Heart failure (HF) is a common diagnosis, facing approximately 4,900,000 people.¹ Over the past 3 decades we have seen a significant rise in the number of hospital discharges for HF,¹ and because the majority of admitted patients enter through the emergency department (ED),² proper initial management is important. Several studies on the use of the B-type natriuretic peptide (BNP) assay have indicated that earlier treatment in the ED can significantly impact hospital length of stay and cost.³

Patients may present to the ED with minimal symptoms, such as mild dyspnea or weight gain. Conversely, they may present to the ED with overt pulmonary edema. In addition to their fluid status, evaluation for adequate perfusion or evidence of shock should be considered. Recognition that HF patients may fall into different hemodynamic categories allows the clinician to tailor treatment based on the initial assessment. Using components of the history and physical examination, the clinician can develop a treatment plan individualized to that patient. Diuretics, vasodilators, angiotensin-converting enzyme inhibitors (ACEI), noninvasive ventilation, and natriuretic peptides can be used for hemodynamic and symptomatic needs.

Because of improvements in the treatment of HF that have resulted in improved survival, the emergency physician will see increased instances of acute exacerbations of HF. This chapter provides the reader with an understanding of the principles of initial acute HF management and examine specific therapeutic agents.

The first step when a patient presents with presumed HF is to stabilize the clinical condition. This is followed by an evaluation including laboratory tests, radiographs, consideration of advance directives, and a search for reversible causes including ischemia and arrhythmias. Finally, treatment is instituted based on an assessment of the hemodynamic status.

Patients presenting with presumed HF should be initially assessed and stabilized. Those with impending respiratory failure should be treated with supplemental oxygen and the physician should consider the use of noninvasive ventilation. Patients who are unable to control their airway, cannot tolerate noninvasive ventilation, or worsen despite these measures should be considered for endotracheal intubation.

When HF is considered the most likely etiology of the patient’s symptoms, the initial workup should include establishment of intravenous (IV) access, a focused history and physical examination, assessment of the degree of fluid overload and perfusion, evaluation of oxygenation, assessment of the cardiac rhythm, evaluation for cardiac ischemia with a 12-lead electrocardiogram, and a chest radiography. Blood work should be based on clinical suspicion and may include a complete blood cell count, electrolytes, BNP or N-terminal pro-BNP levels, and cardiac markers.

Advance directives should be discussed with the patient or family, especially in those with severe exacerbations of chronic disease. This information will help direct the management plan.

The clinician should look for precipitants of the HF (Table 4-1). The identifiable reversible causes should be treated in conjunction with the treatment of the HF. Unfortunately, in one study the authors could not identify a precipitant in 40% of the HF presentations.⁴ Patient-related factors such as noncompliance with medication and diet should be addressed. In several studies, poor compliance was the precipitant of the acute exacerbation, ranging from 21% to 41.9%.^4,5 Patient and family education cannot be underestimated. Several studies have investigated the impact of education and find that it significantly decreases hospital readmissions.⁶, ⁷ and ⁸

Cardiac ischemia is a leading cause of HF and an important cause of acute exacerbation.⁹ Although not every exacerbation of chronic HF will require a workup of an ischemic etiology, the clinician should be aware of the potential and consider it accordingly. Cardiac arrhythmias are associated with a worse prognosis in HF.¹⁰ In the acute care setting, cardiac arrhythmias such as atrial fibrillation, ventricular arrhythmias, and conduction abnormalities can be precipitants of exacerbations. Treatment should be focused on the hemodynamic effects and not correction of every arrhythmia. Patients with chronic HF are at significant risk for ventricular arrhythmias.

The classic picture of an HF patient with acute pulmonary edema frothing at the mouth and appearing cyanotic is only one possible presentation. Some individuals present with respiratory distress, but others may have
only mild symptomatic dyspnea and others have only fatigue. Some present hypotensive and others with significant hypertension.

Categorizing HF patients using a hemodynamic classification system (Figure 4-1) is a useful approach. Based on the initial history and physical examination, patients can be placed into a hemodynamic category and then appropriate therapy can be selected. Fluid overload can be assessed by the presence or absence of dyspnea, orthopnea, pulmonary rales, elevated jugular venous pressure, the presence of a third heart sound S₃, and hepatomegaly. Perfusion can be estimated by evaluating for the presence or absence of fatigue, nausea, symptomatic hypotension, and cool extremities (Table 4-2).

The physician must recognize that these signs and symptoms can be inaccurate and have a low inter-rater reliability.¹¹ Assessment using these historical and physical diagnostic clues needs to be considered in aggregate and supplemented with more objective diagnostic testing (chest radiograph, BNP or pro-BNP level, bioimpedance measurements, digital S₃detection) to improve accuracy. At this point, this clinical assessment strategy provides the best estimate of the patient’s hemodynamic status.

Most patients presenting with HF are fluid overloaded but have adequate perfusion, that is, “wet and warm.” These patients require diuretics and vasodilation. The fluid-overloaded patient could also present with diminished perfusion, called “wet and cold.” Those with elevated systemic vascular resistance (SVR) will require vasodilation. Those with symptomatic hypotension and diminished SVR may require inotropic support. The least common patient is the patient that has been overdiuresed and has evidence of hypoperfusion, the “dry and cold.” If manifesting symptomatic hypotension, this patient may require a fluid bolus and the addition of inotropic support. As a guiding principle, chronic HF patients are best served by lower blood pressures, with a systolic blood pressure as low as 80 to 90 mm Hg. As long as they are asymptomatic, continue to mentate, and have appropriate urine output, no further blood pressure treatment is necessary.

This hemodynamic classification system provides the physician with a framework for the initial assessment and treatment of the HF patient. However, this framework is based on imprecise measures; therefore, the initial treatment must be guided by good clinical judgment and must be adjusted depending on the initial response to the therapeutic interventions. Until better and more accurate diagnostic modalities are available, the physician should use the framework presented in this section to develop the therapeutic plan.