The patient in this case is having an acute exacerbation of his chronic systolic heart failure termed acute decompensated heart failure (ADHF).

ADHF is a clinical syndrome defined by the acute onset of symptoms from heart failure due to congestion with or without a reduction in cardiac output.¹ ADHF can be the initial presentation of heart failure, but more commonly the patient presents with an acute worsening of chronic heart failure. It reflects a disorder of myocardial dysfunction, although overall ejection fraction could be preserved. ADHF is the leading cause of cardiac-related hospital admissions in the United States.² In addition, patients discharged after ADHF have high rates of unscheduled clinician visits and emergency department visits as well as 30-day readmission rates.³ Thus, ADHF represents a remarkable economic burden, drawing on an increasing portion of healthcare resources. There is emerging emphasis on comprehensive treatment strategies that are specifically tailored for ADHF management.

Initial evaluation of ADHF should focus on assessment of the patient’s hemodynamic status as well as identification of any reversible causes of the exacerbation. A commonly used strategy is the rapid bedside assessment of volume and perfusion status of the patient, first described by Stevenson.⁴ Evaluation of volume status allows for assessment of the cardiac filling pressures to classify the patient as “wet” or “dry” and evaluation of adequacy of perfusion allows for assessment of end-organ perfusion to classify the patient as either “warm” or “cold.” Based on this evaluation, patients can then be divided into the following four profiles: warm and dry (profile A), warm and wet (profile B), cold and dry (profile L), and cold and wet (profile C)⁴ (Figure 37-1). This classification carries prognostic significance and also allows for targeted therapies according to each group.

Initial assessment should include a through and careful history and physical examination with some ancillary testing that should be focused on signs and symptoms related to volume overload and end-organ hypoperfusion (Figure 37-2).

Assessment of Volume Status

Volume overload can manifest as weight gain, dyspnea, orthopnea, bendopnea, elevated jugular venous pulse (JVP), rales, pedal edema, ascites, or an S3 heart sound. Most of the findings, when considered in isolation, have limited sensitivity and specificity. For example, there might not be a net weight gain in a patient with fluid retention in the setting of progressive cardiac cachexia. Of all the findings mentioned, an elevated JVP is the most accurate bedside finding that correlates well to elevated left-sided filling pressures.^5,6 However, this method is limited by its interobserver variability, depending on the clinician’s level of training and experience. The examination can also be limited by body habitus or anatomy, and there are a few situations where JVP is actually not reflective of an elevated left-sided filling pressures such as acute myocardial infarction, pulmonary embolism, a primary lung disease, and an isolated right ventricular failure.⁷

Edema, the most visible finding on physical examination is a marker of volume overload, but is nonspecific for ADHF and often is insensitive in younger patients who have excellent venous and lymphatic return. There are many iatrogenic causes of peripheral edema, which could potentially confuse the clinician when evaluating for heart failure. For example, valproate can cause peripheral edema in the absence of myocardial dysfunction that frequently remits after the discontinuation of the drug.⁸ The presence of rales on physical examination is also used as a marker of volume overload, but in reality rales are absent in more than 80% of patients with chronically elevated filling pressures.⁴ Thus, the absence of rales is not sufficient enough to exclude ADHF, particularly in patients with chronic heart failure who have baseline elevated filling pressures.

Assessment of Adequacy of Perfusion

Decreased blood flow can manifest with signs and symptoms of hypoperfusion to the specific organ involved. For example, poor cerebral perfusion results in confusion and somnolence, poor renal perfusion results in oliguria, and poor hepatic perfusion results in shock liver with elevated transaminases. It is also possible to observe hypotension, sinus tachycardia, and cool extremities as systemic manifestations of hypoperfusion. Hypotension is a less common initial presentation in decompensated heart failure, as most patients are hypertensive or normotensive on admission.⁹ However, the presence of hypotension is an important marker of increased morbidity and mortality in patients with ADHF.

