6 responses to “Diuretic strategies in patients with acute decompensated heart failure”

  1. This goes against what is trending in Emergency Medicine

    From EMDocs: http://www.emdocs.net/furosemide-treatment-acute-pulmonary-edema/

    “There’s minimal or no role for the administration of loop diuretics early in the management of APE. The majority of patients aren’t volume overloaded.”

    And here: http://socmob.org/2013/04/evidence-based-management-of-acute-heart-failure-forget-lmnop-think-pond/

    These authors de-emphasize the importance of loop diuretic treatment over nitrates and NIPPV

  2. Creatinine level: to what level will you allow the creatinine to escalate on diuresis, before you reduce the dose?
    20 or 30 % from baseline, or a specific number?

    Not really the scope of your article, but not to be seen in isolation, should we not use an ACE inhibitor, and or a vasodilator ex Nitro in the acute setting, before embarking on flogging the horse, say 30 min before the diuretic?

    Take home message:
    Doubling of the home dose for a few days, monitoring the clinical and lab outcome.
    Also changing the po / home dose to the same mg but IVI on admission.

  3. As mentioned earlier, we are getting further away from using diuretics as the mainstay of therapy for acute heart failure. Nitrates and BIPAP appear to be much more effective and diuretics mainly serve to disrupt renal function. I think the fact that there were minimal differences between the low dose group and the high dose group in the DOSE trial supports this. Diuretics should be used with caution in these patients!

  4. My understanding is that IV furosemide works faster but not better than PO. I use for acute decompensated, but once 02 saturation and dyspnea improve I change to oral. (Hospitalist)

  5. It seems incredible that such a study has not been done previously. I can well recall arguments between residents in my training hospital more than 40 years ago about this matter, with strong feelings on both sides.


    Dear Dr. Mitchell,

    We thank you for reviewing our article and your comments. Regarding your discussion point regarding loop diuretics, we have reviewed the articles that you linked and certainly agree that the management of acute pulmonary edema may require non-invasive positive pressure ventilation and nitrates. This is usually dictated by the severity of the presentation – patients with severe respiratory distress may benefit from non-invasive positive pressure ventilation.

    However, in patients presenting with decompensated heart failure due to acute-on-chronic fluid overload, these patients will likely benefit from diuretic therapy. The 2013 ACCF/AHA Guidelines recommend prompt treatment with intravenous loop diuretics for patients admitted with HF and evidence of significant fluid overload. These guidelines are available here: http://circ.ahajournals.org/content/128/16/e240.long

    Dear Dr. Le Roux,

    We thank you for reviewing our article and your comments. Typically for diuresis, we will consider dose adjustment when there is evidence of an acute kidney injury or signs of hypovolemia suggestive of over-aggressive diuresis. The Acute Kidney Injury Network (AKIN) defines an acute kidney injury as a percentage increase in serum creatinine more than 50% from baseline, or an absolute increase of more than 26 µmol/L. However, patients with chronic volume overload and impaired renal function at baseline may also require a larger dose of intravenous diuretics to facilitate diuresis.

    Nitrates (ie. nitroglycerin) can be considered as an adjuvant to diuretic therapy for symptomatic relief of dyspnea in patients admitted with acute decompensated heart failure. This is discussed in detail in the 2013 ACCF/AHA Guidelines, available here: http://circ.ahajournals.org/content/128/16/e240.long.

    Regarding ACE inhibitors, we typically initiate these agents once the decompensated heart failure has been managed. The use of ACE inhibitors combined with diuretics can increase the likelihood for precipitating an acute kidney injury. Also, patients presenting with decompensated heart failure often already have an element of acute kidney injury as well (ie. cardiorenal syndrome). Certainly, ACE inhibitors are critical in the long-term management of patients with heart failure with reduced ejection fraction.

    Dear Dr. Turner,

    We thank you for reviewing our article and your comments. Please see above for our response to a similar comment. Non-invasive positive pressure ventilation and diuretics all have role in decompensated heart failure, depending on the severity of presentation. The 2013 ACCF/AHA Guidelines are available here: http://circ.ahajournals.org/content/128/16/e240.long

    Dear Dr. Moher,

    We thank you for reviewing our article and your comments. Certainly, intravenous furosemide may be necessary in patients with acute decompensated heart failure as their profound tissue edema can impair gastrointestinal absorption of oral furosemide. We agree with your management – once these patients are stabilized, they should be transitioned to oral furosemide.

    Dear Dr. Toews,

    We thank you for reviewing our article and your comments. This is certainly a very interesting study, just published in the NEJM a few years ago. How the times have changed!

    Thank you for your comments,
    Christopher Cheung and Dr. Mustafa Toma

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