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Acutely Decompensated HeartFailure: Diagnostic andTherapeutic StrategiesYou start your shift. An elderly woman with shortness of breath has congestiveheart failure written all over her and her chart. She takes beta-blockers, an ACEinhibitor, and Lasix. She looks and sounds wet. She receives oxygen,furosemide, morphine, and nitrate therapy. When you return 20 minutes later, shelooks and feels much better. As you reach for the phone to speak with the admit-ting physician, you ask yourself, Do I need to get cardiac enzymes? She reallylooks so good nowdoes she even need to be admitted?
In the next room, you see an obese woman with shortness of breath, COPD,CAD, but no known history of CHF, and she does not take Lasix. Her lungssound wheezy and you hear crackles. Her legs are edematous and she describesorthopnea. Does she have a COPD exacerbation or new onset CHF? Should yousend a BNP level? Will her obesity affect this test?
The next evening you see a patient with severe CHF and an ejection frac-tion of 20%. Her family describes recent fatigue and progressive mild confusion.She is not edematous and her lungs are clear. Her creatinine has increased from2.5 to 3.2 g/dl. Is this a CHF exacerbation? What are your treatment options?Are ionotropes indicated?
Acutely Decompensated Heart Failure (ADHF) is one of themost common cardiac emergencies encountered in the emer-gency department (ED). Because patients with heart failure areseen so frequently, there can be a tendency for the emergencyphysician to become complacent with a perfunctory diagnosticevaluation and a one-size-fits-all therapeutic approach. The fact is,patients with ADHF represent a diverse group with a single com-mon feature: High morbidity and mortality. Heart failure accountsfor 286,700 deaths a year, and, in 2006, the treatment of heart failureis expected to cost approximately $29.6 billion. Failure to appreci-
December 2006Volume 8, Number 12
AuthorsJoshua M. Kosowsky, MDClinical Director, Department of EmergencyMedicine, Brigham & Womens Hospital, AssistantProfessor Harvard Medical School, MA
Jennifer L. Chan, MD, MPHSenior Resident, Harvard Affiliated EmergencyMedicine Residency, Brigham and WomensHospital/ Massachusetts General Hospital, Boston,MA
Peer ReviewersLuke K. Hermann, MDDirector, Chest Pain Unit, Assistant Professor,Department of Emergency Medicine, Mount SinaiSchool of Medicine, New York, NY
Joseph D. Toscano, MDEmergency PhysicianSan Ramon, CA
Upon completion of this article, you should be able to: 1. Describe the basic pathophysiology of acutely
decompensated heart failure and identify its com-mon and life-threatening precipitants.
2. Understand the diagnostic tools used in differenti-ating ADHF from other disease entities.
3. Understand the management of ADHF in the pre-hospital and ED settings, including the role ofdiuretics, vasodilators, inotropes, and non-inva-sive ventilatory support.
4. Appreciate the role of risk-stratification in deter-mining the disposition of patients with acutelydecompensated heart failure.
Date of original release: December 1, 2006.Date of most recent review: November 20, 2006.See Physician CME Information on back page.
Andy Jagoda, MD, FACEP, Professor and Vice-Chair of Academic Affairs,Department of Emergency Medicine;Mount Sinai School of Medicine;Medical Director, Mount Sinai Hospital,New York, NY.
John M Howell, MD, FACEP, Clinical Professor of Emergency Medicine,George Washington University,Washington, DC; Director of AcademicAffairs, Best Practices, Inc, InovaFairfax Hospital, Falls Church, VA.
William J Brady, MD, Associate Professor and Vice Chair, Departmentof Emergency Medicine, University ofVirginia, Charlottesville, VA.
Peter DeBlieux, MD, LSUHSC Professor of Clinical Medicine; LSU
Health Science Center, New Orleans,LA.
Wyatt W Decker, MD, Chair and Associate Professor of EmergencyMedicine, Mayo Clinic College ofMedicine, Rochester, MN.
Francis M Fesmire, MD, FACEP, Director, Heart-Stroke Center,Erlanger Medical Center; AssistantProfessor, UT College of Medicine,Chattanooga, TN.
Michael J Gerardi, MD, FAAP, FACEP, Director, Pediatric EmergencyMedicine, Childrens Medical Center,Atlantic Health System; Department ofEmergency Medicine, MorristownMemorial Hospital, NJ.
Michael A Gibbs, MD, FACEP, Chief, Department of Emergency Medicine,Maine Medical Center, Portland, ME.
Steven A Godwin, MD, FACEP, Assistant Professor and EmergencyMedicine Residency Director,University of Florida
Gregory L Henry, MD, FACEP, CEO, Medical Practice Risk Assessment,Inc; Clinical Professor of EmergencyMedicine, University of Michigan, AnnArbor.
Keith A Marill, MD, Instructor, Department of Emergency Medicine,Massachusetts General Hospital,Harvard Medical School, Boston, MA.
Charles V Pollack, Jr, MA, MD, FACEP,Professor and Chair, Department ofEmergency Medicine, PennsylvaniaHospital, University of PennsylvaniaHealth System, Philadelphia, PA.
Michael S Radeos, MD, MPH, Assistant Professor of EmergencyMedicine, Lincoln Health Center,Bronx, NY.
Robert L Rogers, MD, FAAEM, Assistant Professor and ResidencyDirector, Combined EM/IM Program,University of Maryland, Baltimore,MD.
Alfred Sacchetti, MD, FACEP, Assistant Clinical Professor,Department of Emergency Medicine,Thomas Jefferson University,Philadelphia, PA.
Corey M Slovis, MD, FACP, FACEP,Professor and Chair, Department ofEmergency Medicine, VanderbiltUniversity Medical Center, Nashville,TN.
Jenny Walker, MD, MPH, MSW, Assistant Professor; Division Chief,Family Medicine, Department ofCommunity and Preventive Medicine,Mount Sinai Medical Center, NewYork, NY.
Ron M Walls, MD, Professor and Chair, Department of Emergency Medicine,Brigham & Womens Hospital, Boston,MA.
Research EditorsNicholas Genes, MD, PhD, Mount Sinai Emergency Medicine Residency.
Beth Wicklund, MD, Regions Hospital Emergency Medicine Residency,EMRA Representative.
International EditorsValerio Gai, MD, Senior Editor,
Professor and Chair, Dept of EM,University of Turin, Italy.
Peter Cameron, MD, Chair, Emergency Medicine, Monash University; AlfredHospital, Melbourne, Australia.
Amin Antoine Kazzi, MD, FAAEM, Associate Professor and Vice Chair,Department of Emergency Medicine,University of California, Irvine;American University, Beirut, Lebanon.
Hugo Peralta, MD, Chair of Emergency Services, Hospital Italiano, BuenosAires, Argentina.
Maarten Simons, MD, PhD,Emergency Medicine ResidencyDirector, OLVG Hospital, Amsterdam,The Netherlands.
ate and address the subtleties of a patient withADHF can have dire consequences.
This issue of Emergency Medicine Practice presentsa comprehensive, evidence-based approach to themanagement of acutely decompensated heart failure.It focuses on the identification of major syndromes ofADHF, stabilization, treatment, and appropriate dis-position of the individual patient while highlightingemergency diagnostic and therapeutic options.
Abbreviations In This Article
ACC: American College of CardiologyACE: Angiotensin Converting EnzymeACS: Acute Coronary SyndromeADHERE: The Acute Decompensated Heart
Failure National RegistryADHF: Acutely Decompensated Heart FailureAHA: American Heart AssociationBiPAP: Biphasic Positive Airway PressureBNP: B-Type Natriuretic Peptide: CBC: Complete Blood CountCHF: Congestive Heart FailureCPAP: Continuous Positive Airway PressureCOPD: Chronic Obstructive Pulmonary DiseaseCVP: Central Venous PressureHFSA: The Heart Failure Society of AmericaIABC: Intra-Aortic Balloon Counterpulsation ESC: European Society of CardiologyETCO2: End-Tidal Carbon Dioxide LevelsICG: Impedence CardiographyJVD: Jugular Venous DistensionNIV: Noninvasive VentilationPCWP: Pulmonary Capillary Wedge PressurePEEP: Positive End-Expiratory PressureRSI: Rapid Sequence IntubationVMAC: Vasodilation in the Management of
Critical Appraisal Of The Literature
Despite its overwhelming prevalence and burden onthe healthcare system, evidence-based literature forADHF continues to lag behind that of other emergentconditions such as acute coronary syndrome andstroke. Although consensus guidelines provideinstruction to practicing physicians, there are fewcontrolled studies that have determined the optimaltreatment regimen for ADHF. The Heart FailureSociety of America (HFSA), and the European Societyof Cardiology (ESC) provide recommendations on the
diagnosis and treatment of ADHF.3 Although theAmerican Heart Association and the AmericanCollege of Cardiology (AHA/ACC) provide compre-hensive guidelines on chronic heart failure, they haveyet to publish guidelines that focus upon ADHF.
Since the February 2002 issue of EmergencyMedicine Practice: Acutely Decompensated HeartFailure, multi-center ED and hospital-based studieshave contributed data on the epidemiology, diagno-sis, and treatment of ADHF. The AcuteDecompensated Heart Failure National Registry is aregistry of medical information from patients withADHF from over 275 hospitals.4 Results from thisregistry have confirmed the high prevalence ofunderlying comorbidities such as coronary arterydisease and renal dysfunction. It has also shownthat many patients with ADHF have preserved ven-tricular systolic function. Results from the registryalso highlight the importance of early accurate man-agement beginning in the ED.
The Breathing Not Properly Multinational Studyinvestigated the diagnostic role of B-natriuretic pep-tide (BNP) in patients presenting to EDs with acutedyspnea.5 At least 13 studies have been publishedfrom the multinational data. Results from this studycontinue to provide data on the diagnostic power ofBNP and its role in determining the prognosis ofpatients presenting with ADHF.
