You are here

Responses

Article menu
Download PDFPDF
Review
Inpatient management of acute decompensated heart failure
Compose a Response to This Article
Compose Response

More information about text formats

Plain text

  • No HTML tags allowed.
  • Web page addresses and e-mail addresses turn into links automatically.
  • Lines and paragraphs break automatically.
Author Information
First or given name, e.g. 'Peter'.
Your last, or family, name, e.g. 'MacMoody'.
Your email address, e.g. higgs-boson@gmail.com
Your role and/or occupation, e.g. 'Orthopedic Surgeon'.
Your organization or institution (if applicable), e.g. 'Royal Free Hospital'.
Statement of Competing Interests

PLEASE NOTE:

  • A rapid response is a moderated but not peer reviewed online response to a published article in a BMJ journal; it will not receive a DOI and will not be indexed unless it is also republished as a Letter, Correspondence or as other content. Find out more about rapid responses.
  • We intend to post all responses which are approved by the Editor, within 14 days (BMJ Journals) or 24 hours (The BMJ), however timeframes cannot be guaranteed. Responses must comply with our requirements and should contribute substantially to the topic, but it is at our absolute discretion whether we publish a response, and we reserve the right to edit or remove responses before and after publication and also republish some or all in other BMJ publications, including third party local editions in other countries and languages
  • Our requirements are stated in our rapid response terms and conditions and must be read. These include ensuring that: i) you do not include any illustrative content including tables and graphs, ii) you do not include any information that includes specifics about any patients,iii) you do not include any original data, unless it has already been published in a peer reviewed journal and you have included a reference, iv) your response is lawful, not defamatory, original and accurate, v) you declare any competing interests, vi) you understand that your name and other personal details set out in our rapid response terms and conditions will be published with any responses we publish and vii) you understand that once a response is published, we may continue to publish your response and/or edit or remove it in the future.
  • By submitting this rapid response you are agreeing to our terms and conditions for rapid responses and understand that your personal data will be processed in accordance with those terms and our privacy notice.
CAPTCHA
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.

Vertical Tabs

Other responses

Jump to comment:

  • Published on: 8 November 2019
    Other treatment opportunities in acute decompensated heart failure

    Among the recommendations for inpatient management of acute decompensated heart failure(1), special mention should be made of those patients who present with the association of congestive heart failure (CHF) of left ventricular origin, chronic obstructive pulmonary disease (COPD) and hypoxia (with or without hypercapnia). This diagnostic triad is easily overlooked because the obstructive ventilatory defect of COPD is simulated by the obstructive ventilatory defect of left ventricular failure (LVF) even in the absence of COPD(2). The obstructive ventilatory defect is more likely to be attributable to COPD when hypoxia is associated with hypercapnia, as was the case in a 70 year old woman who presented, not only with radiographically validated LVF, but also with the association of hypoxia and hypercapnia(3).
    The management of patients with combined left ventricular failure and suspected hypoxic COPD includes standard antifailure treatment (such as diuretics and angiotensin converting enzyme inhibitors) and adjunctive supplemental oxygen, the latter for a minimum of 15 hours a day(3)(4). Crucially, such patients should undergo formal assessment for long term oxygen therapy(LTOT) after a period of stability of at least 8 weeks from their lat exacerbation. This evaluation involves two arterial blood gas measurements at least 3 weeks apart(4). This might also be an opportunity to repeat the lung function tests so as to ascertain if the obstructive ventilatory defect has pe...

    Show More
    Conflict of Interest:
    None declared.
  • Published on: 4 November 2019
    acute heart failure in diabetic ketoacidosis

    The emergency management of acute decompensated heart failure(1) would be incomplete without mention of the unique problems posed by the simultaneous occurrence of acute heart failure and diabetic ketoacidosis (DKA). Myocardial infarction, a recognised precipitating factor for DKA(2)(3), is a potential cause of the association of DKA and acute heart failure. This association poses the challenge of simultaneous management of fluid overload, ketoacidosis, and potassium status.
    In the acutely breathless patient the priority is to relieve symptoms of fluid overload(4)(5), fundamentally by avoiding the imposition of an additional fluid burden, while simultaneously relieving the patient's symptoms. This approach flies in the face of the equivocal guideline advice that "fluid replacement may need to be modified"(6). Treatment choices for symptomatic relief include bolus intravenous frusemide(4)(without supplementary intravenous fluids) or simply initiating intravenous insulin infusion, again "without supplementary intravenous fluids"(5). The latter strategy works especially well in DKA-related patients in whom chronic renal failure has impaired the patient's ability to excrete the excessive amount of fluid that has accumulated in the extracellular fluid compartment as a result of osmotic shifts generated by DKA-related hyperglycaemia. Restoring the optimum osmotic balance by lowering the blood glucose concentration generates relief of the sympt...

    Show More
    Conflict of Interest:
    None declared.
  • Published on: 29 October 2019
    raising the index of suspicion for constrictive pericarditis and index of suspicion for iron deficiency

    The point is well made that monitoring of the response to congestive heart failure(CHF) treatment should include documentation of changes in jugular venous pressure (JVP) and changes in body weight. That should especially be the case in patients with markedly elevated JVP, especially in the presence of ascites. There should be a heightened index of suspicion for constrictive pericarditis when a patient with those characteristics experiences a significant fall in body weight without a concurrent fall in JVP(2).
    Coexistence of CHF and iron deficiency(ID) is the other issue that requires a heightened index of suspicion when certain parameters are operative. Notwithstanding the fact that the work-up of suspected ID recommended by Guyatt et al highlighted mean corpuscular volume(MCV) to the total exclusion of mean corpuscular haemoglobin concentration(MCHC)(3), there is now overwhelming evidence that MCHC outperforms MCV in predicting ID, both in non anaemic and in anaemic subjects(4)(5)(6). Among non anaemic female athletes aged 15-20, when a comparison was made between 33 ID subjects(characterised by serum ferritin < 30 mcg/L) vs 87 non-ID subjects, mean MCHC amounted to 327 g/L vs 340 g/L(p < 0.001), whereas MCV( 85.5 fl vs 87.2 fl) did not significantly differentiate between the two subgroups(4). In a smaller study comprising 41 CHF subjects(including 17 with ID validated by bone marrow studies) the Receiver Operating Curve for ID generated an area under the cur...

    Show More
    Conflict of Interest:
    None declared.