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Heart%20 failure

  1. 1. February 2002 Volume 4, Number 2 Authors Joshua M. Kosowsky, MD Department of Emergency Medicine,Brigham and Women’s Hospital, Boston, MA. Leo Kobayashi, MD Department of Emergency Medicine,Brigham and Women’s Hospital, Boston, MA. Peer Reviewers Francis M. Fesmire, MD Director, Heart-Stroke Center, Chattanooga,TN. Christopher J. Rosko, MD, FACEP Medical Director, Department of Emergency Medicine,University of Alabama at Birmingham, Birmingham,AL. CME Objectives Upon completing this article, you should be able to: 1. describe the basic pathophysiology of acutely decompensated heart failure; 2. identify the common and life-threatening precipitants of acutely decompensated heart failure; 3. explain the management of acutely decompensated heart failure in the prehospital and ED settings, including the role of diuretics,vasodilators,inotropes,and noninvasive ventilatory support; and 4. describe the role of risk stratification in determining the disposition of patients with acutely decompensated heart failure. Date of original release: February 1,2002. Date of most recent review: January 18,2002. See“Physician CME Information”on back page. EMERGENCY MEDICINE PRACTICE A N E V I D E N C E - B A S E D A P P R O A C H T O E M E R G E N C Y M E D I C I N E Editor-in-Chief Stephen A. Colucciello, MD, FACEP, Assistant Chair, Director of Clinical Services, Department of Emergency Medicine, Carolinas Medical Center, Charlotte, NC; Associate Clinical Professor, Department of Emergency Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC. Associate Editor Andy Jagoda, MD, FACEP, Professor of Emergency Medicine; Director, International Studies Program, Mount Sinai School of Medicine, New York, NY. Editorial Board Judith C. Brillman, MD, Residency Director,Associate Professor, Department of Emergency Medicine,The University of New Mexico Health Sciences Center School of Medicine, Albuquerque,NM. W. Richard Bukata, MD, Assistant Clinical Professor, Emergency Medicine, Los Angeles County/ USC Medical Center, Los Angeles, CA; Medical Director, Emergency Department, San Gabriel Valley Medical Center, San Gabriel, CA. Francis M. Fesmire, MD, FACEP, Director, Chest Pain—Stroke Center, Erlanger Medical Center; Assistant Professor of Medicine, UT College of Medicine, Chattanooga,TN. Valerio Gai,MD,Professor and Chair, Department of Emergency Medicine,University of Turin,Italy. Michael J. Gerardi, MD, FACEP, Clinical Assistant Professor, Medicine, University of Medicine and Dentistry of New Jersey; Director, Pediatric Emergency Medicine, Children’s Medical Center, Atlantic Health System; Vice-Chairman, Department of Emergency Medicine, Morristown Memorial Hospital. Michael A. Gibbs, MD, FACEP, Residency Program Director; Medical Director, MedCenter Air, Department of Emergency Medicine, Carolinas Medical Center; Associate Professor of Emergency Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC. Gregory L.Henry,MD,FACEP, CEO,Medical Practice Risk Assessment,Inc.,Ann Arbor, MI;Clinical Professor,Department of Emergency Medicine,University of Michigan Medical School,Ann Arbor,MI;President,American Physicians Assurance Society,Ltd., Bridgetown,Barbados,West Indies; Past President,ACEP. Jerome R.Hoffman, MA, MD, FACEP, Professor of Medicine/ Emergency Medicine, UCLA School of Medicine; Attending Physician, UCLA Emergency Medicine Center;Co-Director, The Doctoring Program, UCLA School of Medicine, Los Angeles, CA. John A. Marx, MD, Chair and Chief, Department of Emergency Medicine, Carolinas Medical Center, Charlotte, NC; Clinical Professor, Department of Emergency Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC. Michael S. Radeos, MD, MPH,FACEP, Attending Physician in Emergency Medicine, Lincoln Hospital, Bronx, NY; Research Fellow in Emergency Medicine, Massachusetts General Hospital, Boston, MA; Research Fellow in Respiratory Epidemiology, Channing Lab, Boston, MA. Steven G.Rothrock,MD,FACEP,FAAP, Associate Professor of Emergency Medicine,University of Florida;Orlando Regional Medical Center;Medical Director of Orange County Emergency Medical Service,Orlando,FL. Alfred Sacchetti, MD,FACEP, Research Director, Our Lady of Lourdes Medical Center, Camden, NJ; Assistant Clinical Professor of Emergency Medicine, Thomas Jefferson University, Philadelphia, PA. Corey M. Slovis, MD, FACP, FACEP, Department of Emergency Medicine,Vanderbilt University Hospital, Nashville,TN. Mark Smith, MD,Chairman, Department of Emergency Medicine,Washington Hospital Center,Washington, DC. Charles Stewart,MD,FACEP, Colorado Springs, CO. Thomas E.Terndrup, MD, Professor and Chair, Department of Emergency Medicine, University of Alabama at Birmingham, Birmingham, AL. Acutely Decompensated Heart Failure:Diagnostic AndTherapeutic Strategies ForThe New Millennium 11 p.m.: You begin your shift. An elderly patient with shortness of breath has “CHF” written all over her. She looks and sounds “wet.” She gets the usual: oxygen, furo- semide, and nitrates. When you return 20 minutes later, she looks and feels much better. As you reach for the phone to speak with the admitting physician, you start to wonder, “Do I need to get cardiac enzymes? She really looks so good now—does she even need to be admitted?” ACUTELY decompensated heart failure is one of the most common cardiac emergencies encountered in the ED. Because patients with heart failure are seen so frequently, our evaluations can become perfunctory and our therapy homogenized. The fact is, patients with acutely decompensated heart failure represent a diverse group that share common features, among them high morbidity and mortality. Failure to appreciate and address the subtleties of an individual exacerbation of heart failure 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 stabilization, differential diagnosis, pharmacologic and adjunctive therapies, and appropriate disposition of the individual patient. Epidemiology, Etiology,And Definitions As a result of the aging of the U.S. population, the overall prevalence of heart failure is rising.1 At the same time, advances in outpatient medical therapy are allowing patients with chronic heart failure to survive despite advanced stages of hemodynamic compromise. Nearly 5 million Americans have heart failure, and approximately 550,000 new cases arise each year.2 Heart failure now accounts for close to 1 million inpatient admissions annually and represents the