The B-Type Natriuretic Peptide for AcuteShortness of Breath Evaluation (BASEL) study foundthat using BNP as a diagnostic tool decreases lengthof stay and cost of treatment among patients present-ing to the ED with acute dyspnea.6
The Organized Program to Initiate LifesavingTreatment in Hospitalized Patients with HeartFailure (OPTIMIZE-HF) registry collects data ondemographics, treatment approaches, and followup of patients with heart failure.7 Data fromOPTIMIZE-HF will be used to measure currenttreatment outcomes and therefore improve thequality of care for patients admitted with heart fail-ure. Lastly, the Vasodilation in the Management ofAcute CHF (VMAC) trial was a randomized double-blind trial of dyspneic patients with ADHF. Thisstudy compared two vasoactive agents, nesiritideand nitroglycerin with a placebo, and their effectupon pulmonary capillary wedge pressure (PCWP)and dyspnea. Nesiritide was shown to be superiorto placebo but of marginal benefit compared to intra-venous nitrates. (Discussed in depth in theTreatment section).8
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As a result of the aging of the United States popula-tion and improved survival following myocardialinfarction, the overall prevalence of heart failure isrising.9,10 At the same time, advances in outpatientmedical therapy are allowing patients with chronicheart failure to live longer. Over 5 millionAmericans with heart failure are alive today, and by2037, an estimated 10 million people in the UnitedStates will have a diagnosis of heart failure.1,11 Heartfailure now accounts for over one million in-patientadmissions annually, and is the number one reasonfor hospitalization among the growing elderly popu-lation.1 In 2006, the estimated cost of direct hospitalmanagement for heart failure will be $15.4 billiondollars.13 According to data from ADHERE, 80% ofpatients hospitalized for ADHF will initially presentto the emergency department.14 One retrospectiveanalysis of 2 million ED visits over an eleven-yearperiod revealed approximately 1.1% of visits to havea primary diagnosis of heart failure or pulmonaryedema.15
The Euro Heart Failure survey and the AcuteDecompensated Heart Failure National Registry(ADHERE) add to the current knowledge on the epi-demiology of heart failure. The mean age of patientswith ADHF is between 71-75 years with an equalratio of men to women.4, 16 New studies have shownthat almost half of all patients presenting with ADHFhave preserved systolic function, coronary artery dis-ease, hypertension and diabetes.4
There is no universally accepted definition of ADHF,
reflecting at least in part its heterogeneous patho-physiology and presentation. Some experts describedecompensated heart failure as a syndrome where-by; a patient with an established diagnosis of heartfailure develops increasing signs and symptoms ofthe disease after a period of relative stability,17 whileothers define acute heart failure syndrome as, [the]gradual or rapid change in heart failure signs andsymptoms resulting in the need for urgent therapy.Additional terms used by physicians for this syn-drome are CHF exacerbation and acute CHF. Thecommon theme among these definitions is an abrupt
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Table 1. Guidelines, Registries, And Studies
Table 2. Etiologies Of Heart Failure
Coronary artery disease Hypertension Valvular disease Cardiomyopathy
Idiopathic cardiomyopathyAlcoholic cardiomyopathyToxin-related cardiomyopathy
(e.g., adriamycin)Post-partum cardiomyopathyHypertrophic obstructive cardiomyopathy
Infiltrative disorders (e.g., amyloid) Congenital heart disease Pericardial disease Hyperkinetic states
AnemiaArterio-venous fistulaThyroid diseaseBeri-beri
clinical change from baseline affecting the cardiopul-monary system that requires emergent or urgentintervention. Regardless of terminology, this articlewill refer to this acute clinical presentation asAcutely Decompensated Heart Failure or ADHF.
Chronic heart failure is itself a complex syn-drome, and is characterized by inadequate cardiacoutput at physiologic filling pressures. The etiolo-gies of chronic heart failure are numerous anddiverse (Table 2). In the United States, the vastmajority of heart failure arises as a consequence ofcoronary artery disease and/or long-standing hyper-tension. Table 3 describes the American HeartAssociation classification and the commonly usedNew York Heart Association (NYHA) classificationsystem. Understanding the differences in both classi-fication systems can be helpful in evaluating andmanaging individual patients when they presentwith ADHF.
In the ED, heart failure can present de novo asan acute process or as an acute decompensation ofchronic heart failure. For example, acute myocardialinfarction (MI) with or without valvular dysfunctioncan cause acute heart failure. More commonly,patients seen in the ED have chronic heart failurethat has decompensated as the result of one or moreprecipitating factors.
Each episode of ADHF contributes to diseaseprogression and the gradual decline in clinical statusthat characterizes chronic heart failure. Non-adher-ence to medications, dietary indiscretion, physiologicstress, or lack of access to medication are frequentprecipitants of ADHF (Table 4).
Regardless of etiology, inadequate cardiac function
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Table 3. Classifications Of Heart Failure
American Heart Association ClassificationClass DescriptionStage A Patients are at high risk for heart failure but have not developed structural heart disease
and have no symptoms.Stage B Patients have developed structural heart disease but have not (yet) developed symptoms.Stage C Patients with past or current heart failure symptoms in association with structural damage
to the heart.Stage D Patients with end-stage, or terminal, heart failure requiring specialized treatment strategies.
New York Heart Association ClassificationClass Functional state SymptomsI No limitation Asymptomatic during usual daily activitiesII Slight limitation Mild symptoms (dyspnea, fatigue, or chest pain) with
ordinary daily activitiesIII Moderate limitation Symptoms noted with minimal activityIV Severe limitation Symptoms at rest
Sources: Hunt SA, Abraham WT, Chin MH, et al. ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic HeartFailure in the Adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines(Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure): developed in collaboration withthe American College of Chest Physicians and the International Society for Heart and Lung Transplantation: endorsed by the HeartRhythm Society. Circulation 2005; 112:e154-235.
Table 4. Common Precipitants ofAcutely Decompensated Heart Failure
Medication non-compliance Dietary indiscretion Myocardial ischemia / infarction Uncontrolled hypertension Cardiac arrhythmias Pulmonary and other infections Administration of inappropriate medications
(e.g., negative inotropes) Fluid overload Thyrotoxicosis Anemia Alcohol withdrawal
sets in motion a common set of compensatory mech-anisms, brought about by neurohormonal activationand characterized by elevated sympathetic tone,fluid and salt retention, and ventricular remodeling.These adaptations can allow heart failure to remainstable (or compensated) for a period of time, butalso provide the final common pathway for decom-pensationa downward spiral that can acceleratedramatically in response to a particular precipitantor stress. High circulating levels of aldosterone, vaso-pressin, epinephrine, and norepinephrine are ulti-mately maladaptive, as tachycardia and vasocon-striction compromise the intrinsic performance of theleft ventricle (LV) and simultaneously worsenmyocardial oxygen balance. Deterioration of leftventricular function results in further neurohormon-al activation and self-perpetuation of this adversecycle (Figure 1). An acute decompensation candevelop over a period of minutes, hours, or days andcan range in severity from mild symptoms of volumeoverload or decreased cardiac output to frank pul-monary edema or cardiogenic shock.
ADHF can be viewed as three overlapping syn-
dromes. Systemic volume overload, acute diastolicdysfunction, and low-output failure (Figure 2 andTable 5).
Systemic volume overload, accounting for themajority of cases of ADHF, occurs commonly in thesetting of non-adherence to medical regimens,dietary indiscretion, and/or progression of disease.Volume overload combined with poor left ventricu-lar performance results in gradual worsening of con-gestive symptoms. Patients with ADHF due prima-rily to systemic volume overload will often describea slow increase in lower extremity edema, dyspnea,and fatigue.
Acute diastolic dysfunction results in an abruptincrease in left ventricular pressure producing symp-toms of congestion. Contrary to the common percep-tion that a depressed ejection fraction is the maincause of ADHF, acute diastolic dysfunction oftenoccurs in the setting of a preserved ejection fraction.Many situations cause de novo or worsening dias-tolic dysfunction. Myocardial infarction causes ven-tricular wall stiffness that can maintain cardiac out-put but result in congestive symptoms. Patients withlong standing hypertension may have existing dias-tolic dysfunction as a result of left ventricular hyper-
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Figure 1: Heart Failure Pathophysiology Diagram
Figure 2: Syndromes of AcutelyDecompensated Heart Failure
Table 5. Syndromes of AcutelyDecompensated Heart Failure
trophy. During events such as sepsis, trauma, andarrhythmias, myocardial relaxation is impaired pre-venting proper ventricular filling resulting in pul-monary congestion and pulmonary edema. Thecoexistence of hypertension, CAD and even ACS cancause a complex pathophysiological picture duringacute diastolic dysfunction.
Low output heart failure refers to severelydepressed left ventricular function which impairsend organ perfusion. Patients with low output heartfailure may or may not have congestive symptomsbut may present with worsening fatigue, decline inrenal function, and confusion all due to decreasedperfusion of vital organs.
The severity of failure can be described in manyways, which may include a measure of how chronicheart failure affects the quality of life or more acuteclinical parameters.
Acutely decompensated heart failure can coexistwith or closely mimic a number of other cardiac, res-piratory, and systemic illnesses (Table 6). In fact,when patients present to the ED with undifferentiat-ed dyspnea, the diagnosis of heart failure is oftenoverlooked.18 Patients who present with mild ornon-specific symptoms pose a particular diagnosticchallenge. Symptoms such as weakness, lethargy,fatigue, anorexia, or lightheadedness may actually bea manifestation of decreased cardiac output and lowoutput ADHF. Older patients frequently lack typicalsigns and symptoms of heart failure.20 These featuresmay be obscured by the aging process itself or by thepresence of coexisting medical conditions.