Ancillary Testing in Diagnosis and Management of ADHF

History and physical examination findings can further be corroborated with the use of ancillary laboratory testing and imaging. Serum biomarkers, such as brain natriuretic peptide (BNP), can be used in setting of dyspnea of uncertain etiology to rule out ADHF. BNP of cardiac myocyte origin is released by any disease process that causes myocardial strain such as ventricular dysfunction, acute coronary syndrome (ACS), valvular heart disease, and tachyarrhythmias. Noncardiac causes of BNP release include advanced age, anemia, renal failure, obstructive sleep apnea, pulmonary hypertension, sepsis, critical illness, and severe burns. Some studies have shown that BNP levels improve with treatment of underlying cause, which has prompted to a strategy of BNP-guided heart failure treatment.^10,11 However, recent studies have not clearly established a benefit for this strategy.^11-14 Currently, BNP levels are best utilized as a rule-out marker: to rule out ADHF as the cause of dyspnea in patients with heart failure if levels are very low. Cutoff levels vary depending on laboratory studies, commonly used levels are BNP < 100 pg/mL or NT pro-BNP level < 300 pg/mL.¹⁵

Troponin levels are another laboratory study that is useful in diagnosis and management of ADHF. Elevated troponin levels are suggestive of myocyte necrosis and portend a worse prognosis. In chronic CHF, troponin release is associated with hemodynamic derangements, progressive ventricular dysfunction, and continued myocardial injury often in the absence of obvious ischemia or underlying CAD.¹ In ADHF, elevated troponin levels are associated with worse clinical outcomes and increased morbidity and mortality.^16,17 Similarly, decrease in levels over time has been associated with better prognosis compared with persistent troponin elevation.^18,19

A chest radiograph is an essential tool in the assessment of patients with suspected decompensated heart failure. Common findings include pleural effusions, cardiomegaly, pulmonary congestion, enlarged pulmonary arteries, and engorged upper pulmonary veins (Figure 37-3). However, a chest radiograph has poor sensitivity in detecting signs of chronic congestion²⁰ A normal chest radiograph should not exclude ADHF from the differential. It is useful for identifying alternative pulmonary etiology for a patient’s dyspnea such as pneumonia, pneumothorax, or pleural effusions.¹⁵

Inferior vena cava (IVC) diameter measurement has recently gained popularity as a quick, noninvasive method of evaluating filling pressures with less interobserver variation. The underlying principle of this technique is that elevated filling pressures in the right heart causes the distention of the IVC in the same way as it causes the distension of the internal jugular vein, commonly seen on physical examination. IVC diameter and collapsibility can be evaluated quickly by a bedside ultrasound. Several studies have demonstrated the usefulness of this technique and its correlation to heart failure and prognosis. Larger IVC diameters associate with severity of signs and symptoms of congestion and an increased risk of adverse events within 1 year.^7,21

Echocardiography is another irreplaceable tool in the initial assessment of ADHF as it gives quintessential information on the severity of heart failure, its potential etiologies, and can also provide useful data on intracardiac filling pressures. First, echocardiography should be used to establish if the ventricular function is preserved or diminished, as clinical assessment is limited in its ability to distinguish between systolic and diastolic heart failure.²² Further, the chronicity of heart failure can be inferred by the severity of ventricular dilation. A nondilated ventricle likely has an acute etiology (eg, myocarditis) that has not had the time to remodel. Segmental wall motion abnormalities can be suggestive of underlying CAD. The presence of significant valvular disease should be assessed to determine its role in the acute decompensation. Finally, filling pressures can also be estimated by echocardiography (eg, left atrial filling pressure and pulmonary artery pressures).^23,24

Precipitating Causes of ADHF

There are several principal cardiac and noncardiac causes that should be considered during initial evaluation of a patient with ADHF. Of particular importance is the identification of potential reversible causes that allow for targeted intervention. Acute myocardial infarction is one of the most common causes of ADHF. The constellation of ECG changes, troponin elevation, and symptoms of ischemia is suggestive of myocardial infarction. However, each of these individual signs is nonspecific for acute plaque rupture. Troponin elevation may be present from any cause of myocyte death, and chest pain frequently occurs in heart failure due to subendocardial ischemia in the setting of increased wall stress, so caution should be used. Other causes of ADHF include hypertension, arrhythmias, valvular disease, and myocarditis. Nonadherence or changes to medication regimen or dietary indiscretion with sodium and fluid restriction can also precipitate ADHF. These changes may include addition of drugs that cause direct myocardial injury (eg, doxorubicin), increase salt retention (eg, steroids, NSAIDs), or cause negative inotropic effects (eg, calcium channel blockers). Another example of a drug with myocardial-depressant effect is propofol, often used as a general sedative or in status epilepticus, which can cause diminished cardiac output and lead to hypotension.²⁵ Dilantin, can also cause hypotension and arrhythmias when infused rapidly.^25,26 Other causes of ADHF include right ventricular failure due to pulmonary processes such as pulmonary hypertension, lung disease, or pulmonary embolism, endocrine disturbances such as hyper- and hypothyroidism, infection, sepsis, and substance abuse (alcohol or illicit drug use).

