Acute heart failure covers a wide spectrum of illness, ranging from a gradual increase in leg swelling, shortness of breath, or decreased exercise tolerance to the abrupt onset of pulmonary edema. While alternative terms such as decompensated heart failure, acute heart failure syndrome, or hospitalized with heart failure have been used nearly interchangeably over the last decade, we refer to patients with either an acute exacerbation of chronic heart failure or a new-onset heart failure as having acute heart failure. The term congestive heart failure is outdated and describes patients with signs and symptoms of fluid accumulation.

Most ED visits for acute heart failure result in hospital admission.¹ With the aging population, increased survival from acute myocardial infarction, and evidence-based outpatient treatment options, the prevalence of heart failure is expected to increase over the next decade.^2,3,4 ED physicians drive most disposition decisions.^5,6 There have been tremendous advances in outpatient management of heart failure patients. While long-term heart failure management has improved through the use of β-blockers, angiotensin-converting enzyme inhibitors, spironolactone, and cardiac resynchronization therapy,^2,3 acute therapy is largely unchanged. Acute therapies include nitrates, diuretics, and positive-pressure ventilation, the same as in 1974.⁷ Only one therapy, nesiritide, has been approved for heart failure treatment in the last three decades, but it is not significantly better than standard treatment.⁸

Heart failure has a poor prognosis, with approximately 50% of patients diagnosed dying within 5 years.⁹ Hospitalization also marks an inflection point in a patient’s HF trajectory, with those hospitalized having higher mortality than a matched nonhospitalized cohort.¹⁰

Heart failure is a complicated syndrome manifested by cardinal symptoms (shortness of breath, edema, and fatigue) occurring from functional or structural cardiac damage, impairing the ability of the heart to act as an efficient pump. A clinically useful definition of heart failure is as follows: a complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood. The cardinal manifestations of heart failure are dyspnea and fatigue, which may limit exercise tolerance, and fluid retention, which may lead to pulmonary and/or splanchnic congestion and/or peripheral edema.² There are numerous responsive adaptations in the kidney, peripheral circulation, skeletal muscle, and other organs to maintain short-term circulatory function. Eventually, these responses may become maladaptive, contribute to long-term disease progression, and contribute to acute exacerbations.

Threats to cardiac output from myocardial injury or stress trigger a neurohormonally mediated cascade that includes activation of the renin-angiotensin-aldosterone system and the sympathetic nervous systems. Levels of norepinephrine, vasopressin, endothelin (a potent vasoconstrictor), and tumor necrosis factor-α are increased. Although not measured in routine care, elevated levels of these hormones correlate with higher mortality.

The combined clinical effects of neurohormonal activation are sodium and water retention coupled with increased systemic vascular resistance. These maintain blood pressure and perfusion, but at the cost of increasing myocardial workload, wall tension, and myocardial oxygen demand. Although some patients are initially asymptomatic, a secondary pathologic process called cardiac remodeling begins to occur, eventually triggering more dysfunction.

Natriuretic peptides are the endogenous counterregulatory response to neurohormonal activation in heart failure. Three types are recognized: atrial natriuretic peptide, primarily secreted from the atria; B-type natriuretic peptide, secreted mainly from the cardiac ventricle; and C-type natriuretic peptide, localized in the endothelium. Natriuretic peptides produce vasodilation, natriuresis, decreased levels of endothelin, and inhibition of the renin-angiotensin-aldosterone system and the sympathetic nervous systems. B-type natriuretic peptide is synthesized as N-terminal pre–pro-B-type natriuretic peptide, which is cleaved into two substances, inactive N-terminal pro-B-type natriuretic peptide, with a half-life of approximately 2 hours, and physiologically active B-type natriuretic peptide, with a half-life of about 20 minutes. Assays for both B-type natriuretic peptide and N-terminal pro-B-type natriuretic peptide are available for ED use. Because elevated levels of neurohormones portend a worse prognosis in heart failure, their attenuation provides the basis for most chronic therapies proven to delay heart failure morbidity and mortality. These include treatment with angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, aldosterone antagonists, and β-blockers.

