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Acutely Decompensated Heart Failure: Diagnostic and Therapeutic Strategies You start your shift. An elderly woman

Acutely Decompensated Heart Failure: Diagnostic and Therapeutic Strategies

You start your shift. An elderly woman with shortness of breath has congestive heart failure written all over her and her chart. She takes beta-blockers, an ACE inhibitor, and Lasix®. She looks and sounds “wet.” She receives oxygen, furosemide, morphine, and nitrate therapy. When you return 20 minutes later, she looks 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 really looks so good now—does 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 lungs

sound “wheezy” and you hear crackles.

orthopnea. Does she have a COPD exacerbation or new onset CHF?

send a BNP level?

Her legs are edematous and she describes

Should you

Will her obesity affect this test?

The next evening you see a patient with “severe CHF” and an ejection frac-

tion of 20%.

She is not edematous and her lungs are clear. Her creatinine has increased from

2.5 to 3.2 g/dl. Is this a CHF exacerbation? What are your treatment options? Are ionotropes indicated?

Her family describes recent fatigue and progressive mild confusion.

A cutely Decompensated Heart Failure (ADHF) is one of the most common cardiac emergencies encountered in the emer-

gency department (ED). Because patients with heart failure are seen so frequently, there can be a tendency for the emergency physician to become complacent with a perfunctory diagnostic evaluation 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 accounts for 286,700 deaths a year, and, in 2006, the treatment of heart failure

is expected to cost approximately $29.6 billion. Failure to appreci-

December 2006

Volume 8, Number 12

Authors

Joshua M. Kosowsky, MD Clinical Director, Department of Emergency Medicine, Brigham & Women’s Hospital, Assistant Professor Harvard Medical School, MA

Jennifer L. Chan, MD, MPH Senior Resident, Harvard Affiliated Emergency Medicine Residency, Brigham and Women’s Hospital/ Massachusetts General Hospital, Boston, MA

Peer Reviewers

Luke K. Hermann, MD Director, Chest Pain Unit, Assistant Professor, Department of Emergency Medicine, Mount Sinai School of Medicine, New York, NY

Joseph D. Toscano, MD Emergency Physician San Ramon, CA

CME Objectives

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 of diuretics, vasodilators, inotropes, and non-inva- sive ventilatory support.

4. Appreciate the role of risk-stratification in deter- mining the disposition of patients with acutely decompensated heart failure.

Date of original release: December 1, 2006. Date of most recent review: November 20, 2006. See “Physician CME Information” on back page.

Editor-in-Chief

Health Science Center, New Orleans, LA. Wyatt W Decker, MD, Chair and Associate Professor of Emergency

Medicine, Mayo Clinic College of Medicine, Rochester, MN.

HSC/Jacksonville, FL.

Alfred Sacchetti, MD, FACEP, Assistant Clinical Professor, Department of Emergency Medicine, Thomas Jefferson University, Philadelphia, PA.

 

Beth Wicklund, MD, Regions Hospital Emergency Medicine Residency, EMRA Representative.

International Editors

 

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.

Associate Editor

 

Gregory L Henry, MD, FACEP, CEO, Medical Practice Risk Assessment, Inc; Clinical Professor of Emergency

Medicine, University of Michigan, Ann

Arbor.

Corey M Slovis, MD, FACP, FACEP, Professor and Chair, Department of Emergency Medicine, Vanderbilt University Medical Center, Nashville, TN.

 

Francis M Fesmire, MD, FACEP, Director, Heart-Stroke Center,

Keith A Marill, MD, Instructor, Department of Emergency Medicine,

 

Valerio Gai, MD, Senior Editor, Professor and Chair, Dept of EM, University of Turin, Italy.

Peter Cameron, MD, Chair, Emergency Medicine, Monash University; Alfred Hospital, Melbourne, Australia.

Amin Antoine Kazzi, MD, FAAEM, Associate Professor and Vice Chair, Department of Emergency Medicine, University of California, Irvine; American University, Beirut, Lebanon.

John M Howell, MD, FACEP, Clinical Professor of Emergency Medicine, George Washington University, Washington, DC; Director of Academic Affairs, Best Practices, Inc, Inova Fairfax Hospital, Falls Church, VA.

Editorial Board

Erlanger Medical Center; Assistant Professor, UT College of Medicine, Chattanooga, TN.

Michael J Gerardi, MD, FAAP, FACEP, Director, Pediatric Emergency Medicine, Children’s Medical Center, Atlantic Health System; Department of Emergency Medicine, Morristown Memorial Hospital, NJ.

Massachusetts General Hospital, Harvard Medical School, Boston, MA.

Charles V Pollack, Jr, MA, MD, FACEP, Professor and Chair, Department of Emergency Medicine, Pennsylvania Hospital, University of Pennsylvania Health System, Philadelphia, PA.

Michael S Radeos, MD, MPH,

Jenny Walker, MD, MPH, MSW, Assistant Professor; Division Chief, Family Medicine, Department of Community and Preventive Medicine, Mount Sinai Medical Center, New York, NY.

 

Assistant Professor of Emergency Medicine, Lincoln Health Center, Bronx, NY.

Ron M Walls, MD, Professor and Chair, Department of Emergency Medicine, Brigham & Women’s Hospital, Boston, MA.

 

William J Brady, MD, Associate Professor and Vice Chair, Department of Emergency Medicine, University of Virginia, Charlottesville, VA.

Michael A Gibbs, MD, FACEP, Chief, Department of Emergency Medicine, Maine Medical Center, Portland, ME.

Hugo Peralta, MD, Chair of Emergency Services, Hospital Italiano, Buenos Aires, Argentina.

Steven A Godwin, MD, FACEP, Assistant Professor and Emergency Medicine Residency Director, University of Florida

Robert L Rogers, MD, FAAEM, Assistant Professor and Residency Director, Combined EM/IM Program,

University of Maryland, Baltimore,

MD.

Research Editors

Maarten Simons, MD, PhD, Emergency Medicine Residency Director, OLVG Hospital, Amsterdam, The Netherlands.

Peter DeBlieux, MD, LSUHSC Professor of Clinical Medicine; LSU

Nicholas Genes, MD, PhD, Mount

Sinai Emergency Medicine Residency.

ate and address the subtleties of a patient with ADHF can have dire consequences.

This issue of Emergency Medicine Practice presents

a comprehensive, evidence-based approach to the management of acutely decompensated heart failure.

It focuses on the identification of major syndromes of

ADHF, stabilization, treatment, and appropriate dis- position of the individual patient while highlighting emergency diagnostic and therapeutic options.

Abbreviations In This Article

ACC: American College of Cardiology ACE: Angiotensin Converting Enzyme ACS: Acute Coronary Syndrome ADHERE: The Acute Decompensated Heart Failure National Registry ADHF: Acutely Decompensated Heart Failure AHA: American Heart Association BiPAP: Biphasic Positive Airway Pressure BNP: B-Type Natriuretic Peptide:

CBC: Complete Blood Count CHF: Congestive Heart Failure CPAP: Continuous Positive Airway Pressure COPD: Chronic Obstructive Pulmonary Disease CVP: Central Venous Pressure HFSA: The Heart Failure Society of America IABC: Intra-Aortic Balloon Counterpulsation ESC: European Society of Cardiology ETCO 2 : End-Tidal Carbon Dioxide Levels ICG: Impedence Cardiography JVD: Jugular Venous Distension NIV: Noninvasive Ventilation PCWP: Pulmonary Capillary Wedge Pressure PEEP: Positive End-Expiratory Pressure RSI: Rapid Sequence Intubation VMAC: Vasodilation in the Management of Acute CHF

Critical Appraisal Of The Literature

Despite its overwhelming prevalence and burden on the healthcare system, evidence-based literature for ADHF continues to lag behind that of other emergent conditions such as acute coronary syndrome and stroke. Although consensus guidelines provide instruction to practicing physicians, there are few controlled studies that have determined the optimal treatment regimen for ADHF. The Heart Failure Society of America (HFSA), and the European Society of Cardiology (ESC) provide recommendations on the

diagnosis and treatment of ADHF. 3 Although the American Heart Association and the American College of Cardiology (AHA/ACC) provide compre- hensive guidelines on chronic heart failure, they have yet to publish guidelines that focus upon ADHF. Since the February 2002 issue of Emergency Medicine Practice: “Acutely Decompensated Heart Failure,” multi-center ED and hospital-based studies have contributed data on the epidemiology, diagno- sis, and treatment of ADHF. The Acute Decompensated Heart Failure National Registry is a registry of medical information from patients with ADHF from over 275 hospitals. 4 Results from this registry have confirmed the high prevalence of underlying comorbidities such as coronary artery

disease and renal dysfunction.

that many patients with ADHF have preserved ven- tricular systolic function. Results from the registry also highlight the importance of early accurate man- agement beginning in the ED. The Breathing Not Properly Multinational Study investigated the diagnostic role of B-natriuretic pep- tide (BNP) in patients presenting to EDs with acute dyspnea. 5 At least 13 studies have been published from the multinational data. Results from this study continue to provide data on the diagnostic power of BNP and its role in determining the prognosis of patients presenting with ADHF. The B-Type Natriuretic Peptide for Acute Shortness of Breath Evaluation (BASEL) study found that using BNP as a diagnostic tool decreases length of stay and cost of treatment among patients present- ing to the ED with acute dyspnea. 6

The Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure (OPTIMIZE-HF) registry collects data on demographics, treatment approaches, and follow up of patients with heart failure. 7 Data from OPTIMIZE-HF will be used to measure current treatment outcomes and therefore improve the quality of care for patients admitted with heart fail- ure. Lastly, the Vasodilation in the Management of Acute CHF (VMAC) trial was a randomized double- blind trial of dyspneic patients with ADHF. This study compared two vasoactive agents, nesiritide and nitroglycerin with a placebo, and their effect upon pulmonary capillary wedge pressure (PCWP) and dyspnea. Nesiritide was shown to be superior to placebo but of marginal benefit compared to intra- venous nitrates. (Discussed in depth in the Treatment section). 8

