Elsevier

Progress in Cardiovascular Diseases

Volume 60, Issue 2, September–October 2017, Pages 178-186
Progress in Cardiovascular Diseases

Approach to Acute Heart Failure in the Emergency Department

https://doi.org/10.1016/j.pcad.2017.08.008Get rights and content

Abstract

Acute heart failure (AHF) patients rarely present complaining of ‘acute heart failure.’ Rather, they initially present to the emergency department (ED) with a myriad of chief complaints, symptoms, and physical exam findings. Such heterogeneity prompts an initially broad differential diagnosis; securing the correct diagnosis can be challenging. Although AHF may be the ultimate diagnosis, the precipitant of decompensation must also be sought and addressed. For those AHF patients who present in respiratory or circulatory failure requiring immediate stabilization, treatment begins even while the diagnosis is uncertain.

The initial diagnostic workup consists of a thorough history and exam (with a particular focus on the cause of decompensation), an EKG, chest X-ray, laboratory testing, and point-of-care ultrasonography performed by a qualified clinician or technologist. We recommend initial treatment be guided by presenting phenotype. Hypertensive patients, particularly those in severe distress and markedly elevated blood pressure, should be treated aggressively with vasodilators, most commonly nitroglycerin. Normotensive patients generally require significant diuresis with intravenous loop diuretics. A small minority of patients present with hypotension or circulatory collapse. These patients are the most difficult to manage and require careful assessment of intra- and extra-vascular volume status. After stabilization, diagnosis, and management, most ED patients with AHF in the United States (US) are admitted. While this is understandable, it may be unnecessary. Ongoing research to improve diagnosis, initial treatment, risk stratification, and disposition may help ease the tremendous public health burden of AHF.

Section snippets

Stabilization

Occasionally, patients with possible AHF present in extremis or near respiratory failure. In these instances, the diagnostic work up and management occur in parallel. Importantly, the precipitating cause of the patient's dramatic presentation must be simultaneously identified and treated. Arrhythmias, infection, and acute coronary syndromes are just a few potential precipitants. The classical teaching of ensuring “Airway, Breathing, and Circulation” first is worth reiterating.

Obtunded patients

Initial diagnosis and assessment

Fortunately, most AHF patients do not present in extremis. Establishing the diagnosis is the sine qua non of medicine, but is not always easy. It is worth noting the myriad of different patient complaints: Fatigue, dizziness, shortness of breath, chest pain, weakness, exercise intolerance, swelling, and weight gain are all symptoms prompting consideration of AHF as the cause.

The clinical presentation of AHF varies widely, ranging from mildly worsening heart failure, de novo or new onset HF, to

Initial management

Once the diagnosis is made, presenting phenotype and cause of exacerbation guides initial treatment. As mentioned earlier, first assuring respiratory and hemodynamic stability is paramount (see Table 1 for goals of ED management). While addressing the patient's respiratory status, the precipitant of AHF should be sought and treated. For example, rapid atrial fibrillation (AF), ACS, pulmonary embolism, underlying infection or dietary indiscretion can all trigger AHF.57 Often the precipitant is

Initial classification

As an initial guide, we recommend grouping patients with suspected AHF by systolic BP (SBP).58., 59. As evidenced by registries, SBP is often high (> 140 mm Hg) at the time of presentation.60 We recommend using cutpoints of > 140 mm Hg, 100–140 mm Hg, and < 100 mm Hg to guide initial selection of pharmacologic therapy.58., 59. While there is considerable overlap, simple categorization aids the busy clinician. As such, it is reasonable to assume the predominant pathophysiologic derangement in a patient

Initial therapy

At the present time, no AHF therapy receives a Level I, Class A recommendation from guidelines,1., 2. highlighting the lack of robust evidence from randomized studies. Therapies used today are largely the same as those employed 4 decades ago (Table 2). Rotating tourniquets and phlebotomy are no longer used; whether this represents a major advance is debatable. Importantly, lack of high quality evidence from robust, randomized controlled trials does not equate with ineffectiveness in achieving

