The American Journal of Medicine (2007) 120, 121-127 REVIEW Diagnostic and Therapeutic Approach to Acute Decompensated Heart Failure John R Kapoor, MD, PhD,a Mark A Perazella, MD, FACPb a Division of Cardiology, Department of Medicine, Stanford University School of Medicine, Stanford, Calif, and bSection of Nephrology, Department of Medicine, Yale University School of Medicine, New Haven, Conn ABSTRACT Heart failure afflicts large numbers of patients and is the leading cause for hospitalizations in the United States Diagnosis and management of decompensated heart failure present a clinical challenge, requiring complex decision-making History and physical examination findings are important in the diagnosis of heart failure Diagnostically, B-type natriuretic peptide levels appear very useful to separate cardiac from noncardiac causes of dyspnea and provide information about heart failure severity and prognosis Immediate management goals include improvement of symptoms and hemodynamic parameters Diuretics, vasodilators, and inotropic agents are useful in the acute setting This article provides a systematic approach to the diagnosis and management of acute decompensated heart failure © 2007 Elsevier Inc All rights reserved KEYWORDS: Heart failure; Diuretics; Dobutamine; Nesiritide; B-type natriuretic peptide Heart failure affects 4-5 million people in the United States, more than 500,000 new cases are diagnosed annually, resulting in substantial morbidity and mortality.1 Heart failure prevalence increases with age, occurring in up to 10% of patients over age 75 years It is the leading cause for hospitalizations in the United States, with over million each year.2 Heart failure hospitalizations increased approximately 150% over the last 20 years More than 80% of emergency department visits for heart failure result in hospitalization, and approximately 50% of these were hospitalized in the prior months High inpatient and postdischarge mortality rates, approaching 5% and 10%, respectively, are noted.1,3 It is estimated that 50% of such patients die within years of diagnosis Frequent hospitalizations and return visits for heart failure result in an enormous economic burden, including disability, direct medical costs, and lost employment It is the most expensive diagnosis to have, with costs exceeding those of combined lung and breast cancers, and twice that Requests for reprints should be addressed to Mark A Perazella, MD, FACP, Section of Nephrology, Department of Medicine, Yale University School of Medicine, FMP 107, 330 Cedar Street, New Haven, CT, 06511 E-mail address: mark.perazella@yale.edu 0002-9343/$ -see front matter © 2007 Elsevier Inc All rights reserved doi:10.1016/j.amjmed.2006.05.066 for combined myocardial infarction and cancer treatment Hospitalizations cost nearly $25 billion yearly and account for approximately 60% of total costs for heart failure.1,3 A hospital loses an estimated $1300 per patient admitted for this diagnosis.4 Great emotional and physical burden of hospitalization among patients and their families also occurs Effective management of acute decompensated heart failure is paramount in reducing length of stay, revisits, complications, and expenditures Guidelines abound for treatment of acute coronary syndrome and chronic congestive heart failure Although national guidelines for treatment of acute decompensated heart failure exist, clear consensus and guidance for drug therapy is lacking Review of recently published studies on acute decompensated heart failure serves to guide formulation of an effective approach DIAGNOSIS Assuring the correct diagnosis of acute decompensated heart failure is a clinical challenge Surveyed physicians were uncertain about the diagnosis in approximately 60% of cases; the misdiagnosis rate is as high as 10%-20%.5,6 A carefully completed history and physical examination is the 122 The American Journal of Medicine, Vol 120, No 2, February 2007 cornerstone of diagnosis Symptoms of worsening fluid reis variably present depending on the degree of volume tention or decreasing exercise tolerance related to increasing overload left or right ventricular filling pressures are often present Although a good history and physical examination are They are usually attributable to depressed cardiac output key to diagnosis and useful for providing prognostic infor(fatigue, cool extremities), elevated right-sided (nausea, mation,12 alone they are insufficient Diagnostic studies