It has also shown

Table 1. Guidelines, Registries, And Studies Epidemiology As a result of the aging of the
Table 1. Guidelines, Registries, And Studies
Epidemiology
As a result of the aging of the United States’ popula-
tion and improved survival following myocardial
infarction, the overall prevalence of heart failure is
rising. 9,10 At the same time, advances in outpatient
medical therapy are allowing patients with chronic
heart failure to live longer. Over 5 million
Americans with heart failure are alive today, and by
2037, an estimated 10 million people in the United
States will have a diagnosis of heart failure. 1,11 Heart
failure now accounts for over one million in-patient
admissions annually, and is the number one reason
for hospitalization among the growing elderly popu-
lation. 1 In 2006, the estimated cost of direct hospital
management for heart failure will be $15.4 billion
dollars. 13 According to data from ADHERE, 80% of
patients hospitalized for ADHF will initially present
to the emergency department. 14 One retrospective
analysis of 2 million ED visits over an eleven-year
period revealed approximately 1.1% of visits to have
a primary diagnosis of heart failure or pulmonary
edema. 15
The Euro Heart Failure survey and the Acute
Decompensated Heart Failure National Registry
(ADHERE) add to the current knowledge on the epi-
demiology of heart failure. The mean age of patients
with ADHF is between 71-75 years with an equal
ratio of men to women. 4, 16 New studies have shown
that almost half of all patients presenting with ADHF
have preserved systolic function, coronary artery dis-
ease, hypertension and diabetes. 4
reflecting at least in part its heterogeneous patho-
physiology and presentation. Some experts describe
decompensated heart failure as a syndrome where-
by; “ a patient with an established diagnosis of heart
failure develops increasing signs and symptoms of
the disease after a period of relative stability,” 17 while
others define acute heart failure syndrome as, “[the]
gradual or rapid change in heart failure signs and
symptoms resulting in the need for urgent therapy.”
Additional terms used by physicians for this syn-
drome are CHF exacerbation” and “acute CHF.” The
common theme among these definitions is an abrupt
Table 2. Etiologies Of Heart Failure
• Coronary artery disease
• Hypertension
• Valvular disease
• Cardiomyopathy
Idiopathic cardiomyopathy
Alcoholic cardiomyopathy
Toxin-related cardiomyopathy
(e.g., adriamycin)
Post-partum cardiomyopathy
Hypertrophic obstructive cardiomyopathy
(HOCM)
Tachyarrhythmia-induced cardiomyopathy
• Infiltrative disorders (e.g., amyloid)
• Congenital heart disease
• Pericardial disease
Definitions, Etiology
• Hyperkinetic states
Anemia
Arterio-venous fistula
Thyroid disease
Beri-beri
There is no universally accepted definition of ADHF,

clinical change from baseline affecting the cardiopul- monary system that requires emergent or urgent intervention. Regardless of terminology, this article will refer to this acute clinical presentation as Acutely Decompensated Heart Failure or ADHF. Chronic heart failure is itself a complex syn- drome, and is characterized by inadequate cardiac output at physiologic filling pressures. The etiolo- gies of chronic heart failure are numerous and diverse (Table 2). In the United States, the vast majority of heart failure arises as a consequence of coronary artery disease and/or long-standing hyper- tension. Table 3 describes the American Heart Association classification and the commonly used New York Heart Association (NYHA) classification system. Understanding the differences in both classi- fication systems can be helpful in evaluating and managing individual patients when they present with ADHF. In the ED, heart failure can present de novo as an acute process or as an acute decompensation of chronic heart failure. For example, acute myocardial infarction (MI) with or without valvular dysfunction can cause acute heart failure. More commonly, patients seen in the ED have chronic heart failure that has decompensated as the result of one or more precipitating factors.

 

Each episode of ADHF contributes to disease progression and the gradual decline in clinical status that characterizes chronic heart failure. Non-adher- ence to medications, dietary indiscretion, physiologic stress, or lack of access to medication are frequent precipitants of ADHF (Table 4).

Pathophysiology

 

Regardless of etiology, inadequate cardiac function

 
 

Table 4. Common Precipitants of Acutely 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

 
 

Table 3. Classifications Of Heart Failure

   

American Heart Association Classification

 

Class

Description

Stage A

Patients are at high risk for heart failure but have not developed structural heart disease

 
 

Stage B

and have no symptoms. Patients have developed structural heart disease but have not (yet) developed symptoms. Patients with past or current heart failure symptoms in association with structural damage to the heart. Patients with end-stage, or terminal, heart failure requiring specialized treatment strategies.

Stage C

Stage D

New York Heart Association Classification

Class

Functional state

Symptoms

I

No limitation

Asymptomatic during usual daily activities

II

Slight limitation

Mild symptoms (dyspnea, fatigue, or chest pain) with ordinary daily activities

III

Moderate limitation

Symptoms noted with minimal activity

IV

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 Heart Failure 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 with the American College of Chest Physicians and the International Society for Heart and Lung Transplantation: endorsed by the Heart Rhythm Society. Circulation 2005; 112:e154-235.

Figure 1: Heart Failure Pathophysiology Diagram

Figure 1: Heart Failure Pathophysiology Diagram sets in motion a common set of compensatory mech- anisms,
Figure 1: Heart Failure Pathophysiology Diagram sets in motion a common set of compensatory mech- anisms,
Figure 1: Heart Failure Pathophysiology Diagram sets in motion a common set of compensatory mech- anisms,
Figure 1: Heart Failure Pathophysiology Diagram sets in motion a common set of compensatory mech- anisms,
Figure 1: Heart Failure Pathophysiology Diagram sets in motion a common set of compensatory mech- anisms,
Figure 1: Heart Failure Pathophysiology Diagram sets in motion a common set of compensatory mech- anisms,
Figure 1: Heart Failure Pathophysiology Diagram sets in motion a common set of compensatory mech- anisms,
Figure 1: Heart Failure Pathophysiology Diagram sets in motion a common set of compensatory mech- anisms,
Figure 1: Heart Failure Pathophysiology Diagram sets in motion a common set of compensatory mech- anisms,

sets in motion a common set of compensatory mech- anisms, brought about by neurohormonal activation and characterized by elevated sympathetic tone, fluid and salt retention, and ventricular remodeling. These adaptations can allow heart failure to remain stable (or “compensated”) for a period of time, but also provide the final common pathway for decom- pensation—a downward spiral that can accelerate dramatically in response to a particular precipitant or 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 the left ventricle (LV) and simultaneously worsen myocardial oxygen balance. Deterioration of left ventricular function results in further neurohormon- al activation and self-perpetuation of this adverse cycle (Figure 1). An acute decompensation can develop over a period of minutes, hours, or days and can range in severity from mild symptoms of volume overload or decreased cardiac output to frank pul- monary edema or cardiogenic shock. ADHF can be viewed as three overlapping syn-

Figure 2: Syndromes of Acutely Decompensated Heart Failure

Figure 2: Syndromes of Acutely Decompensated Heart Failure dromes. Systemic volume overload, acute diastolic

dromes. Systemic volume overload, acute diastolic dysfunction, and low-output failure (Figure 2 and Table 5). Systemic volume overload, accounting for the majority of cases of ADHF, occurs commonly in the setting 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 describe a slow increase in lower extremity edema, dyspnea, and fatigue. Acute diastolic dysfunction results in an abrupt increase in left ventricular pressure producing symp- toms of congestion. Contrary to the common percep- tion that a depressed ejection fraction is the main cause of ADHF, acute diastolic dysfunction often occurs 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 with long standing hypertension may have existing dias- tolic dysfunction as a result of left ventricular hyper-

Table 5. Syndromes of Acutely Decompensated Heart Failure
Table 5. Syndromes of Acutely
Decompensated Heart Failure

trophy. During events such as sepsis, trauma, and arrhythmias, myocardial relaxation is impaired pre- venting proper ventricular filling resulting in pul- monary congestion and pulmonary edema. The coexistence of hypertension, CAD and even ACS can cause a complex pathophysiological picture during acute diastolic dysfunction. Low output heart failure refers to severely depressed left ventricular function which impairs end organ perfusion. Patients with low output heart failure may or may not have congestive symptoms but may present with worsening fatigue, decline in renal function, and confusion all due to decreased perfusion of vital organs. The severity of failure can be described in many ways, which may include a measure of how chronic heart failure affects the quality of life or more acute clinical parameters.

Differential Diagnosis

Acutely decompensated heart failure can coexist with 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 often overlooked. 18 Patients who present with mild or non-specific symptoms pose a particular diagnostic challenge. Symptoms such as weakness, lethargy, fatigue, anorexia, or lightheadedness may actually be a manifestation of decreased cardiac output and low output ADHF. Older patients frequently lack typical signs and symptoms of heart failure. 20 These features may be obscured by the aging process itself or by the presence of coexisting medical conditions. Patients presenting with acute exacerbations of either cardiac dysfunction or COPD may have wheezing on pulmonary auscultation with signs of chronic right-sided heart failure and non-diagnostic chest radiographs. In heart failure patients, pul- monary embolism may be clinically indistinguish- able from ADHF. 21 Precipitating factors for decompensation should be sought in a careful and deliberate fashion

(Table 4).

non-compliance with medications or dietary indis- crition are the most common causes of clinical decom- pensation. 22-27 Often, the cause-effect relationship of ADHF is difficult to determine due to the co-preva- lence of diseases such as coronary artery disease, hypertension, and atrial fibrillation. 14 The exact

Myocardial ischemia or infarction and

prevalence of these coexisting diseases varies depending on the particular population. Nevertheless, in almost all cases, the possibility of an acute 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 ADHF could arise as a consequence of non-cardiac condi- tions such as sepsis, anemia, alcohol withdrawal, uncontrolled diabetes, or thyroid disease (Tables 4 and 6).

