Author’s Disclosure Statement: Dr. Peacock reports that he has received research grants from Abbott Laboratories, Janssen Pharmaceuticals, Inc, Hoffman LaRoche, and ZS Pharma Inc; serves as a consultant for Bayer Corporation, Beckman Coulter Life Sciences, Boehringer Ingelheim, Instrumentation Laboratory, Janssen Pharmaceuticals, Relypsa Inc, Hoffman LaRoche, and ZS Pharma Inc; has provided expert testimony for Johnson and Johnson; and has ownership interests in Comprehensive Research Associates LLC, Emergencies in Medicine LLC, and Ischemia DX, LLC.
A focused history and physical examination that is part of all ED evaluations should be expedited whenever there is evidence of hemodynamic instability or respiratory compromise. An early working diagnosis is essential to avoid a delay in appropriate treatment, which is associated with increased mortality.
When HF is likely, the potential etiology and precipitants for decompensation must be considered. This list is long, but medication noncompliance and dietary indiscretion are the most common causes.
Symptoms and Prior History of HF
The classic symptoms for AHF include dyspnea at rest or exertion, and orthopnea, both of which unfortunately have poor sensitivity and specificity for AHF. As an isolated symptom, dyspnea is of marginal diagnostic utility (sensitivity and specificity for an HF diagnosis is 56% and 53%, respectively), and orthopnea is only slightly better (sensitivity and specificity 77% and 50%, respectively). A prior HF diagnosis makes repeat presentations much more likely (sensitivity and specificity 60% and 90%, respectively).17
Physical Examination
Simple observation and a directed examination can rapidly point to the diagnosis (Figure 2).
Figure 2.
The examination findings of AHF include jugular venous distention (JVD), dependent edema, rales, and a third heart sound (S3) on cardiac auscultation. While edema and rales have limited diagnostic sensitivity (50%-78%), and specificity (60%-78%), the presence of JVD makes HF much more likely (sensitivity and specificity of 39% and 92%, respectively). Although the absence of an S3 sound cannot exclude its presence (sensitivity 13%), detection of an S3 (ventricular gallop) is one of the best clinical indicators for HF (specificity 99%).17 Ultimately, most AHF signs/symptoms have low sensitivity to exclude its diagnosis, but greater specificity in identifying AHF.
Electrocardiography
Because CAD is one of the most common underlying AHF etiologies, an electrocardiogram (ECG) should always be obtained early for a patient presenting with potential AHF. Although the ECG does not usually contribute to ED management, the identification of new ST-segment changes or a malignant arrhythmia will guide critical management decisions.
Imaging Studies
Chest X-ray Imaging.A chest X-ray (CXR) study must be considered early when a patient presents with signs and symptoms suggestive of AHF. Although the classic findings of HF (eg, Kerley B lines [short horizontal lines perpendicular to the pleural surface],18 interstitial congestion, pulmonary effusion) can lag behind the clinical presentation, and also be nondiagnostic in the setting of mild HF, the CXR is an effective aid in identifying other causes of dyspnea such as pneumonia. Ultimately, the utility of the CXR for diagnosis is similar to that of the history and physical examination in that it will be diagnostic when positive but cannot exclude AHF if normal.
Ultrasound.Because it is fast, inexpensive, noninvasive, and readily available in the ED, ultrasound is frequently used to evaluate potential HF patients. Several studies have demonstrated that the presence of B lines in two or more regions is specific for AHF (specificity 75%-100%), although the sensitivity may be limited (40%-91%).19-21 The presence of inferior vena cava (IVC) dilation is also associated with adverse outcomes.22 In 80 patients hospitalized with acute decompensated HF (ADHF), a dilated IVC (≥1.9 cm) at admission was associated with higher 90-day mortality (25.4% vs 3.4%, P = 0.009).23 These findings may be considered in groups: In an evaluation of the combination of LV EF, IVC collapsibility, and B lines for an HF diagnosis, the combination of all three had a poor sensitivity (36%) but an excellent specificity (100%), and any two of the three had a specificity of at least 93%.24
Laboratory Evaluation
Myocardial Strain: BNP/NTproBNP. Natriuretic peptides (NPs) are not AHF-specific, but rather they are synthesized and released by the myocardium in the setting of myocardial pressure or volume stress. They are manufactured as preproBNP,then enzymatically cleaved into the active BNP and the inactive fragment N-terminal proBNP (NTproBNP). The predominant hormonal effects of BNP are vasodilation and natriuresis, as well as antagonism of the hormones associated with sodium retention (aldosterone) and vasoconstriction (endothelin, norepinephrine).