Patients presenting with acute exacerbations ofeither cardiac dysfunction or COPD may havewheezing on pulmonary auscultation with signs ofchronic right-sided heart failure and non-diagnosticchest radiographs. In heart failure patients, pul-monary embolism may be clinically indistinguish-able from ADHF.21
Precipitating factors for decompensationshould be sought in a careful and deliberate fashion(Table 4). Myocardial ischemia or infarction andnon-compliance with medications or dietary indis-crition are the most common causes of clinical decom-pensation.22-27 Often, the cause-effect relationship ofADHF is difficult to determine due to the co-preva-lence of diseases such as coronary artery disease,hypertension, and atrial fibrillation.14 The exact
prevalence of these coexisting diseases variesdepending on the particular population.Nevertheless, in almost all cases, the possibility of anacute coronary syndrome should be considered.Other cardiovascular precipitants, such as arrhyth-mia, high-grade heart block, severe valvular dys-function, or hypertensive crisis, must not be over-looked. It should also be recognized that ADHFcould arise as a consequence of non-cardiac condi-tions such as sepsis, anemia, alcohol withdrawal,uncontrolled diabetes, or thyroid disease (Tables 4and 6).
Even before patients reach the hospital, ADHF isassociated with significant morbidity and mortalityincluding malignant arrhythmias and prehospitalcardiac arrest.28 All patients should have continuouscardiac monitoring and intravenous access estab-lished if possible (See also Clinical Pathway:Prehospital Therapy For Acutely DecompensatedHeart Failure). Because successful managementdepends on reversal of hypoxia, pulse oximetry andsupplemental oxygen should be utilized routinely inthe prehospital care of patients with ADHF.Prehospital personnel should alert ED staff of any
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Table 6. Differential Diagnosis OfAcutely Decompensated Heart Failure
CardiovascularAcute Coronary SyndromeAcute valvular / septal ruptureAortic dissectionArrhythmiaCritical aortic stenosisEndocarditis / MyocarditisHypertensive crisisPericardial tamponade / effusion
PulmonaryCOPD (chronic obstructive pulmonary disease)Pulmonary thromboembolismMulti-lobar pneumoniaARDS (acute respiratory distress syndrome)
OtherPure volume overload
renal failureiatrogenic (e.g., post-transfusion)
patient presenting with symptoms suggestive of pul-monary edema or cardiogenic shock, and receive on-line medical advice when appropriate. Prehospitalstaff trained to interpret electrocardiograms shouldobtain a 12-lead electrocardiogram and, if ACS isidentified, ED staff or medical control should beimmediately informed.
The decision to treat a patient in the relativelyuncontrolled prehospital environment carries somerisks that must be weighed against expected benefits.With few exceptions, the safety and efficacy of pre-hospital medications have been poorly studied.29
Prehospital therapy for ADHF should be undertakenwith particular caution in light of the relatively highnumber of inaccurate diagnoses made in the field.As many as 50% of patients with assumed cardiacassociated respiratory distress are diagnosed with adifferent condition once they arrive at the hospital.28,30,31
Despite these concerns, evidence suggests that pre-hospital therapy for presumed ADHF can preventserious complications and improve survival, particu-larly for critically ill patients.28,30,31 In a large retro-spective case series of 493 patients, there was adecrease in mortality among critical and non criticalpatients who received treatment (nitroglycerin,Lasix and/or morphine) compared to no pharma-cologic intervention.30 In European countries, wherephysicians commonly staff ambulances, intensiveprehospital treatment of patients with severe heartfailure confers short-term benefits.32-34 A retrospectivereview of 640 patients that presented in the prehospi-tal setting with acute pulmonary edema (APE)revealed that the use of nitrates were associated witha trend toward decreased mortality.32
Sublingual nitroglycerin appears to be the safestand most effective of the prehospital medicationsused for presumed pulmonary edema.31 A prospec-tive, randomized, double blind study of 57 patientscomparing morphine, nitroglygerin, and furosemidefound nitroglycerin to be the safest and most effec-tive intervention in the prehospital management ofADHF.31 Prehospital intravenous (IV) nitrates alsoyield positive short-term results. The role of othermedications for heart failure in the prehospital set-ting is less clear. Early administration of furosemideappears to have very little benefit, and may result inshort-term complications.31,35 The prehospital use ofmorphine sulfate for presumed pulmonary edema isassociated with an increased rate of endotrachealintubation, particularly among patients who turn outto have been misdiagnosed in the field.31,36 A
prospective, randomized study of 57 patients admin-istered four different drug regimens found that theadministration of morphine and Lasix showed littleimprovement.31
Emergency Department Evaluation
Initial ApproachThe approach to the patient with ADHF begins withstabilization of respiratory and hemodynamic statusand with the rapid exclusion or treatment ofreversible conditions. Clinical evaluation and empir-ic therapy begin simultaneously with supplementaloxygen, cardiac monitoring, pulse oximetry, andintravenous access. Patients with clinical signs ofexhaustion or cyanosis, despite supplemental oxygen,require respiratory support by either invasive or non-invasive means. Those with hypotension, obtunda-tion, cool extremities, or other signs of poor perfusionshould be presumed to be in or near cardiogenicshock and managed accordingly (see SpecialCircumstances). Once the initial resuscitation isunderway, further efforts should be made to identifythe underlying cause of acute decompensation.
HistoryMost patients presenting with heart failure complainof dyspnea; therefore, determining its degree andprecipitants are important. Dyspnea with exertionand at rest, paroxysmal nocturnal dyspnea (PND),and orthopnea are common symptoms. Inquiringabout the number of pillows used while sleepingmay help identify the presence of orthopnea. A largemeta-analysis in 2005 reported that these symptomsare not only specific, but are more likely to occurduring ADHF37 (Table 8). Patients who present withPND, orthopnea, or edema are two time mores likelythan others to have ADHF.37 The rapidity of symp-tom onset may suggest an underlying etiology forthe decompensation. An abrupt deterioration shouldraise concern for arrhythmia, acute MI, or valvularrupture (see Special Circumstances). Prior episodesof a similar nature can provide important clues.
Associated symptoms are important and the EPshould determine whether the patient has had anychest pain or other anginal equivalent such as shoul-der, neck, arm or epigastric discomfort. In a retro-spective analysis of 491 patients, the combination ofsyncope and heart failure was found to be associatedwith a mortality rate of 50%, which was ten timesgreater than those patients without ADHF.38 Recent
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weight gain, leg swelling, change in urinary output,exercise tolerance, fatigue, and compliance with dietshould be elicited.
Medication history is also important in determin-ing the etiology of ADHF and may also guide thera-py. Non-adherence with prescribed medications isoften a precipitating factor and is associated with 15to 64% of cases of ADHF.39,40 New prescriptions orchanges in dosage of medications such as NSAIDs,ophthalmic beta-blockers, herbals, and over thecounter drugs are important as well. Male patients
with congestive failure may take sildenafil (Viagra),and the administration of nitrates may cause life-threatening hypotension in such individuals.41
The most valuable historical information to elicitfrom patients with ADHF is a prior history of heartfailure, myocardial infarction, and/or coronaryartery disease37 (Table 8). A history of heart failurehas a specificity of 90%, and patients with prior heartfailure are approximately four times more likely tohave ADHF when presenting to the ED with acutedyspnea.37 Prior myocardial infarction is one of thebest predictors of impaired left ventricular systolicdysfunction.42 Patients often can tell you if they havehad prior episodes of ADHF. A common term syn-onymous to ADHF for patients with the syndrome ofsystemic volume overload or acute diastolic dysfunc-tion is fluid on the lungs. More sophisticatedpatients may be able to provide details of previousechocardiograms or cardiac catheterizations.
PhysicalVital signs provide a sense of the severity of illnessand can suggest etiologic factors for decompensa-tion. Hyperthermia or hypothermia may indicatesepsis or thyroid disease. In the absence of rate-con-trolling pharmacologic agents, tachycardia is nearlyuniversal in ADHF. Bradycardia should raise con-cern for high-degree AV block, hyperkalemia, drugtoxicity (digoxin, calcium channel, beta blocker), orsevere hypoxia. Hypertension is commonly seen inboth systemic volume overload and acute diastolicdysfunction syndromes of ADHF. Hypotension canbe baseline for patients with end-stage cardiomyopa-thy or low output heart failure, but otherwise shouldraise concern for sepsis, massive pulmonaryembolism, or cardiogenic shock.
Signs of congestion may be detected by carefulattention to heart and lung sounds, jugular venousdistention (JVD), hepatomegaly, and peripheraledema. Elevated central venous pressure (CVP) ispresent when the top of the external or internal jugu-lar veins is more than 3 cm of vertical distance abovethe sternal angle.43 The diagnostic utility of this physi-cal exam finding is well documented for chronic heartfailure, but less so for ADHF in the ED setting.44, 45
JVD, abdominojugular reflux, and an audible 3rdheart sound are very specific. Patients who presentwith these exam findings are at least five times morelikely to have ADHF37 (Table 8). A new cardiac mur-mur in the proper context must be presumed to sig-nal acute valvular or papillary muscle dysfunction.
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Table 8. Signs, Symptoms AndDiagnostic Studies In Determining
Acutely Decompensated Heart Failure.
Table 7. Key Historical Questions
Have you been able to take your prescribedmedications?
Have you adhered to a prescribed dietregimen?
Has your primary care doctor or cardiologistchanged any of your medications lately?
Have you gained or lost weight in the past3 to 5 days?
Do you have difficulty breathing? While lyingflat? While walking? In the middle of the night?
Do these symptoms feel like any prior episodesof fluid in your lungs, or heart failure?
Are you having any chest pain? Have youpassed out?