  2. 2. EmergencyMedicinePractice 2 February 2002 number-one reason for hospitalization among the growing elderly population.2 Symptoms of decompensated heart failure commonly cause patients to seek emergency care. The National Hospital Ambulatory Medical Care Survey reported 1.5 million ED visits in 1999 for non-ischemic heart disease, of which a significant proportion were related to heart failure.3 One retrospective analysis of 2 million ED visits over an 11- year period revealed approximately 1.1% of visits to have a primary diagnosis of heart failure or pulmonary edema.4 Short-term outcomes for patients admitted to the hospital with decompensated heart failure have held fairly constant over the past two decades. In-hospital mortality remains approximately 7%, with major adverse events occurring in up to 18% of patients.5-7 For those patients who present with frank pulmonary edema, the corresponding rates of morbidity and mortality are approximately double.8-11 Patients who present with acute myocardial infarction and cardiogenic shock have a mortality rate of 70% or more despite aggressive therapy.12 Less is known about the outcomes of patients who are sent home from the ED. In a recent study of 112 patients discharged from the ED with a primary diagnosis of heart failure, more than 60% experienced another ED visit, hospitalization, or death within 90 days of the index visit.13 The etiologies of heart failure are numerous and diverse. (See Table 1.) In the United States, the vast majority of heart failure arises as a consequence of coronary artery disease and/or long-standing hypertension. In the ED, acute heart failure can present de novo—for example, in acute myocardial infarction (MI) or with acute valvular insufficiency. Much more commonly, patients seen in the ED have chronic heart failure that has decompensated as the result of one or more precipitating factors. Chronic heart failure is a complex and multifaceted syndrome with variable clinical presentations and overlap- ping systems of classification. Differentiating among these can be helpful in evaluating and managing individual patients. Systolic failure is a physiologic state characterized by impaired cardiac contractility—typically defined as an ejection fraction less than 40%. In the case of diastolic failure, the ejection fraction is normal or supranormal, but myocar- dial relaxation is impaired, preventing proper filling of the ventricle. Forward failure is a clinical constellation of symptoms representing inadequate tissue perfusion, the extreme example of which is cardiogenic shock. Pulmonary edema, peripheral edema, and congestive hepatomegaly distin- guish backward failure. Right heart failure involves impaired return of blood to central venous circulation (as evidenced by neck vein distention, dependent extremity edema, and hepatomegaly). It is most commonly a consequence of severe left heart failure but can also occur in isolation (as in the case of cor pulmon- ale) or result from right ventricular infarction. High-output failure is caused by excessive demand for tissue perfusion resulting in hyperdynamic cardiac dysfunction, as seen with sepsis, thyrotoxicosis, and beri-beri. Low output failure, distinguished by a low cardiac output, is the more common presentation of heart failure. The severity of failure can be described in many ways, which may include a measure of how chronic failure affects the quality of life or more acute clinical parameters. Table 2 on page 3 describes the new American Heart Association classification, the commonly used New York Heart Associa- tion (NYHA) classification, and the Killip classification (originally used to predict outcome after acute MI). Pathophysiology Regardless of etiology, inadequate cardiac function triggers a common set of compensatory mechanisms. These are brought about by neurohormonal activation and character- ized 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 decompensation—a downward spiral resulting from some precipitant or stress. High circulating levels of aldosterone, vasopressin, epinephrine, and norepinephrine are ultimately maladap- tive, as tachycardia and vasoconstriction compromise the performance of the left ventricle (LV) and simultaneously worsen myocardial oxygen balance. Deteriorating left ventricular function results in further neurohormonal activation and self-perpetuation of this adverse cycle. (See Figure 1 on page 3.) Pathophysiologic considerations notwithstanding, acutely decompensated heart failure is a poorly defined clinical entity, and no universal definition exists.14 An acute decompensation can develop over a period of minutes, hours, or days and can range in severity from mild symp- toms of volume overload or decreased cardiac output to frank pulmonary edema or cardiogenic shock. However it is defined, the number of heart failure patients who present to the ED with clinical decompensation is likely to increase over the coming years. Table 1.Etiologies Of Heart Failure. Coronary artery disease Hypertension Valvular disease Cardiomyopathy • Idiopathic cardiomyopathy • Alcoholic cardiomyopathy • Toxin-related cardiomyopathy (e.g., adriamycin) • Postpartum cardiomyopathy • Hypertrophic obstructive cardiomyopathy (HOCM) • Tachyarrhythmia-induced cardiomyopathy Infiltrative disorders (e.g.,amyloid) Congenital heart disease Pericardial disease Hyperkinetic states • Anemia • Arteriovenous fistula • Thyroid disease • Beri-beri
