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Figure 1. RA = right atrial pressures, PCWP = pulmonary capillary wedge pressure
Her current medications included:
- Furosemide, 60 mg by mouth two times daily;
- Carvedilol, 12.5 mg by mouth in the morning, 6.25 mg in the evening;
- Amiodarone, 200 mg by mouth daily; and
- Digoxin, 0.125 mg by mouth daily.
Laboratory findings included normal electrolytes, blood urea nitrogen, and serum creatinine. Her hemoglobin was 11.3 gm/L, and her B-type natriuretic peptide (BNP) level was 4,837 pg/ml. Initial cardiac enzymes were negative (troponin I of <0. 03).
Her chest X-ray demonstrated moderate cardiac enlargement with bilateral thickening of subpleural septal lines and blurring of the pulmonary vasculature consistent with developing cardiogenic pulmonary edema. A 12-lead electrocardiogram indicated sinus tachycardia with a rate of 110 beats per minute and nonspecific ST-T wave changes in the inferior leads, but no Q waves were noted. Echocardiography showed severely reduced left ventricular systolic function with severe global hypokinesis of the left ventricle and a measured ejection fraction of 25%-30%. There was no pericardial effusion.
She was admitted to the telemetry floor with the diagnosis of ADHF. She was placed on supplemental oxygen and serial cardiac enzymes, and her electrocardiogram remained negative for injury or ischemia. Intravenous furosemide was initiated at 40 mg every 12 hours. After 24 hours, she was given a bolus of nesiritide (2 mcg/kg), followed by a continuous infusion at 0.01 mcg/kg/min. Cardiac medications were continued, and the dosage of carvedilol was reduced to 6.25 mg by mouth twice daily.
After a period of diuresis, the patient remained highly symptomatic; therefore, a right heart catheterization was done. The hemodynamics indicated a cardiac output of three liters per minute, a right atrial pressure of 20 mm Hg, a right ventricular pressure of 70/20 mm Hg, pulmonary artery pressure of 66/20 mm Hg with a mean pressure of 52 mm Hg, and a pulmonary capillary wedge pressure of 25 mm Hg. (See Figures 1 and 2, p. 23).
Over the next 24 hours, the patient had more than three liters of urine output and was significantly improved. The nesiritide infusion was discontinued after 48 hours of therapy, and the patient was weaned from supplemental oxygen. Lisinopril was started at 2.5 mg daily by mouth. On hospital day four, the patient walked around the nurses’ station without supplemental oxygen, and she was returned to the previous dose of furosemide, 60 mg twice daily.
The patient was enrolled in the Heart Success Program (HSP), a collaborative interdisciplinary program that is available in the institution for cancer patients with heart failure. She was provided with patient education materials that included educational videotapes on heart failure management, daily weight monitoring, diet, medications, exercise, and the emotional aspects of heart failure. Nurses with heart failure training were available to answer questions for the patient and to provide further instruction for follow-up after the patient’s discharge. The patient improved enough that she was able to enroll in a New York Heart Association (NYHA) class II and was discharged after five days, with a follow-up appointment to the outpatient clinic one week after hospital discharge.
Discussion
This case illustrates the challenges inherent in the diagnosis and management of ADHF in a cancer patient with a known history of heart failure. Rapid assessment is critical in establishing a diagnosis and initiating appropriate intervention. The goals of managing ADHF remain the same regardless of etiology. These 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. The same principles apply—even if the patient has a major comorbidity such as cancer, and suspicion for the diagnosis must remain high.