bloating) and elevated left-sided such as the electrocardiogram, filling pressures (dyspnea, orthopchest radiographs, and laboratory nea) The Framingham Heart Failtests (B-type natriuretic peptide CLINICAL SIGNIFICANCE ure criteria are useful for identifyassay, chemistry panel and coming chronic heart failure but are plete blood count) are used to sup● Acute decompensated heart failure is a less helpful for identifying acute port the diagnosis Electrocardiohighly morbid complication, which is asdecompensated heart failure (Tagram is usually abnormal (not sociated with prolonged hospitalizable 1) Orthopnea has the highest specific for heart failure) and may tions, excessive costs, and increased sensitivity (ϳ90%) for elevated reveal Q-waves, left ventricular hospital mortality rates pulmonary capillary wedge preshypertrophy, ST-T wave changes sures, but its specificity remains a and bundle branch block Cardio● History and physical examination, along problem.7 A history of previous megaly, interstitial and alveolar with directed imaging and laboratory heart failure has the best predicedema along with pleural effutesting, are useful to categorize patients tive value Potential precipitants sions may be demonstrable on with acute decompensated heart failure, such as ischemia, progressive left chest radiograph However, up to allowing a rational approach to therapy 20% of patients with acute decomventricular dysfunction, medical pensated heart failure may lack noncompliance, dietary indiscre● Patients with acute decompensated congestion on chest radiograph, tions, high-dose beta-blockers, arheart failure manifested clinically as volespecially those with end-stage rhythmias, hypertension, pulmoume overload are treated initially with heart failure.7 Increased wall nary hypoxemia, and alcohol intravenous diuretics, and in more seintake should be investigated stress results in localized areas of vere cases, intravenous vasodilators in Identification of potential culprit ischemia and troponin elevathe absence of severe hypotension etiologies forms the basis for a tions, despite patent coronary artargeted approach to treatment teries.13 Evidence supports that ● Patients with hypotensive heart failure Past medical records should be retroponin elevations have prognosor a low cardiac output state may require viewed carefully, especially for tic value.14 intravenous inotropic therapy with dorelated comorbidities (chronic Capitalizing on the known role butamine or milrinone (patients on obstructive pulmonary disease, of neurohormones in the pathobeta-blockers) diabetes) and possible inciting physiology of heart failure, assays medications (nonsteroidal anti-infor B-type natriuretic peptide flammatory drugs).8 (BNP) are valuable adjuncts to Carefully performed physical examination adds imporclinical data Pro-BNP is produced in response to increased tant clues to the diagnosis Examination relies on findings ventricular wall stress It is cleaved to an inactive N-termiresulting from changes in filling pressures and end organ nal brain natriuretic peptide (NT-pro BNP) and the active perfusion; and can be used not only for initial assessment, C-terminal, BNP.15 Both peptides serve as markers of heart but also to monitor response to treatment These findings, failure Both BNP and NT-proBNP have similar diagnostic however, can underestimate the severity of hemodynamic test characteristics and are most useful with an intermediate abnormalities Rales and wheezing may be present during pretest likelihood of disease.16 BNP assays have higher acute decompensation but are often absent in chronic heart sensitivity compared with NT-BNP assays, which have failure because of compensatory increased lymphatic drainhigher specificity Thus, BNP assays exclude heart failure, age.7 Increased pulmonary component of the second heart whereas NT-BNP assays have better positive predictive sound (P2) heard along the lower left sternal border reflects value.17 elevations in pulmonary capillary wedge pressure The most Increased BNP levels correlate with New York Heart specific signs of decompensated heart failure are elevated Association (NYHA) Functional Class, implying that levels jugular venous pressures and an S3 gallop (specificity, 95% correlate with congestive heart failure severity Changes in and sensitivity, 20%).9 Elevated jugular venous pressures BNP levels also correlate with changes in pulmonary capprimarily reflect elevated right-sided filling pressures, illary