Prehospital Care

Even before patients reach the hospital, ADHF is associated with significant morbidity and mortality including malignant arrhythmias and prehospital cardiac arrest. 28 All patients should have continuous cardiac monitoring and intravenous access estab- lished if possible (See also “Clinical Pathway:

Prehospital Therapy For Acutely Decompensated Heart Failure”). Because successful management depends on reversal of hypoxia, pulse oximetry and supplemental oxygen should be utilized routinely in the prehospital care of patients with ADHF. Prehospital personnel should alert ED staff of any

Table 6. Differential Diagnosis Of Acutely Decompensated Heart Failure

Cardiovascular Acute Coronary Syndrome Acute valvular / septal rupture Aortic dissection Arrhythmia Critical aortic stenosis Endocarditis / Myocarditis Hypertensive crisis Pericardial tamponade / effusion Pulmonary COPD (chronic obstructive pulmonary disease) Pulmonary thromboembolism Multi-lobar pneumonia ARDS (acute respiratory distress syndrome) Other Pure volume overload renal failure iatrogenic (e.g., post-transfusion) Sepsis

patient presenting with symptoms suggestive of pul- monary edema or cardiogenic shock, and receive on- line medical advice when appropriate. Prehospital staff trained to interpret electrocardiograms should obtain a 12-lead electrocardiogram and, if ACS is identified, ED staff or medical control should be immediately informed. The decision to treat a patient in the relatively uncontrolled prehospital environment carries some risks 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 undertaken with particular caution in light of the relatively high number of inaccurate diagnoses made in the field. As many as 50% of patients with assumed cardiac associated respiratory distress are diagnosed with a different condition once they arrive at the hospital. 28,30,31 Despite these concerns, evidence suggests that pre- hospital therapy for presumed ADHF can prevent serious 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 a decrease in mortality among critical and non critical patients who received treatment (nitroglycerin, Lasix® and/or morphine) compared to no pharma- cologic intervention. 30 In European countries, where physicians commonly staff ambulances, intensive prehospital treatment of patients with severe heart failure confers short-term benefits. 32-34 A retrospective review of 640 patients that presented in the prehospi- tal setting with acute pulmonary edema (APE) revealed that the use of nitrates were associated with a trend toward decreased mortality. 32 Sublingual nitroglycerin appears to be the safest and most effective of the prehospital medications used for presumed pulmonary edema. 31 A prospec- tive, randomized, double blind study of 57 patients comparing morphine, nitroglygerin, and furosemide found nitroglycerin to be the safest and most effec- tive intervention in the prehospital management of ADHF. 31 Prehospital intravenous (IV) nitrates also yield positive short-term results. The role of other medications for heart failure in the prehospital set- ting is less clear. Early administration of furosemide appears to have very little benefit, and may result in short-term complications. 31,35 The prehospital use of morphine sulfate for presumed pulmonary edema is associated with an increased rate of endotracheal intubation, particularly among patients who turn out to have been misdiagnosed in the field. 31,36 A

prospective, randomized study of 57 patients admin- istered four different drug regimens found that the administration of morphine and Lasix® showed little improvement. 31

Emergency Department Evaluation

Initial Approach The approach to the patient with ADHF begins with stabilization of respiratory and hemodynamic status and with the rapid exclusion or treatment of reversible conditions. Clinical evaluation and empir- ic therapy begin simultaneously with supplemental oxygen, cardiac monitoring, pulse oximetry, and intravenous access. Patients with clinical signs of exhaustion 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 perfusion should be presumed to be in or near cardiogenic shock and managed accordingly (see Special Circumstances). Once the initial resuscitation is underway, further efforts should be made to identify the underlying cause of acute decompensation.

History Most patients presenting with heart failure complain of dyspnea; therefore, determining its degree and precipitants are important. Dyspnea with exertion and at rest, paroxysmal nocturnal dyspnea (PND), and orthopnea are common symptoms. Inquiring about the number of pillows used while sleeping may help identify the presence of orthopnea. A large meta-analysis in 2005 reported that these symptoms are not only specific, but are more likely to occur during ADHF 37 (Table 8). Patients who present with PND, orthopnea, or edema are two time mores likely than others to have ADHF. 37 The rapidity of symp- tom onset may suggest an underlying etiology for the decompensation. An abrupt deterioration should raise concern for arrhythmia, acute MI, or valvular rupture (see Special Circumstances). Prior episodes of a similar nature can provide important clues. Associated symptoms are important and the EP should determine whether the patient has had any chest pain or other anginal equivalent such as shoul- der, neck, arm or epigastric discomfort. In a retro- spective analysis of 491 patients, the combination of syncope and heart failure was found to be associated with a mortality rate of 50%, which was ten times greater than those patients without ADHF. 38 Recent

weight gain, leg swelling, change in urinary output, exercise tolerance, fatigue, and compliance with diet should 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 is often a precipitating factor and is associated with 15 to 64% of cases of ADHF. 39,40 New prescriptions or changes in dosage of medications such as NSAIDs, ophthalmic beta-blockers, herbals, and over the counter drugs are important as well. Male patients

Table 7. Key Historical Questions

• Have you been able to take your prescribed medications?

• Have you adhered to a prescribed diet regimen?

• Has your primary care doctor or cardiologist changed any of your medications lately?

• Have you gained or lost weight in the past 3 to 5 days?

• Do you have difficulty breathing? While lying flat? While walking? In the middle of the night?

• Do these symptoms feel like any prior episodes of “fluid in your lungs,” or “heart failure?

• Are you having any chest pain? Have you passed out?

Table 8. Signs, Symptoms And Diagnostic Studies In Determining Acutely Decompensated Heart Failure.

Studies In Determining Acutely Decompensated Heart Fail ure. with congestive failure may take sildenafil (Viagra), and

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 elicit from patients with ADHF is a prior history of heart failure, myocardial infarction, and/or coronary artery disease 37 (Table 8). A history of heart failure has a specificity of 90%, and patients with prior heart failure are approximately four times more likely to have ADHF when presenting to the ED with acute dyspnea. 37 Prior myocardial infarction is one of the best predictors of impaired left ventricular systolic dysfunction. 42 Patients often can tell you if they have had prior episodes of ADHF. A common term syn- onymous to ADHF for patients with the syndrome of systemic volume overload or acute diastolic dysfunc- tion is “fluid on the lungs.” More sophisticated patients may be able to provide details of previous echocardiograms or cardiac catheterizations.

Physical Vital signs provide a sense of the severity of illness and can suggest etiologic factors for decompensa- tion. Hyperthermia or hypothermia may indicate sepsis or thyroid disease. In the absence of rate-con- trolling pharmacologic agents, tachycardia is nearly universal in ADHF. Bradycardia should raise con- cern for high-degree AV block, hyperkalemia, drug toxicity (digoxin, calcium channel, beta blocker), or severe hypoxia. Hypertension is commonly seen in both systemic volume overload and acute diastolic dysfunction syndromes of ADHF. Hypotension can be baseline for patients with end-stage cardiomyopa- thy or low output heart failure, but otherwise should raise concern for sepsis, massive pulmonary

embolism, or cardiogenic shock.

Signs of congestion may be detected by careful

attention to heart and lung sounds, jugular venous

distention (JVD), hepatomegaly, and peripheral

edema. Elevated central venous pressure (CVP) is

present when the top of the external or internal jugu-

lar veins is more than 3 cm of vertical distance above

the sternal angle. 43 The diagnostic utility of this physi-

cal exam finding is well documented for chronic heart

failure, but less so for ADHF in the ED setting. 44, 45

JVD, abdominojugular reflux, and an audible 3rd

heart sound are very specific. Patients who present

with these exam findings are at least five times more

likely to have ADHF 37 (Table 8). A new cardiac mur-

mur in the proper context must be presumed to sig- nal acute valvular or papillary muscle dysfunction.

The pulmonary exam is usually helpful, but can be misleading. Rales, a classic finding in heart fail- ure, may also occur with pneumonia, interstitial lung disease, 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 sensitivity 37 (Table 8). The leg exam is routine in the evaluation of patients with suspected heart failure and may repre- sent a degree of systemic volume overload. While peripherial edema is moderately specific for increased filling pressures, it has poor sensitivity 37,45 (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.

Diagnostic Studies

Laboratory tests The majority of patients who present with com- plaints suggestive of ADHF will need basic laborato- ry testing. A complete blood count (CBC) is useful for ruling out anemia as a cause for decompensation. Some believe that an elevated white blood count may suggest the presence of an infectious process, especially if bands are present. However, this is not well studied in the patient who presents with dysp- nea. Serum chemistries help assess renal function and overall fluid and electrolyte balance.

Cardiac Markers The question as to which patients with ADHF require screening for cardiac enzymes is not well studied. Additional information from the history (e.g., chest discomfort, new-onset heart failure, or significant risk factors for coronary artery disease) should heighten the suspicion of associated cardiac ischemia. Although not always clear, a high level of suspicion for acute coronary syndrome (ACS) should be considered in patients presenting with ADHF. Several studies have shown that elevated cardiac tro- ponins are found in up to one-third of patients with severe heart failure and help to identify those with worse short-term prognosis. 46, 47 According to one review of 151 patients with a discharge diagnosis of heart failure, 70% of patients did not report chest pain. 47 Therefore, the ED physician should strongly consider screening for cardiac enzymes in any patient who presents with ADHF, regardless of the presence or absence of chest pain.

