Approach to Acute Heart Failure in the Emergency Department
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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2019, International Journal of CardiologyCitation 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].
Acute Heart Failure Risk Stratification in the Emergency Department: Are We There Yet?
2019, Revista Espanola de Cardiologia
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.