wedge pressures.18 Using a BNP cutoff of 100 pg/mL 10 which are associated with increased left-sided pressures in patients presenting to the emergency department with The abdominojugular reflux enhances the sensitivity and dyspnea, the BNP assay has a diagnostic sensitivity of 90% specificity (Ͼ80%) of jugular venous distension.11 A third and a specificity of 76%.19 Patients without heart failure heart sound suggests left ventricular dysfunction, which secrete low levels of BNP (Ͻ100 pg/mL) Levels in the Kapoor and Perazella Acute Decompensated Heart Failure Table Framingham Criteria for the Diagnosis of Chronic Heart Failure (CHF)* Major criteria Paroxysmal nocturnal dyspnea Neck vein distension Rales Cardiomegaly on chest radiograph Pulmonary edema on chest radiograph S3 gallop Central venous pressureϾ16 cm H2O Hepatojugular reflux Weight loss Ͼ4.5 kg in days in response to treatment Minor criteria Bilateral ankle edema Night-time cough Dyspnea on ordinary exertion Hepatomegaly Pleural effusion Heart rate Ͼ120 beats/min Decrease in vital capacity by one third from maximum recorded *The diagnosis of heart failure requires that major or major and minor criteria be present (Adapted from McKee PA, et al N Engl J Med 1971;285:1441-1446) range of 100-200 pg/mL are seen for class I heart failure patients, and may increase Ͼ700 pg/mL in class IV heart failure Marked increases in BNP levels over baseline values or levels Ͼ400 pg/mL are seen in acute decompensated heart failure BNP levels in dyspneic patients presenting in the emergency department also have prognostic value.20 They predict risk for future cardiovascular events, whereas decreases in levels during hospitalization are associated with lower rates of death and 30-day readmissions In fact, BNP levels at discharge are predictive of survival (Figure 1).21 Although rapid BNP assays are useful diagnostically, certain caveats remain Elevated levels occur in noncardiac conditions, including chronic kidney disease, acute pulmonary embolism, and pulmonary hypertension.19 Higher levels are seen with older age and in women compared with men, and are affected by certain drugs.16 There is substantial interassay and intraindividual variation in BNP levels, such that only serial measurements revealing a 100% change are considered significant.22 Notwithstanding such limitations, BNP should be used in the context of other previously reviewed clinical and diagnostic data Along with clinical assessment, the rapid BNP assay reduces the number of hospital admissions, decreases length of stay, and reduces costs in patients presenting with dyspnea.23 123 tilation decreases pulmonary edema, because increases in intrathoracic pressure decrease venous return Symptomatic treatment strategies, namely relief of dyspnea and exercise intolerance, are mainstays of acute therapy in the decompensated patient Intravenous diuretics, vasodilators, and inotropes are used to achieve these goals Morphine decreases sympathetically mediated vasoconstriction, leading to vasodilation and, therefore, a fall in cardiac filling pressures.24 Reversible etiologies for decompensation should be rapidly addressed DIURETICS Because patients with acute decompensated heart failure present with signs of circulatory congestion, intravenous diuretic therapy is first-line therapy Loop diuretics relieve volume overload by promoting a net diuresis by inhibiting sodium reabsorption in the loop of Henle Greater diuresis is achieved with loop diuretics when compared with distalacting diuretics because of their proximal site of action in the kidney Diuretics should be administered as an intravenous bolus to ensure maximal bioavailability and to circumvent decreases in oral absorption due to gastrointestinal edema Dosing recommendations are not based on randomized clinical trials and are largely empiric Intravenous bolus doses of furosemide can be as high as 180-360 mg; patients with kidney failure require such high doses.25 Caution should be exercised in patients with hypotension The effectiveness of administered diuretic therapy is gauged on the basis of symptomatic improvement and urine output Typically, Ͼ250-500 cc of urine output is expected within the first several hours, depending upon underlying kidney function.25 Repeat boluses of furosemide in higher doses may be required if urine output is inadequate Continuous infusion of furosemide, addition of a diuretic that acts at THERAPEUTIC APPROACHES Attention should