Acute Heart Failure Syndromes: Emergency Department Presentation, Treatment, and Disposition: Current Approaches and Future Aims
2010; Lippincott Williams & Wilkins; Volume: 122; Issue: 19 Linguagem: Inglês
10.1161/cir.0b013e3181f9a223
ISSN1524-4539
AutoresNeal L. Weintraub, Sean P. Collins, Peter S. Pang, Phillip D. Levy, Allen S. Anderson, Cynthia Arslanian‐Engoren, W. Brian Gibler, James McCord, Mark B. Parshall, Gary S. Francis, Mihai Gheorghiade,
Tópico(s)Gastroesophageal reflux and treatments
ResumoHomeCirculationVol. 122, No. 19Acute Heart Failure Syndromes: Emergency Department Presentation, Treatment, and Disposition: Current Approaches and Future Aims Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplemental MaterialFree AccessResearch ArticlePDF/EPUBAcute Heart Failure Syndromes: Emergency Department Presentation, Treatment, and Disposition: Current Approaches and Future AimsA Scientific Statement From the American Heart Association Neal L. Weintraub, Sean P. Collins, Peter S. Pang, Phillip D. Levy, Allen S. Anderson, Cynthia Arslanian-Engoren, W. Brian Gibler, James K. McCord, Mark B. Parshall, Gary S. Francis, Mihai Gheorghiade and on behalf of the American Heart Association Council on Clinical Cardiology and Council on Cardiopulmonary, Critical Care, Perioperative and Resuscitation Neal L. WeintraubNeal L. Weintraub , Sean P. CollinsSean P. Collins , Peter S. PangPeter S. Pang , Phillip D. LevyPhillip D. Levy , Allen S. AndersonAllen S. Anderson , Cynthia Arslanian-EngorenCynthia Arslanian-Engoren , W. Brian GiblerW. Brian Gibler , James K. McCordJames K. McCord , Mark B. ParshallMark B. Parshall , Gary S. FrancisGary S. Francis , Mihai GheorghiadeMihai Gheorghiade and on behalf of the American Heart Association Council on Clinical Cardiology and Council on Cardiopulmonary, Critical Care, Perioperative and Resuscitation Originally published11 Oct 2010https://doi.org/10.1161/CIR.0b013e3181f9a223Circulation. 2010;122:1975–1996Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: October 11, 2010: Previous Version 1 With a prevalence of 5 800 000 (≈2% of the entire populace) in 2009 and an estimated yearly incidence of 550 000, the burden of heart failure (HF) in the United States is tremendous.1 Although HF is largely a condition defined by chronic debility, virtually all patients experience, at some point, acute symptoms that trigger a visit to the emergency department (ED). These symptoms may vary in severity but, for the most part, they necessitate early intervention, often with intravenous medication and, less frequently, respiratory support. As shown by combined data from the National Ambulatory Medical Care Survey (NAMCS) and the National Hospital Ambulatory Medical Care Survey (NHAMCS), this is a common occurrence; there are nearly 658 000 annual ED encounters primarily for acute HF in the United States—a figure that represents almost 20% of the total HF-specific ambulatory care delivered each year.2It is noteworthy that few settings other than the ED can offer open access to treatment or provide the level and intensity of care required to effectively manage the acute phase of decompensation, also referred to as episodes of acute heart failure syndromes (AHFS). Nearly 80% of those treated for AHFS in the ED are ultimately admitted to the hospital and, accordingly, the ED serves as the principal portal of entry for hospitalized AHFS patients.34 The ED therefore plays a unique role in the continuum of AHFS treatment, functioning for most patients as the initial point of definitive healthcare contact, the location where primary stabilization is achieved, and the site where disposition decisions are generally made.4 Whereas the ED is a pivotal place for the vast majority of hospitalized patients with acute HF, the evidence base on which this foundation of acute care is built is astonishingly thin. The purpose of this scientific statement, therefore, is to describe current standard practice for HF clinicians, to highlight the knowledge gaps that are present, and to serve as a call to action for ED-based research as a future endeavor for those with a vested interest in AHFS care.The need for improvement in our approach to AHFS management was recognized in the recently published 2009 Focused Update to the 2005 American College of Cardiology (ACC)/American Heart Association (AHA) Guidelines for the Diagnosis and Management of Heart Failure in Adults. For the first time recommendations relevant to the hospitalized AHFS patient were included.5 Developed using guideline methodology standardized by the ACC/AHA (Table 1),6 these recommendations represent an important step forward in the ongoing effort to optimize the care of patients with AHFS. With respect to the ED several key points warrant mention: (1) the included procedures and treatments represent a combination that target acute (24 to 48 hours) and subacute (≥48 hours) stages of AHFS and are not specific to the immediate management; (2) although they provide general guidance for treatment, there is limited direction for the care of particular subgroups or phenotypes commonly seen in the ED setting, especially those who have acute hypertension with fluid redistribution rather than excess