The pulmonary exam is usually helpful, but canbe misleading. Rales, a classic finding in heart fail-ure, may also occur with pneumonia, interstitial lungdisease, or COPD. The presence of rales has moder-ate specificity and is more likely to occur in ADHF(Table 8). Wheezing, or cardiac asthma, is com-mon in ADHF but has poor sensitivity37 (Table 8).
The leg exam is routine in the evaluation ofpatients with suspected heart failure and may repre-sent a degree of systemic volume overload. Whileperipherial edema is moderately specific forincreased filling pressures, it has poor sensitivity37,45
(Table 8). Unilateral extremity swelling and espe-cially the presence of a venous cord should raise sus-picion for deep venous thrombosis and possible pul-monary embolism.
Laboratory testsThe majority of patients who present with com-plaints suggestive of ADHF will need basic laborato-ry testing. A complete blood count (CBC) is usefulfor ruling out anemia as a cause for decompensation.Some believe that an elevated white blood countmay suggest the presence of an infectious process,especially if bands are present. However, this is notwell studied in the patient who presents with dysp-nea. Serum chemistries help assess renal functionand overall fluid and electrolyte balance.
Cardiac MarkersThe question as to which patients with ADHFrequire screening for cardiac enzymes is not wellstudied. Additional information from the history(e.g., chest discomfort, new-onset heart failure, orsignificant risk factors for coronary artery disease)should heighten the suspicion of associated cardiacischemia. Although not always clear, a high level ofsuspicion for acute coronary syndrome (ACS) shouldbe considered in patients presenting with ADHF.Several studies have shown that elevated cardiac tro-ponins are found in up to one-third of patients withsevere heart failure and help to identify those withworse short-term prognosis.46, 47 According to onereview of 151 patients with a discharge diagnosis ofheart failure, 70% of patients did not report chestpain.47 Therefore, the ED physician should stronglyconsider screening for cardiac enzymes in anypatient who presents with ADHF, regardless of thepresence or absence of chest pain.
B-Natriuretic Peptide and NT-proBNPB-type natriuretic peptide (BNP) and NT-proBNPcorrelate with the presence and severity of heart fail-ure. BNP is produced by cardiac myocytes inresponse to myocardial stretch and increased end-diastolic pressure and occurs in the setting of heartfailure. Pre-proBNP is synthesized within myocytesand is cleaved to proBNP. The latter is released intothe circulation and then cleaved to the active BNPand an inactive N-terminal fragment, called NT-proBNP.48 The half-life of BNP is approximately 20minutes and the half-life of NT-proBNP is three tosix times that of BNP.
BNP is a counter-regulatory hormone that offsetsthe effects of neurohormonal activation by promot-ing diuresis, natriuresis, and vasodilation and sup-pressing the renin-angiotensin system. Plasma levelsof BNP have been shown to correlate with the degreeof left ventricular overload, severity of clinical heartfailure, and both short- and long-term cardiovascularmortality.49-53
Plasma BNP and NT-proBNP levels can be usedto distinguish between cardiac and non-cardiac caus-es of dyspnea.5,54-56 Studies have shown that the twopeptides have a high degree of correlation.57-60
Acutely dyspneic patients with plasma BNP levels ofless than 100 pg/dl and NT-proBNP levels less than300 pg/dl are unlikely to have ADHF, and thosewith BNP greater than 500 pg/dl and NT-proBNPlevels greater than 1000 pg/dl are very likely to haveADHF. BNP levels above 100 pg/dl have 90% sensi-tivity for identifying ADHF, and BNP levels of 500pg/dl have 87% specificity for identifying ADHF.61
A BNP cut point of 100 pg/ml predicts the diagnosisADHF with 81 to 91% accuracy.5,10,61 Fewer studieshave been performed on NT-proBNP, but a prospec-tive, observational study showed a cut point of 300pg/ml with 99% sensitivity.62
In general, clinicians are 80% accurate in clinical-ly differentiating ADHF from other disease process-es.10,63 Data from the Breathing Not ProperlyMultinational Study indicate that BNP levels can beused to improve diagnostic accuracy beyond clinicaljudgment.5,10,61 BNP levels will not add significantdiagnostic value for patients with classic findingsfrom history and physical exam of ADHF; therefore,diagnostic BNP levels should be used on a case-by-case basis. It is unclear how indeterminate BNP lev-els affect the management of patients with suspectedADHF.
BNP and NT-proBNP levels are elevated in non-
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cardiac conditions (i.e., age, renal insufficiency, pul-monary embolism, and cor pulmonale).58, 64-67 SinceBNP and NT-proBNP levels increase with age, cut-points for diagnosing ADHF are elevated among theelderly and have discriminatory value.58,65,67 Datafrom the Breathing Not Properly Multinational Studyindicate that BNP is a better indicator at youngerages.65 In a prospective, observational study of elder-ly patients greater than 65 years of age with acutedyspnea, a higher BNP level of 250 pg/ml has aspecificity of 90% in diagnosing ADHF.58
The role of BNP in patients with severe renalfailure is less studied. Patients with severe renal fail-ure have reduced ability to clear metabolites and vol-ume overload resulting in higher levels of circulatingBNP. These proposed elevated cut-points have dis-criminatory value, but actual cut points are yet to bedetermined.59
Obese patients with elevated filling pressuresmay have less myocardial stretch which lowersmeasured BNP and NT-proBNP levels. This may bedue to increased extracardiac pressure associatedwith an elevated BMI. The sensitivity of BNP andNT-proBNP at existing cut points for obese patientsmay be lower than expected and a true cut-point inthis setting is unclear.68 The Breathing Not ProperlyMultinational Study found an inverse relationshipbetween BMI and BNP.69 For overweight and obesepatients, BNP is 80% sensitive at a cut point of 100pg/ml. In addition, 20% of these patients withADHF had BNP levels less than the standard cutoff.68 NT-proBNP may also lose discriminatory valueamong obese patients. The ProBNP Investigation ofDyspnea in the Emergency Department (PRIDE)study identified significantly lower ProBNP andBNP levels in overweight and obese patients present-ing with ADHF.68
For patients with classic signs of ADHF (i.e.prior episodes of ADHF, volume overload, dyspnea,and orthopnea) or those with shortness of breathconsistent with other etiologies (i.e. asthma, COPD),BNP is not likely to assist in the diagnostic workup.Checking BNP levels in indeterminate cases may aidin diagnosing or excluding ADHF, but results mayleave the EP with additional questions.
A provocative single-center study used BNP todiagnose ADHF and showed beneficial effects onpatient outcomes. In the B-Type Natriuretic Peptidefor Acute Shortness of Breath Evaluation (BASEL)study, patients presenting to the ED with acute dysp-nea were randomized to standard clinical evaluation
versus a clinical evaluation including BNP. The BNPgroup had reduced time to treatment, reduced hospi-tal costs, and reduced time to discharge.6
Approximately one-third of the cost saving was asso-ciated with identifying an alternate diagnosis.
ECG While the ECG is admittedly a relatively insensitivetool, it remains useful for detecting ischemia,arrhythmias, and electrolyte disturbances. Given thehigh proportion of heart failure exacerbations precip-itated or accompanied by ischemia, it is difficult tojustify not obtaining an ECG on all such patients.22
In a meta-analysis of 22 studies differentiating car-dio-pulmonary cause of dyspnea, atrial fibrillationwas the most likely associated ECG finding amongpatients presenting to the ED with ADHF37 (Table 8).
The ECG is likely to be abnormal in patientswith chronic heart failure. In a clinic population,approximately 40% of 19,877 clinic patients had ECGwith left ventricular hypertrophy, and approximately70% had electrocardiographic evidence of cardiacischemia or a prior MI.70 Conversely, an entirely nor-mal ECG is strong evidence against the presence ofleft ventricular dysfunction and should thereforeprompt consideration of alternative diagnoses.20,37,71
Also, a prolonged QRS has been shown to be anindependent predictor of LV dysfunction.
Chest X-rayThe chest x-ray should be obtained in patients withsuspected ADHF.3 Findings suggestive of ADHFinclude cardiomegaly, vascular redistribution (e.g.,cephalization, fullness of hilar vessels), interstitial orpulmonary edema, and pleural effusions. Pleuraleffusions in heart failure tend to be bilateral or local-ized to the right side.73 The presence of pulmonarycongestion and cardiomegaly is associated with avery high likelihood of ADHF37 (Table 8). The chestfilm may also be useful in identifying alternative orcontributing causes of the patients symptomatology.
There are several pitfalls that await the unwaryphysician who uses the chest film to diagnose acuteheart failure. Heart size may be normal in acute fail-ure, especially if the failure originates from acutediastolic dysfunction.45 COPD patients may haveminimal radiographic evidence of concurrent heartfailure. Also, patients with longstanding chronicheart failure may have well developed lymphaticdrainage of the pulmonary interstitium and, there-fore, little radiographic evidence of congestion.
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Recent studies have shown that a normal chest radi-ograph alone cannot exclude ADHF. According to arecent ADHERE study, one in five patients withoutradiographic findings of interstitial edema, pul-monary edema, or vascular congestion received afinal diagnosis of ADHF.73
Cardiac EchocardiographyEchocardiography is invaluable and is, in somesense, considered the gold standard for assessingthe status of left ventricular function, distinguishingbetween systolic and diastolic failure, and identify-ing regional wall motion abnormalities.Echocardiography can also assist in diagnosing orexcluding potentially reversible etiologies of an acutedecompensation such as pericardial tamponade,massive pulmonary embolus, ruptured chordaetendineae, or ruptured ventricular septum (seeSpecial Circumstances).