B-Natriuretic Peptide and NT-proBNP B-type natriuretic peptide (BNP) and NT-proBNP correlate with the presence and severity of heart fail- ure. BNP is produced by cardiac myocytes in response to myocardial stretch and increased end- diastolic pressure and occurs in the setting of heart failure. Pre-proBNP is synthesized within myocytes and is cleaved to proBNP. The latter is released into the circulation and then cleaved to the active BNP and an inactive N-terminal fragment, called NT- proBNP. 48 The half-life of BNP is approximately 20 minutes and the half-life of NT-proBNP is three to six times that of BNP. BNP is a counter-regulatory hormone that offsets the effects of neurohormonal activation by promot- ing diuresis, natriuresis, and vasodilation and sup- pressing the renin-angiotensin system. Plasma levels

of

BNP have been shown to correlate with the degree

of

left ventricular overload, severity of clinical heart

failure, and both short- and long-term cardiovascular mortality. 49-53

Plasma BNP and NT-proBNP levels can be used

to

distinguish between cardiac and non-cardiac caus-

es

of dyspnea. 5,54-56 Studies have shown that the two

peptides have a high degree of correlation. 57-60 Acutely dyspneic patients with plasma BNP levels of less than 100 pg/dl and NT-proBNP levels less than 300 pg/dl are unlikely to have ADHF, and those with BNP greater than 500 pg/dl and NT-proBNP

levels greater than 1000 pg/dl are very likely to have ADHF. BNP levels above 100 pg/dl have 90% sensi- tivity for identifying ADHF, and BNP levels of 500 pg/dl have 87% specificity for identifying ADHF. 61

A BNP cut point of 100 pg/ml predicts the diagnosis

ADHF with 81 to 91% accuracy. 5,10,61

have been performed on NT-proBNP, but a prospec- tive, observational study showed a cut point of 300

pg/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 Properly Multinational Study indicate that BNP levels can be used to improve diagnostic accuracy beyond clinical judgment. 5,10,61 BNP levels will not add significant diagnostic value for patients with classic findings from 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 suspected ADHF. BNP and NT-proBNP levels are elevated in non-

Fewer studies

cardiac conditions (i.e., age, renal insufficiency, pul- monary embolism, and cor pulmonale). 58, 64-67 Since BNP and NT-proBNP levels increase with age, cut- points for diagnosing ADHF are elevated among the elderly and have discriminatory value. 58,65,67 Data from the Breathing Not Properly Multinational Study indicate that BNP is a better indicator at younger ages. 65 In a prospective, observational study of elder- ly patients greater than 65 years of age with acute dyspnea, a higher BNP level of 250 pg/ml has a specificity of 90% in diagnosing ADHF. 58 The role of BNP in patients with severe renal failure is less studied. Patients with severe renal fail- ure have reduced ability to clear metabolites and vol- ume overload resulting in higher levels of circulating BNP. These proposed elevated cut-points have dis- criminatory value, but actual cut points are yet to be determined. 59 Obese patients with elevated filling pressures may have less myocardial stretch which lowers measured BNP and NT-proBNP levels. This may be due to increased extracardiac pressure associated with an elevated BMI. The sensitivity of BNP and NT-proBNP at existing cut points for obese patients may be lower than expected and a true cut-point in this setting is unclear. 68 The Breathing Not Properly Multinational Study found an inverse relationship between BMI and BNP. 69 For overweight and obese patients, BNP is 80% sensitive at a cut point of 100 pg/ml. In addition, 20% of these patients with ADHF had BNP levels less than the standard cut off. 68 NT-proBNP may also lose discriminatory value among obese patients. The ProBNP Investigation of Dyspnea in the Emergency Department (PRIDE) study identified significantly lower ProBNP and BNP 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 breath consistent with other etiologies (i.e. asthma, COPD), BNP is not likely to assist in the diagnostic workup. Checking BNP levels in indeterminate cases may aid in diagnosing or excluding ADHF, but results may leave the EP with additional questions. A provocative single-center study used BNP to diagnose ADHF and showed beneficial effects on patient outcomes. In the B-Type Natriuretic Peptide for 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 BNP group 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 insensitive tool, it remains useful for detecting ischemia, arrhythmias, and electrolyte disturbances. Given the high proportion of heart failure exacerbations precip- itated or accompanied by ischemia, it is difficult to justify not obtaining an ECG on all such patients. 22 In a meta-analysis of 22 studies differentiating car- dio-pulmonary cause of dyspnea, atrial fibrillation was the most likely associated ECG finding among patients presenting to the ED with ADHF 37 (Table 8). The ECG is likely to be abnormal in patients with chronic heart failure. In a clinic population, approximately 40% of 19,877 clinic patients had ECG with left ventricular hypertrophy, and approximately 70% had electrocardiographic evidence of cardiac ischemia or a prior MI. 70 Conversely, an entirely nor- mal ECG is strong evidence against the presence of left ventricular dysfunction and should therefore prompt consideration of alternative diagnoses. 20,37,71 Also, a prolonged QRS has been shown to be an independent predictor of LV dysfunction.

Chest X-ray The chest x-ray should be obtained in patients with suspected ADHF. 3 Findings suggestive of ADHF include cardiomegaly, vascular redistribution (e.g., cephalization, fullness of hilar vessels), interstitial or pulmonary edema, and pleural effusions. Pleural effusions in heart failure tend to be bilateral or local- ized to the right side. 73 The presence of pulmonary congestion and cardiomegaly is associated with a very high likelihood of ADHF 37 (Table 8). The chest film may also be useful in identifying alternative or contributing causes of the patient’s symptomatology. There are several pitfalls that await the unwary physician who uses the chest film to diagnose acute heart failure. Heart size may be normal in acute fail- ure, especially if the failure originates from acute diastolic dysfunction. 45 COPD patients may have minimal radiographic evidence of concurrent heart failure. Also, patients with longstanding chronic heart failure may have well developed lymphatic drainage of the pulmonary interstitium and, there- fore, little radiographic evidence of congestion.

Recent studies have shown that a normal chest radi- ograph alone cannot exclude ADHF. According to a recent ADHERE study, one in five patients without radiographic findings of interstitial edema, pul- monary edema, or vascular congestion received a final diagnosis of ADHF. 73

Cardiac Echocardiography Echocardiography is invaluable and is, in some sense, considered the “gold standard” for assessing the status of left ventricular function, distinguishing between systolic and diastolic failure, and identify- ing regional wall motion abnormalities. Echocardiography can also assist in diagnosing or excluding potentially reversible etiologies of an acute decompensation such as pericardial tamponade, massive pulmonary embolus, ruptured chordae tendineae, or ruptured ventricular septum (see Special Circumstances). Echocardiography is probably not indicated in all instances of ADHF, particularly if a patient has had a recent echocardiogram and a clear precipitant for decompensation. ACC/AHA guidelines recommend transthoracic echocardiography as soon as possible after initial stabilization for any patient who presents with acute pulmonary edema, unless there are obvi- ous precipitating factors and the patient’s cardiac sta- tus has been adequately evaluated previously. 74 Guidelines for establishing an effective system for emergency echocardiography have been published. 75 Experience with emergency physicians performing bedside echocardiography has generally been limited to ruling out pericardial effusion / tamponade. 76-78

Pulmonary Artery Catheterization (Swan-Ganz) Swan-Ganz catheters provide considerable data on cardiopulmonary function that are thought to improve management and clinical outcomes; howev- er, recent trials have not demonstrated significant patient benefit associated with their use. 79 The Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness (ESCAPE) trial, a randomized, controlled trial of 433 patients, showed no difference in six-month mortali- ty or return for hospitalization compared to clinical assessment. 79 On the other hand, the use of invasive monitoring in this study was associated with more adverse events. Nevertheless, published consensus guidelines advise the use of PA catheters in patients who do not respond to initial therapies. 2,3

Other Diagnostic Modalities

Peak Flow/End Tidal CO 2 Peak flow and end tidal CO 2 are two additional diag- nostic modalities that may help identify ADHF in the undifferentiated patient. In a study of 56 acutely dyspneic patients, peak expiratory flow rates of those with heart failure were found to be twice those of patients with COPD; however, no single cut-off provided for perfectly accurate classification. 80 While end-tidal carbon dioxide levels (ETCO 2 ) for heart failure patients differ significantly from those of asthma/COPD patients, there is no single ETCO 2 level that can reliably differentiate between the two conditions. 81

Treatment

As with any ill patient, the initial focus of treatment will be on airway and breathing (see Clinical Pathway: Treatment For Acutely Decompensated Heart Failure). Although many patients can be man- aged with oxygen, with or without non-invasive ventilatory support, the presence of agonal respira- tions or profoundly depressed mental status will mandate emergent intubation with the caveat that the respiratory symptoms that accompany ADHF reflect cardiovascular rather than pulmonary pathol- ogy and are therefore often rapidly reversible with aggressive medical therapy (see Respiratory Therapy). Sitting the patient upright may reduce pulmonary congestion and improve respiratory dynamics. Studies in patients with chronic heart failure show a large rise in airflow resistance after lying supine for five minutes, a condition that is reversed by sitting erect. 82 Practice guidelines recommend early use of pulse oximetry, noninvasive blood pressure monitor- ing, and continuous cardiac monitoring as these can provide early warnings of decompensation. 3

Pharmacologic Therapy The main objectives of pharmacologic therapy for ADHF are relief of pulmonary congestion and improvement in systemic tissue perfusion. The goal of therapy is to reduce preload and enhance left ven- tricular function, while maintaining or improving myocardial oxygen balance. While the basic approach to treating ADHF has not changed over the past two decades, there has been increasing empha- sis on afterload reduction and other means of coun- teracting the adverse cycle of neurohormonal activa-

tion (see Table 9 and Clinical Pathway: Emergency Department Therapy for Acutely Decompensated Heart Failure).

Nitrates

Nitrates are recommended as initial therapy for ADHF of both ischemic and non-ischemic origin, par-

ticularly for patients with hypertension or with presumed 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 dilation of the coronary arteries. 85 Significantly, in patients with severe underlying left ventricular dysfunction,

