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Heart Failure in the Emergency Department

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References

Volume Assessment

Objective volume assessment is useful for diagnosis and prognosis in AHF. Bioimpedance vector analysis (BIVA) is a rapid, inexpensive, noninvasive technique that measures total body water by placing a pair of electrodes on the wrist and ipsilateral ankle. The BIVA measurements have strong correlations with the gold standard volume-assessment technique of deuterium dilution (r > 0.99).36 In HF, BIVA can assess volume depletion37 and overload,38 and identifies differences in hydration status between 90-day survivors and non-survivors (P < 0.01).39

Used in combination with BNP, one prospective study of 292 dyspneic patients found that, while BIVA was a strong predictor of AHF (c-statistic 0.93, P = 0.016), the most accurate volume status determination was the combination of both (c-statistic, 0.99; P = 0.005), for which the combined accuracy exceeded either alone.40 Finally, in 166 hospitalized HF patients discharged by BNP and BIVA parameters, vs 149 discharged based on clinical impressions, those assessed with BNP and BIVA had lower 6-month readmissions (23% vs 35%, P = 0.02) and overall cost of care.41

Combination Technologies

Obviously, EPs may consider multiple technologies to arrive at an accurate diagnosis. One prospective evaluation enrolled 236 patients to determine the diagnostic accuracy for AHF in the ED and reported lung ultrasound, CXR, and NTproBNP had a sensitivity of 57.7% and 88.0%, 74.5% and 86.3%, and a specificity of 97.6% and 28.0%. The best overall combination was the CXR with lung ultrasound (sensitivity 84.7%, specificity 77.7%).42

Another prospective study evaluated IVC diameter, bioelectrical impedance analysis (BIA), and NTproBNP in 96 elderly patients. ADHF patients had higher IVC diameters and lower collapsibility index, lower resistance and reactance, and higher NTproBNP levels. While all had high and statistically similar C-statistics (range 0.8 to 0.9) for an ADHF diagnosis, they concluded that IVC ultrasonography and BIA were as useful as NT-proBNP for diagnosing ADHF. 24

Diagnostic Scoring Systems

A scoring system has been proposed to improve diagnosis in the ED. Unfortunately, the value over clinical impression has not been clearly proven, though one randomized, controlled trial did not show statistically significant improvement in diagnostic accuracy when compared to standard care (77% vs 74%, P = 0.77).43

Differential Diagnosis

The differential diagnosis for acute dyspnea is long and potentially arcane. Efforts should focus on excluding non-HF causes of dyspnea, while considering the high risk of alternative etiologies for signs and symptoms. These include asthma, COPD, pneumonia, and pulmonary embolism, which may represent the primary pathologies in a patient with a history of HF, or be the cause of a HF exacerbation. Additional causes of noncardiogenic pulmonary edema should also be considered (eg, acute respiratory distress syndrome, toxins, etc). Acute coronary syndrome and dyspnea may be angina equivalents—one important consideration.

Treatment and Management

Airway Management

Treatment of CH in the ED must always start with an immediate airway evaluation, with the possible need for endotracheal intubation preceding all diagnostic or other management considerations. Intubation is a decision most successfully based on physician clinical assessment, including oxygen (O2) selection rather than waiting for the results of objective measures such as arterial blood gas analysis.

Oxygen

Supplemental O2 should be administered to maintain an O2 saturation above 95%, but obviously is unnecessary in the absence of hypoxia.

Noninvasive Ventilation

Two kinds of noninvasive ventilation (NIV) are available, continuous positive airway pressure and bilevel positive airway pressure ventilation. The physiological differences between these types of NIV have little bearing on ED treatment.

Noninvasive ventilation has not been clearly shown to provide long-term mortality benefit. Large registry data44 report that outcomes are no worse than the alternative of endotracheal intubation, while multiple systematic reviews,45,46meta-analysis,47and Cochrane reviews48,49have established NIV as an acute pulmonary edema intervention that provides reductions in hospital mortality (numbers needed to treat [NNT] 13) and intubation (NNT 8), the prospective randomized C3PO (Congenital Cardiac Catheterization Project on Outcomes) trial50 failed to demonstrate any mortality reduction.

In patients with severe respiratory distress, NIV is a reasonable strategy during the aggressive administration of medical therapy in an attempt to avoid endotracheal intubation. However, NIV is not a stand-alone therapy and though its use may obviate the need for immediate intubation, its implementation should not be considered definitive management.

Correction of Abnormal Vital Signs: Abnormal SBP

Vital signs are an important determinant of therapy, driving treatment strategies. Interventions for HF are based on the patient’s SBP, in particular correction of symptomatic hypotension and hypertensive HF (Table 3).51

Table 3.

Symptomatic Hypotension. The presence of symptomatic hypotension is an extremely poor prognostic finding in AHF. Inotrope therapy may be considered, but it does not reduce mortality except as a bridge to mechanical interventions (LV assist device or transplant).52-54 Temporary inotropic support is recommended for cardiogenic shock to maintain systemic perfusion and prevent end organ damage.3 The inotropic support includes administration of dopamine, dobutamine, or milrinone, though none have been proven to be superior over the other. The lowest possible dose of the selected inotrope should be used to limit arrhythmogenic effects. Inotropic agents should not be used in the absence of severe systolic dysfunction, or low BP, or impaired perfusion, or evidence of significantly decreased cardiac output.

Hypertensive Heart Failure. Defined as the rapid onset of pulmonary congestion with an SBP greater than 140 mm Hg, and commonly greater than 160 mm Hg, these patients may have profound dyspnea, requiring endotracheal intubation. However, in this situation, aggressive vasodilation is typically rapidly effective. Overall, patients presenting with an elevated SBP have lower rates of in-hospital mortality, 30-day myocardial infarction (MI), death, or rehospitalization, and a greater likelihood of discharge within 24 hours—as long as the elevated SBP is aggressively and rapidly treated.

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