Decompensated Heart Failure: Ten Things to Remember From Updated ACCF/AHA Guidelines 2013 ACCF/AHA guideline for the management of heart failure. A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Major Recommendations Biomarkers Hospitalized/Acute Class I 1. Measurement of BNP or NT-proBNP is useful to support clinical judgment for the diagnosis of acutely decompensated HF, especially in the setting of uncertainty for the diagnosis . (Level of Evidence: A) 2. Measurement of BNP or NT-proBNP and/or cardiac troponin is useful for establishing prognosis or disease severity in acutely decompensated HF ). (Level of Evidence: A) Class IIb 1. The usefulness of BNP- or NT-proBNP–guided therapy for acutely decompensated HF is not well established . (Level of Evidence: C) 2. Measurement of other clinically available tests such as biomarkers of myocardial injury or fibrosis may be considered for additive risk stratification in patients with acutely decompensated HF. (Level of Evidence: A) Noninvasive Cardiac Imaging Class I 1. Patients with suspected or new-onset HF, or those presenting with acute decompensated HF, should undergo a chest x-ray to assess heart size and pulmonary congestion and to detect alternative cardiac, pulmonary, and other diseases that may cause or contribute to the patients symptoms. (Level of Evidence: C) 2. A 2-dimensional echocardiogram with Doppler should be performed during initial evaluation of patients presenting with HF to assess ventricular function, size, wall thickness, wall motion, and valve function. (Level of Evidence: C) 3. Repeat measurement of ejection fraction (EF) and measurement of the severity of structural remodeling are useful to provide information in patients with HF who have had a significant change in clinical status; who have experienced or recovered from a clinical event; or who have received treatment, including GDMT, that might have had a significant effect on cardiac function; or who may be candidates for device therapy. (Level of Evidence: C) Class IIa 1. Noninvasive imaging to detect myocardial ischemia and viability is reasonable in patients presenting with de novo HF, who have known coronary artery disease (CAD) and no angina, unless the patient is not eligible for revascularization of any kind. (Level of Evidence: C) 2. Viability assessment is reasonable in select situations when planning revascularization in HF patients with CAD . (Level of Evidence: B) 3. Radionuclide ventriculography or magnetic resonance imaging can be useful to assess left ventricular ejection fraction (LVEF) and volume when echocardiography is inadequate. (Level of Evidence: C) 4. Magnetic resonance imaging is reasonable when assessing myocardial infiltrative processes or scar burden (Level of Evidence: B) Class III: No Benefit 1. Routine repeat measurement of LV function assessment in the absence of clinical status change or treatment interventions should not be performed . (Level of Evidence: B) The Hospitalized Patient Precipitating Causes of Decompensated HF Class I 1. ACS precipitating acute HF decompensation should be promptly identified by ECG and serum biomarkers, including cardiac troponin testing, and treated optimally as appropriate to the overall condition and prognosis of the patient. (Level of Evidence: C) 2. Common precipitating factors for acute HF should be considered during initial evaluation, as recognition of these conditions is critical to guide appropriate therapy. (Level of Evidence: C) Maintenance of GDMT during Hospitalizations Class I 1. In patients with HFrEF experiencing a symptomatic exacerbation of HF requiring hospitalization during chronic maintenance treatment with GDMT, it is recommended that GDMT be continued in the absence of hemodynamic instability or contraindications (Level of Evidence: B) 2. Initiation of beta-blocker therapy is recommended after optimization of volume status and successful discontinuation of intravenous diuretics, vasodilators, and inotropic agents. Beta-blocker therapy should be initiated at a low dose and only in stable patients. Caution should be used when initiating beta blockers in patients who have required inotropes during their hospital course (Level of Evidence: B) Diuretics in Hospitalized Patients Class I 1. Patients with HF admitted with evidence of significant fluid overload should be promptly treated with intravenous loop diuretics to reduce morbidity . (Level of Evidence: B) 2. If patients are already receiving loop diuretic therapy, the initial intravenous dose should equal or exceed their chronic oral daily dose and should be given as either intermittent boluses or continuous infusion. Urine output and signs and symptoms of congestion should be serially assessed, and the diuretic dose should be adjusted accordingly to relieve symptoms, reduce volume excess, and avoid hypotension . (Level of Evidence: B) 3. The effect of HF treatment should be monitored with careful measurement of fluid intake and output, vital signs, body