first be directed to the ABCs of airway, breathing, and circulation in patients with acute pulmonary edema Supplemental oxygen, noninvasive positive pressure ventilation, and mechanical ventilation are considered for hypoxemic and hypercarbic patients Positive pressure ven- Figure Cumulative hospitalization-free survival according to NT-proBNP plasma level at discharge (median, 4137.0 pg/mL) (With permission, Bettencourt P, et al Circulation 2004;110: 2168-2174) 124 The American Journal of Medicine, Vol 120, No 2, February 2007 another site (thiazide-type), or addition of vasodilators or positive ionotropic agents may be necessary to overcome diuretic resistance in the late stages of heart failure or advanced kidney disease.26,27 Renal function and electrolytes should be monitored during diuresis Loop diuretics can promote prerenal azotemia, cause orthostatic hypotension, and decrease tolerability to angiotensin-converting enzyme (ACE) inhibitors Renal failure following diuretics predicts worsening outcomes.28 Diuresis can furthermore result in hypokalemia, hypocalcemia, hypomagnesemia, and a metabolic alkalosis, increasing arrhythmia risk By decreasing plasma volume, loop diuretics also increase neurohormonal activation, which may paradoxically worsen heart failure Intravenous loop diuretics also produce an initial increase in pulmonary capillary wedge pressure and systemic vascular resistance.29 Studies have linked diuretics to increased mortality.30,31 Data from the Acute Decompensated Heart Failure National Registry (ADHERE) reveal an association between intravenous diuretic use and higher in-hospital mortality and longer length of stay both in hospitals and in intensive care units.32 Further research is required before definitive conclusions can be made about the safety of diuretics Moderate to severe volume overload states or low cardiac output states may not adequately respond to aggressive diuretic management These situations necessitate use of more aggressive pharmacologic regimens Specifically, the additional use of vasoactive drugs, such as vasodilators and inotropes should be strongly considered VASODILATORS Patients demonstrating an inadequate response to diuretic therapy as evidenced by continued symptomatic deterioration (increased oxygen requirements, fatigue), congestion (orthopnea, jugular venous distension, rales, S3 gallop, edema) and preserved perfusion (warm extremities) are classified as “warm and wet” (Figure 2).33 Such patients are moderately to severely volume-overloaded with elevated left ventricular filling pressures and require more aggressive treatment with vasodilators provided they have adequate systolic blood pressure Symptomatic patients with hypertension may also benefit from vasodilator use Nitroglycerin and Nitroprusside Nitroglycerin and nitroprusside act on arterial and venous smooth muscle to increase levels of cGMP, resulting in vasodilation This effect reduces preload, myocardial oxygen consumption, systemic vascular resistance, and the workload of the ventricles, thus increasing the efficiency of cardiac function, cardiac index, and stroke volume They also reduce harmful neurohormones, such as norepinephrine.34 At low doses, nitroglycerin increases the capacity of the venous system and, thus, decreases ventricular filling pressures and volume Nitroglycerin also decreases coronary vascular resistance, further augmenting perfusion to a failing heart At higher doses, nitroglycerin reduces after- Figure Description of hemodynamic profiles based on evidence of resting congestion or hypoperfusion Most ‘B’ patients (Wet and Warm) require only diuresis in addition to their regular regimen of ACE inhibitors and digoxin ‘C’ patients (Cold and Wet) in general cannot be effectively ‘dried out’ until they have ‘warmed up’, usually with monitored vasodilation, rarely requiring inotropic therapy as well ‘L’ patients, if correctly classified with low resting cardiac output without congestion (Cold and Dry), are generally comfortable at rest but have no cardiac reserve or exercise capacity Adjustment of the oral regimen for L patients is unlikely to yield direct improvement, although chronic therapy with beta-blockers, if tolerated, or amiodarone will, in some cases, improve function after several months (With permission, Stevenson LN Eur J Heart Fail 1999;1:251-257) load by affecting arterial resistance Nitroglycerin is very effective in treating acute decompensated heart failure, and