Assessment and treatment of acute heart failure-Case study: Wet and warm profile-Diuretic refractory

Abstract

A 62-year-old man presented to the emergency department (ED) with severe shortness of breath. His symptoms had begun 4 days previously when he ran out of his "water pills." He also complained of dyspnea on exertion, difficulty breathing when lying supine, and swelling of his feet. His past medical history was significant for hypertension and congestive heart failure (CHF). His normal medications included furosemide 40 mg b.i.d. and a clonidine 0.4 mg patch. He reported having no money to refill any of his prescriptions, and he had not taken any of his medications for almost a week. ExaminationIn general, he appeared anxious and in mild respiratory distress. His vital signs were: temperature 36.8°C, heart rate 119 beats/min, respiratory rate 32 breaths/min, blood pressure 178/86 mmHg, and SO 2 by pulse oximetry 89% on room air. His neck veins were grossly distended with elevated jugular venous pressure (JVP). Lungs demonstrated diffuse wheezes and crackles in all lung fields. Cardiac examination showed tachycardia. Abdominal and neurological examinations were normal. Lower extremities showed 3+ peripheral edema bilaterally. Laboratory Findings• Hemoglobin 11.4 mg/dl • Serum creatinine 1.6 mg/dl • Blood urea nitrogen 35 mg/dl • Sodium 139 mEq/l • B-type natriuretic peptide (BNP) 1740 pg/ml • Troponin T < 0.02 ng/ml Hospital CourseChest radiography was consistent with pulmonary edema, and an electrocardiogram showed sinus tachycardia with left ventricular strain. The patient was started on supplemental oxygen and given furosemide 60 mg intravenously (IV). He was admitted to a telemetry unit, and the furosemide was continued every 12 h. Enalapril was initiated at 10 mg orally b.i.d., and a clonidine patch delivering 0.4 mg/h was replaced. By the next morning, the patient was still short of breath with signs of volume overload. Diuresis was ineffective, with only a 500 cc net negative fluid balance. Cardiac enzymes remained normal. His furosemide was increased to 80 mg IV q 12 h, and a nesiritide bolus of 2 mcg/kg was given followed by a continuous infusion at 0.01 mcg/kg/min. Over the next 12 h the patient had 1.5 l of urine output, and by the next hospital day he was on room air with good oxygen saturations. Total fluid balance was now 3 l net negative, and his systolic blood pressure was now controlled at 135 mmHg. A social work consult was obtained, and the patient was provided with a temporary Medicaid number so his prescriptions would be filled. The nesiritide infusion was stopped at a total of 20 h of therapy. A repeat BNP was 356 pg/ml at the time of discharge. He was discharged home on clonidine, enalapril, and furosemide. DiscussionPatients can become diuretic refractory (clinically defined as the failure to remove edema despite a high diuretic dose) over time with increased diuretic dosage requirements; this typically occurs in one out of every three patients with CHF. 1 It can be caused by a host of factors, including excessive sodium intake, decreased renal function, 2 and reduced/delayed peak concentrat...

The Benefits of Early Vasoactive Therapy in the Treatment of Acute Decompensated Heart Failure

“…diuretic therapy ( p < .001) (Colucci et al, 2000). The use of nesiritide to increase urine output is particularly relevant in the treatment of volume‐overloaded (“warm and wet”) patients with elevated pulmonary capillary wedge pressure (PCWP), as they may have reduced responsiveness to diuretics or may be refractory to diuretic therapy (Figure 3) (Michota, 2004a, 2004b).…”

“…CI, cardiac index; PCWP, pulmonary capillary wedge pressure; SVR, systemic vascular resistance. Adapted with permission from Michota (2004a, 2004b) .…”