The hypotensive AHF patient

Shock due solely to worsening HF rarely occurs relative to other types of AHF.15 Given its relatively uncommon presentation combined with the complexity of these patients' underlying pathophysiology, precipitant, cardiac structure, function, and resultant hemodynamic status, management can be challenging. Patients with advanced HF may present with alarmingly low SBP. This may, in fact, reflect their baseline SBP. Even when resuscitating shock, a common mistake is attempting to normalize SBP and

Inotropes and vasopressors

Table 3 shows commonly used inotropes and vasoactive agents. Although inotropes and vasopressors improve hemodynamics, to date, none are associated with better clinical outcomes. In fact, available inotropes have been associated with harm, though the evidence base is small and inconsistent.68., 69., 70., 71. In terms of vasopressors, there is a paucity of robust data to strongly recommend one vasopressor over another. Subgroup analysis from a large randomized trial found increased mortality in

The hypertensive patient

Approximately half of patients admitted with AHF present with hypertension (SBP  140 mm Hg).15., 60. In general, these patients tend to be older, have preserved EF,60 and present with a more acute onset of symptoms, often < 24 h. Pulmonary edema in such patients is more likely to be caused by vascular redistribution than by hypervolemia. As such, vasodilators are the mainstay of treatment.

Of the guideline-recommended vasodilator options [nitroglycerin (NTG), nitroprusside, or nesiritide], we

The normotensive patient (SBP 100–140 mm Hg)

AHF patients presenting with SBP ranging from 100 to 140 mm Hg rarely arrive to the ED in extremis.60 The prototypical patient reports an indolent course over days or even weeks, and may report significant weight gain. Decongestion with intravenous (IV) loop diuretics is the primary therapy. Bolus or continuous infusion diuretic administration makes no difference.80 A randomized trial comparing IV doses of the patient's standard oral dose to larger IV doses (2.5 times the standard oral dose)

Disposition and outcomes

Contrary to commonly held belief, most patients who visit the ED are sent home; only 9.3% of the annual 130 million ED visits in the US result in hospitalization. However, nearly all ED patients with AHF are hospitalized. From 2006 to 2011, the annual US hospitalization rate for AHF patients in the ED has consistently been around 85%.86 Given financial penalties tied to excess re-hospitalization, this admission rate warrants scrutiny.

Administrative data analyses suggest up to 50% of patients

Conclusion

The ED management of AHF centers around diagnosis, stabilization, identification of the precipitant of AHF, initial treatment, and risk-stratification. We recommend initial ED treatment be guided by presenting phenotype but treatment largely centers around diuretics and vasodilators. Although currently available therapies improve symptoms, none definitively improve outcomes. Identification of life saving therapies for the early treatment of AHF remains an unmet need, though whether a short-term

Statement of conflict of interest

Benton Hunter has no conflicts of interest.

Osama Abdel Hafez has no conflicts of interest.

Jennifer Martindale has no conflicts of interest.

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      Citation Excerpt :

      Acute heart failure (AHF) is one of the most common reasons for admission to the Emergency Department (ED) and dyspnea is one of its most frequent clinical presentation [1]. For patients with acute respiratory failure, recognition of AHF is sometimes challenging and requires a complete diagnostic workup including history, physical exam, EKG, chest X-ray, laboratory tests and point-of-care ultrasound [2]. The importance of lung and multi-organ ultrasound examination in the diagnosis of AHF has been established [3–5].

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    Statement of Conflict of Interest: see page 184.

    1

    Peter Pang is or has been in the last one year a Consultant for: BMS, Novartis, Trevena, scPharmaceuticals, Roche Diagnostics, Relypsa and Research Support: Roche, Novartis, AHA, NIH, PCORI, AHRQ.

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