Table 9. Medications For Acutely Decompensated Heart Failure

9. Medications For Acutely Decompensated Heart Failure Emergency M M edicine P P ractice © 12

afterload reduction appears to predominate over preload 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 treatment of ADHF. To date, no prospective studies on its effects on mortality have been published. In the Vasodilation in the Management of Acute Congestive Heart failure (VMAC) trial, intravenous nitroglycerin improved dyspnea scores compared to placebo dur- ing early therapy. 8 In another randomized, controlled trial involving subjects with pulmonary edema, a reg- imen of high-dose nitrates and low-dose diuretics provided more consistent clinical improvement than a regimen of high-dose diuretic and low-dose nitrates. It was also associated with lower rates of mechanical ventilation and MI. 87 Because many of the patients in this study had underlying coronary artery disease, it is likely that the anti-ischemic effects of nitrates also played a role. Data from ADHERE show a lower mortality rate among patients treated with nitrates compared to inotropic agents, but did not compare nitrates to diuretic therapy. 88 Single doses of 0.4 mg sublingual nitroglycerin can be given repeatedly every five to ten minutes, provided the patient has stable blood pressures. In the hospital setting, continuous IV administration of nitroglycerin is generally more convenient and allows for titration to specific clinical or hemody- namic end-points. Nitroglycerin can be started at 0.3 to 0.5 mcg/kg/min but may require much higher doses (up to 3 to 5 mcg/kg/min), so long as the blood pressure is above 95 to 100 mm Hg. 89 Alternative regimens and formulations for adminis- tering IV nitrates have been described, but offer no clear advantages. 83,90,91 Oral or transdernal nitroglyc- erin have comparable hemodynamic effects to IV nitroglycerin but are less amenable to rapid titration and may be less effective in patients with poor gas- trointestinal absorption or poor skin perfusion. 92 Hypotension with standard nitrate therapy is generally mild and transient. Severe or persistent hypotension should raise suspicion for hypovolemia, stenotic valvular disease such as aortic stenosis, car- diac tamponade, right ventricular infarction, or recent use of sildenafil (Viagra®). If these conditions are known or suspected, nitrates should be avoided or used with extreme caution. Nitrate therapy may not be particularly effective in patients with massive peripheral 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 with marked systemic hypertension, severe mitral or aor- tic valvular regurgitation, or pulmonary edema not responsive 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 to 0.3 mcg/kg/min and advanced as needed to improve clinical and hemodynamic status, maintain- ing a SBP greater than 90 or mean arterial pressure greater 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 patients with systemic volume overload. 2,3 Although this practice is recommended by societies and is a com- monly accepted approach, there have not been multi- ple randomized, controlled trials or meta-analysis to support it use. On the other hand, it is important to recognize that patients who present with ADHF are not always volume overloaded. Patients with acute diastolic dysfunction may benefit more from redistri- bution of circulating volume by using vasodilators. The indiscriminate use of diuretics carries the risk of overdiuresis and detrimental effects on renal func- tion, particularly among elderly patients. Even with- out overdiuresis, there is growing evidence that the higher doses of diuretics required to treat advanced heart failure correlate to worsening renal function, which has been tied to both longer hospi- talizations and increased mortality after discharge. This adds strength to the argument that the focus should be on changing loading conditions with vasodilators rather than diuresis as the stand alone therapy it often is. Evidence from a large number of in vitro and in vivo experiments suggest that direct vascular actions also contribute to the clinical effects of furosemide. 94-97 These actions are not necessarily advantageous, in that their net effect may promote further activation of the sympathetic and renin-angiotensin systems characterized by reflex vasoconstriction, worsening of cardiac loading conditions, and a decline in car- diac output. 98,99 Studies comparing the acute effects of diuretics and nitrates have emphasized the more favorable overall hemodynamic effects of the latter group, as described earlier.

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(continued from page 13)

Depending on the patient’s clinical condition, state of hydration, and previous use of diuretics, an initial IV dose of 40 to 200 mg of furosemide can be administered. For patients on chronic diuretic thera- py, a common strategy is to begin with the usual daily dose (typically 40 to 80 mg) given as an IV bolus, and to double the dose if there is inadequate diuresis. Although IV boluses of furosemide are a common practice, there is a trend toward using IV furosemide infusions. 100-102 A randomized crossover study compared continuous furosemide to bolus administration and showed that those treated with continuous furosemide resulted in greater urine out-

put and fewer adverse effects. 96 A recent meta-analy-

sis reviewing eight randomized, controlled trials

compared bolus versus continuous intravenous diuretics. These small heterogeneous studies showed that continuous IV diuretics improved diuresis and carried a better safety profile. 103 Although these findings are encouraging, larger

studies to definitively support one over the other are needed. In cases of volume overload that fail to respond

to standard therapy, substitute a more potent loop

diuretic such as torsemide (Demadex®) 10 to 20 mg

IV or bumetanide (Bumex®) 1 to 4 mg IV. The use of

these medications among patients with ADHF in the ED setting has not been published. Combining furosemide with a thiazide agent such as metolazone

(5 to 20 mg PO) or chlorothiazide (Diuril®) 500 to 1000 mg IV) may improve diuresis. 104,105 While not all patients 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 hypokalemia and hypomagnesemia occur with chronic diuretic

use and may worsen with subsequent administration

of 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

Nesiritide

Nesiritide (recombinant BNP) is FDA approved for the treatment of ADHF symptoms. BNP has vasodilatory as well as mild diuretic and natriuretic properties. When administered in supraphysiologic doses, it exerts favorable hemodynamic, natriuretic, and neurohormonal effects. 106-109 Nesiritide can be administered 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 be

more effective than placebo in improving hemody-

namics. 110-112 The VMAC trial compared nesiritide to nitroglycerin in the treatment of ADHF. At three hours, PCWP was lower in the nesiritide group ver- sus the nitroglycerin group but dyspnea scores at 3 and 24 hours were not statistically significant between the two groups. 8 A study from ADHERE showed that treatment with nitroglycerin or nesiri- tide had lower in-hospital mortality than ionotropic treatments with milrinone or dobutamine. 88 There was no in-hospital difference in mortality between nitroglycerin and nesiritide. Studies have yet to show improvement in length of stay, hospital costs,

or mortality. Recent studies have emphasized potential risks

associated with nesiritide. 113,114 Pooled data and meta- analysis suggest an increase in creatinine levels with nesiritide, which required additional medical inter- vention. Another meta-analysis suggested that nesir- itide carries a greater 30-day risk of death compared

to conventional therapy. 113 Prospective trials address-

ing these questions have not yet been published. Although there are recent studies questioning the safety of nesiritide and consensus guidelines rec- ommend its use, the Heart Failure Society of America notes the need for additional prospective studies. 2

ACE Inhibitors

Angiotensin converting enzyme inhibitors (ACE inhibitors) represent a logical extension of vasodila- tor therapy. The beneficial hemodynamic effects of ACE inhibitors in acute heart failure have been appreciated for two decades. 115 Acutely, ACE inhibitors 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 the European Society of Cardiology or the Heart Failure Society of America in the setting of acute heart fail- ure, drug regimens that include an ACE inhibitor appear to have hemodynamic advantages over those based upon other vasodilators. 119-121 For acutely decompensated heart failure, ACE inhibitors can be administered intravenously (e.g., enalaprilat), orally (e.g., captopril) or sublingually (e.g., emptied captopril capsules contents).

Depending on the drug, the dose, and the route of administration, hemodynamic effects may be seen within 10 to 60 minutes. 116,117,119 Safe dosing regimens of enalaprilat include 0.004 mg/kg as an intravenous bolus, or 1 mg by continuous intravenous infusion over two hours. The suggested one-time dose of oral or sublingual captopril is 12.5 to 25 mg. The safety of administering an ACE inhibitor in the setting of ADHF is of concern to some clinicians who fear potentially deleterious effects on blood pressure, renal function, and electrolyte balance. However, clinical trials have consistently demonstrated the safety of administering ACE inhibitors to patients with ADHF. 118,122 Few studies of ACE inhibitors for ADHF have been performed in the ED setting. Small studies have demonstrated that sublingual captopril is safe and effective for ED patients with pulmonary edema. 123,124 In one retrospective analysis, the use of sublingual captopril in the ED was associated with lower rates of mechanical ventilation and CCU admission. 125 ACE inhibitors are contraindicated in the context of pregnancy, hyperkalemia, or a history of ACE- inhibitor-induced angioedema. For patients with evidence of poor systemic perfusion, ACE inhibitors should be used cautiously, because additional vasodilation may not be tolerated. Unlike nitrates, ACE inhibitors have a relatively prolonged duration of action, making dosage less easily titratable.

Inotropes

Short-term therapy with ionotropes may benefit patients presenting with low output failure, which are considered acceptable treatment modalities, although with notable risks. 2,3 Classically, inotropic agents have been reserved for the treatment of car- diogenic shock. However, short-term inotropic sup- port may also be seen as beneficial for patients with low output failure who fail to respond to conven- tional therapy. While short-term inotropic therapy clearly improves hemodynamic performance, the impact on clinical outcomes is less sanguine. Inotropic therapy has deleterious effects upon patients with preserved or moderately depressed ventricular function and congestion. The Outcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic Heart Failure, a random- ized, controlled trial, showed no increased benefit over standard therapy with the use of milrinone. 126,127 ADHERE also supports this finding indicating an

increase in mortality among patients with volume overload and diastolic dysfunction who were treated with ionotropes. 88 It is important to understand the expected hemo- dynamic effects of inotropic agents and to set clear goals for therapy. Most inotropic agents have multi- ple pharmacologic actions, some of which may be deleterious. Undesirable chronotropic effects, arrhythmogenesis, or ischemia resulting from increased 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 of digoxin are modest, unpredictable, and delayed for at least 90 minutes after intravenous loading. 128 For patients with ADHF, the only reasonable use for digoxin is to help control the ventricular response to atrial fibrillation (see Special CircumstancesAtrial Fibrillation).

Morphine

Morphine is one of the oldest drugs still in use for the treatment of acute heart failure and remains an adjunct for treating the anxiety and discomfort asso- ciated with pulmonary edema. With high doses of morphine, direct vasodilation may result from hista- mine release, but the predominant hemodynamic effects of morphine appear to be mediated through the central nervous system. 129 Morphine can be administered safely to most patients. However, because of its sedative properties and potential to depress respirations, caution should be exercised when administering morphine in the setting of chronic pulmonary insufficiency or suspected acido- sis. One retrospective study found that ED adminis- tration of morphine to patients with pulmonary edema was associated with an increased rate of endotracheal intubation and CCU admission. 125

Respiratory Therapy The majority of patients with respiratory distress respond to supplemental oxygen and standard phar- macologic therapy, but patients with persistent hypoxemia or progressive fatigue will require at least temporary respiratory support (see also the July 2001 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 atelectatic alveoli, improving pulmonary compliance, and

reducing the work of breathing. 130 At the same time, particularly in patients with congestive heart failure, CPAP improves hemodynamics by reducing preload and afterload, thereby enhancing left ventricular per- formance. 131-134 Nasal or face mask-applied CPAP of 5 to 10 cm H 2 0 has been shown to improve oxygena- tion, reduce heart rate and reduce blood pressure compared to standard oxygen treatment. 135-141 In sev- eral randomized, controlled clinical trials, CPAP reduced the need for endotracheal intubation in patients with severe cardiogenic pulmonary edema. 135,137,138,142 Pooled data and one randomized, controlled trial also suggest that the use of CPAP in this 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 assistance with the inspiratory work of breathing. Evidence from several case series and a recent randomized trial support the use of this therapy in patients with acute cardiogenic pulmonary edema; 144-147 however, another randomized, controlled trial and small series did not show benefit. 148,149 A small, randomized trial compar- ing BiPAP with CPAP demonstrated a more rapid clinical improvement with BiPAP but no difference in the rates of intubation. 150 Of concern in this trial was an unexpectedly high rate of acute MI associated with the use of BiPAP, which prompted premature termination of the study. One other clinical trial involving BiPAP was also terminated early because

Cost Effective Strategies For Acutely Decompensated Heart Failure

1. Don’t admit every patient with heart failure.

Some patients with acutely decompensated heart failure may only require an ED “tune-up” and

will be appropriate for discharge. Patients with

a past history of failure who have a reassuring

history and physical examination, normal labora- tory values, and an ECG unchanged from previ- ous tracings may be candidates for outpatient follow up (especially if their decompensation

occurred because they ran out of their medicine).