Neurogenic pulmonary edema (NPE) is a clinical syndrome of acute-onset pulmonary edema that occurs in setting of significant CNS insult or stress causing raised intracranial pressure such as intracerebral hemorrhage, traumatic brain injury, status epilepticus, and meningitis. Although considered a noncardiac cause of pulmonary edema, there are cases of associated direct cardiac injury that are likely mediated by an abnormal sympathetic response.²⁷ Therefore, the diagnosis of this condition requires the assessment of cardiac function with an echocardiogram and possible pulmonary artery catheter placement to exclude the cardiac cause of pulmonary edema. Treatment of this condition in the absence of cardiac dysfunction involves reduction of intracranial pressure and supportive ARDS ventilator management.

Takotsubo cardiomyopathy is a clinical syndrome of sudden-onset ventricular dysfunction in the absence of coronary artery disease that is usually precipitated by an emotional or physical stressor. Although the prototypical precipitant is an emotional stressor such as a funeral, cases have been described with physical precipitants including acute strokes and seizures.^28,29 Echocardiography or ventriculography will demonstrate regional wall motion abnormalities in a noncoronary distribution. The typical patient has apical hypokinesis and ballooning, although other patterns have been described. Management is largely supportive as recovery of left ventricular function is expected independent of early therapy.³⁰ However, early complications including cardiogenic shock (CS), ventricular thrombus, and arrhythmias can occur.

The ADHERE and OPTIMIZE-HF registries evaluated a range of variables to identify the causes of HF decompensation and their impact on mortality. According to these registries, the top three precipitating factors of ADHF hospitalization were pneumonia and respiratory processes followed by ischemia and uncontrolled arrhythmias.⁹ The individual precipitating factor for decompensation also has an impact on its prognosis. For example, ischemia was associated with higher risk of follow-up mortality and rehospitalization, whereas uncontrolled hypertension was associated with lower follow-up mortality and rehospitalization.³¹ These studies also found admission serum creatinine, admission systolic blood pressure, and patient age to be strongly predictive of in-hospital mortality. There was an associated increase of in-hospital mortality as serum creatinine increased to 3.5 mg/dL.³² In regard to blood pressure, elevated systolic pressure up to 160 mm Hg on admission was associated with lower risk of in-hospital mortality, with each 10 mm Hg increase over systolic pressure of 100 mm Hg being associated with a 17% reduction in mortality.^31,32 In this case, elevated systolic pressure may be a marker of greater myocardial reserve and thus indicate lower short-term mortality risk. Finally, advanced age was associated with increased mortality, with a 34% increase in mortality per 10 years of age increase.^31,33

The aim of therapy is to relieve symptoms, optimize cardiac filling pressures, and manage any reversible etiology responsible for the decompensation. Therapeutic management can be guided by the defined hemodynamic profile.

Symptom management in acutely decompensated heart failure generally involves management of dyspnea. The use of supplemental oxygen can improve dyspnea due to hypoxia and acts as a pulmonary vasodilator. Noninvasive positive pressure ventilation (NIPPV) in the form of bi-level positive airway pressure (BiPAP) can also be used. BiPAP can relieve dyspnea and improve oxygen saturation in patients with acute pulmonary edema by increasing intrathoracic pressure and decreasing preload. Despite these advantages, NIPPV has not shown to reduce mortality or rate of intubation compared with standard therapy with vasodilators.³⁴ Contraindications to use of BiPAP include hypotension, vomiting, pneumothorax, and depressed consciousness. Intubation and mechanical ventilation provides complete respiratory support and can correct oxygenation, reduce hypercarbia, and reduce the work of breathing, thereby significantly decreasing the myocardial demand.

With stabilization of the respiratory status of the patients, therapy can be guided by the clinical assessment of the volume status and adequacy of perfusion of the patient. In the past, invasive hemodynamic monitoring with right heart catheterization and pulmonary artery catheter (PAC) placement was routinely used in ADHF patients. The idea behind its use was that therapy guided by PAC would allow for a more accurate hemodynamic assessment than clinical assessment alone. However, the landmark ESCAPE trial showed no significant difference on days alive out of the hospital during the first 6 months after admission in PAC-guided therapy vs clinically driven therapy and was terminated early.³⁵ Therefore, there is no role for routine placement of PAC in initial ADHF management. An invasive hemodynamic assessment is useful when patients do not improve with initial medical therapy or if the clinician is unsure of the hemodynamics by noninvasive evaluation and is the standard of care in cardiogenic shock.