  3. 3. 3 Emergency Medicine PracticeFebruary 2002 State Of The Literature Unfortunately, controlled trials provide few data to direct the optimal diagnosis and management of patients with acutely decompensated heart failure. In general, clinical trials have focused on heart failure arising in the context of acute MI, although this subgroup represents 15% or fewer of patients hospitalized with heart failure.11,15 Much of the literature on severely decompensated heart failure concerns the management of patients after they have been admitted to the CCU. Care of patients in the ED—particularly for those with mild-to-moderate symptoms—remains largely empiric or based on observational studies and small case- series reports. The American College of Cardiology/ American Heart Association (ACC/AHA) and the Agency for Health Care Policy and Research (AHCPR) have published practice guidelines that are based, in part, on the aforementioned literature.16,17 Differential Diagnosis Decompensated heart failure can coexist with or closely mimic a number of other cardiac, respiratory, and systemic illnesses. (See Table 3 on page 4.) In fact, when patients Table 2.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 and have no symptoms. Stage B Patients have developed structural heart disease but have not (yet) developed symptoms. Stage C Patients with past or current heart failure symptoms in association with structural damage to the heart. Stage D Patients with end-stage,or terminal,heart failure requiring specialized treatment strategies. New York Heart Association 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 Killip Classification Class Description Killip class I No evidence of pulmonary congestion or shock. Killip class II Mild pulmonary congestion (patients had rales up to 50% of each lung field ) or an isolated S3 gallop. Killip class III Pulmonary edema (rales more than 50% up). Killip class IV Hypotension and evidence of shock. Sources: Hunt HA, Baker DW, Chin MH, et al. ACC/AHA guidelines for the evaluation and management of chronic heart failure in the adult: executive summary.A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1995 Guidelines for the Evaluation and Management of Heart Failure).Circulation 2001;104: 2996-3007; and Killip T, Kimball JT.Treatment of myocardial infarction in coronary care unit. A two-year experience with 250 patients. Am J Cardiol 1967;20:457-467. Figure 1. Heart Failure Pathophysiology Diagram. symptomatic decompensation activation of renin-angiotensin system activation of sympathetic nervous system cardiac ischemia decreased left ventricle function decreased cardiac output increased pulmonary capillary wedge pressure increased heart rate increased systemic vascular resistance increased preload ➤ ➤ ➤ ➤ ➤
  4. 4. EmergencyMedicinePractice 4 February 2002 present to the ED with undifferentiated dyspnea, the diagnosis of heart failure is often overlooked.19 Patients who present with mild or nonspecific symptoms pose a particular diagnostic challenge. Symptoms such as weakness, lethargy, fatigue, anorexia, or lightheadedness may actually be a manifestation of decreased cardiac output.20 Older patients frequently lack typical signs and symptoms of heart failure.21 These features may be obscured by the aging process itself or by the presence of coexisting medical conditions. Distinguishing heart failure from other life-threatening conditions may be as difficult as identifying its atypical or subtle presentations. However, if an adequate history and physical exam are not suggestive of heart failure, and both the chest radiograph and the ECG are normal, heart failure is unlikely. Patients presenting with acute exacerbations of either cardiac dysfunction or chronic obstructive pulmonary disease (COPD) may have wheezing on pulmonary auscultation with signs of chronic right-sided heart failure and non-diagnostic chest radiographs. Bedside peak flow measurements may prove useful in these cases.22 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.22 While ETCO2 levels for heart failure patients differ significantly from those of asthma/COPD patients, once again, there is no single ETCO2 level that can reliably differentiate between the two conditions.23 In heart failure patients, pulmonary embolism may be clinically indistinguishable from an acute deteriora- tion of underlying failure.24 Precipitating factors for decompensation should be sought in a careful and deliberate fashion. (See Table 4.) Ischemia/infarction and noncompliance with medications or dietary restrictions are the most common causes of clinical decompensation.10,15,25-28 The exact prevalence of such precipitants varies depending on the particular population. Nevertheless, in almost all cases, the possibility of an acute coronary syndrome should be considered. Other cardiovas- cular precipitants, such as arrhythmia, high-grade heart block, severe valvular dysfunction, or hypertensive crisis must not be overlooked. It should also be recognized that decompensated heart failure can arise as a consequence of non-cardiac conditions such as sepsis, anemia, alcohol withdrawal, uncontrolled diabetes, or thyroid disease. “Out-worn heart, in a time out-worn, Come clear of the nets of wrong and right; Laugh, heart, again in the gray twilight.” —William Butler Yeats (1865–1939), “Into the Twilight.”29 Prehospital Care Even before patients reach the hospital, decompensated heart failure is associated with significant morbidity and mortality, including malignant arrhythmias and prehospital cardiac arrest.30 All patients should have continuous cardiac monitoring and intravenous access established if possible. (See also “Clinical Pathway: Prehospital Therapy For Acutely Decompensated Heart Failure” on page 13.) Because successful management depends on reversal of hypoxia, pulse oximetry and supplemental oxygen should be utilized routinely in the prehospital care of patients with decompensated heart failure. Prehospital personnel should radio ED staff for any patient presenting with symptoms suggestive of pulmonary edema or cardiogenic shock and receive on-line medical advice when appropriate. The decision to treat a patient in the relatively