of 180 mg to promote urine output. If a patient is not currently on a diuretic, 40 mg of furosemide is usually adequate [4,58,59,65,68]. Urine output and serum electrolytes are monitored to track diuresis volume and to screen for treatment-induced hypokalemia. If target urine outputs are not met, the diuretic dose is doubled and repeated at 2 hours. Adequate output should exceed 500 cc within 2 hours, unless the creatinine exceeds 2.5 mg/dL. With elevated creatinine, 2-hour urine output goals are halved. Failure to meet output goals suggests inpatient hospitalization may be needed [4,58,59,65,68].
Diuretics prevent hospitalization and provide symptomatic relief. They are indicated for all patients with congestive findings, but not as chronic monotherapy (diuretics should be combined with ACE inhibitors and beta-blockers) because alone they provide no mortality benefit [1,5,27,29]. With aggressive diuresis, potassium supplementation is frequently required. However, if loop diuretics are used in concert with nesiritide, potassium supplements are less often needed. Standing orders for oral or IV potassium supplementation with the goal of maintaining a K+ between 4.0 and 5.0 meq/dL may be useful.
Magnesium is an important cofactor for myo-cardial function and should be supplemented if the patient is deficient. Give magnesium if the creatinine is < 1.5 mg/dL; otherwise, therapy should be individualized. Magnesium may be given as 140 mg magnesium oxide orally once.
Limited data suggest that combining loop diuretics treatment with IV vasoactive agents has benefit. In 1442 patients from 42 hospitals, patients receiving intermittent IV bolus therapy (eg, furosemide bolus) of any type while in the ED had a mean hospitalization LOS of 9.9 days. This compared with an LOS of 6.6 days (P — .004) for those treated with IV infusion therapy (eg, nesiri-tide or nitroglycerin) while still in the ED. In this registry analysis, early infusion therapy with a va-soactive agent, as opposed to intermittent bolus therapy, was associated with a significantly shorter hospital LOS .
Certain vasodilators have the potential to provide both symptomatic improvement and mortality reduction in HF. Although hemodynamic improvements are the direct result of the effect on the vascular tree, mortality improvements in long-term outcomes are not a universal feature of all vasodilators. For mortality reduction to occur, the vasodilator must also have the characteristic of neurohormonal antagonism directed at the pathologic hormonal excesses of HF [69-72]. With regard to specific agents, ACE inhibitors, with both vasodilation and neurohormonal antagonistic effects, represent a class of medications with a mortality reduction benefit of such magnitude that all HF patients deserve a therapeutic trial [1,29,5,69-72]. ARBs, predicted to have similar physiologic effects as ACE inhibitors, may have fewer side effects than ACE inhibitors. However, as the preponderance of the current mortality reduction data uses ACEI, they should be replaced by ARBs only if significant intolerance or a contraindication to the ACE inhibitor exists [1,29].
Improvement of hemodynamic parameters in the acutely decompensated HF patient, reflected by improvements in vital signs and in the clinical presentation of dyspnea, may be obtained with the use of intravenous vasodilators. The appropriate candidate usually has a blood pressure in excess of 90 mm Hg and no contraindications to vasodila-tion. Vasodilation can result in hypotension in selected populations, including those conditions where there is either an impediment to outflow (eg, aortic stenosis), situations where cardiac output depends on adequate or elevated pre-load (eg, right ventricular infarct, pericardial tamponade), or when preload is already abnormally decreased (eg, volume depletion).
Because their optimal use in HF requires invasive monitoring, nitroprusside and nitroglyc-erin are generally discouraged from use in the OU environment. Conversely, nesiritide, which can be used safely and efficaciously without invasive hemodynamic monitoring, is permissible in the OU.
Nesiritide is an IV medication for the treatment of decompensated HF. It provides hemody-namic [73,74] and clinical benefits [75-77] from the combination of vasodilation , natriuresis, and neurohormonal antagonism . It has been shown to decrease costs and hospital readmissions  and lower 6-month mortality as compared with dobutamine [75,76]. Compared with nitro-glycerin, nesiritide improves dyspnea and hemo-dynamics more rapidly and to a greater extent . Nesiritide is appropriate for use in the ED OU. Once stabilized in the ED, patients on the recommended fixed dose of nesiritide (2 ^g/kg IV bolus, then a 0.01 ^g/kg infusion) are candidates for OU admission.