accumulation7; (3) potential applicability of critically important acute interventions typically initiated in the ED, such as noninvasive ventilatory measures8 and endotracheal intubation, are not discussed; (4) there is no consideration of risk stratification or proposal to provide objective measures for disposition decision making, which has crucial bearing on resource utilization, in particular, for those patients whose condition may be amenable to a short-term, observation stay; and (5) the vast majority of recommendations are considered class I, yet, overall, and in contrast to those presented in the sections for chronic management, only one was based on level A evidence. This final point is perhaps the most pressing and serves to highlight a critical limitation in the quest to develop data-driven, best-practice approaches to the care of AHFS patients in the ED.Table 1. Classification of Recommendations and Level of Evidence6Table 1. Classification of Recommendations and Level of Evidence6*Data available from clinical trials or registries about the usefulness/efficacy in different subpopulations, such as gender, age, history of diabetes, history of prior myocardial infarction, history of heart failure, and prior aspirin use. A recommendation with Level of Evidence B or C does not imply that the recommendation is weak. Many important clinical questions addressed in the guidelines do not lend themselves to clinical trials. Even though randomized trials are not available, there may be a very clear clinical consensus that a particular test or therapy is useful or effective.†In 2003, the ACCF/AHA Task Force on Practice Guidelines developed a list of suggested phrases to use when writing recommendations. All guideline recommendations have been written in full sentences that express a complete thought, such that a recommendation, even if separated and presented apart from the rest of the document (including headings above sets of recommendations), would still convey the full intent of the recommendation. It is hoped that this will increase readers' comprehension of the guidelines and will allow queries at the individual recommendation level.Reasons for the lack of definitive evidence for AHFS management are multifactorial but can be largely attributed to the absence of a cohesive research agenda among respective stakeholders. Whereas registry databases such as ADHERE (Acute Decompensated Heart Failure National Registry)9,10 and OPTIMIZE-HF (Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients With Heart Failure)11,12 have compiled important information on initial presentation and treatment, large-scale clinical trials, utilizing prospective data collection, have not been designed to recruit patients in the ED setting. Factors contributing to this include a long-standing difficulty establishing consensus on reasonable end points4 as well as a desire to ensure accurate diagnosis before enrollment. More importantly, there has been a misperception by HF specialists that identification and enrollment of ED patients is problematic.3 The net result is a lingering uncertainty with regard to the impact of early intervention on outcomes and de facto inclusion of patients who have refractory symptoms.3,4 The latter, in particular, may be responsible for the predominantly neutral findings associated with the majority of AHFS investigations that have been conducted to date.As highlighted in this Introduction, a paradigm shift in the clinical practice and investigative agenda surrounding AHFS is warranted. Sensing the urgency of this matter, the National Heart, Lung, and Blood Institute recently convened a multidisciplinary working group of individuals with expertise in AHFS management and tasked them with development of the Institute's future research focus for AHFS.13 Although the proceedings were published elsewhere, there was firm resolve among all participants regarding the need to improve the evidence base in AHFS by initiating study of these patients in the ED, and that a better understanding of AHFS could only be achieved through broad collaboration.Organization of Writing Group and Relationships With IndustryExperts in the subject of AHFS were selected and charged with examining subject-specific data and writing this scientific statement. The writing group performed a formal literature review and weighed the strength of evidence for or against existing treatments or procedures using established AHA statement and guideline methodology. Discussion of patient-specific modifiers, comorbidities, and issues of patient preference that might influence the choice of particular tests or therapies were considered, as were frequency of follow-up and cost-effectiveness. When available, information from studies on cost was considered; however, review of data on efficacy and clinical outcomes constituted the primary basis for any related recommendations. To ensure that any actual, potential, or perceived conflicts of interest were identified, all members of the writing group, as well as peer reviewers of the document, completed "Relationship with Industry" forms when the writing group was formed. Writing group members were also required to review and update their disclosure