uncon- trolled prehospital environment carries some risks that must be weighed against expected benefits. With few exceptions, the safety and efficacy of prehospital medications have been poorly studied.32 Prehospital therapy for decompensated heart failure requires particular caution in light of the relatively high number of inaccurate diagnoses made in the field. Nearly 30% of patients with respiratory distress (presumed in the field to be cardiac in origin) are diagnosed with a different condition once they arrive at the hospi- tal.30,33,34 Despite these concerns, available evidence suggests Table 4.Common Precipitants Of CHF Decompensation. • Medication noncompliance • Dietary indiscretion • Uncontrolled hypertension • Myocardial ischemia/infarction • Acute valvular dysfunction • Cardiac arrhythmias • Pulmonary and other infections • Administration of inappropriate medications (e.g., negative inotropes) • Fluid overload • Missed dialysis • Thyrotoxicosis • Anemia • Alcohol withdrawal Table 3.Differential Diagnosis Of Acutely Decompensated Heart Failure. Cardiovascular • Acute myocardial infarction • Unstable angina • Acute valvular/septal rupture • Aortic dissection • Arrhythmia • Critical aortic stenosis • Endocarditis/myocarditis • Hypertensive crisis • Pericardial tamponade/effusion Pulmonary • COPD • Pulmonary thromboembolism • Multilobar pneumonia • Acute respiratory distress syndrome (ARDS) Other • Pure volume overload • Renal failure • Iatrogenic (e.g., post-transfusion) • Sepsis
  5. 5. 5 Emergency Medicine PracticeFebruary 2002 that prehospital therapy for presumed heart failure can prevent serious complications and improve survival, particularly for critically ill patients.30,33,34 In European countries, where physicians commonly staff ambulances, intensive prehospital treatment of patients with severe heart failure confers short-term benefits.35,36 Sublingual nitroglycerin appears to be safest and most effective of the prehospital medications used for presumed pulmonary edema.33 Prehospital intravenous (IV) nitrates also yield positive short-term results. The role of other medica- tions for heart failure in the prehospital setting is less clear. Early administration of furosemide appears to have very little benefit and may result in short-term complications.33 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.33,37 There are few data on the prehospital use of noninvasive ventilation (NIV). In one non-randomized study, patients presumed to have congestive heart failure (CHF) were given biphasic positive airway pressure (BiPAP) by the medics during transport and compared to matched controls treated without NIV.38 In this trial, 97% of emer- gency medicine technicians who used BiPAP 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. “The heart monitor, the death cricket bleeping.” —Anne Sexton (1928-1974), U.S. poet. “The Twelve Dancing Princesses.”29 ED Evaluation Initial Approach The approach to the patient with acutely decompensated heart failure begins with stabilization of respiratory and hemodynamic status. The emergency physician must then rapidly exclude or treat reversible conditions. Clinical evaluation and empiric therapy begin simultaneously with supplemental oxygen, cardiac monitoring, pulse oximetry, and IV access. Patients with clinical signs of exhaustion or cyanosis despite supplemental oxygen require respiratory support by either invasive or noninvasive means (which is described later in the text). Those with hypotension, obtundation, cool extremities, or other signs of poor perfusion should be presumed to be in or near cardiogenic shock and managed accordingly (which is also described later in the text). Once the initial resuscitation is under way, further efforts should be made to identify the underlying cause of decompensation. History Most patients with heart failure complain of dyspnea or trouble sleeping. It is important to determine the degree of dyspnea and its precipitants. Does it occur at rest? Does the patient have paroxysmal nocturnal dyspnea (PND)? Ask the patient how he or she has been sleeping and on how many pillows. (Spending the night erect on the sofa is a suspicious finding except in the most severe addict of CNN.) The rapidity of symptom onset may suggest an etiology for the decompensation. An abrupt deterioration raises concern for arrhythmia, acute coronary syndrome, or Cost-EffectiveStrategiesForAcutelyDecompensatedHeartFailure 1. Don’t admit every patient with heart failure. Certain patients with heart failure may require only an ED“tune-up”and discharge. Patients with a past history of failure who have a reassuring history and physical examination,normal laboratory values, and an ECG unchanged from previous tracings may be candidates for outpatient follow-up (especially if their decompensation occurred because they ran out of their medicines).ED observation units for select patients may also be a cost- effective alternative to traditional admission.202,203 Caveat: Most patients who present with acutely decompensated heart failure will need hospital admission—especially those with abnormal vital signs, chest pain,or acute exacerbations. 2. Consider the use of CPAP. CPAP may prevent the need for intubation in some patients with acute 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 noninvasive ventilation—especially those who are agitated or those who have altered mental status, unstable vital signs, or evidence of acute MI. 3. Consider the use of furosemide infusions. While many patients in acute heart failure respond quickly to nitrates and bolus diuretics, some do not. According to one study, intravenous infusions of furosemide for class IV heart failure are a safe, effective,and economic mode of therapy, especially in the elderly.98 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 BNPs when appropriate. Of all of the tests available to determine the presence of acute heart failure, BNP may be the single best investigation. It is very sensitive and specific and can be performed at the bedside. In the acute setting, elevated BNP levels correlate with the diagnosis of heart failure.58 v
