Initial Evaluation
Early diagnosis and effective management of ADHF are critically important, as these have been shown to reduce hospitalizations and intensive care unit admissions, to decrease length of stay, and to decrease cost of hospitalization.4 A comprehensive history and physical examination must be performed to identify signs and symptoms that lead to a heart failure diagnosis.
We must evaluate such potential risk factors as history of hypertension, dyslipidemia, diabetes mellitus, coronary artery disease, valvular disease, peripheral vascular disease, a family history of cardiomyopathy, smoking, alcohol use, thyroid problems, sleep apnea, and any recent history of infection (particularly upper respiratory tract infection, which can cause viral cardiomyopathy).
As part of further investigation with cancer patients, include the patient’s possible past exposure to cardiotoxic agents (e.g., anthracyclines, trastuzumab, high-dose cyclophosphamide) or mediastinal irradiation. Chemotherapy-induced cardiomyopathy is increasingly becoming an issue in heart failure management as a result of the growing number of long-term cancer survivors who have received treatment with anthracycline-containing chemotherapy or other aggressive therapy.
Focus on volume and perfusion status during the physical assessment of each patient. Most patients presenting to the ED with acute decompensation are volume overloaded. Volume overload is manifested by symptoms of dyspnea, orthopnea, and paroxysmal nocturnal dyspnea, as well as jugular venous distention, hepatojugular reflux, ascites, edema, and crackles in the lungs.5 Crackles are not always present in chronic heart failure patients, however, because of the continuous movement of fluid into the interstitium associated with increased lymphatic drainage, leaving the alveoli relatively dry.6
In addition to a comprehensive history and physical examination, several tests will help establish the diagnosis. (See Table 1, top left.) A measurement of a B-type natriuretic peptide (BNP) facilitates the diagnosis of ADHF. BNP is an endogenously generated natriuretic peptide that is activated in response to atrial or ventricular expansion due to volume overload and increased wall tension.7,8 Circulating levels of endogenous BNP are significantly elevated in ADHF patients and are a valuable tool for diagnosis of heart failure in the ED.9-11 In Karen A., the BNP level was 4,837 pg/mL, which is indicative of Stage D heart failure. This diagnosis was confirmed by chest X-ray findings of cardiogenic pulmonary edema in the setting of severe left ventricular hypokinesis and an ejection fraction of 25%-30%.
Although history and physical examination may provide important clues regarding the underlying cardiac abnormality, both invasive and noninvasive testing are necessary to provide a definitive diagnosis of heart failure and to evaluate potential exacerbating conditions. A two-dimensional echocardiogram with Doppler flow study is an essential diagnostic test for evaluating myocardial contractility or ejection fraction. Echocardiogram can also evaluate other structural components such as the pericardium, valvular status, and hemodynamic parameters that may contribute to the development of ADHF. In patients with cardiac risk factors, a myocardial perfusion stress test or catheterization may identify the presence of coronary artery disease as a contributor.
A 12-lead electrocardiogram is necessary to establish the rhythm and to show evidence of acute or prior myocardial infarction, pericarditis, conduction abnormalities, or left ventricular hypertrophy as a result of prolonged uncontrolled hypertension. It is known that rhythm disturbances such as atrial fibrillation can be a precipitating factor for ADHF.
A chest X-ray is needed to uncover pulmonary edema in cases of fluid overload and to show an enlarged cardiac silhouette in cases of dilated cardiomyopathy. Identification of a definitive cause or causes that precipitate the occurrence of ADHF is crucial in devising a management plan and initiating appropriate intervention. (See Table 2, p. 22.)
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Figure 1. RA = right atrial pressures, PCWP = pulmonary capillary wedge pressure