Echocardiography is probably not indicated in allinstances of ADHF, particularly if a patient has had arecent echocardiogram and a clear precipitant fordecompensation. ACC/AHA guidelines recommendtransthoracic echocardiography as soon as possibleafter initial stabilization for any patient who presentswith acute pulmonary edema, unless there are obvi-ous precipitating factors and the patients cardiac sta-tus has been adequately evaluated previously.74
Guidelines for establishing an effective system foremergency echocardiography have been published.75
Experience with emergency physicians performingbedside echocardiography has generally been limitedto ruling out pericardial effusion / tamponade.76-78
Pulmonary Artery Catheterization (Swan-Ganz)Swan-Ganz catheters provide considerable data oncardiopulmonary function that are thought toimprove management and clinical outcomes; howev-er, recent trials have not demonstrated significantpatient benefit associated with their use.79 TheEvaluation Study of Congestive Heart Failure andPulmonary Artery Catheterization Effectiveness(ESCAPE) trial, a randomized, controlled trial of 433patients, showed no difference in six-month mortali-ty or return for hospitalization compared to clinicalassessment.79 On the other hand, the use of invasivemonitoring in this study was associated with moreadverse events. Nevertheless, published consensusguidelines advise the use of PA catheters in patientswho do not respond to initial therapies.2,3
Other Diagnostic Modalities
Peak Flow/End Tidal CO2Peak flow and end tidal CO2 are two additional diag-nostic modalities that may help identify ADHF in theundifferentiated patient. In a study of 56 acutelydyspneic patients, peak expiratory flow rates ofthose with heart failure were found to be twice thoseof patients with COPD; however, no single cut-offprovided for perfectly accurate classification.80 Whileend-tidal carbon dioxide levels (ETCO2) for heartfailure patients differ significantly from those ofasthma/COPD patients, there is no single ETCO2level that can reliably differentiate between the twoconditions.81
As with any ill patient, the initial focus of treatmentwill be on airway and breathing (see ClinicalPathway: Treatment For Acutely DecompensatedHeart Failure). Although many patients can be man-aged with oxygen, with or without non-invasiveventilatory support, the presence of agonal respira-tions or profoundly depressed mental status willmandate emergent intubation with the caveat thatthe respiratory symptoms that accompany ADHFreflect cardiovascular rather than pulmonary pathol-ogy and are therefore often rapidly reversible withaggressive medical therapy (see RespiratoryTherapy).
Sitting the patient upright may reduce pulmonarycongestion and improve respiratory dynamics.Studies in patients with chronic heart failure show alarge rise in airflow resistance after lying supine forfive minutes, a condition that is reversed by sittingerect.82 Practice guidelines recommend early use ofpulse oximetry, noninvasive blood pressure monitor-ing, and continuous cardiac monitoring as these canprovide early warnings of decompensation.3
Pharmacologic Therapy The main objectives of pharmacologic therapy forADHF are relief of pulmonary congestion andimprovement in systemic tissue perfusion. The goalof therapy is to reduce preload and enhance left ven-tricular function, while maintaining or improvingmyocardial oxygen balance. While the basicapproach to treating ADHF has not changed over thepast two decades, there has been increasing empha-sis on afterload reduction and other means of coun-teracting the adverse cycle of neurohormonal activa-
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tion (see Table 9 and Clinical Pathway: EmergencyDepartment Therapy for Acutely DecompensatedHeart Failure).
Nitrates Nitrates are recommended as initial therapy forADHF of both ischemic and non-ischemic origin, par-
ticularly for patients with hypertension or withpresumed pulmonary edema.2,3 The beneficial hemo-dynamic effects of nitrates in the setting of heart fail-ure have long been appreciated.83,84 At low doses,nitroglycerin induces venodilation; at high doses,nitroglycerin causes arteriodilation including dilationof the coronary arteries.85 Significantly, in patientswith severe underlying left ventricular dysfunction,
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Table 9. Medications For Acutely Decompensated Heart Failure
afterload reduction appears to predominate overpreload reduction, even at moderate doses of nitro-glycerin.86
Despite its common use, few studies have rigor-ously addressed the role of nitrates in the treatmentof ADHF. To date, no prospective studies on itseffects on mortality have been published. In theVasodilation in the Management of Acute CongestiveHeart failure (VMAC) trial, intravenous nitroglycerinimproved dyspnea scores compared to placebo dur-ing early therapy.8 In another randomized, controlledtrial involving subjects with pulmonary edema, a reg-imen of high-dose nitrates and low-dose diureticsprovided more consistent clinical improvement thana regimen of high-dose diuretic and low-dosenitrates. It was also associated with lower rates ofmechanical ventilation and MI.87 Because many ofthe patients in this study had underlying coronaryartery disease, it is likely that the anti-ischemic effectsof nitrates also played a role. Data from ADHEREshow a lower mortality rate among patients treatedwith nitrates compared to inotropic agents, but didnot compare nitrates to diuretic therapy.88
Single doses of 0.4 mg sublingual nitroglycerincan be given repeatedly every five to ten minutes,provided the patient has stable blood pressures. Inthe hospital setting, continuous IV administration ofnitroglycerin is generally more convenient andallows for titration to specific clinical or hemody-namic end-points. Nitroglycerin can be started at 0.3to 0.5 mcg/kg/min but may require much higherdoses (up to 3 to 5 mcg/kg/min), so long as theblood pressure is above 95 to 100 mm Hg.89
Alternative regimens and formulations for adminis-tering IV nitrates have been described, but offer noclear advantages.83,90,91 Oral or transdernal nitroglyc-erin have comparable hemodynamic effects to IVnitroglycerin but are less amenable to rapid titrationand may be less effective in patients with poor gas-trointestinal absorption or poor skin perfusion.92
Hypotension with standard nitrate therapy isgenerally mild and transient. Severe or persistenthypotension should raise suspicion for hypovolemia,stenotic valvular disease such as aortic stenosis, car-diac tamponade, right ventricular infarction, orrecent use of sildenafil (Viagra). If these conditionsare known or suspected, nitrates should be avoidedor used with extreme caution. Nitrate therapy maynot be particularly effective in patients with massiveperipheral edema.93 In such cases, aggressive diuret-ic therapy is more likely to be of benefit.
The European Society of Cardiology (ESC) rec-ommends sodium nitroprusside for patients withmarked systemic hypertension, severe mitral or aor-tic valvular regurgitation, or pulmonary edema notresponsive to standard nitrate therapy.3
Nitroprusside directly dilates resistance vessels,rapidly reducing blood pressure and afterload.83
Typically, nitroprusside is started at a dose of 0.1 to0.3 mcg/kg/min and advanced as needed toimprove clinical and hemodynamic status, maintain-ing a SBP greater than 90 or mean arterial pressuregreater than 65 mm Hg. In patients with renal fail-ure, long-term use of nitroprusside carries the poten-tial for cyanide toxicity as metabolites accumulate.
Diuretics Diuretics are the mainstay of therapy for patientswith systemic volume overload.2,3 Although thispractice is recommended by societies and is a com-monly accepted approach, there have not been multi-ple randomized, controlled trials or meta-analysis tosupport it use. On the other hand, it is important torecognize that patients who present with ADHF arenot always volume overloaded. Patients with acutediastolic dysfunction may benefit more from redistri-bution of circulating volume by using vasodilators.The indiscriminate use of diuretics carries the risk ofoverdiuresis and detrimental effects on renal func-tion, particularly among elderly patients. Even with-out overdiuresis, there is growing evidence thatthe higher doses of diuretics required to treatadvanced heart failure correlate to worsening renalfunction, which has been tied to both longer hospi-talizations and increased mortality after discharge.This adds strength to the argument that the focusshould be on changing loading conditions withvasodilators rather than diuresis as the stand alonetherapy it often is.
Evidence from a large number of in vitro and invivo experiments suggest that direct vascular actionsalso contribute to the clinical effects of furosemide.94-97
These actions are not necessarily advantageous, inthat their net effect may promote further activationof the sympathetic and renin-angiotensin systemscharacterized by reflex vasoconstriction, worseningof cardiac loading conditions, and a decline in car-diac output.98,99 Studies comparing the acute effectsof diuretics and nitrates have emphasized the morefavorable overall hemodynamic effects of the lattergroup, as described earlier.
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(continued from page 13)
Depending on the patients clinical condition,state of hydration, and previous use of diuretics, aninitial IV dose of 40 to 200 mg of furosemide can beadministered. For patients on chronic diuretic thera-py, a common strategy is to begin with the usualdaily dose (typically 40 to 80 mg) given as an IVbolus, and to double the dose if there is inadequatediuresis. Although IV boluses of furosemide are acommon practice, there is a trend toward using IVfurosemide infusions.100-102 A randomized crossoverstudy compared continuous furosemide to bolusadministration and showed that those treated withcontinuous furosemide resulted in greater urine out-put and fewer adverse effects.96 A recent meta-analy-sis reviewing eight randomized, controlled trialscompared bolus versus continuous intravenousdiuretics. These small heterogeneous studiesshowed that continuous IV diuretics improveddiuresis and carried a better safety profile.103
Although these findings are encouraging, largerstudies to definitively support one over the other areneeded.
In cases of volume overload that fail to respondto standard therapy, substitute a more potent loopdiuretic such as torsemide (Demadex) 10 to 20 mgIV or bumetanide (Bumex) 1 to 4 mg IV. The use ofthese medications among patients with ADHF in theED setting has not been published. Combiningfurosemide with a thiazide agent such as metolazone(5 to 20 mg PO) or chlorothiazide (Diuril) 500 to1000 mg IV) may improve diuresis.104,105 While not allpatients in ADHF require a Foley catheter, monitor-ing of urinary output with a urinometer can be help-ful in those with severe symptoms.