  6. 6. EmergencyMedicinePractice 6 February 2002 valvular rupture. Prior episodes of a similar nature can provide important clues. Associated symptoms are also important. Determine whether the patient has had any chest pain or other anginal equivalent such as shoulder, neck, arm or epigastric discomfort. The combination of syncope and heart failure is worrisome and is associated with high one-year mortality rate.39 Ask the patient and family about recent weight gain, leg swelling, urinary output, exercise tolerance, fatigue, and compliance with diet and medications. New prescriptions or changes in dosage of suspect drugs such as NSAIDs, ophthalmic beta-blockers, herbals, and over-the-counter agents should be sought. Medication history is also important in determining therapy. Specifically ask male patients with congestive failure if they are currently taking sildenafil (Viagra). The administration of nitrates may cause life-threatening hypotension in such individuals.40 Most patients presenting with decompensated heart failure will have a prior cardiac history. Patients can generally tell you if they have had “fluid on the lungs” in the past. More sophisticated patients may be able to provide details of previous echocardiograms or cardiac catheterizations. “heart, n. Figuratively, this useful organ is said to be the seat of emotions and sentiments . . . . It is now known that sentiments and emotions reside in the stomach, being evolved from food by chemical action of the gastric fluid.” —Ambrose Bierce (1842-1914) U.S. journalist, short-story writer; The Devil’s Dictionary, 1911.29 Physical Examination The patient’s degree of distress should be determined early in the encounter; severe pulmonary edema can be a “doorway diagnosis.” Confusion, cyanosis, diaphoresis, inability to speak, falling over on the stretcher, and so on should prompt a call for the airway cart. Vital signs not only suggest the severity of illness but can also indicate etiologic factors. Hyperthermia or hypoth- ermia can occur with sepsis or thyroid disease. In the absence of rate-controlling pharmacologic agents, tachycar- dia is nearly universal in decompensated heart failure. Bradycardia should raise concern for high-degree AV block, hyperkalemia, digoxin (or other drug) toxicity, or severe hypoxia. Hypertension is common in both systolic and diastolic failure. While hypotension can be baseline for patients with end-stage cardiomyopathy, in the symptom- atic patient it should raise concern for sepsis, massive pulmonary embolism, or cardiogenic shock. The propor- tional pulse pressure (PPP)—i.e., pulse pressure (systolic minus diastolic pressure) divided by systolic blood pres- sure—provides an approximation of left ventricular function, a PPP of less than 25% correlating with a cardiac index less than 2.2 L/min/m2 .19,41 Signs of congestion may be detected by careful attention to heart and lung sounds, jugular venous disten- tion (JVD), hepatomegaly, and peripheral edema. The diagnostic utility of these physical exam findings and related maneuvers is well-documented for chronic heart failure.42,43 Studies performed in the acute setting are scarce and tend to be limited by the lack of “gold-standard” diagnostic criteria. Inter-observer agreement on some of these findings is marginal, even in ideal settings.44,45 The pulmonary exam is usually helpful, but it can sometimes be misleading. Rales, a classic finding in heart failure, may also occur with pneumonia, interstitial lung disease, or COPD. On the other hand, wheezing, or “cardiac asthma,” is not uncommon in acute heart failure. In acutely dyspneic patients, the sensitivity and specificity of rales for LV dysfunction appears to be quite poor, whereas the constellation of rales, an S3 gallop, and JVD is more accurate.24 Elevated CVP is present when the top of the external or internal jugular veins is more than 3 cm vertical distance above the sternal angle.46 A positive hepatojugular reflux sign is defined by a rise in the neck veins of greater than 3 cm, sustained for more than 15 seconds, that occurs when the physician pushes firmly on the patient’s epigastrium.47 In one study, ED patients with acute dyspnea, presence of hepatojugular reflux had a reported sensitivity and specific- ity of 24% and 96%, respectively, for heart failure.19 A MEDLINE review of the hepatojugular sign found that it is positive in a variety of conditions, including constrictive pericarditis, right ventricular infarction, restrictive cardi- omyopathy, and left ventricular failure (but only when the pulmonary capillary wedge pressure is greater than 15).47 Heart sounds can be helpful in confirming the diagno- sis of heart failure. In one study of patients with chronic heart failure, an S3 gallop was highly predictive of an abnormal ejection fraction. The absence of an S3, however, was not uncommon in those with a mildly impaired ejection fraction.48 A new cardiac murmur in the proper context must be presumed to signal acute valvular or papillary muscle dysfunction. The leg examination is routine in the evaluation of patients with suspected heart failure. While pedal edema is highly specific for increased filling pressures, it has poor sensitivity.43 Unilateral extremity swelling and especially the presence of a venous cord should raise suspicion for deep venous thrombosis and possible pulmonary embolism. Diagnostic Studies Laboratory Tests The majority of patients who present with complaints consistent with heart failure will need basic laboratory testing. A complete blood count (CBC) or other measure- ment of hemoglobin is useful for ruling out anemia as a cause for decompensation. Some believe that an elevated white blood cell count may suggest an infectious process, especially if bands are present. However, this is not well- studied in the patient who presents with dyspnea. Serum chemistries help assess renal function and overall fluid and electrolyte balance.
