. In line with this, the Heart Failure Society of America also recommends intravenous loop diuretics for acute pulmonary oedema.3

On their introduction, loop diuretics revolutionised the management of congestive cardiac failure. Their role remains important today. The recommendation against the use of frusemide as first-line treatment in acute heart failure in appropriately selected patients is potentially dangerous. Non-invasive ventilation strategies and intravenous nitrate therapy do have a role in acute heart failure. Evidence for their efficacy is largely based on studies where they were used with intravenous loop diuretics. The role of these therapies without the concomitant use of loop diuretics has not been established.4–6

In summary, intravenous loop diuretics remain a first-line component in the management of acute heart failure and suggestions to the contrary are not based on sound evidence nor supported by internationally recognised guidelines on the subject.

Anthony C Camuglia
Advanced trainee in cardiology

Darren L Walters
Director of cardiology

The Prince Charles Hospital

Author's comments

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.


  1. Dickstein K, Cohen-Solal A, Filippatos G, McMurray JJ, Ponikowski P, Poole-Wilson PA, et al; ESC Committee for Practice Guidelines. ESC guidelines for the diagnosis and treatment of acute and chronic heart failure 2008. Eur J Heart Fail 2008;10:933-89.
  2. Jessup M, Abraham WT, Casey DE, Feldman AM, Francis GS, Ganiats TG, et al. 2009 focused update: ACC/AHA guidelines for the diagnosis and management of heart failure in adults. J Am Coll Cardiol 2009;53:1343-82.
  3. Lindenfeld J, Albert NM, Boehmer JP, Collins SP, Ezekowitz JA, Givertz MM, et al; Heart Failure Society of America. HFSA 2010 Comprehensive Heart Failure Practice Guideline. J Card Fail 2010;16:e1-194.
  4. Crane SD, Elliott MW, Gilligan P, Richards K, Gray AJ. Randomised controlled comparison of continuous positive airways pressure, bilevel non-invasive ventilation, and standard treatment in emergency department patients with acute cardiogenic pulmonary oedema. Emerg Med J 2004;21:155-61.
  5. Gray A, Goodacre S, Newby DE, Masson M, Sampson F, Nicholl J; 3CPO Trialists. Noninvasive ventilation in acute cardiogenic pulmonary edema. N Engl J Med 2008;359:142-51.
  6. Kelly CA, Newby DE, McDonagh TA, Mackay TW, Barr J, Boon NA, et al. Randomised controlled trial of continuous positive airway pressure and standard oxygen therapy in acute pulmonary oedema. Eur Heart J 2002;23:1379-86.
  7. Cotter G, Metzkor E, Kaluski E, Faigenberg Z, Miller R, Simovitz A, et al. Randomised trial of high-dose isosorbide dinitrate plus low-dose furosemide versus high-dose furosemide plus low-dose isosorbide dinitrate in severe pulmonary oedema. Lancet 1998;351:389-93.
  8. Nelson GI, Silke B, Ahuja RC, Hussain M, Taylor S. Haemodynamic advantages of isosorbide dinitrate over frusemide in acute heart-failure following myocardial infarction. Lancet 1983;1:730-3.
  9. Crane SD. Epidemiology, treatment and outcomes of acidotic, acute, cardiogenic pulmonary oedema presenting to an emergency department. Eur J Emerg Med 2002;9:320-4.
  10. Peter JV, Moran JL, Phillips-Hughes J, Graham P, Bersten AD. Effect of non-invasive positive pressure ventilation (NIPPV) on mortality in patients with acute cardiogenic pulmonary oedema. Lancet 2006;367:1155-63.
  11. Masip J, Roque M, Sanchez B, Fernandez R, Subirana M, Exposito J. Non-invasive ventilation in acute cardiogenic pulmonary edema. JAMA 2005;294:3124-30.
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