As AHF results in myocardial stress, NP elevation provides diagnostic and prognostic information. Clinical judgment supported by a BNP greater than 100 pg/mL is a better predictor of AHF than clinical judgment alone (accuracy 81% vs 74%, respectively).25 While low levels (BNP <100 pg/mL or NTproBNP <300 pg/mL) reliably exclude the diagnosis of HF (sensitivities >95%), higher levels (BNP >500 pg/mL, NTproBNP >900 pg/mL) are useful as “rule-in” markers, with specificity greater than 95%. The NTproBNP also requires adjustment for patients older than age 75 years, with a higher level (>1,800 pg/mL) to rule-in HF. The NP grey zone (BNP 100-500 pg/mL, NTproBNP 300-900 pg/mL)requires additional testing for accurate diagnoses (Figure 3).25-29
Figure 3.
There are several confounders to the interpretation of NP results: NPs are negatively confounded by the presence of obesity, resulting in a lowering of the value as compared to the clinical presentation.Thus, the measured BNP level should be doubled if the patient’s body mass index exceeds 35 kg/m2.30 Secondly, because NP metabolism is partially renal dependent, elevated levels may not reflect AHF in the presence of renal failure. If the estimated glomerular filtration rate is less than 60 mL/min, measured BNP levels should be halved.31
AHF vs Myocardial Ischemia: Troponin Levels. Large registry data using contemporary troponin assays clearly identify the association between elevated troponin levels (>99th percentile in a healthy population) and increased short-term risk. With the US Food and Drug Association (FDA) approval of a high-sensitivity troponin (hs-cTnT) assay, a greater frequency of elevated cardiac troponin T (cTnT) and cardiac troponin I (cTnl) will be identified in AHF patients in the ED.
In one retrospective study of 4,705 AHF patients in the ED, hs-cTnT were elevated in 48.4% of cases (25.3% in cTnI, 37.9% in cTnT, and 82.2% in hs-cTnT). Although 1-year mortality was higher in those with elevated troponin (adjusted heart rate [HR] 1.61; CI 95% 1.38-1.88), elevated troponin was not associated with 30-day revisits to the ED (1.01; 0.87-1.19) and high sensitive elevations less than double the reference value had no impact on outcomes.32 Thus, in terms of management of AHF in the ED, slightly elevated stable serial troponins are more consistent with underlying HF, and should be managed as such. This is not true of rising/falling troponin levels, which should still engender concern for underlying myocardial ischemia and a different management pathway.
Renal function.Comprised renal function is an important predictor of AHF outcome. Large registry data from hospitalized HF patients demonstrate that a presenting blood urea nitrogen level greater than 43 mg/dL is one of the most important predictors of increased acute mortality,33 and levels below 30 mg/dL identify a cohort likely to be successfully managed in an observation environment.34 Creatinine is a helpful lagging indicator of mortality, with higher levels (>2.75 mg/dL) associated with increased short-term adverse outcomes and decreased therapeutic responsiveness (Figure 4).
Figure 4.
For patients presenting with ADHF, a newer test recently approved by the FDA uses the product of the urine markers tissue inhibitor of metalloproteinase-2 and insulin-like growth factor-binding protein 7, to generate a score predictive of acute kidney injury.35 While promising, no studies of ED outcomes are currently available.