If discharge is considered, communicating with

the patient’s cardiologist and/or primary care provider is necessary for close follow-up. ED

observation units for select patients may also be

a cost-effective alternative to traditional admis- sion.

Caveat: Most patients who present with acutely decompenesated heart failure will need hospital admission—especially those with abnormal vital signs, 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 and length of stay in the intensive care unit. Keeping

a machine in the ED and using it frequently can promote early use.

Caveat: Some patients are not good candidates for non-invasive ventilation—especially those

who are agitated or those who have altered men- tal status, unstable vital signs, or evidence of acute MI.

3. Consider the use of furosemide infusions.

While many patients in acutely decompensated heart failure respond quickly to nitrates and bolus diuretics, some do not. Some studies do show that intravenous infusions of furosemide for NYHA class IV heart failure are a safe, effec- tive, and economic mode of therapy, especially in the elderly. The increased cost of the infusion would be more than offset by savings accrued by a shorter hospital stay. Since this trial was small and non-randomized, further study is needed to ensure 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 decompensated heart failure, BNP may be the single best investi- gation. It is relatively sensitive and specific and can be performed at the bedside. In the acute setting, elevated BNP levels correlate with the diagnosis of heart failure, reduce time to treat- ment, decrease length of hospital stay, and decrease cost of care.

Caveats: Levels of BNP or NT-proBNP are affect- ed by their half-lives. BNP levels may also be elevated in eldery patients and patients with renal insufficiency and lower in obese patients.

of similar safety concerns. 151 Recent studies provide

evidence to suggest no advantage of BiPAP/NPPV over CPAP for patients with cardiogenic pulmonary edema and hypoxemic respiratory failure. 152-154

However, recent meta-analysis shows a small benefit

in CPAP, but no significant changes in clinical out-

comes. 155 The success of non-invasive respiratory support depends upon appropriate patient selection. For patients with compromised upper airway function or significantly altered level of consciousness, intuba- tion and mechanical ventilation remain the definitive therapy. Patients with a history of cardiac arrest, unstable cardiac rhythms, or cardiogenic shock are generally not felt to be candidates for non-invasive approaches. Likewise, in the setting of severe myocardial ischemia or infarction, full ventilatory support may be preferable in order to decrease the myocardial oxygen demand associated with respira- tory effort. Although the decision to initiate non-invasive respiratory support is dependent on a variety of fac- tors, the presumption is that the earlier therapy is instituted, 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 patients with presumed cardiogenic pulmonary edema. 156, 157

A small case series showed an increase in mean

pulse oximetry of patients treated with CPAP. 157 In one 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 BiPAP on patients with suspected CHF thought it improved the patients’ dyspnea; however, data analysis showed no statistical difference between groups in the length of subsequent hospital stay, intubation, or mortality. 156

In either the prehospital or ED setting, if there is progressive respiratory failure in spite of non-inva- sive support, the patient requires intubation and mechanical ventilation. In general, airway manage- ment should be accomplished with rapid sequence intubation (RSI). This involves using an induction agent in combination with a short-acting paralytic such as succinylcholine so as to maximize the rate of success on the initial attempt. 158 Maintaining the patient in an upright position as long as possible prior to intubation may assist in maximizing pre-

oxygenation. Prolonged episodes of hypoxia or hypotension during intubation risk further cardiac decompensation and cardiopulmonary arrest. In one study, all induction agents used (thiopental, fentanyl, and midazolam) were associated with a significant risk of hypotension for patients with pulmonary edema. However, the authors admit that the small numbers of patients with pulmonary edema in this study preclude a valid post hoc comparison. 159 On the other hand, induction with etomidate appears to be safe and effective for a range of patients undergoing RSI, including those with underlying heart disease. 160 Once mechanical ventilation is instituted for cardio- genic pulmonary edema, it is not certain whether positive end-expiratory pressure (PEEP) confers any additional hemodynamic benefit. 161-164

Special Circumstances

Cardiogenic Shock Cardiogenic shock in the setting of heart failure is most often seen in the setting of acute ST-segment elevation MI and acute valvular diseases. Mortality rates for patients with frank cardiogenic shock remain alarmingly high, ranging from 50 to 80% 165 Stat echocardiograms play a pivotal role in diagnos- tics and treatment, as many etiologies of cardiogenic shock will require surgical management. In the con- text of acute MI, emergent cardiac catheterization and revascularization have been shown to be of ben- efit.

Other potentially reversible causes of cardiogenic shock, such as acute valvular dysfunction, ventricu- lar septal wall rupture, and pericardial tamponade, need to be excluded or addressed promptly. Acute valvular dysfunction can occur in the setting of ACS (ischemic papillary muscle dysfunction/rupture) or independently in acute mitral/aortic insufficiency, aortic dissection, or prosthetic valve thrombosis causing cardiogenic shock. Free wall rupture and ventricular septal wall rupture are uncommon com- plications of AMI that require rapid recognition. Once the diagnosis is made, surgical management provides an opportunity for survival. Again, the eti- ology of these types of cardiogenic shock should be promptly identified with emergent echocardiogra- phy. 2 Once acute surgical causes of cardiogenic shock are ruled out, non-cardiac etiologies of shock, such as hypovolemia, sepsis, poisoning, and massive pulmonary embolism must also be entertained. Aside from addressing reversible causes of car-

3,166,167

diogenic shock, the overarching goal in treating patients who present with evidence of inadequate

tissue perfusion (i.e., cool skin, altered mental status) from acute heart failure or ADHF should be to restore and maintain perfusion of vital organs. Patients who present in shock with a normal blood pressure or with mild hypotension may respond favorably to dobutamine (starting at 2 to 3 mcg/kg/min). Prior to initiation of vasopressor agents or ionotropes, small fluid bolus can be admin- istered as an initial measure. Compared with dopamine, dobutamine is associated with a lower incidence 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 patients

who

have severe hypotension (SBP less than 70 to 80

mm

Hg) in the presence of volume overload or after

bolus administration of saline. At moderate doses (4 to 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 of dopamine reduced, with the goal of reducing myocardial oxygen demand. Intra-aortic balloon counterpulsation (IABC) should be considered for patients with a potentially reversible condition, when initial management of ADHF fails, or when stabilizing measures are needed as a bridge to definitive management. 3 IABC can be an effective temporizing measure in anticipation of coronary revascularization or cardiac valve repair.

The patients least likely to benefit from the IABC are

those with multiple previous infarctions, massive irreversible myocardial necrosis, aortic dissection, advanced stages of cardiogenic shock, and elderly patients with peripheral vascular disease (because of complications from insertion of the device). If IABC is not immediately available, norepinephrine can be added to increase systolic pressure to acceptable lev- els (80 or more mm Hg). Because of the adverse effects on renal and mesenteric perfusion, the use of high-dose dopamine or norepinephrine should be considered only as a temporizing measure until a definitive therapy can be substituted. It is important for the EP to distinguish between acute heart failure with cardiogenic shock and low output ADHF, both which present with hypotension. Low output ADHF tends to present subacutely in patients with end stage systolic heart failure (see Pathophysiology section, and Figure 1 on page 5).

Patients may describe symptoms of fatigue, loss of appetite and lethargy. Management of these patients can be extremely challenging for the EP; therefore, optimal treatment may require the involvement of a heart failure specialist. Frequently, the key to man- agement is identifying the etiology of decompensa- tion. Although the EP’s impulse may be to aggres- sively fluid bolus or aggressively diurese patients with low output ADHF, a “do nothing” management style is often the best approach.

Renal Dysfunction ADHF and chronic renal insufficiency frequently co- exist. 169,170 One out of every three patients admitted for ADHF have renal insufficiency, with one of every five patients with creatinine levels greater than 2.0 mg/dl. Renal hypoperfusion from poor cardiac out- put is aggravated by the use of diuretics and ace inhibitors which, in turn, contribute to worsening renal function. Both pre-existing renal insufficiency and decline in renal function while managing ADHF are associated with increased mortality. There is a greater risk of in-hospital mortality among patients treated for ADHF with interval worsening of renal function. 171 Heart failure is present in about one third of patients who begin dialysis and will develop over time in an additional 25%. 172 Among anuric hemodialysis patients, heart failure is the most com- mon cause of ED visits. 173 In these patients, ADHF is most often due to volume overload between dialysis treatments. Although hemodialysis is the treatment of choice for these patients, it may not be immediate- ly available. ED treatment is directed at stabilizing these patients until hemodialysis can be performed (Table 10). Because of their direct vascular effects, diuretics may still have a role in managing anuric patients with volume overload. 174 Vasodilator thera- py with nitrates and ACE inhibitors has been shown to be particularly effective. 123 In a descriptive study of 46 renal dialysis patients, the administration of preload and afterload reducing agents including cap- topril and nitroglycerin resulted in no deaths. In any dialysis patient with an unstable cardiac rhythm, hyperkalemia and digoxin toxicity must be consid- ered.