is the preferred nitrate given its lower toxicity profile It is limited by frequent titration requirement and the rapid emergence of tachyphylaxis with high doses or long infusions.35 Headache (20%) and dose-dependent hypotension (5%) are also adverse effects These characteristics necessitate intensive care monitoring Although infrequently used, nitroprusside is an effective vasodilator that rapidly reduces systemic vascular resistance It dilates both venous and arterial vessels at all doses Small studies have demonstrated that it decreases PCWP, increases diuresis and natriuresis, increases cardiac output, improves renal function, and in conjunction with diuretics, decreases neurohormonal activation.36,37 There are several concerns with use of nitroprusside In patients with left ventricular failure after an acute myocardial infarction, nitroprusside reduced survival at 13 weeks when initiated Ͻ9 hours after the onset of pain, but improved survival when initiated after this time period.38 The truncated survival in patients suffering from myocardial infarction may be due to the shunting of blood away from ischemic areas following vasodilation in nonischemic areas.39 Another concern is cyanide and thiocyanate toxicity (with renal or hepatic dysfunction) Hypotension with reduced coronary perfusion in patients with coronary artery disease is another concern Nitroprusside is best used in an intensive care unit with invasive monitoring Kapoor and Perazella Acute Decompensated Heart Failure 125 Figure Kaplan-Meier estimate of mortality Circles ϭ dobutamine (n ϭ 58); squares ϭ nesiritide 0.6 g/kg 0.030 g/kg per (n ϭ 100); triangles ϭ nesiritide 0.3 g/kg 0.015 g/kg per (n ϭ 103) (With permission, Silver MA, et al J Am Coll Cardiol 2002;39:798-803) Brain Natriuretic Peptide (Nesiritide) Nesiritide is a 32-amino acid synthetic BNP that induces beneficial hemodynamic and neurohormonal effects in heart failure patients Receptor engagement by nesiritide increases cGMP, which in turn results in dilation of arterial and venous beds, unloading the heart by decreasing right atrial pressure and systemic vascular resistance, and leading to reflex increases in cardiac output and cardiac index.40 Nesiritide has desirable effects on the disturbed neurohormonal mileu, decreasing levels of aldosterone, angiotensin II, norepinephrine, and endothelin.41 Administration does not require invasive monitoring, and nesiritide is not associated with tachyphylaxis or drug toxicity Nesiritide improves patient symptoms when compared with either nitroglycerin or placebo.42,43 It improves patient-assessed dyspnea and exhibits a trend in the reduction Table Therapeutic Goals in Acute Heart Failure Syndromes Stabilization phase (early management) Improve symptoms Blood pressure control in hypertensive patients Improve PCWP and CO without causing: Decreased coronary perfusion (hypotension) Myocyte damage (ischemia, necrosis, apoptosis) Further kidney dysfunction Arrhythmias (including increased heart rate) Achieve euvolemia Implementation phase Administer life-saving therapies (eg, ACE-inhibitor, betablockers, aldosterone-receptor antagonists, ICD, etc) ACE ϭ angiotensin-converting enzyme; CO ϭ cardiac output; ICD ϭ implantable cardiac defibrillator; PCWP ϭ pulmonary capillary wedge pressure (Reproduced with permission, Gheorghiade et al Am J Cardiol 2005;96(suppl):11G-17G) of rates of hospital re-admission within 30 days when compared with placebo.44 Dyspnea, 6-month mortality, and rehospitalization rates were similar to that of nitroglycerin.45 Nesiritide causes less adverse effects when compared with nitroglycerin, but hypotension is similar between the drugs.45 Nesiritide decreases mortality rates when compared with dobutamine in acute decompensated heart failure.46 Nesiritide therapy is limited by high cost, hypotension, and recent concerns that it worsens kidney function and decreases survival at 30 days.47,48 The survival disadvantage may be due to induction of kidney failure, which is associated with poor outcomes in acute decompensated heart failure Patients with aortic stenosis, hypertrophic cardiomyopathy, or cardiogenic shock are not candidates for nesiritide Large prospective trials are needed to further assess nesiritide’s effect on outcomes INOTROPIC AGENTS Patients with decreased urine output, cool extremities, narrow pulse pressure, prerenal physiology, and altered mental status are likely suffering from low cardiac output This represents