TY - CHAP M1 - Book, Section TI - Acute Decompensated Heart Failure A1 - Rodgers, Jo E. A1 - Reed, Brent N. A2 - DiPiro, Joseph T. A2 - Talbert, Robert L. A2 - Yee, Gary C. A2 - Matzke, Gary R. A2 - Wells, Barbara G. A2 - Posey, L. Michael PY - 2017 T2 - Pharmacotherapy: A Pathophysiologic Approach, 10e AB - KEY CONCEPTS Patients presenting to the hospital with acute decompensated heart failure (ADHF) can be categorized into four hemodynamic subsets based on volume status (euvolemic or “dry” vs volume overloaded or “wet”) and cardiac output (adequate cardiac output or “warm” vs hypoperfusion or “cold”). Patients may be warm and dry, warm and wet, cold and dry, or cold and wet. While invasive hemodynamic monitoring using a pulmonary artery (PA) catheter does not alter outcomes in a broad population of ADHF patients, it may be considered in those who are refractory to initial therapy, whose volume status is unclear, or in those with clinically significant hypotension (ie, systolic blood pressure <80 mm Hg) or worsening renal function despite standard therapy. Key hemodynamic parameters monitored with a PA catheter include pulmonary capillary wedge pressure (PCWP; reflecting fluid status or “preload”), cardiac output or cardiac index (CI; reflecting the innate contractility of the heart), and systemic vascular resistance (SVR; reflecting vascular tone or “afterload”). Although a normal PCWP (6-12 mm Hg) is desirable in healthy patients, higher ventricular filling pressures (15-18 mm Hg) are often necessary in patients with heart failure (HF). Treatment goals for ADHF include relief of congestive symptoms, restoration of systemic tissue perfusion via improved cardiac output, and minimization of further cardiac damage and other adverse effects. Optimizing oral chronic HF therapy in the setting of ADHF may assist with improving cardiac output, relieving congestion, and preventing hospital readmission. Pharmacologic therapies used in the management of ADHF can be broadly classified according to whether they improve volume overload and/or low cardiac output. No therapy studied to date has conclusively been shown to reduce mortality and several may potentially worsen outcomes. Intravenous (IV) loop diuretics are considered first-line therapy for the management of ADHF associated with volume overload refractory to orally administered diuretics. Administration as a bolus or continuous infusion appears to be equally efficacious and safe when selected as initial therapy, although high-dose loop diuretic therapy (ie, up to 2.5-times the oral regimen prior to admission) is associated with greater volume removal. The addition of a thiazide-type diuretic may be considered in patients with diuretic resistance. If patients continue to be refractory to, or experience worsening renal function with diuretic therapy, IV vasodilators and/or inotropes may be indicated. Placement of a PA catheter may be helpful in guiding therapy in such patients. Intravenous vasodilators may be added to diuretics for rapid resolution of congestive symptoms, especially in patients with acute pulmonary edema or severe hypertension. Such therapy may also be considered in patients who fail to respond to aggressive treatment with diuretics. Vasodilators should be avoided in patients with symptomatic hypotension or reduced left ventricular filling pressure. Frequent blood pressure monitoring is necessary to ensure their safe use. Vasopressin antagonists such as tolvaptan may be considered in patients with severe euvolemic or hypervolemic hyponatremia. Therapy should only be initiated in a hospital setting to allow for monitoring of volume status and serum sodium concentrations, as rapid correction of serum sodium may result ... SN - PB - McGraw-Hill Education CY - New York, NY Y2 - 2024/03/29 UR - accesspharmacy.mhmedical.com/content.aspx?aid=1145177519 ER -