The Proaction Trial was a multicenter, doubleblind, randomized, placebo-controlled safety and efficacy trial of standard OU therapy, with and without nesiritide . In this trial, OU patients with acute decompensated HF and receiving standard therapy were treated with at least 12 hours of either standard dose-blinded nesiritide or placebo. In the safety analysis, there were no differences in adverse outcomes between the standard care and nesiritide cohorts. NYHA class III or IV HF patients receiving nesiritide had a 29% decrease in revisit rates (P — .057). Days in the hospital in the month after study entry were markedly lower in patients receiving nesiritide compared with standard therapy (2.5 versus 6.5, respectively; P — .03).
Similar to diuretics, digoxin decreases hospital-izations but does not alter mortality. It is recommended for LV systolic dysfunction and rate control in atrial fibrillation [1,5,29]. Toxicity manifests as cardiac arrhythmia (heart block, ectopy, or re-entrant rhythms), gastrointestinal symptoms, or neurologic complaints (eg, visual disturbances and confusion). Serum levels can suggest toxicity if they exceed 2.0 ng/mL, but toxicity can also occur at lower levels if there is coexistent hypokalemia or hypomagnesemia. Digoxin should be used at a dose of 0.125 to 0.250 mg daily [1,5,29].
Beta-blockers prolong life in HF patients  but should only be initiated if the patient is he-modynamically stable [1,29]. They should not be started in decompensated HF; consequently, this generally precludes OU initiation. Conversely, abruptly stopping a beta-blocker has the potential to worsen hemodynamics. Recommended therapy for decompensated HF patients presenting to the ED while on a beta-blocker is to hold the dose or continue it at one dosing level lower than the maintenance dose. If inotropes are required, the beta-blocker may be withheld [1,29]. Patients at this stage of their disease are not usually ideal OU candidates.
The aldosterone antagonist spironolactone decreases the relative risk of mortality in end stage HF . These patients should receive 12.5 to 25.0 mg qid [1,29]. It is not recommend if the creatinine exceeds 2.5 mg/dL or the K+ is > 5.0 mEq/L. If a patient is already on an aldosterone antagonist, it should be continued in OU patients.
The risk of thromboembolism in the clinically stable HF outpatient is low, estimated at 1% to 3% per year, and is greatest patients with the lowest EF [87,88]. However, hospitalized HF patients are at significant risk for sustaining deep vein thrombosis (DVT) and its complications. In the MEDENOX (prophylaxis in MEDical patients with ENOXaparin) study of hospitalized patients, subcutaneous enoxaparin decreased ve-nographically documented DVT, from 14.9% in the placebo group to 5.5% in the 40-mg every day enoxaparin prophylaxis group . Empiric
DVT prevention in hospitalized, bedridden HF patients must be balanced against the relatively low risk of complications associated with anticoagulant prophylaxis. The precise value of prophylactic anticoagulation has never been reported in ED OU HF management. However, as it is anticipated that this cohort of patients will be discharged in a relatively limited time frame, anticoagulation is usually not performed.
Calcium channel blockers (CCBs) are not routinely recommended in HF [1,90]. This is because short-term use may result in pulmonary edema and cardiogenic shock, whereas in the long-term, they may increase the risk of worsening HF and death [91-94]. These adverse effects have been attributed to the negative inotropic effects of CCBs. If necessary, amlodipine, the CCB with no clear adverse mortality effect, may be used for compelling clinical reasons (eg, as an anti-anginal agent despite maximal therapy with nitrates and beta-blockers).
Nonsteroidal anti-inflammatory drugs should be avoided in HF [1,90]. They inhibit the effects of diuretics and ACE inhibitors and can worsen cardiac and renal function .
HF is an important risk factor for sudden cardiac death, and its likelihood increases in proportion to the decrease in EF and HF severity . Premature ventricular contractions occur in 95% of dilated cardiomyopathy patients, and nonsustained VT may be seen in up to 30% to 40% of cases. Prophylactic administration of anti-arrhythmics is not effective and may actually increase mortality . Therefore, their routine use to suppress asymptomatic ventricular arrhythmias is not warranted.
OU patients may be discharged at any time, once there has been a good therapeutic response. Although there are very few studies that have determined predictors of successful ED discharge, a net volume output of greater than 1 L is associated with a higher rate of successful discharge from the ED OU .
Discharge criteria may aid in selecting candidates who may be sent home (Box 8). Most important in the disposition determination is the clinical assessment, but a post-treatment BNP level can help to guide this decision. If nesiritide
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