Ͻ1% of all presentations.49 Inotropic therapy should be considered in patients with this “cool and dry” type of heart failure Dobutamine and milrinone usually produce short-term symptomatic and hemodynamic improvement.50 Dobutamine increases cardiac output by stimulating cardiac beta-receptors This increases pulse and blood pressure, without significantly lowering filling pressure It also increases myocardial oxygen demand and may induce arrhythmias Several small studies report improved hemodynamics with dobutamine use in acute decompensated heart failure.51,52 Milrinone improves cardiac output by increasing intracellular concentrations of cAMP through its ability to inhibit phosphodiesterase activity It also 126 The American Journal of Medicine, Vol 120, No 2, February 2007 lowers central filling pressures and may precipitate hypotension When patients with acute decompensated heart failure have low cardiac output and low blood pressure (systolic blood pressure Ͻ90 mm Hg), therapy with dobutamine or milrinone should be started Initial use of a peripheral vasoconstrictor may be necessary to prevent severe hypotension Patients on chronic beta-blocker therapy, with low cardiac outputs, should receive milrinone, because its effect would not be abrogated by beta-blocker therapy.53,54 Because dobutamine acts on cardiac beta-receptors, it would be a poor choice in this circumstance as beta-blockers would offset beneficial cardiac effects Either milrinone or dobutamine could be used in normotensive patients without beta-blocker therapy Although the short-term benefits of inotropic therapy should be evident, there are increasing lines of evidence for worsened patient outcomes.55 Milrinone increased the incidence of sustained hypotension, as well as new atrial and ventricular arrhythmias, worsened heart failure, and showed an increased trend in the number of in-hospital deaths at 60 days (10.3% milrinone vs 8.9% placebo, P ϭ 41).56,57 Furthermore, milrinone did not improve length of stay or readmission rates Dobutamine increased risk of adverse clinical events and was an independent predictor of death (Figure 3).58,59 Dobutamine also increased ventricular ectopy when compared with nesiritide.60 Inotropic therapy is therefore not routinely recommended for acute decompensated heart failure, as the risks appear to outweigh the benefits It may, however, be used short-term in patients with low cardiac output states or where there is associated cardiogenic shock These agents are also approved as a bridge for cardiac transplantation and for palliation in stage IV heart failure CONCLUSIONS Acute decompensated heart failure presents a challenge to the clinician that usually requires complex decision-making The diagnosis requires a thorough history and physical examination, often with adjunctive tests Immediate management goals include improvement of symptoms and hemodynamic parameters (Table 2) Current treatment standards demonstrate beneficial effects on both parameters, although effects on long-term mortality are lacking Future studies need to better address how to reduce readmission rates and decrease overall mortality Effective neurohormonal antagonism with ACE-inhibitors/angiotensin receptor blocker and beta-blockers might prevent cardiac and renal deterioration during acute decompensated heart failure Finally, newer investigational agents including calcium sensitizers, vasopressin antagonists, and adenosine 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advanced heart failure: insights from the Flolan International Randomized Survival Trial (FIRST) Am Heart J 1999;138:78-86 60 Burger AJ, Horton DP, LeJemtel T, et al Effect of nesiritide (B-type natriuretic peptide) and dobutamine on ventricular arrhythmias in the treatment of patients with acutely decompensated congestive heart failure: the PRECEDENT study Am Heart J 2002;144:1102-1108 ... Electrocardiohighly morbid complication, which is asdecompensated heart failure (Tagram is usually abnormal (not sociated with prolonged hospitalizable 1) Orthopnea has the highest specific for heart... a and bundle branch block Cardio● History and physical examination, along problem.7 A history of previous megaly, interstitial and alveolar with directed imaging and laboratory heart failure has... IV heart failure CONCLUSIONS Acute decompensated heart failure presents a challenge to the clinician that usually requires complex decision-making The diagnosis requires a thorough history and