  7. 7. 7 Emergency Medicine PracticeFebruary 2002 Cardiac Markers The question as to which patients with acutely decompen- sated heart failure should get cardiac enzymes is not well- studied. If an acute coronary syndrome is a consideration (e.g., history of chest discomfort or other anginal equivalent, new-onset heart failure, or significant risk factors for coronary artery disease), serum markers for cardiac ischemia/infarction (CK, CK-MB, and troponin) are indicated. Elevated troponins may detect cardiac myolysis (possibly secondary to myocardial wall strain) even in the absence of coronary artery disease.49 Other studies show that elevated cardiac troponins may be found in the blood of 25%-33% of patients with severe heart failure and help to identify those with poor short-term prognosis.50 B-Natriuretic Peptide B-type natriuretic peptide (BNP) is an endogenous hormone released from the ventricles in response to stretch. BNP is a counter-regulatory hormone, offsetting the effects of neurohormonal activation by promoting diuresis and vasodilation. Plasma levels of BNP have been shown to correlate with degree of left ventricular overload, severity of clinical heart failure, and both short- and long-term cardiovascular mortality.51-55 Of significance from an ED standpoint, plasma BNP levels can be used to distinguish between cardiac and non- cardiac causes of dyspnea.56,57 Among patients presenting with acute dyspnea, a serum BNP level above 94 pg/mL predicts a diagnosis of heart failure with 91% accuracy.58 In a prospective study of 250 patients with acute dyspnea possibly due to CHF, the mean BNP level was 1076 pg/mL in the CHF group compared with 38 pg/mL in patients without CHF. In this study, BNP measurement was more accurate than any other single variable, including history, physical, chest x-ray, or ECG.58 Using standard clinical criteria, the treating physicians misdiagnosed heart failure in 15 patients subsequently found to have other conditions and failed to recognize it in 15 additional patients. BNP would have accurately classified 29 of these 30 patients using an 80 pg/mL cut-off.59 For patients with known heart failure, BNP levels at any given point in time can be compared with baseline measurements to form an independent assessment of clinical severity and may be useful for tailoring specific therapies.60,61,164 Other Tests Arterial blood gases should not be routine in those with acutely decompensated heart failure. They may be useful if there is a concern for hypoxia and pulse oximetry is not available or if the physician suspects hypercapnia. Patients on digoxin should have serum levels checked. “But the heart refuses to be imprisoned; in its first and narrowest pulses it already tends outward with a vast force and to immense and innumerable expansions.” —Ralph Waldo Emerson (1803–1882), U.S. essayist, poet, philosopher. “Circles,” in Essays, First Series (1841, repr. 1847).29 Electrocardiogram While the ECG is admittedly a relatively insensitive tool, it remains useful for detecting ischemia, arrhythmias, or electrolyte disturbances. Given the high proportion of heart failure exacerbations precipitated by ischemic events, it is difficult to justify not obtaining an ECG on all such patients.15 The ECG is likely to be abnormal in patients with heart failure. In one study using a clinic population, left ventricu- lar hypertrophy on resting ECG was noted in 42% and electrocardiographic evidence of cardiac ischemia or a prior MI was present in approximately 70%.62 Comparison with prior ECGs may be critical, especially with patients who have subtle changes or “baseline abnormal” tracings. Patients with ECG evidence of acute ischemia or infarction should be considered for emergent coronary reperfusion therapy. Importantly, a completely normal ECG is strong evidence against the presence of left ventricular dysfunction and should therefore prompt consideration of alternative diagnoses.24,63 Chest X-ray Combined with a clinical assessment, chest radiography has been reported to be 92% sensitive and 91% specific for detecting systolic dysfunction.24 The chest film may also be useful in identifying alternative or contributing causes of the patient’s symptomatology. Findings on chest radiograph can include cardiome- galy, 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 localized to the right side.64 There are several pitfalls that await the unwary physician who uses the chest film to diagnose acute heart failure. Most importantly, heart size may be normal in acute failure, especially if the failure originates from acute diastolic dysfunction.43 It is also important to recognize that radio- graphic findings can lag several hours behind clinical signs and symptoms.64 COPD patients may have minimal radiographic evidence of concurrent heart failure, and patients with prior lung injury may develop focal infiltrates mimicking pneumonia. Cardiac Echocardiography Formal echocardiography is invaluable for assessing the status of left ventricular function, distinguishing between systolic and diastolic failure, and identifying 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. Whether or not echocardiography is indicated in all instances of decompensated heart failure remains open to debate.24,64 ACC/AHA guidelines recommend transthoracic echocardiography as soon as possible after initial stabiliza- tion for any patient who presents with acute pulmonary edema, unless there are obvious precipitating factors and