Electrolyte abnormalities such as hypokalemiaand hypomagnesemia occur with chronic diureticuse and may worsen with subsequent administrationof diuretics in the ED. Daily monitoring of potassi-um, magnesium, and sodium levels are recommend-ed for patients admitted to the hospital for ADHF.2
NesiritideNesiritide (recombinant BNP) is FDA approved forthe treatment of ADHF symptoms. BNP hasvasodilatory as well as mild diuretic and natriureticproperties. When administered in supraphysiologicdoses, it exerts favorable hemodynamic, natriuretic,and neurohormonal effects.106-109 Nesiritide can beadministered intravenously with a 2 mcg/kg bolus
followed by a continuous drip of 0.01 mcg/kg/hr. Randomized, controlled trials of NYHA class II-
IV patients with ADHF have shown nesiritide to bemore effective than placebo in improving hemody-namics.110-112 The VMAC trial compared nesiritide tonitroglycerin in the treatment of ADHF. At threehours, PCWP was lower in the nesiritide group ver-sus the nitroglycerin group but dyspnea scores at 3and 24 hours were not statistically significantbetween the two groups.8 A study from ADHEREshowed that treatment with nitroglycerin or nesiri-tide had lower in-hospital mortality than ionotropictreatments with milrinone or dobutamine.88 Therewas no in-hospital difference in mortality betweennitroglycerin and nesiritide. Studies have yet toshow improvement in length of stay, hospital costs,or mortality.
Recent studies have emphasized potential risksassociated with nesiritide.113,114 Pooled data and meta-analysis suggest an increase in creatinine levels withnesiritide, which required additional medical inter-vention. Another meta-analysis suggested that nesir-itide carries a greater 30-day risk of death comparedto conventional therapy.113 Prospective trials address-ing these questions have not yet been published.
Although there are recent studies questioningthe safety of nesiritide and consensus guidelines rec-ommend its use, the Heart Failure Society ofAmerica notes the need for additional prospectivestudies.2
ACE InhibitorsAngiotensin converting enzyme inhibitors (ACEinhibitors) represent a logical extension of vasodila-tor therapy. The beneficial hemodynamic effects ofACE inhibitors in acute heart failure have beenappreciated for two decades.115 Acutely, ACEinhibitors reduce both preload and afterload,improve renal hemodynamics, impair sodium reten-tion, attenuate sympathetic stimulation, and main-tain or enhance left ventricular function.116-118
Although not currently recommended by theEuropean Society of Cardiology or the Heart FailureSociety of America in the setting of acute heart fail-ure, drug regimens that include an ACE inhibitorappear to have hemodynamic advantages over thosebased upon other vasodilators.119-121
For acutely decompensated heart failure, ACEinhibitors can be administered intravenously (e.g.,enalaprilat), orally (e.g., captopril) or sublingually(e.g., emptied captopril capsules contents).
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Depending on the drug, the dose, and the route ofadministration, hemodynamic effects may be seenwithin 10 to 60 minutes.116,117,119 Safe dosing regimensof enalaprilat include 0.004 mg/kg as an intravenousbolus, or 1 mg by continuous intravenous infusionover two hours. The suggested one-time dose of oralor sublingual captopril is 12.5 to 25 mg. The safetyof administering an ACE inhibitor in the setting ofADHF is of concern to some clinicians who fearpotentially deleterious effects on blood pressure,renal function, and electrolyte balance. However,clinical trials have consistently demonstrated thesafety of administering ACE inhibitors to patientswith ADHF.118,122
Few studies of ACE inhibitors for ADHF havebeen performed in the ED setting. Small studieshave demonstrated that sublingual captopril is safeand effective for ED patients with pulmonaryedema.123,124 In one retrospective analysis, the use ofsublingual captopril in the ED was associated withlower rates of mechanical ventilation and CCUadmission.125
ACE inhibitors are contraindicated in the contextof pregnancy, hyperkalemia, or a history of ACE-inhibitor-induced angioedema. For patients withevidence of poor systemic perfusion, ACE inhibitorsshould be used cautiously, because additionalvasodilation may not be tolerated. Unlike nitrates,ACE inhibitors have a relatively prolonged durationof action, making dosage less easily titratable.
Inotropes Short-term therapy with ionotropes may benefitpatients presenting with low output failure, whichare considered acceptable treatment modalities,although with notable risks.2,3 Classically, inotropicagents have been reserved for the treatment of car-diogenic shock. However, short-term inotropic sup-port may also be seen as beneficial for patients withlow output failure who fail to respond to conven-tional therapy. While short-term inotropic therapyclearly improves hemodynamic performance, theimpact on clinical outcomes is less sanguine.
Inotropic therapy has deleterious effects uponpatients with preserved or moderately depressedventricular function and congestion. The Outcomesof a Prospective Trial of Intravenous Milrinone forExacerbations of Chronic Heart Failure, a random-ized, controlled trial, showed no increased benefitover standard therapy with the use of milrinone.126,127
ADHERE also supports this finding indicating an
increase in mortality among patients with volumeoverload and diastolic dysfunction who were treatedwith ionotropes.88
It is important to understand the expected hemo-dynamic effects of inotropic agents and to set cleargoals for therapy. Most inotropic agents have multi-ple pharmacologic actions, some of which may bedeleterious. Undesirable chronotropic effects,arrhythmogenesis, or ischemia resulting fromincreased myocardial oxygen consumption may cur-tail the use of any particular drug.
Digoxin has a very limited role in the ED man-agement of heart failure. The inotropic effects ofdigoxin are modest, unpredictable, and delayed forat least 90 minutes after intravenous loading.128 Forpatients with ADHF, the only reasonable use fordigoxin is to help control the ventricular response toatrial fibrillation (see Special CircumstancesAtrialFibrillation).
MorphineMorphine is one of the oldest drugs still in use forthe treatment of acute heart failure and remains anadjunct for treating the anxiety and discomfort asso-ciated with pulmonary edema. With high doses ofmorphine, direct vasodilation may result from hista-mine release, but the predominant hemodynamiceffects of morphine appear to be mediated throughthe central nervous system.129 Morphine can beadministered safely to most patients. However,because of its sedative properties and potential todepress respirations, caution should be exercisedwhen administering morphine in the setting ofchronic pulmonary insufficiency or suspected acido-sis. One retrospective study found that ED adminis-tration of morphine to patients with pulmonaryedema was associated with an increased rate ofendotracheal intubation and CCU admission.125
Respiratory TherapyThe majority of patients with respiratory distressrespond to supplemental oxygen and standard phar-macologic therapy, but patients with persistenthypoxemia or progressive fatigue will require at leasttemporary respiratory support (see also the July2001 issue of Emergency Medicine Practice,Noninvasive Airway Management Techniques:How And When To Use Them).
Continuous positive airway pressure (CPAP)improves lung mechanics by recruiting atelectaticalveoli, improving pulmonary compliance, and
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reducing the work of breathing.130 At the same time,particularly in patients with congestive heart failure,CPAP improves hemodynamics by reducing preloadand afterload, thereby enhancing left ventricular per-formance.131-134 Nasal or face mask-applied CPAP of 5to 10 cm H20 has been shown to improve oxygena-tion, reduce heart rate and reduce blood pressurecompared to standard oxygen treatment.135-141 In sev-eral randomized, controlled clinical trials, CPAPreduced the need for endotracheal intubation inpatients with severe cardiogenic pulmonaryedema.135,137,138,142 Pooled data and one randomized,controlled trial also suggest that the use of CPAP inthis setting may be associated with decreased mor-tality.142,143
Biphasic positive airway pressure (BiPAP)or
non-invasive positive pressure ventilation (NPPV)provides the physiological advantages of CPAP dur-ing expiration and also provides additional assistancewith the inspiratory work of breathing. Evidencefrom several case series and a recent randomized trialsupport the use of this therapy in patients with acutecardiogenic pulmonary edema;144-147 however, anotherrandomized, controlled trial and small series did notshow benefit.148,149 A small, randomized trial compar-ing BiPAP with CPAP demonstrated a more rapidclinical improvement with BiPAP but no difference inthe rates of intubation.150 Of concern in this trial wasan unexpectedly high rate of acute MI associatedwith the use of BiPAP, which prompted prematuretermination of the study. One other clinical trialinvolving BiPAP was also terminated early because
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1. Dont admit every patient with heart failure.
Some patients with acutely decompensated heartfailure may only require an ED tune-up andwill be appropriate for discharge. Patients witha past history of failure who have a reassuringhistory and physical examination, normal labora-tory values, and an ECG unchanged from previ-ous tracings may be candidates for outpatientfollow up (especially if their decompensationoccurred because they ran out of their medicine).If discharge is considered, communicating withthe patients cardiologist and/or primary careprovider is necessary for close follow-up. EDobservation units for select patients may also bea cost-effective alternative to traditional admis-sion.
Caveat: Most patients who present with acutelydecompenesated heart failure will need hospitaladmissionespecially those with abnormal vitalsigns, worsening renal function, or chest pain.
2. Consider the use of CPAP/BIPAP.
CPAP or BIPAP may prevent the need for intuba-tion in some patients with acutely decompensat-ed heart failure and can decrease the cost andlength of stay in the intensive care unit. Keepinga machine in the ED and using it frequently canpromote early use.
Caveat: Some patients are not good candidatesfor non-invasive ventilationespecially those
who are agitated or those who have altered men-tal status, unstable vital signs, or evidence ofacute MI.
3. Consider the use of furosemide infusions.
While many patients in acutely decompensatedheart failure respond quickly to nitrates andbolus diuretics, some do not. Some studies doshow that intravenous infusions of furosemidefor NYHA class IV heart failure are a safe, effec-tive, and economic mode of therapy, especially inthe elderly. The increased cost of the infusionwould be more than offset by savings accrued bya shorter hospital stay. Since this trial was smalland non-randomized, further study is needed toensure the cost-effectiveness of this intervention.
4. Utilize BNP or NT-proBNP when appropriate.
Of all of the diagnostic tests available to deter-mine the presence of acutely decompensatedheart failure, BNP may be the single best investi-gation. It is relatively sensitive and specific andcan be performed at the bedside. In the acutesetting, elevated BNP levels correlate with thediagnosis of heart failure, reduce time to treat-ment, decrease length of hospital stay, anddecrease cost of care.