information before publication. The writing group used the "Methodology Manual for ACC/AHA Guideline Writing Committees"14 as a guide for developing this statement. Writing group and reviewer disclosures that are pertinent to this scientific statement are provided at the end of this statement.What Happens Currently in the ED: Diagnosis, Treatment, and Disposition?Diagnosis and treatment of AHFS in the ED is a clinical challenge that requires complex decision-making skills to achieve hemodynamic balance, improve functional capacity, and decrease mortality and length of stay.15–19 This difficult task is further compounded by the organizational structure and operations of most EDs, which tend to be better suited for rapid stabilization, treatment, and disposition of acute emergencies such as shock, arrhythmias, or ST-segment myocardial infarction, as opposed to the timely recognition and treatment of more subtle or complicated forms of AHFS which most often are related to decompensation of underlying, chronic HF.20 It may be easier to judge how seriously ill patients are when their baseline has deviated from a previously healthy state, than when their condition represents deterioration of a chronic illness that is protean in nature, especially when the emergency physician is unfamiliar with the patient.The ED phase of AHFS management concludes with a disposition decision (admit to ED observation unit, in-hospital telemetry unit, intensive care unit, or discharge to the outpatient environment).21 Because it is challenging to identify patients at risk for poor outcomes in the ED, including acute and 30-day adverse cardiac events,22 and because definitive resolution of symptoms is seldom achieved in the ED, 80% of patients who present to the ED with AHFS are hospitalized.23 At present, however, there is little evidence to guide disposition decisions, and imprecise risk stratification and uncertainty regarding the etiology of AHFS often prompts the decision to admit for further treatment and testing.21Current DiagnosticsThe evaluation of the patient in the ED with possible AHFS includes history, physical examination, chest radiography, 12-lead ECG, cardiac troponin testing (I or T), electrolytes, and a complete blood cell count. The chest radiograph remains a cornerstone for diagnostic testing, but can lack signs of congestion in over 15% of patients, thus limiting its ability as a screening tool.24 In select cases, liver and thyroid function tests may be considered. The natriuretic peptides b-type natriuretic peptide (BNP) and N-terminal (NT)-proBNP have demonstrated diagnostic utility in this patient population when clinical uncertainty remains after initial history, physical examination, and chest radiography. These biomarkers are generated from a prohormone released from cardiac myocytes in response to ventricular dilatation and pressure overload.25–27 After release from the cardiac myocyte, the prohormone proBNP is cleaved into BNP, which is metabolically active, and NT-proBNP, which is metabolically inactive. Both BNP and NT-proBNP are elevated in AHFS and the magnitude of marker elevation is correlated with severity of illness.28–32A large study that investigated the diagnostic utility of natriuretic peptides was the Breathing Not Properly trial which enrolled 1586 patients, and evaluated BNP measurement in ED patients with possible AHFS.28 Using a cutoff of 100 pg/mL, BNP had a sensitivity, specificity, negative predictive, and positive predictive value of 90%, 76%, 79%, and 89%, respectively. In this capacity, BNP is highly useful to exclude AHFS. In a multiple logistic regression analysis including history, physical examination, and chest x-ray findings, an elevated BNP was the strongest independent predictor of AHFS, with an odds ratio of 29.6 (95% confidence interval [CI] 17.75 to 49.37). In a secondary analysis from this study, BNP correctly classified 74% of the patients with an intermediate probability of AHFS.33 When BNP was added to clinical judgment after routine evaluation, the area under the receiver operating characteristic curve (AUC) rose significantly from 0.86 to 0.93 (P<0.0001). Similarly, a single-center investigation evaluated the diagnostic utility of NT-proBNP in the ED in 600 patients with dyspnea.31 The AUC rose from 0.90 to 0.96 when NT-proBNP was added to clinical judgment. The authors suggest a single cut point of 300 pg/mL to rule out AHFS, but 2 cut points to rule in AHFS depending on age: 450 pg/mL)and >50 years old (>900 pg/mL). Subsequent studies suggested even further delineation as follows: (1) either an age-independent cutoff of 900 pg/mL, or (2) the more accurate (but more complex) age-stratified approach of 450/900/1800 for patients aged 75 years.34,35 Other smaller studies have also demonstrated the diagnostic utility of BNP and NT-proBNP for AHFS.29,30,36,37The majority of studies suggest that BNP and NT-proBNP are of equal diagnostic utility. However, subtle differences in patient characteristics may favor one biomarker over the other. BNP and NT-proBNP both can be elevated in patients with renal insufficiency, which is more commonly found in older patients.38,39 Levels of NT-proBNP appear to be more affected by renal