  8. 8. EmergencyMedicinePractice 8 February 2002 the patient’s cardiac status has been adequately evaluated previously.16 With the availability of on-call sonographers and timely interpretation via telemedicine, echocardiography can be made operational around the clock.65 Guidelines for establishing an effective system for emergency echocardiography have recently been pub- lished.66 Experience with emergency physicians performing bedside echocardiography has generally been limited to ruling out pericardial effusion/tamponade.67-69 Pulmonary Artery Catheterization Most patients with decompensated heart failure can be evaluated and stabilized in the ED without the introduction of a pulmonary artery (PA) catheter. The literature on the risks and benefits of PA catheterization (also called Swan- Ganz catheterization) in critical illness continues to evolve, but in the case of patients with decompensated heart failure, little is known. ACC/AHA guidelines recommend place- ment of a PA catheter in the setting of acutely decompen- sated heart failure if improvement is not proceeding as expected, if high-dose nitrates are required for clinical stabilization, or if inotropic support is needed to augment systemic perfusion.16 However, these guidelines were first issued in 1995, before the publication of more recent data regarding the dangers of PA catheterization in the critically ill.70,71 When it is believed necessary, invasive hemodynamic monitoring can generally be initiated in the CCU. “I am dying from the treatment of too many physicians.” —Alexander the Great Treatment The most important initial interventions will involve management of the airway. Patients with inadequate respirations will most likely need emergent intubation. In general, airway management 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.72 Prolonged episodes of hypoxia or hypotension during intubation risk further cardiac decom- pensation 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.73 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.74 Once mechanical ventilation is instituted for cardiogenic pulmonary edema, it is not certain whether positive end-expiratory pressure (PEEP) confers any additional hemodynamic benefit.75-77 For patients in respiratory distress, application of high- flow oxygen appears beneficial. Although there have been reports that excessive oxygen can adversely affect left ventricular function, hypoxia is by far the greater concern in the acute setting.31 Sitting the patient bolt upright may 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.78 Early application of monitors such as pulse oximetry, noninvasive blood pressure, and continuous cardiac monitoring may provide early warnings of decompensation. While not all patients in acutely decompensated heart failure require a Foley catheter, monitoring of urinary output with a urinometer can be helpful in those with severe symptoms. Once immediate threats to airway and breathing are addressed, the physician must deal with blood pressure emergencies. While hypertensive emergencies resulting in pulmonary edema are life-threatening, they are in general more easily amenable to pharmacologic therapy than hypotensive emergencies associated with acute heart failure. In most cases of shock, fluid challenge is routine and generally not harmful, yet in the case of cardiogenic shock the literature is mute. Pharmacologic Therapy The twin objectives of pharmacologic therapy for acutely decompensated heart failure are relief of pulmonary congestion and improvement in systemic tissue perfusion. An ideal drug (or drug combination) would reduce preload, enhance left ventricular function, and at the same time maintain or improve myocardial oxygen balance. While the basic approach to treating acutely decompensated heart failure has not changed over the past two decades, there has been increasing emphasis on afterload reduction and other means of counteracting the adverse cycle of neurohormonal activation. (See Table 5 on page 9; see also “Clinical Pathway: Emergency Department Therapy For Acutely Decompensated Heart Failure” on page 14.) Nitrates Nitrates are recommended as first-line therapy for acutely decompensated heart failure of both ischemic and non- ischemic origin.16 The beneficial hemodynamic effects of nitrates in the setting of heart failure have long been appreciated.80,81 At low doses, nitroglycerin induces venodilation; at high doses, nitroglycerin causes arteriodilation, including dilation of the coronary arteries.82 Significantly, in patients with severe underlying left ventricular dysfunction, afterload reduction appears to predominate over preload reduction, even at moderate doses of nitroglycerin.83 A number of studies have compared the hemodynamic effects of nitrates and diuretics in acutely decompensated heart failure. In contrast to furosemide, nitrates reduce both preload and afterload, and maintain or improve cardiac output.84-86 In one head-to-head comparison, a regimen of high-dose nitrates and low-dose diuretics provided more consistent clinical improvement than a regimen of high-dose diuretics and low-dose nitrates and was 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 played a role.
  9. 9. 9 Emergency Medicine PracticeFebruary 2002 No other group of agents improves the symptoms of congestion as rapidly as nitrates. Treatment with sublingual nitroglycerin (tablets or spray) results in noticeable hemody- namic and clinical improvement within five minutes.88-90 Single doses of 0.4 mg can be given repeatedly every 5-10 minutes provided the patient has stable blood pressures. In the hospital setting, continuous IV administration of nitroglycerin is generally more convenient and appropriate for the more severely ill patient and allows for titration to specific clinical or hemodynamic end-points. Nitroglycerin can be started at 0.3-0.5 mcg/kg/min so long as the blood pressure is above 95-100 mmHg.16 Alternative regimens and formulations for administering IV nitrates have been described, but they offer no clear advantages.80,91,92 Transdermal nitroglycerin has comparable hemodynamic effects to IV nitroglycerin but is less amenable to rapid titration and may be less effective in patients with poor skin perfusion.93 Hypotension with standard nitrate therapy is generally mild and transient. Severe or persistent hypotension should raise suspicion for hypovolemia, stenotic valvular disease, cardiac 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.94 In such cases, aggressive diuretic therapy is more likely to be of benefit. Sodium nitroprusside is recommended for patients with marked systemic hypertension, severe mitral or aortic valvular regurgitation, or pulmonary edema not responsive to standard nitrate therapy.16 Nitroprusside directly dilates resistance vessels, rapidly reducing blood pressure and afterload.80 Typically, nitroprusside is started at a dose of 0.1 mcg/kg/min and advanced as needed to improve clinical and hemodynamic status. Use a systolic pressure of 85-90 mmHg as a lower limit provided that adequate systemic perfusion is maintained. In patients with renal failure, long- term use of nitroprusside carries the potential for cyanide toxicity, as metabolites accumulate. However, this is extremely unlikely during the course of emergency therapy. Nitroprusside has been safely used in the ED treatment of dialysis patients who presented in acute heart failure.95 Diuretics Diuretics represent the mainstay of therapy for patients with volume overload. On the other hand, it is important to recognize that patients who present with acutely decompensated heart failure are not necessarily volume overloaded. Patients with acute diastolic dysfunction, for example, may benefit more from redistribution of circulating volume (using nitrates) rather than from diuresis. The indiscriminate use of diuretics carries the risk of overdiuresis, particularly among elderly patients. 