Patients with heart failure (HF) present daily to busy EDs. An estimated 6.5 million Americans are living with this diagnosis, and the number is predicted to grow to 8 million by 2023.1 Most HF patients (82.1%) who present to EDs are hospitalized, while a selected minority are either managed in the ED and discharged (11.6%) or managed in observation units (OU) (6.3%).2 The prognosis after HF is initially diagnosed is poor, with a 5-year mortality of 50%,3 and after a single HF hospitalization, 29% will die within 1 year.4
One-third of the total Medicare budget is spent on HF, despite the fact that HF represents only 10.5% of the Medicare population.2 Up to 80% of HF costs are for hospitalizations, which cost an average of $11,840 per inpatient admission.5,6 The high costs are due to an average length of stay (LOS) of 5.2 days7 (Table 1).
Adding to hospital costs is the degree of “reactivism,” with approximately 20% of patients discharged from the ED returning within 2 weeks, of whom nearly 50% will be hospitalized.11 Following HF hospitalization and discharge, the 30-day readmission rate is 26.2%,2 increasing to 36% by 90 days.12 The Centers for Medicare & Medicaid Services (CMS) has incentivized hospitals and providers to reduce admissions, but penalize hospitals that do not. Overall, CMS will reduce payments by up to 3% to hospitals with excess readmissions for select conditions, including HF.13
Causes of Heart Failure
Heart failure represents a final common pathway, which in the United States is most often due to coronary artery disease (CAD). Many types of pathology ultimately result in left ventricular (LV) dysfunction, and much of its rising prevalence is a result of the success we now have in managing historically fatal cardiovascular (CV) conditions. These include hypertension, diabetes mellitus (DM), CAD, and valvular and other CV structural conditions.
Heart failure is caused by either a dilated ventricle with a reduced ejection fraction (HFrEF) and inability to eject volume, or a stiffened ventricle with a preserved EF (HFpEF) that is unable to receive increased venous return. Both conditions acutely decompensate pulmonary congestion. A preserved EF is defined as an EF at or greater than 50%, whereas a reduced EF is at or less than 40%, with the 41% to 49% range considered as borderline preserved EF.3
While there are important differences in the treatment of chronic and subacute HF, driven by the EF, the effect of EF on early decision-making and treatment in the ED is negligible: Although the probability of HFpEF increases with increasing initial ED systolic blood pressure (SBP), clinical presentation and treatment in the ED are initially identical—regardless of the EF.
Noninvasive continuous transcutaneous hemodynamic monitoring is available for ED use, and may provide further insight into the underlying pathophysiology. A study of 127 acute heart failure (AHF) ED patients identified three hemodynamic AHF phenotypes. These include normal cardiac index (CI) and systemic vascular resistance index (SVRI), low CI and SVRI, and low CI and elevated SVRI.14 While it is attractive to suggest therapeutic interventions based on these measurements, outcome data are lacking.
The most common ED presentation of patients suffering from AHF is dyspnea secondary to volume overload, or as the result of acute hypertension with relatively less volume overload. However, regardless of the cause of dyspnea, it is not only the most common resulting complaint, but one that requires immediate treatment. Ultimately, 59% of all HF admissions are attributed to volume overload and dyspnea (Figure 1).15
Heart failure can also present in a more protean manner, with cough, fatigue, and edema, as well as more subtle symptoms predominating and resulting in a complicated differential diagnosis (Table 2).16
Because HF is a disease that most significantly affects older patients who frequently have concomitant morbidities (eg, myocardial ischemia, chronic obstructive pulmonary disease [COPD] exacerbation, uncontrolled DM), other less clinically obvious disease presentations may actually be the cause of the AHF exacerbation.