Caveats: Levels of BNP or NT-proBNP are affect-ed by their half-lives. BNP levels may also beelevated in eldery patients and patients withrenal insufficiency and lower in obese patients.
Cost Effective Strategies For Acutely Decompensated Heart Failure
of similar safety concerns.151 Recent studies provideevidence to suggest no advantage of BiPAP/NPPVover CPAP for patients with cardiogenic pulmonaryedema and hypoxemic respiratory failure.152-154
However, recent meta-analysis shows a small benefitin CPAP, but no significant changes in clinical out-comes.155
The success of non-invasive respiratory supportdepends upon appropriate patient selection. Forpatients with compromised upper airway function orsignificantly altered level of consciousness, intuba-tion and mechanical ventilation remain the definitivetherapy. Patients with a history of cardiac arrest,unstable cardiac rhythms, or cardiogenic shock aregenerally not felt to be candidates for non-invasiveapproaches. Likewise, in the setting of severemyocardial ischemia or infarction, full ventilatorysupport may be preferable in order to decrease themyocardial oxygen demand associated with respira-tory effort.
Although the decision to initiate non-invasiverespiratory support is dependent on a variety of fac-tors, the presumption is that the earlier therapy isinstituted, the greater the likelihood of averting intu-bation. Recent studies suggest that the use of non-invasive ventilatory support in the prehospital set-ting is feasible and potentially beneficial for patientswith presumed cardiogenic pulmonary edema.156, 157
A small case series showed an increase in meanpulse oximetry of patients treated with CPAP.157 Inone convenience sample, matched control study,patients presumed to have congestive heart failure(CHF) were given BiPAP by the medics during trans-port and compared to matched controls treated with-out NIV. In this trial, 97% of EMTs who used BiPAPon patients with suspected CHF thought it improvedthe patients dyspnea; however, data analysisshowed no statistical difference between groups inthe length of subsequent hospital stay, intubation, ormortality.156
In either the prehospital or ED setting, if there isprogressive respiratory failure in spite of non-inva-sive support, the patient requires intubation andmechanical ventilation. In general, airway manage-ment should be accomplished with rapid sequenceintubation (RSI). This involves using an inductionagent in combination with a short-acting paralyticsuch as succinylcholine so as to maximize the rate ofsuccess on the initial attempt.158 Maintaining thepatient in an upright position as long as possibleprior to intubation may assist in maximizing pre-
oxygenation. Prolonged episodes of hypoxia orhypotension during intubation risk further cardiacdecompensation and cardiopulmonary arrest. In onestudy, all induction agents used (thiopental, fentanyl,and midazolam) were associated with a significantrisk of hypotension for patients with pulmonaryedema. However, the authors admit that the smallnumbers of patients with pulmonary edema in thisstudy preclude a valid post hoc comparison.159 On theother hand, induction with etomidate appears to besafe and effective for a range of patients undergoingRSI, including those with underlying heart disease.160
Once mechanical ventilation is instituted for cardio-genic pulmonary edema, it is not certain whetherpositive end-expiratory pressure (PEEP) confers anyadditional hemodynamic benefit.161-164
Cardiogenic ShockCardiogenic shock in the setting of heart failure ismost often seen in the setting of acute ST-segmentelevation MI and acute valvular diseases. Mortalityrates for patients with frank cardiogenic shockremain alarmingly high, ranging from 50 to 80%165
Stat echocardiograms play a pivotal role in diagnos-tics and treatment, as many etiologies of cardiogenicshock will require surgical management. In the con-text of acute MI, emergent cardiac catheterizationand revascularization have been shown to be of ben-efit.3,166,167
Other potentially reversible causes of cardiogenicshock, such as acute valvular dysfunction, ventricu-lar septal wall rupture, and pericardial tamponade,need to be excluded or addressed promptly. Acutevalvular dysfunction can occur in the setting of ACS(ischemic papillary muscle dysfunction/rupture) orindependently in acute mitral/aortic insufficiency,aortic dissection, or prosthetic valve thrombosiscausing cardiogenic shock. Free wall rupture andventricular septal wall rupture are uncommon com-plications of AMI that require rapid recognition.Once the diagnosis is made, surgical managementprovides an opportunity for survival. Again, the eti-ology of these types of cardiogenic shock should bepromptly identified with emergent echocardiogra-phy.2 Once acute surgical causes of cardiogenicshock are ruled out, non-cardiac etiologies of shock,such as hypovolemia, sepsis, poisoning, and massivepulmonary embolism must also be entertained.
Aside from addressing reversible causes of car-
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diogenic shock, the overarching goal in treatingpatients who present with evidence of inadequatetissue perfusion (i.e., cool skin, altered mental status)from acute heart failure or ADHF should be torestore and maintain perfusion of vital organs.
Patients who present in shock with a normalblood pressure or with mild hypotension mayrespond favorably to dobutamine (starting at 2 to 3mcg/kg/min). Prior to initiation of vasopressoragents or ionotropes, small fluid bolus can be admin-istered as an initial measure. Compared withdopamine, dobutamine is associated with a lowerincidence of arrhythmias, less peripheral vasocon-striction, and more consistent reduction in left ven-tricular filling pressure for a comparable rise in car-diac output.168 Dopamine is required for patientswho have severe hypotension (SBP less than 70 to 80mm Hg) in the presence of volume overload or afterbolus administration of saline. At moderate doses (4to 5 mcg/kg/min), dopamine improves cardiac out-put without causing excessive systemic vasoconstric-tion. If the patient can be stabilized with dopamine,dobutamine can then be added and the dose ofdopamine reduced, with the goal of reducingmyocardial oxygen demand.
Intra-aortic balloon counterpulsation (IABC)should be considered for patients with a potentiallyreversible condition, when initial management ofADHF fails, or when stabilizing measures are neededas a bridge to definitive management.3 IABC can bean effective temporizing measure in anticipation ofcoronary revascularization or cardiac valve repair.The patients least likely to benefit from the IABC arethose with multiple previous infarctions, massiveirreversible myocardial necrosis, aortic dissection,advanced stages of cardiogenic shock, and elderlypatients with peripheral vascular disease (because ofcomplications from insertion of the device). If IABCis not immediately available, norepinephrine can beadded to increase systolic pressure to acceptable lev-els (80 or more mm Hg). Because of the adverseeffects on renal and mesenteric perfusion, the use ofhigh-dose dopamine or norepinephrine should beconsidered only as a temporizing measure until adefinitive therapy can be substituted.
It is important for the EP to distinguish betweenacute heart failure with cardiogenic shock and lowoutput ADHF, both which present with hypotension.Low output ADHF tends to present subacutely inpatients with end stage systolic heart failure (seePathophysiology section, and Figure 1 on page 5).
Patients may describe symptoms of fatigue, loss ofappetite and lethargy. Management of these patientscan be extremely challenging for the EP; therefore,optimal treatment may require the involvement of aheart failure specialist. Frequently, the key to man-agement is identifying the etiology of decompensa-tion. Although the EPs impulse may be to aggres-sively fluid bolus or aggressively diurese patientswith low output ADHF, a do nothing managementstyle is often the best approach.
Renal DysfunctionADHF and chronic renal insufficiency frequently co-exist.169,170 One out of every three patients admittedfor ADHF have renal insufficiency, with one of everyfive patients with creatinine levels greater than 2.0mg/dl. Renal hypoperfusion from poor cardiac out-put is aggravated by the use of diuretics and aceinhibitors which, in turn, contribute to worseningrenal function. Both pre-existing renal insufficiencyand decline in renal function while managing ADHFare associated with increased mortality. There is agreater risk of in-hospital mortality among patientstreated for ADHF with interval worsening of renalfunction.171
Heart failure is present in about one third ofpatients who begin dialysis and will develop overtime in an additional 25%.172 Among anurichemodialysis patients, heart failure is the most com-mon cause of ED visits.173 In these patients, ADHF ismost often due to volume overload between dialysistreatments. Although hemodialysis is the treatmentof choice for these patients, it may not be immediate-ly available. ED treatment is directed at stabilizingthese patients until hemodialysis can be performed(Table 10). Because of their direct vascular effects,diuretics may still have a role in managing anuricpatients with volume overload.174 Vasodilator thera-py with nitrates and ACE inhibitors has been shownto be particularly effective.123 In a descriptive studyof 46 renal dialysis patients, the administration ofpreload and afterload reducing agents including cap-topril and nitroglycerin resulted in no deaths. In anydialysis patient with an unstable cardiac rhythm,hyperkalemia and digoxin toxicity must be consid-ered.
Atrial Fibrillation Atrial fibrillation is commonly seen in patients withchronic heart failure and its co-prevalence is likelyassociated with underlying hypertension and coro-
Emergency MMedicine PPractice 22 December 2006 EBMedicine.net
nary artery disease. In patients presenting withADHF, atrial fibrillation is seen in approximatelyone-third of patients.3,4,8
In the context of normal ventricular function,loss of synchronized atrial contractions is of minimalhemodynamic significance. However, in patientswho have abnormal systolic or diastolic function, theloss of atrial kick can have profound conse-quences. When atrial fibrillation is accompanied bya rapid ventricular response, the reduced filling timeand increased myocardial oxygen demand lead tofurther decline in cardiac performance.
