Acute decompensated heart failure (ADHF) remains one of the most common reasons for hospitalization. ADHF patients who have co-morbid conditions present stubborn challenges for hospitalists. And ADHF is frequently observed in patients 65 and older. The neurohormonal activation that results as a consequence of myocardial dysfunction leads to progressive cardiac deterioration and hemodynamic disturbances that ultimately become manifest as acute decompensated heart failure.
ADHG management goals include stabilizing the patient, managing acute hemodynamic abnormalities, reversing the symptoms of dyspnea caused by fluid overload, and initiating evidence-based therapies to decrease disease progression and improve survival.
In this article we present the case of a 26-year-old female with ADHF and highlight the management strategies that can result in stabilization and improved long-term outcome.
Despite major advances in the treatment of heart disease, heart failure remains a growing public health problem of epidemic proportions in the United States. Approximately five million Americans have heart failure, and more than 550,000 patients are diagnosed with the disease each year.1 The annual number of hospitalizations for heart failure as a primary diagnosis has increased from approximately 810,000 in 1990 to more than 1 million in 1999, and it is the most common discharge diagnosis-related group for patients 65 and older.2 Medicare spent more dollars on the diagnosis and treatment of heart failure than on any other diagnosis—more than $27.9 billion in 2005.1
Patients presenting to the emergency department (ED) with ADHF are often hemodynamically unstable, with severe symptoms of dyspnea and fluid overload. Rapid assessment and prompt initiation of appropriate interventions are necessary to achieve clinical stability and prevent prolonged hospital stay if hospitalization is required. The in-hospital mortality rate for ADHF is 5%-8%; median duration of hospitalization is five days, and the six-month re-hospitalization rate is about 50%.1,3 Thus, it is clear that improved recognition and treatment are of paramount importance. With these goals in mind, we present a recent case that highlights many of the concerns about and treatment options for ADHF.
Karen A. is a 26-year-old black female with stage III Hodgkin’s disease, diagnosed in 2000. She received chemotherapy (cisplatin, cytarabine, doxorubicin, rituxan, gemcitabine) and, as a result, in 2001 developed chemotherapy-induced cardiomyopathy with an ejection fraction of <20%. Her condition stabilized, and she remained in clinical remission until September 2002.
In 2003 she received an autologous stem cell transplant and subsequently presented to the ED with complaints of fatigue, progressive shortness of breath in the previous seven days, and lower extremity edema. She also reported right-sided pleuritic chest pain, but denied associated nausea, vomiting, or diaphoresis. In the three days preceding admission, she had gained 10 pounds. In the past six months, she had had multiple admissions for ADHF.
Her physical examination revealed an alert, obese female in moderate respiratory distress with dry mucous membranes. Her vital signs indicated a temperature of 36.5° C, a heart rate of 110 beats per minute, a respiratory rate of 20 breaths per minute, blood pressure measuring 111/73 mm Hg, and an oxygen saturation of 92%. She had no scleral icterus, but did have jugular venous distention to the angle of the mandible at 45° upright. Her cardiac examination indicated tachycardia with distant heart sounds and an audible third heart sound (S3), as well as a grade 2/6 systolic ejection murmur at the left sternal border. Her lung examination demonstrated diffuse crackles present in both lung fields, but no wheezes. Abdominal examination was notable for tenderness to palpation at the right hypogastric region and for hepatomegaly, her skin was warm and dry with no cyanosis, and her extremities demonstrated significant bilateral pitting pre-tibial edema to her knees.