function.40 Four studies have directly compared the diagnostic utility of BNP and NT-proBNP.29,36,41,42 Both natriuretic peptides demonstrated similar accuracy in 3 studies, but in 1 study BNP was superior to NT-proBNP.42 The AUC for the diagnosis of AHFS was 0.80 for NT-proBNP and 0.85 for BNP, P 65 years old were enrolled, suggesting that BNP may be superior in older patients. This finding will need to be confirmed in other studies. The natriuretic peptides are particularly good at ruling out AHFS; the negative likelihood ratio of BNP at 100 pg/mL is 0.13,28 and of NT-proBNP at 300 pg/mL is 0.015.31 However, the positive likelihood ratio of the natriuretic peptides is more limited (3.8 and 3.1, respectively, for BNP and NT-proBNP) because they can be elevated in numerous conditions including sepsis, pulmonary hypertension, older age, renal insufficiency, atrial fibrillation, and pulmonary embolism.43–47 Obesity is actually associated with disproportionately low BNP levels.48 Mechanisms that have been postulated for these low BNP levels include reduced peptide synthesis and/or secretion in subjects with obesity; increased expression of natriuretic peptide clearance receptors in adipose tissue; and increased circulating neutral endopeptidases, which are secreted by adipocytes, may contribute to a lesser extent.49 Patients with a history of HF can have chronically elevated BNP or NT-proBNP levels. An elevation above their baseline, or dry weight level, may help identify a patient with AHFS. What constitutes a significant change above the baseline level in any particular patient is uncertain at the present time. Biological variability further complicates this situation. Studies suggest that BNP may need to change by at least 70% and NT-proBNP may need to change by 50% to identify a patient with a diagnostically meaningful change.50–53The clinical utility and resource utilization of BNP testing were evaluated in a single-center randomized trial of 453 patients with dyspnea in an ED in Switzerland.32 Two hundred twenty-five patients were randomly assigned to a standard diagnostic strategy, and 227 patients were randomly assigned to a standard diagnostic strategy plus BNP measurement. In comparison with the standard strategy, BNP testing led to reductions in the number of patients hospitalized (75% versus 85%, P=0.008), time to discharge (8.0 days versus 11.0 days, P=0.001), cost ($5410 versus $7264, P=0.006), and time to treatment (63 minutes versus 90 minutes, P=0.03) In a separate analysis from the same trial, the cost-effectiveness of BNP measurement in the ED was maintained at 180 days.54 However, the dramatically different lengths of stay compared with centers in the United States makes extrapolation of these results problematic. Another trial of 500 patients with dyspnea presenting to EDs in Canada randomly assigned 250 patients to a standard diagnostic strategy and 250 patients to a standard diagnostic strategy plus NT-proBNP measurement.55 The AUC of the emergency physician's diagnostic accuracy without knowledge of NT-proBNP results was 0.83 (95% CI 0.80 to 0.84), which increased to 0.90 (95% CI 0.90 to 0.93, P 140 mm Hg) and 2 normotensive (<140 mm Hg). Hypotension (<90 mm Hg) and cardiogenic shock are rare and make up less than 5% of ED presentations.12,65 Those who present with hypertension may appear to be the most acutely ill, but aggressive blood pressure management often results in rapid resolution of symptoms. More importantly, once their acute symptoms are adequately managed, patients presenting with hypertension often have 60- to 90-day mortality rates that are much lower than those who present with normotension.12,18,71,72 Although both of these subsets have signs and symptoms of pulmonary congestion, the actual mechanisms and volume status may differ. Traditional AHFS models describe fluid accumulation and acute symptoms as being almost synonymous. Recent data suggest that those patients who present with hypertension (ie, vascular crisis) may have congestion caused by a mismatch between rapidly increasing afterload and impaired systolic performance leading to volume redistribution.7,73–75 Nevertheless, both groups of patients present with similar symptoms and are often treated solely with intravenous diuretics despite differences in underlying pathophysiology and volume status.Further subcategorization can be made based on underlying etiologies and reasons for decompensation such as AHFS related to dietary and medication nonadherence, ischemia, worsening renal function, arrhythmias, or a concomitant pulmonary process.76 In select cases this may help direct further therapy such as anitarrhythmics; however, regardless of the etiology, the majority of patients are admitted to the hospital for further therapy targeting congestion reduction.12,77–79 Very few changes are made to medication regimens during hospitalization, and only a minority of patients receive a therapeutic procedure or device during their inpatient stay.80–82According to the recently completed URGENT (Ularitide Global Evaluation in Acute Decompensated Heart Failure) dyspnea study, the ED approach does improve overt symptoms of breathlessness in most patients by 6 hours.83 