Heart failure may also result from pump dysfunction from acute myocardial infarction. Mechanistically, loss of a critical mass of myocardium results in immediate symptoms. If there is symptomatic hypotension with inadequate perfusion, cardiogenic shock is present (see chapter 50 “Cardiogenic Shock”). Acute pulmonary edema may be precipitous and is the clinical manifestation of a downward spiral of rapidly decreasing cardiac output and rising systemic vascular resistance on top of underlying cardiac dysfunction. Even relatively small elevations of blood pressure can result in decreased cardiac output. Decreasing cardiac output triggers increasing systemic vascular resistance, which further decreases cardiac output. Acute pulmonary edema can present acutely with severe symptoms, and if not promptly reversed, it may be a terminal event.

ACUTE HEART FAILURE CLASSIFICATION

There are many causes for heart failure (Table 53-1).

Patients can be categorized into six phenotypes to assist with investigating the causes and precipitants for the acute presentation, as well as directing initial therapy (Table 53-2).¹¹ Those with acute heart failure and hypertension often have a precipitous presentation and may have significant pulmonary edema and hypoxia. Symptoms may be due to fluid redistribution more than fluid overload, and treatment initially focuses on antihypertensive therapy.^12,13 Pulmonary edema may benefit from noninvasive ventilation to decrease the work of breathing and avoid intubation.^14,15 For heart failure accompanied by hypotension or poor perfusion without another cause, think of an ischemic or structural heart trigger creating cardiogenic shock; patients often benefit from inotropic agents and invasive hemodynamic monitoring to guide other therapies.

Patients with acute-on-chronic heart failure tend to present with gradual symptoms and weight gain over days to weeks. High-output heart failure is distinguished by a relatively normal ejection fraction and is often caused by anemia or thyrotoxicosis. Isolated right heart failure is characterized by lower extremity edema and jugular venous distension but little or no pulmonary congestion, and the cause is usually from pulmonary disease, valvular disease such as tricuspid regurgitation, or obstructive sleep apnea. Treatment approaches center on identifying and treating the underlying cause, often without volume removal because low-output states may coexist.

SYSTOLIC AND DIASTOLIC HEART FAILURE

Heart failure is classified as systolic or diastolic by ejection fraction, which is normally 60%. Systolic dysfunction, or heart failure with reduced ejection fraction, is defined as an ejection fraction <50%. Mechanistically, the ventricle has difficulty ejecting blood, leading to increased intracardiac volume and afterload sensitivity. With circulatory stress (e.g., walking), failure to improve contractility despite increasing venous return results in increased cardiac pressures, pulmonary congestion, and edema.

Diastolic dysfunction, or heart failure with is preserved ejection fraction, is characterized by impaired ventricular relaxation, causing an abnormal relation between diastolic pressure and volume. This results in a left ventricle that has difficulty receiving blood. Decreased left ventricular compliance necessitates higher atrial pressures to ensure adequate left ventricular diastolic filling, creating a preload sensitivity. The frequency of diastolic dysfunction increases with age and is more common in chronic hypertension, which leads to left ventricular hypertrophy. Coronary artery disease also contributes, as diastolic dysfunction is an early event in the ischemic cascade.

Most hospitalized patients with heart failure are admitted through the ED. Commonly, patients will present with dyspnea, which has a large differential diagnosis including heart failure, chronic obstructive pulmonary disease, asthma, pneumonia, and acute coronary syndrome. Misdiagnosis increases mortality, prolongs hospital stay, and increases treatment costs.^{16,17,18,19,20} Table 53-3 lists common causes of dyspnea in ED patients. There is no single diagnostic test for heart failure; it is a clinical diagnosis based on the history and physical examination. Having an understanding of the diagnostic certainty regarding the history, physical examination, and laboratory and radiographic testing is extremely important when caring for ED patients with undifferentiated dyspnea.

