Guidelines for Acute Decompensated Heart Failure Treatment

DiDomenico, Robert J.; Park, Hayley Y; Southworth, Mary Ross; Eyrich, Heather M; Lewis, Richard Kurt; Finley, Jamie M; Schumock, Glen T.

doi:10.1345/aph.1d481

Cited by 74 publications

(56 citation statements)

References 44 publications

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“…At present, there is only one national or international consensus guideline for the management of AHF (66). An accurate and rapid diagnosis of AHF is important to the timely institution of appropriate therapy and to improve clinical outcomes (67)(68)(69), and is based on a careful evaluation of symptoms and clinical findings, supported by appropriate investigations such as electrocardigraphy, chest radiography and, if available, echocardiography and biomarkers. It is important to classify patients based on the presence or absence of congestion and signs of low cardiac output and impaired tissue perfusion to administer the appropriate therapy (70,71).…”

Section: Recommendationsmentioning

confidence: 99%

See 1 more Smart Citation

Canadian Cardiovascular Society consensus conference recommendations on heart failure 2006: Diagnosis and management

Arnold¹,

Liu²,

Demers³

et al. 2006

Canadian Journal of Cardiology

363

256

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Section: Recommendationsmentioning

confidence: 99%

“…Nesiritide, a peptide identical to human BNP, has been studied in clinical trials but is not available in Canada. Emerging data suggest that early initiation of IV vasoactive therapy reduces the subsequent length of hospital stay (67,68).…”

Section: Vasodilatorsmentioning

confidence: 99%

Canadian Cardiovascular Society consensus conference recommendations on heart failure 2006: Diagnosis and management

Arnold¹,

Liu²,

Demers³

et al. 2006

Canadian Journal of Cardiology

363

256

View full text Add to dashboard Cite

“…[5][6][7] Hospitalization is recommended for patients with evidence of severely decompensated heart failure, dyspnea at rest, hemodynamically significant arrhythmias, and acute coronary syndromes and should be considered in patients with worsening congestion, major electrolyte abnormalities, associated comorbid conditions, and repeated implantable cardioverter-defibrillator firings. 8 However, correctly identifying ADHF at the time of hospital presentation can be challenging.…”

Section: Recognition Of Adhfmentioning

confidence: 99%

“…4 The first guideline to specifically address the management of ADHF was published in 2004. 5 These guidelines, a consensus statement based on expert panel review of the available literature, were created to improve treatment at member hospitals of a national group purchasing organization and focused only on the initial 24 hours of care. They had 2 important components.…”

Section: Therapymentioning

confidence: 99%

Hospitalized patients with acute decompensated heart failure: Recognition, risk stratification, and treatment review

Amin¹

2008

J. Hosp. Med.

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Acute decompensated heart failure (ADHF) has emerged as a major healthcare problem. It causes approximately 3% of all hospitalizations in the United States, with the direct medical cost of these hospitalizations estimated at $18.8 billion per year. Early recognition, risk stratification, and evidence-based treatment are crucial in reducing the morbidity, mortality, and costs associated with this disorder. Classic signs and symptoms of ADHF, such as rales, dyspnea, and peripheral edema, may be absent at hospital presentation and, even when present, are not specific to this disorder. As a result, serum B-type natriuretic peptide level is now used to rapidly and accurately detect ADHF. Multivariate analyses have identified renal dysfunction, hypotension, advanced age, hyponatremia, and comorbidities as significant and independent mortality risk factors. Based on these factors, mortality risk can be stratified from very low to very high using published algorithms that have been validated in independent populations. Evidence-based guidelines for the treatment of ADHF are available from both the European Society of Cardiology and the Heart Failure Society of America. In general, an intravenous loop diuretic, either alone or in combination with a vasodilator, is recommended as initial therapy in patients with volume overload, depending on the patient's clinical status. Use of inotropic agents should be limited to the small subset of patients with low-output syndrome and significant hypotension. In any event, frequent monitoring of clinical response is essential, with subsequent therapy determined by this response. Finally, focused patient education during hospitalization may help reduce readmissions for ADHF. Journal of Hospital Medicine 2008;3(Suppl 6):S16-S24. V

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“…2 -6 More recently, nesiritide, a recombinant human B-type natriuretic peptide (hBNP), has been proposed as an agent that may improve loop diuretic effect. 7 The premise for this empiric use of nesiritide as adjunctive diuretic therapy includes its demonstrated vasodilatory and neuroinhibitory effects, with the latter being marked by reductions in both plasma aldosterone and plasma renin activity. 8 -10 However, the impact of combination therapy with furosemide and nesiritide on urine output and neurohormonal activation in humans with heart failure (HF) has yet to be rigorously investigated in a randomized clinical trial.…”

Section: Introductionmentioning

confidence: 99%

Natriuretic and Neurohormonal Responses to Nesiritide, Furosemide, and Combined Nesiritide and Furosemide in Patients With Stable Systolic Dysfunction

Sica

Oren

Gottwald

et al. 2010

Clinical Cardiology

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Background: In patients with heart failure, few data describe the neurohormonal response to nesiritide and furosemide either alone or in combination. This study systematically compared the effects of nesiritide, furosemide, and their combination on natriuresis/diuresis and plasma aldosterone in patients with chronic stable heart failure who were relatively diuretic resistant. Hypothesis: Natriuretic, diuretic, and neurohormonal responses to furosemide and nesiritide will differ when these agents are administered alone vs. in combination. Methods: Twenty-eight subjects completed a multicenter, open-label, three-arm crossover study. Each subject received the following treatments in random order on alternate days: (1) furosemide, 40 mg intravenousbolus; (2) nesiritide, 2 μg/kg intravenous bolus followed by a 0.01 μg/kg/min infusion for 6 hours; (3) both furosemide and nesiritide, with furosemide given at least 15 minutes after initiation of nesiritide. Results: Plasma aldosterone increased by 2.2 ± 1.6 ng/dL after furosemide alone, decreased by 3.9 ± 1.6 ng/dL after nesiritide alone (P = 0.005 vs furosemide alone and P = 0.56 vs furosemide plus nesiritide), and decreased by 2.8 ± 1.6 ng/dL after furosemide plus nesiritide (P = 0.02 vs furosemide alone). Conclusions: Furosemide alone produced natriuresis/diuresis and a prompt rise in plasma aldosterone values. Nesiritide alone produced no significant natriuresis/diuresis,but decreased plasma aldosterone values. When furosemide was administered on a background of nesiritide infusion, the observed natriuresis/diuresis was similar to that seen with furosemide alone, without the anticipated increase in plasma aldosterone observed with furosemide alone.

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Guidelines for Acute Decompensated Heart Failure Treatment

Cited by 74 publications

References 44 publications

Canadian Cardiovascular Society consensus conference recommendations on heart failure 2006: Diagnosis and management

Canadian Cardiovascular Society consensus conference recommendations on heart failure 2006: Diagnosis and management

Hospitalized patients with acute decompensated heart failure: Recognition, risk stratification, and treatment review

Natriuretic and Neurohormonal Responses to Nesiritide, Furosemide, and Combined Nesiritide and Furosemide in Patients With Stable Systolic Dysfunction

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