Yet, despite improvement in symptoms by 6 hours, registry data also suggest that only 50% of patients have complete resolution of their congestive symptoms at hospital discharge.11 Furthermore, there is little randomized evidence of the benefit of diuretics beyond symptomatic improvement, because randomized trials are nonexistent84 and signals increasingly point to the potential for induction of harm with both acute85,86 and chronic87 usage of diuretic medication. Previous studies of diuretics suggest not only an association with adverse outcomes, but also perhaps direct causality.71,86,–91 The development of in-hospital acute renal injury has been associated with increased in-hospital mortality.92–94 Although, for some, diuresis is important and appropriate, could the nearly universal application of homogeneous therapy to an inherently heterogeneous disorder negatively impact the high rates of short-term recidivism95 and mortality1 associated with AHFS?3,58AHFS has historically been viewed as a transient event, characterized primarily by systolic dysfunction, low cardiac output, and fluid overload. This pathophysiologic model has been thought to be applicable across all patient groups, varying only by degree of severity.96–98 Consequently, short-term treatment strategies such as intravenous diuretics, targeted at rapidly alleviating fluid congestion, were adopted without clinical trials evaluating long-term safety and efficacy. It is noteworthy that emerging data from several HF registries have largely challenged the traditional low cardiac output model exemplified by the prototypical male with ischemic heart disease, revealing a more complex and distinct group of pathophysiologic entities.77,78 Despite the heterogeneous clinical profiles outlined above, suggesting that targeted treatment may be beneficial, the majority of patients with AHFS are treated with homogeneous therapy, namely intravenous diuretics. A next logical step would be to determine whether select subsets of patients, classified via reliable objective measures after initial evaluation, would benefit from targeted therapy aimed at their risk profile, HF etiology, and reason for decompensation.Emergency Department Disposition Decision MakingThe majority of patients who present to the ED with AHFS are admitted to the hospital.99,100 This approach is largely due to the challenge of identifying ED patients at low risk for poor outcomes. Risk stratification of patients with AHFS is traditionally problematic, not only because of the patients' underlying HF, but also because of their multiple comorbidities. Further, even for patients who exhibit no objective markers of high risk, the subsequent inability to ensure close follow-up, provide bedside HF education, and address the importance of adherence to therapeutic recommendations makes direct ED discharge problematic.Those patients who present in extremis with significant dyspnea and elevated blood pressures may appear to be at the greatest risk for short-term adverse events. However, once acute symptoms are controlled their intermediate (30- to 60-day) risk of adverse events is low when compared with the cohort of patients with normal blood pressure who often present with less severe symptoms.12,18,101 Only a minority of patients manifest low-output signs such as diminished urine production or systemic hypoperfusion.12Other admission profiles associated with an increased risk of in-hospital mortality include AHFS related to myocardial infarction or ischemia, worsening renal function, or a concomitant pneumonia.76 Conversely, as many as one-third of patients decompensate because of medication or dietary nonadherence or as a result of poorly controlled hypertension. These individuals have a better short-term prognosis with a reduced risk of early mortality.102 Studies over the past decade have recurrently identified several variables and biomarkers as predictors of adverse events: (1) elevated blood urea nitrogen or creatinine, (2) hyponatremia, (3) ischemic electrocardiogram changes, (4) elevated natriuretic peptide levels, (5) elevated troponins, and (6) low systolic blood pressure.12,65,101,103,104–107 Markers of low-risk AHFS, however, have not been as well delineated. Preliminary work suggests an initial systolic blood pressure over 160 mm Hg and a normal initial cardiac troponin I as markers associated with a decreased risk of adverse events.22 In a large retrospective analysis of a statewide database that utilized recursive partitioning, 17% of ED patients were identified as low risk.108 This somewhat complex model also found systolic blood pressure, serum sodium, and creatinine serving to differentiate between low and high risk. This statistical model was subsequently validated in more than 8300 patients. The model had a negative likelihood ratio of 0.24 (0.18 to 0.32) for identification of 30-day mortality or serious complications.109Although markers of low-risk presentations have remained somewhat elusive, alternatives to hospitalization have also been investigated. Because the majority of hospitalizations originate from the ED, emergency physicians have considerable experience stabilizin
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