Atrial Fibrillation Atrial fibrillation is commonly seen in patients with chronic heart failure and its co-prevalence is likely associated with underlying hypertension and coro-

nary artery disease. In patients presenting with ADHF, atrial fibrillation is seen in approximately one-third of patients. 3,4,8 In the context of normal ventricular function, loss of synchronized atrial contractions is of minimal hemodynamic significance. However, in patients who have abnormal systolic or diastolic function, the loss of “atrial kick” can have profound conse- quences. When atrial fibrillation is accompanied by a rapid ventricular response, the reduced filling time and increased myocardial oxygen demand lead to further decline in cardiac performance. When assessing the patient with rapid atrial fib- rillation and ADHF, it is often difficult to attribute cause and effect. While new onset rapid atrial fibril- lation may be the precipitant of ADHF, more com- monly atrial fibrillation is a response to worsening heart failure (e.g., via neurohormonal activation and/or increased atrial stretch). This distinction can often only be made clinically. In either case, manage- ment focuses upon the treatment of both conditions. 175 Management of atrial fibrillation in the context of ADHF should focus upon treating the underlying cause of ADHF and controlling the ventricular rate to allow for improved ventricular filling / contrac- tion and improved myocardial oxygen balance 2,3 (Table 10). In general, digoxin, diltiazem, and amio- darone are considered acceptable therapies for rate control in patients with left ventricular systolic dys- function. 176-178 The EP should exercise some caution with beta-blockers or calcium-channel blockers for rate control because of potential negative inotropic effects that could worsen existing systolic dysfunc- tion. Although not specifically studied in the setting of ADHF, esmolol would be a reasonable option, given its short duration of action and demonstrated safety in patients with severe chronic heart failure. Cardioversion, whether electrical or chemical, is a reasonable treatment alternative for unstable or “new” atrial fibrillation, but maintaining sinus rhythm may not be possible if the underlying heart failure is not addressed.

Controversies / Cutting Edge

Impedance Cardiography (ICG) Impedance cardiography (ICG) is a non-invasive means of hemodynamic monitoring that provides real-time estimates of cardiac output and pulmonary capillary wedge pressure by employing principles of thoracic bioimpedance. Over the past three decades,

ICG has been investigated in a variety of clinical set- tings and has been found to compare moderately well 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 underlying heart disease; however, serial measurements may still provide useful information, such as monitoring response to therapy. In a small study of 38 patients with undifferentiated dyspnea, incorporation of ICG data increased diagnostic accuracy of patients with cardiac causes of dyspnea. 181 In the Emergency Department Impedance Cardiography–aided Assessment Changes Therapy (ED-IMPACT) trial, the use of ICG affected treatment plans for 24% of patients with acute dyspnea. 182 However, more stud- ies are necessary to determine the overall utility of this diagnostic tool and its effects on morbidity, mor- tality, cost, and length of stay.

Beta-blockers Large, randomized, controlled trials have demon- strated clear morbidity and mortality benefits of long-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 clinical deterioration. 186 There has been no study that specifi- cally addresses the potential benefits of beta-blocker therapy 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 is advised during its use. 3 In the setting of an acute decompensation, chronic beta-blocker therapy should either be temporarily discontinued or admin- istered cautiously at a reduced dose, according to the ESC. On the other hand, in the context of ongoing ischemia, tachycardia, and severe hypertension beta- blockers may be considered. 3 Less is known specifically about the safety and efficacy of beta-blocker therapy for patients with acute diastolic dysfunction. In theory, the value of reducing hypertension and tachycardia would out- weigh any concern about negative inotropy in these patients. Further studies are needed to clarify the role of beta-blockers in this context.

Calcium Sensitizers Calcium sensitizers are a novel class of agents that

modify the configuration of troponin C to promote myofilament sensitivity to calcium, enhancing con- tractility without impeding diastolic relaxation. 186b Levosimendan is the best studied of these agents. In two small, randomized, controlled studies of patients with severe ADHF, these agents were shown to improve hemodynamics and decrease mortality. 187,188 The Levosimendan Versus Dobutamine Trial (LIDO) compared levosimendan to dobutamine with improved hemodynamics and six month mortality among 203 patients. 187 Although encouraging, the study population was restricted to low output heart failure patients and the mortality benefit may be associated with adverse affects of dobutamine. The Calcium Sensitizer or Inotrope or None in Low Output Failure Trial (CASINO) showed a significant mortality benefit with levosimendan compared to dobutamine and placebo. 188 Although these results are 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 is still unclear. Implications for ED use await addition- al clinical trials. Pimobendan is another calcium sensitizer approved for use in Japan. The Pimobenden in Congestive Heart Failure Trial (PICO) showed improved hemodynamics but increased hazards for death compared to placebo. 189 The study population was stable heart failure patients in the clinic setting. Generalization of these findings to patients with ADHF in the ED setting is limited.

Novel Natriuretic Peptides Endogenous natriuretic peptides in addition to nesir- itide have been investigated as potential new agents to treat ADHF. Carperitide, an atrial natriuretic pep- tide, has vasodilatory effects as well as natriuretic properties. 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 showed improved hemodynamics, and symptoms of dysp- nea. The impact of these novel therapies in the ED setting is unknown because previous studies have yet to represent ED patients with ADHF.

Vasopressin Antagonists Elevated vasopressin levels are found in patients with ADHF, and vasopressin antagonists have been proposed as a means to improve diuresis in patients with ADHF. In a hemodynamic trial, conivaptan, a V1a and V2 receptor antagonist, decreased PCWP and right atrial pressures. 191 In a randomized con- trolled trial among patients with ADHF in the setting of systolic dysfunction, tolvaptan, a V2 receptor antagonist, has been shown to decrease body weight with no changes in worsening heart failure at 60 days. 192

Endothelin Antagonists Endothelin one (ET-1), a potent vasoconstrictor and modulator 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, delayed myocyte hypertrophy, and increased myocardial con-

tractility. 193 A randomized, controlled trial comparing tezosentan with placebo among patients with low output ADHF showed improved hemodynamics with the use of tezosentan without significant changes in dyspnea compared to standard thera-

pies. 194

in the treatment of ADHF.

Future studies will clarify tezosentan’s role

Disposition

Even in this era of cost containment, the vast majori- ty of patients who present with ADHF are admitted to the hospital. 195 According to ADHERE, the majority of patients with ADHF are admitted to telemetry and step-down units while 14% of patients are admitted to the ICU during their hospital stay. 14 Meanwhile, hospital costs for in-patient care of ADHF are continuing to rise. In-hospital mortality remains approximately 2.3 to 7%, 14,126,196 with major adverse events occurring in up to 18% of patients. 197,198 In patients with NYHA class III or IV heart failure who are admitted for ADHF, there is a 9.6% mortality rate at 60 days and a 30% combined rate of rehospi- talization and/or death. 6 However, while the realities of modern healthcare economics may not favor rou- tine hospitalization, premature release of inadequate- ly treated patients are likely to result in increased short-term morbidity and mortality. 199 In general, clinicians have great difficulty judg- ing the prognosis of patients with exacerbations of heart failure. 200 Acutely decompensated heart failure

is a dynamic entity, and the ED physician often sees only a snapshot of the patient at any point in time. Some patients are dramatically ill at presentation but respond rapidly to treatment, while other patients go on to develop serious complications after a period of relative stability. Previous studies have found that certain patient characteristics are predictive of in-hospital morbidity and mortality (Table 11). 201-206 In multivariate analysis, independent correlates of major complications or death during hospitalization have included hypoten- sion, tachypnea, jugular venous distention, electrocar- diographic abnormalities, hyponatremia, and poor initial diuresis. 196,201-204 Recent studies have shown that troponin elevations, elevated BNP, and worsening renal function are prognostic factors in post-discharge mortality and risk for rehospitalization. 196,207,208 In one study, 325 patients with acute dyspnea and those with BNP levels greater than 230 pg/ml had a rela- tive risk of 24.1 for death and a 51% probability of an additional 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 mortality among patients admitted with heart failure. 205,206 The Enhanced Feedback for Effective Cardiac Treatment (EFFECT) study, a retrospective, multi-center, com- munity-based study identified predictors of 30-day and one-year mortality among patients admitted to the 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 than 43) and moderately low systolic blood pressures (SBP greater than 115) to have a mortality of greater than 20%. 205 A risk stratification tree has been devel- oped to assist clinicians in determining mortality risk of patients who present with ADHF (Table 12). Disturbingly, some studies have shown that patients without any independent risk factors appear to have substantial rates (6%) of in-hospital morbidity and mortality. 201 The Heart Failure Society of America has estab- lished criteria for hospitalization of patients with heart failure. 2 The recent HFSA criterion includes worsening renal function, altered mentation, and new onset atrial fibrillation as circumstances that merit hospitalization. However, in the Agency for Health Care Policy and Research study, criteria failed to identify up to one-third of the patients who die

within 30 days. 195 Studies on the effectiveness of the HFSA criteria have not yet been studied or pub- lished. Thus, while published criteria and guidelines can help with triage, the significant rate of morbidity even among “low-risk” patients mandates that clini- cal judgment be incorporated into the decision-mak- ing process. For patients who are ultimately discharged home, consultation with the patient’s primary care physician and/or cardiologist is imperative. The EP needs to understand that this is a high-risk situation. Patients and their families need to understand that there is a substantial chance of outpatient failure necessitating a repeat ED visit or hospitalization within the next 30 days. 211 Alarmingly, a recent out- come study of 112 patients discharged from the ED with a primary diagnosis of CHF showed that within three months of initial visit, more than 60% experi- enced a recurrent ED visit, hospitalization, or death. 211 Depending on what precipitated the decom- pensation, the patient’s outpatient drug regimen may require some adjustment. Intensive outpatient fol- low-up has been shown to be successful in prevent- ing repeat visits to the ED. 212-214 Referral to an outpa- tient heart failure program, where available, can reduce the frequency of ED visits and hospitaliza- tions. 215

Heart Failure Observation Units Theoretically, an ED-based observation unit or other subacute care setting can serve patients with ADHF

Table 10. Treatment Recommendations For Special Circumstances
Table 10. Treatment Recommendations
For Special Circumstances

Class of evidence definitions from Emergency Medicine Practice; see back page of this issue.

and accomplish this at substantial cost savings. These units could monitor for patients’ response to therapy and the development of potentially serious adverse events. Observation units have been advanced as a safe and effective means of reducing hospital admissions in general and heart failure admissions in particular. 216,217 There have been sever- al studies that suggest ED-based heart failure obser- vation units may decrease ED return visits and read- missions. 218 Although there is a growing interest to provide ED observation units for patients with ADHF, no randomized studies have been performed to substantiate their use.