HISTORY AND PHYSICAL EXAMINATION

There is no singular historical or physical examination finding that achieves both 70% sensitivity and 70% specificity for the diagnosis of acute heart failure.¹⁹ The initial global clinical judgment has a sensitivity of 61% and specificity of 86%. A history of heart failure is the most useful historical parameter, but only has a sensitivity of 60% and specificity of 90% (positive likelihood ratio [LR+] = 5.8; negative likelihood ratio [LR–] = 0.45). Risk factors for acute heart failure sometimes may be helpful, including hypertension, diabetes, valvular heart disease, old age, male sex, and obesity. The symptom with the highest sensitivity for diagnosis is dyspnea on exertion (84%).^19,20 The most specific symptoms are paroxysmal nocturnal dyspnea, orthopnea, and edema (76% to 84%).^19,20 Evaluation for historical precipitating factors (Table 53-4) is also useful.

On exam, an S₃ has the highest LR+ for acute heart failure (11), but its absence is not useful as a negative predictor (0.88).¹⁹ However, the interrater reliability of an S₃ is not good,^21,22,23 and the ambient noise in a busy ED may interfere with S₃ detection. Abdominojugular reflux (LR+ = 6.4) and jugular venous distension (LR+ = 5.1) are the only other two physical examination findings that have an LR+ greater than 5. Increased neck size, obesity, and rapid breathing may diminish the ability to accurately measure jugular venous distension at the bedside in the ED.

When clinicians are 80% confident of the diagnosis of acute heart failure, the “clinical gestalt” outperforms diagnostic tests available in the ED for the diagnosis¹⁹; however, clinical gestalt may be about 50% accurate in an outpatient setting.²⁴ Data from the Breathing Not Proper Trial found that clinical judgment and a single B-type natriuretic peptide value had a similar accuracy performance.²⁵

CHEST RADIOGRAPHY

Chest radiographs showing pulmonary venous congestion, cardiomegaly, and interstitial edema are most specific for a final diagnosis of acute heart failure,^18,19 but the absence of these does not rule it out, because up to 20% of patients subsequently diagnosed with heart failure have chest radiographs without signs of congestion at the time of prior ED evaluation.²⁶ Particularly in late-stage heart failure, patients may have few radiographic signs, despite symptoms and elevated pulmonary capillary wedge pressure.¹⁸

ECG

The ECG is not useful for diagnosis, but it may reveal an underlying cause or precipitant. ECG signs of ischemia, acute myocardial infarction, or dysrhythmias may point to the precipitating cause. The presence of atrial fibrillation has the highest LR+ for a diagnosis of heart failure; however, new T-wave changes were also associated with the diagnosis.¹⁹

BIOMARKERS

The most widely investigated markers have been the natriuretic peptides, B-type natriuretic peptide, and N-terminal pro-B-type natriuretic peptide. Other novel biomarkers have been explored for both diagnosis and prognosis, such as ST2, galectin 3, and neutrophil gelatinase-associated lipocalin. Their role in the ED is not established; B-type natriuretic peptide and N-terminal pro-B-type natriuretic peptide remain the most important biomarkers in clinical use. Natriuretic peptide tests may add value in the setting of undifferentiated dyspnea in the ED, improving diagnostic discrimination in a variety of settings^25,27 and correlating with cardiac filling pressures and ventricular stretch.²⁸ As a result, B-type natriuretic peptide or N-terminal pro-B-type natriuretic peptide testing is recommended and helpful when the cause of dyspnea is unclear after standard evaluation (Table 53-5).

Despite the established value of natriuretic peptide testing, there are many situations where interpretation of results is unclear. Levels can be affected by age, gender, and body mass, and may elevate later in patients who present with flash pulmonary edema.³⁰ Dyspnea and modest B-type natriuretic peptide elevation are evident in conditions such as pulmonary hypertension, pulmonary embolism, pneumonia, sepsis, and renal failure. As many as 25% of patients will fall into the diagnostic “grey zone” (100 to 500 pg/mL for B-type natriuretic peptide), complicating test interpretation. B-type natriuretic peptide/N-terminal B-type natriuretic peptide testing is best used when diagnostic uncertainty exists and as an addition to the physician assessment, rather than as a routine measurement.

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