When assessing the patient with rapid atrial fib-rillation and ADHF, it is often difficult to attributecause and effect. While new onset rapid atrial fibril-lation may be the precipitant of ADHF, more com-monly atrial fibrillation is a response to worseningheart failure (e.g., via neurohormonal activationand/or increased atrial stretch). This distinction canoften only be made clinically. In either case, manage-ment focuses upon the treatment of both conditions.175
Management of atrial fibrillation in the contextof ADHF should focus upon treating the underlyingcause of ADHF and controlling the ventricular rateto allow for improved ventricular filling / contrac-tion and improved myocardial oxygen balance2,3
(Table 10). In general, digoxin, diltiazem, and amio-darone are considered acceptable therapies for ratecontrol in patients with left ventricular systolic dys-function.176-178 The EP should exercise some cautionwith beta-blockers or calcium-channel blockers forrate control because of potential negative inotropiceffects that could worsen existing systolic dysfunc-tion. Although not specifically studied in the settingof ADHF, esmolol would be a reasonable option,given its short duration of action and demonstratedsafety in patients with severe chronic heart failure.Cardioversion, whether electrical or chemical, is areasonable treatment alternative for unstable ornew atrial fibrillation, but maintaining sinusrhythm may not be possible if the underlying heartfailure is not addressed.
Controversies / Cutting Edge
Impedance Cardiography (ICG)Impedance cardiography (ICG) is a non-invasivemeans of hemodynamic monitoring that providesreal-time estimates of cardiac output and pulmonarycapillary wedge pressure by employing principles ofthoracic bioimpedance. Over the past three decades,
ICG has been investigated in a variety of clinical set-tings and has been found to compare moderatelywell with other modalities for assessing hemody-namics (e.g., echocardiography, Swan-Ganz catheter-ization).179,180 Because the technique is non-invasive,portable, and capable of providing beat-to-beat infor-mation, potential applications in the ED are numer-ous. ICG is less accurate in patients with underlyingheart disease; however, serial measurements maystill provide useful information, such as monitoringresponse to therapy. In a small study of 38 patientswith undifferentiated dyspnea, incorporation of ICGdata increased diagnostic accuracy of patients withcardiac causes of dyspnea.181 In the EmergencyDepartment Impedance CardiographyaidedAssessment Changes Therapy (ED-IMPACT) trial,the use of ICG affected treatment plans for 24% ofpatients with acute dyspnea.182 However, more stud-ies are necessary to determine the overall utility ofthis diagnostic tool and its effects on morbidity, mor-tality, cost, and length of stay.
Beta-blockersLarge, randomized, controlled trials have demon-strated clear morbidity and mortality benefits oflong-term beta-blocker therapy in patients with sys-tolic heart failure.183-185 In contrast, short-term admin-istration of beta-blockers to patients with severe sys-tolic dysfunction can cause life-threatening clinicaldeterioration.186 There has been no study that specifi-cally addresses the potential benefits of beta-blockertherapy in the setting of ADHF. Therefore, beta-block-ers are not routinely recommended by the ESC for treat-ment of acutely decompensated heart failure and caution isadvised during its use.3 In the setting of an acutedecompensation, chronic beta-blocker therapyshould either be temporarily discontinued or admin-istered cautiously at a reduced dose, according to theESC. On the other hand, in the context of ongoingischemia, tachycardia, and severe hypertension beta-blockers may be considered.3
Less is known specifically about the safety andefficacy of beta-blocker therapy for patients withacute diastolic dysfunction. In theory, the value ofreducing hypertension and tachycardia would out-weigh any concern about negative inotropy in thesepatients. Further studies are needed to clarify therole of beta-blockers in this context.
Calcium SensitizersCalcium sensitizers are a novel class of agents that
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modify the configuration of troponin C to promotemyofilament sensitivity to calcium, enhancing con-tractility without impeding diastolic relaxation.186b
Levosimendan is the best studied of these agents. Intwo small, randomized, controlled studies of patientswith severe ADHF, these agents were shown toimprove hemodynamics and decrease mortality.187,188
The Levosimendan Versus Dobutamine Trial (LIDO)compared levosimendan to dobutamine withimproved hemodynamics and six month mortalityamong 203 patients.187 Although encouraging, thestudy population was restricted to low output heartfailure patients and the mortality benefit may beassociated with adverse affects of dobutamine. TheCalcium Sensitizer or Inotrope or None in LowOutput Failure Trial (CASINO) showed a significantmortality benefit with levosimendan compared todobutamine and placebo.188 Although these resultsare encouraging, this study was performed on inpa-tients and the incidence of low output failure requir-ing ionotropes remains low so its use in the ED isstill unclear. Implications for ED use await addition-al clinical trials.
Pimobendan is another calcium sensitizerapproved for use in Japan. The Pimobenden inCongestive Heart Failure Trial (PICO) showedimproved hemodynamics but increased hazards fordeath compared to placebo.189 The study populationwas stable heart failure patients in the clinic setting.Generalization of these findings to patients withADHF in the ED setting is limited.
Novel Natriuretic Peptides Endogenous natriuretic peptides in addition to nesir-itide have been investigated as potential new agentsto treat ADHF. Carperitide, an atrial natriuretic pep-tide, has vasodilatory effects as well as natriureticproperties. Preliminary studies indicated that carper-itide improves hemodynamic parameters and dysp-nea scores among NYHA class III and IV heart fail-ure patients with ADHF.190 Ularitide is a renal natri-uretic peptide that has diuretic and natriuretic prop-erties. One small, randomized study evaluated con-tinuous ularitide compared to placebo in predomi-nantly male patients with ADHF. Results showedimproved hemodynamics, and symptoms of dysp-nea. The impact of these novel therapies in the EDsetting is unknown because previous studies haveyet to represent ED patients with ADHF.
Vasopressin AntagonistsElevated vasopressin levels are found in patientswith ADHF, and vasopressin antagonists have beenproposed as a means to improve diuresis in patientswith ADHF. In a hemodynamic trial, conivaptan, aV1a and V2 receptor antagonist, decreased PCWPand right atrial pressures.191 In a randomized con-trolled trial among patients with ADHF in the settingof systolic dysfunction, tolvaptan, a V2 receptorantagonist, has been shown to decrease body weightwith no changes in worsening heart failure at 60days.192
Endothelin AntagonistsEndothelin one (ET-1), a potent vasoconstrictor andmodulator of the renin-angiotensin-aldosterone sys-tem, are elevated in patients with ADHF. In hemo-dynamic studies, tezosentan, an ET-1 receptor antag-onist, reduced preload and afterload, delayedmyocyte hypertrophy, and increased myocardial con-tractility.193 A randomized, controlled trial comparingtezosentan with placebo among patients with lowoutput ADHF showed improved hemodynamicswith the use of tezosentan without significantchanges in dyspnea compared to standard thera-pies.194 Future studies will clarify tezosentans rolein the treatment of ADHF.
Even in this era of cost containment, the vast majori-ty of patients who present with ADHF are admittedto the hospital.195 According to ADHERE, themajority of patients with ADHF are admitted totelemetry and step-down units while 14% of patientsare admitted to the ICU during their hospital stay.14
Meanwhile, hospital costs for in-patient care ofADHF are continuing to rise. In-hospital mortalityremains approximately 2.3 to 7%,14,126,196 with majoradverse events occurring in up to 18% of patients.197,198
In patients with NYHA class III or IV heart failurewho are admitted for ADHF, there is a 9.6% mortalityrate at 60 days and a 30% combined rate of rehospi-talization and/or death.6 However, while the realitiesof modern healthcare economics may not favor rou-tine hospitalization, premature release of inadequate-ly treated patients are likely to result in increasedshort-term morbidity and mortality.199
In general, clinicians have great difficulty judg-ing the prognosis of patients with exacerbations ofheart failure.200 Acutely decompensated heart failure
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is a dynamic entity, and the ED physician often seesonly a snapshot of the patient at any point in time.Some patients are dramatically ill at presentation butrespond rapidly to treatment, while other patients goon to develop serious complications after a period ofrelative stability.
Previous studies have found that certain patientcharacteristics are predictive of in-hospital morbidityand mortality (Table 11).201-206 In multivariate analysis,independent correlates of major complications ordeath during hospitalization have included hypoten-sion, tachypnea, jugular venous distention, electrocar-diographic abnormalities, hyponatremia, and poorinitial diuresis.196,201-204 Recent studies have shown thattroponin elevations, elevated BNP, and worseningrenal function are prognostic factors in post-dischargemortality and risk for rehospitalization.196,207,208 In onestudy, 325 patients with acute dyspnea and thosewith BNP levels greater than 230 pg/ml had a rela-tive risk of 24.1 for death and a 51% probability of anadditional episode of ADHF within 6 months.207 Pre-discharge BNP for patients treated for ADHF are pre-dictive of readmission and mortality.209,210
Two large, recent studies have further investigat-ed characteristics predictive of increased mortalityamong patients admitted with heart failure.205,206 TheEnhanced Feedback for Effective Cardiac Treatment(EFFECT) study, a retrospective, multi-center, com-munity-based study identified predictors of 30-dayand one-year mortality among patients admitted tothe hospital for heart failure.
A clinical tool developed from ADHERE identi-fied patients admitted with ADHF, renal insufficien-cy (Cr greater than 2.7), elevated BUN (greater than43) and moderately low systolic blood pressures(SBP greater than 115) to have a mortality of greaterthan 20%.205 A risk stratification tree has been devel-oped to assist clinicians in determining mortality riskof patients who present with ADHF (Table 12).Disturbingly, some studies have shown that patientswithout any independent risk factors appear to havesubstantial rates (6%) of in-hospital morbidity andmortality.201
The Heart Failure Society of America has estab-lished criteria for hospitalization of patients withheart failure.2 The recent HFSA criterion includesworsening renal function, altered mentation, andnew onset atrial fibrillation as circumstances thatmerit hospitalization. However, in the Agency forHealth Care Policy and Research study, criteria failedto identify up to one-third of the patients who die
within 30 days.195 Studies on the effectiveness of theHFSA criteria have not yet been studied or pub-lished. Thus, while published criteria and guidelinescan help with triage, the significant rate of morbidityeven among