weight that is determined at the same time each day, and clinical signs and symptoms of systemic perfusion and congestion. Daily serum electrolytes, urea nitrogen, and creatinine concentrations should be measured during the use of intravenous diuretics or active titration of HF medications. (Level of Evidence: C) Class IIa 1. When diuresis is inadequate to relieve symptoms, it is reasonable to intensify the diuretic regimen using either: a. Higher doses of intravenous loop diuretics (Level of Evidence: B); or b. Addition of a second (e.g., thiazide) diuretic (Level of Evidence: B). Class IIb 1. Low-dose dopamine infusion may be considered in addition to loop diuretic therapy to improve diuresis and better preserve renal function and renal blood flow (Level of Evidence: B) Renal Replacement Therapy—Ultrafiltration Class IIb 1. Ultrafiltration may be considered for patients with obvious volume overload to alleviate congestive symptoms and fluid weight . (Level of Evidence: B) 2. Ultrafiltration may be considered for patients with refractory congestion not responding to medical therapy. (Level of Evidence: C) Parenteral Therapy in Hospitalized HF Class IIb 1. If symptomatic hypotension is absent, intravenous nitroglycerin, nitroprusside, or nesiritide may be considered an adjuvant to diuretic therapy for relief of dyspnea in patients admitted with acutely decompensated HF . (Level of Evidence: A) Venous Thromboembolism Prophylaxis in Hospitalized Patients Class I 1. A patient admitted to the hospital with decompensated HF should receive venous thromboembolism prophylaxis with an anticoagulant medication if the risk–benefit ratio is favorable . (Level of Evidence: B) Arginine Vasopressin Antagonists Class IIb 1. In patients hospitalized with volume overload, including HF, who have persistent severe hyponatremia and are at risk for or having active cognitive symptoms despite water restriction and maximization of GDMT, vasopressin antagonists may be considered in the short term to improve serum sodium concentration in hypervolemic, hyponatremic states with either a V2 receptor selective or a nonselective . (Level of Evidence: B) Stage D Water Restriction Class IIa 1. Fluid restriction (1.5 to 2 L/d) is reasonable in stage D, especially in patients with hyponatremia, to reduce congestive symptoms. (Level of Evidence: C) Inotropic Support Class I 1. Until definitive therapy (e.g., coronary revascularization, MCS, heart transplantation) or resolution of the acute precipitating problem, patients with cardiogenic shock should receive temporary intravenous inotropic support to maintain systemic perfusion and preserve end-organ performance. (Level of Evidence: C) Class IIa 1. Continuous intravenous inotropic support is reasonable as bridge therapy in patients with stage D HF refractory to GDMT and device therapy who are eligible for and awaiting MCS or cardiac transplantation . (Level of Evidence: B) Class IIb 1. Short-term, continuous intravenous inotropic support may be reasonable in those hospitalized patients presenting with documented severe systolic dysfunction who present with low blood pressure and significantly depressed cardiac output to maintain systemic perfusion and preserve end-organ performance (Level of Evidence: B) 2. Long-term, continuous intravenous inotropic support may be considered as palliative therapy for symptom control in select patients with stage D HF despite optimal GDMT and device therapy who are not eligible for either MCS or cardiac transplantation (Level of Evidence: B) Class III: Harm 1. Long-term use of either continuous or intermittent, intravenous parenteral positive inotropic agents, in the absence of specific indications or for reasons other than palliative care, is potentially harmful in the patient with HF . (Level of Evidence: B) 2. Use of parenteral inotropic agents in hospitalized patients without documented severe systolic dysfunction, low blood pressure, or impaired perfusion and evidence of significantly depressed cardiac output, with or without congestion, is potentially harmful (Level of Evidence: B) Mechanical Circulatory Support Class IIa 1. MCS is beneficial in carefully selected‡ patients with stage D HFrEF in whom definitive management (e.g., cardiac transplantation) or cardiac recovery is anticipated or planned (Level of Evidence: B) 2. Nondurable MCS, including the use of percutaneous and extracorporeal ventricular assist devices (VADs), is reasonable as a bridge to recovery or bridge to decision for carefully selected‡ patients with HFrEF with acute, profound hemodynamic compromise . (Level of Evidence: B) 3. Durable MCS is reasonable to prolong survival for carefully selected‡ patients with stage D HFrEF (Level of Evidence: B) ‡Although optimal patient selection for MCS remains an active area of investigation, general indications for referral for MCS therapy include patients with LVEF
Posted on: Sat, 05 Jul 2014 21:48:51 +0000
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