 

Table 11. Correlates Of In-Hospital Mortality

• Advanced age

• New onset of heart failure

• Prolonged duration of symptoms

• Poor left ventricular (LV) function

• Chest pain

• Hypotension

• Jugular venous distention

• Non-sinus rhythm and ECG abnormalities

• Elevated creatine kinase levels

• Hyponatremia

 

• Elevated BUN

Conclusion: Case Outcomes

• Systolic Blood Pressure less than 115

 

The elderly woman who “looked and sounded wet” felt much better after receiving furosemide and sup- plemental oxygen. You decided to send off cardiac enzymes and they were positive. She did not have

• BNP level greater than 230 pg/ml

• Digoxin use

• Advanced renal dysfunction

• Poor response to initial therapy

Table 12. Predictors of In-Hospital Mortality

therapy Table 12. Predictors of In-Hospital Mortality Emergency M M edicine P P ractice © 26
therapy Table 12. Predictors of In-Hospital Mortality Emergency M M edicine P P ractice © 26
therapy Table 12. Predictors of In-Hospital Mortality Emergency M M edicine P P ractice © 26
therapy Table 12. Predictors of In-Hospital Mortality Emergency M M edicine P P ractice © 26
therapy Table 12. Predictors of In-Hospital Mortality Emergency M M edicine P P ractice © 26
therapy Table 12. Predictors of In-Hospital Mortality Emergency M M edicine P P ractice © 26
therapy Table 12. Predictors of In-Hospital Mortality Emergency M M edicine P P ractice © 26
therapy Table 12. Predictors of In-Hospital Mortality Emergency M M edicine P P ractice © 26
therapy Table 12. Predictors of In-Hospital Mortality Emergency M M edicine P P ractice © 26
therapy Table 12. Predictors of In-Hospital Mortality Emergency M M edicine P P ractice © 26
therapy Table 12. Predictors of In-Hospital Mortality Emergency M M edicine P P ractice © 26
therapy Table 12. Predictors of In-Hospital Mortality Emergency M M edicine P P ractice © 26
therapy Table 12. Predictors of In-Hospital Mortality Emergency M M edicine P P ractice © 26
therapy Table 12. Predictors of In-Hospital Mortality Emergency M M edicine P P ractice © 26
therapy Table 12. Predictors of In-Hospital Mortality Emergency M M edicine P P ractice © 26
Ten Pitfalls To Avoid 1. “She was just weak and dizzy. How was I sup-
Ten Pitfalls To Avoid
1.
“She was just weak and dizzy. How was I sup-
posed to know she had heart failure?”
You found out when she went into acute pul-
monary edema after the aggressive fluid bolus.
Non-specific symptoms such as weakness, lethar-
gy, fatigue, anorexia, or lightheadedness may be a
manifestation of low output acutely decompen-
sated heart failure. Older patients can be particu-
larly difficult to evaluate because they often lack
typical signs and symptoms of heart failure.
2. “She was only 35, she couldn’t have had heart
failure”
You can’t diagnose post-partum cardiomyopathy
unless you consider it. Myocarditis, alcohol
abuse, and cardiotoxic chemotherapies are among
the other etiologies of heart failure that present in
younger patients. Older age is a major risk factor
for heart failure, but young age should never
exclude it.
3. “He seemed to be wheezing, so I treated him for
COPD.”
Unfortunately, his condition continued to deterio-
rate and you only learned about his history of
heart failure after he was intubated.
Distinguishing between cardiac and pulmonary
causes of dyspnea remains a fundamental clinical
challenge. Careful diagnostic workup can yield
important clues and using BNP or NT-ProBNP
can aid in diagnostics challenges.
4. “I just assumed he hadn’t been taking his med-
ications.”
Medication non-compliance and dietary indiscre-
tion commonly precipitate decompensated heart
failure, but don’t assume this is the case until
other serious causes have been considered. Acute
decompensation may be brought on by a variety
of cardiac and non-cardiac conditions including
ischemia / infarction, arrhythmias, valvular /
septal rupture, sepsis, anemia, and thyrotoxicosis.
5. “He was wide awake, and looked extremely anx-
ious. I thought he could tolerate the 10 mg of
morphine”
Until he stopped breathing and had to be intubat-
ed. Injudicious use of opiates can result in exces-
sive sedation and loss of respiratory drive.
Although useful in small doses for relieving anxi-
ety, opiates provide little or no direct hemody-
namic benefit in patients with pulmonary edema.

6. “She was clearly ‘wet’ and needed to be aggres- sively diuresed. Is it my fault her creatinine doubled by the next day?” Maybe. This elderly woman with acute diastolic dysfunction was not suffering from volume over- load. Her pulmonary congestion may have responded better to vasodilator therapy than to aggressive diuresis which ended up impairing her renal function and prolonging her hospital stay.

7. “I always thought sublingual nitroglycerin was harmless. I didn’t expect his systolic BP to drop to single digits.” Nitrates are fast, effective, and relatively safe; however, patients with preload-dependent condi- tions (e.g., valvular stenosis) do not tolerate them well.

8. ”He was in severe respiratory distress so he had to be intubated. Who would have thought he would spend a week in the CCU?” Maybe if you had considered CPAP, the patient could have avoided the ventilator-associated pneumonia and prolonged CCU stay. For patients with severe cardiogenic pulmonary edema, non- invasive ventilatory support, CPAP in particular, has been shown in multiple controlled trials to reduce the need for endotracheal intubation and to decrease length of ICU stay.

9. “He was in rapid atrial fibrillation and I figured rate-control would improve his cardiac func- tion.” Unfortunately, you failed to consider the negative inotropic effects of verapamil, and the patient’s heart failure further decompensated. When a patient presents with acutely decompensated heart failure in the context of rapid atrial fibrilla- tion, it is important to address the clinical situa- tion as a whole, which means treating for both conditions simultaneously and recognizing that the treatment of one may impact the other.

10. “She felt a little better after the Lasix, so we sent her home.” But when she came back the next day in florid pulmonary edema, she ended up in the CCU. There is growing evidence that premature release of patients with inadequately treated heart failure is associated with increased short-term morbidity and mortality. While published guidelines can help guide the decision to admit, it is important to recognize that even “low-risk” patients have considerable potential for morbidity.

any ischemic ECG changes, but you changed her dis- position to a step-down unit for closer monitoring. You decided to send a BNP test on the obese woman in the next room since it was unclear whether she was presenting with a COPD exacerba- tion or ADHF. The BNP returned at 1100 pg/dl con- firming a diagnosis of ADHF. You informed her of your clinical diagnosis and she improved after administration of nitroglycerin and furosemide. She called you back into the room later to tell you that she remembers taking a “water pill” in the past for similar symptoms but was not restarted on this med- ication when she moved to your town. This further confirmed your clinical diagnosis. Remembering that “less is more” for patients with low output failure, you immediately called the cardiologist of the woman with recent fatigue, confu- sion, and an ejection fraction of 20%. You discussed the role of inotropes with her cardiologist and agreed to “hold off” on inotropes in the ED, but immediate admission to the ICU for monitoring was necessary. Prior to her disposition, you confirmed that her uri- nalysis and chest x-ray did not show signs of infec- tion to account for her fatigue and mild confusion. At the end of your busy shift, you reflected upon the diverse presentation of patients with ADHF and the importance of tailoring therapy to a specific syn- drome.

References

Evidence-based medicine requires a critical appraisal of the literature based upon study methodology and number of subjects. Not all references are equally robust. The findings of a large, prospective, random- ized, and blinded trial should carry more weight than a case report. To help the reader judge the strength of each ref- erence, pertinent information about the study, such as the type of study and the number of patients in the study, will be included in bold type following the reference, where available.

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2. Heart Failure Society of America. Executive summary: HFSA

2006 Comprehensive Heart Failure Practice Guideline. J Card Fail 2006:12(1)10-38. (Review)

3.

Nieminen MS, Bohm M, Cowie MR, et al. Executive summary of the guidelines on the diagnosis and treatment of acute heart failure: the Task Force on Acute Heart Failure of the European Society of Cardiology. Eur Heart J 2005;26(4):384- 416. (Consensus statement)

4.

Maisel AS, Kirsiknaswany P, Nowak R et al. Rapid measure- ment of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Engl J Med 2002;347:161-169. (Retrospective, descriptive; 105,388 patients)

5.

Maisel A. B-type natriuretic peptide measurements in diag- nosing congestive heart failure in the dyspneic emergency department patient. Rev Cardiovasc Med 2002;3 Suppl 4:S10-7. (Prospective, observational; 1586 patients)

6.

Mueller C, Scholer A, Laule-Kilian K, et al. Use of B-type natriuretic peptide in the evaluation and management of acute dyspnea. N Engl J Med 2004;350(7):647-54. (Prospective, randomized, controlled; 452 patients)

7.

Fonarow GC. Strategies to improve the use of evidence-based heart failure therapies: OPTIMIZE-HF. Rev Cardiovasc Med 2004;5 Suppl 1:S45-54. (Review)

8.

Investigators V. Intravenous nesiritide vs nitroglycerin for treatment of decompensated congestive heart failure: a ran- domized controlled trial. JAMA 2002;287(12):1531-40. (Randomized double-blind; 489 patients)

9.

Kannel WB, Belanger AJ. Epidemiology of heart failure. Am Heart J 1991;121(3 Pt 1):951-7. (Retrospective)

10.

McCullough PA, Nowak RM, McCord J, et al. B-type natri- uretic peptide and clinical judgment in emergency diagnosis of heart failure: analysis from Breathing Not Properly (BNP) Multinational Study. Circulation 2002;106:416-22. (Prospective, observational; 1538 patients)

11.

Croft JB, Giles WH, Pollard RA, et al. National trends in the initial hospitalization for heart failure. J Am Geriatr Soc 1997;45(3):270-5. (Retrospective; 1,434, 912 patients)

12.

Koelling TM, Chen RS, Lubwama RN, et al. The expanding national burden of heart failure in the United States: the influ- ence of heart failure in women. Am Heart J 2004;147(1):74-8. (Chart review)

13.

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