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.104-107 These actions are not necessarily altogether advantageous, in that their net effect tends to promote further activation of the sympathetic and renin-angiotensin systems.108,109 Studies comparing the acute effects of diuretics and nitrates have Table 5.Medications For Acutely Decompensated Heart Failure. Oxygen Action:Improvement in systemic and myocardial oxygen balance Indications: Hypoxia and/or dyspnea Cautions/Adverse Effects: Respiratory depression (COPD) Dosing:Titrate to pulse oximetry Morphine Action:Relief of anxiety; preload reduction Indications: Pulmonary edema Cautions/Adverse Effects:Respiratory depression; hypotension Dosing: 2-4 mg IV boluses Furosemide Action:Preload reduction Indications:Volume overload Cautions/Adverse Effects: Hypotension; pre-renal azotemia Dosing: Start 20-40 mg (or twice daily oral dose as IV bolus ) Nitroglycerin Action:Preload and afterload reduction; anti-ischemic Indications: Pulmonary edema; myocardial ischemia Cautions/Adverse Effects: Hypotension; tolerance Dosing: Start 0.3–0.5 mcg/kg/min IV and titrate upward Nitroprusside Action:Afterload reduction Indications: Severe hypertension; refractory pulmonary edema Cautions/Adverse Effects: Hypotension; myocardial ischemia; cyanide toxicity Dosing: Start 0.1-0.2 mcg/kg/min IV and titrate upward Enalaprilat Action:Afterload reduction Indications: Pulmonary edema; hypertension Cautions/Adverse Effects: Hypotension; hyperkalemia Dosing: 1.25 mg IV Dobutamine Action:Positive inotropy; afterload reduction Indications: Low-output heart failure; refractory pulmonary edema Cautions/Adverse Effects:Tachycardia; arrhythmia; hypotension; bronchoconstriction Dosing: Start 2.5 mcg/kg/min IV and titrate upward Milrinone Action:Positive inotropy; afterload reduction Indications: Low-output heart failure; refractory pulmonary edema Cautions/Adverse Effects: Arrhythmia; hypotension Dosing: Bolus 50 mcg/kg over 10 min,then start 0.375 mcg/kg/min IV and titrate upward
  10. 10. EmergencyMedicinePractice 10 February 2002 emphasized the more favorable overall hemodynamic effects of the latter group (as described earlier). Depending on the patient’s clinical condition, state of hydration, and previous use of diuretics, an initial IV dose of 20-200 mg of furosemide can be adminis- tered. For patients on chronic diuretic therapy, a common strategy is to begin with the usual daily dose (typically 40-80 mg) given as an IV bolus, and to double the dose if there is inadequate diuresis. In cases of volume overload that fail to respond to standard therapy, substitute a more potent loop diuretic such as torsemide (Demadex) 10-20 mg IV or bumetanide (Bumex) 1-4 mg IV. Combining furosemide with a thiazide agent such as metolazone (5-20 mg PO) or chlorothiazide (Diuril 500-1000 mg IV) may improve diuresis.96,97 If the patient does not respond to an initial dose or two of diuretics, another alternative is to administer a high-dose, continuous furosemide infusion at 20-40 mg/hr titrated to a urine output of 100 mL/hr. This will maximize diuresis while minimizing the toxicity of comparable bolus furo- semide therapy.98 Other studies support the superiority of continuous furosemide therapy over bolus injection,99,100 with some patients receiving up to 2 grams (yes, 2 grams) of furosemide per day.101 (For a more detailed discussion of this topic and further references, see the Cochrane Database of Systematic Reviews.102 ) In patients with severe chronic heart failure, regular use of spironolactone substantially reduces the risk of both morbidity and death.110 However, there is no evidence supporting its use in the ED during an acute episode of decompensated failure. ACE Inhibitors Angiotensin-converting enzyme (ACE) inhibitors represent a logical extension of vasodilator therapy. The beneficial hemodynamic effects of ACE inhibitors in acute heart failure have been appreciated for two decades.111 Acutely, ACE inhibitors reduce both preload and afterload, improve renal hemodynamics, impair sodium retention, attenuate sympathetic stimulation, and maintain or enhance left ventricular function.112-114 In the setting of acute heart failure, drug regimens that include an ACE inhibitor appear to have hemodynamic advantages over those based on other vasodilators.115-117 For acutely decompensated heart failure, ACE inhibi- tors can be administered intravenously (e.g., enalaprilat [Vasotec IV]), orally (e.g., captopril), or sublingually (e.g., emptied captopril capsules contents). Depending on the drug, dose, and route of administration, hemodynamic effects may be seen within 10-60 minutes.112,113,115 Safe dosing regimens of enalaprilat include 0.004 mg/kg as an IV bolus, or 1.25 mg by infusion over five minutes. The suggested one-time dose of oral or sublingual captopril is 12.5-25.0 mg. The safety of administering an ACE inhibitor in the setting TenExcusesThatDon’tWorkInCourt 1.“She was just weak and dizzy. How was I supposed to know she had heart failure?” You found out when she went into acute pulmonary edema after the aggressive fluid bolus! Nonspecific symptoms such as weakness, lethargy, fatigue, anorexia, or lightheadedness may be a manifestation of decreased cardiac output, especially in the older patient. Geriatric patients can be particularly 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 postpartum cardiomyopathy unless you consider it.Myocarditis,cocaine or alcohol abuse, and cardiotoxic chemotherapies are important causes of heart failure in younger patients.While advanced age is a major risk factor for heart failure, young age should never exclude it. 3.“He seemed to be wheezing,so I treated him for COPD!” Unfortunately, his condition continued to deteriorate 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. A careful diagnostic work-up can yield important clues.Consider the use of BNP if the diagnosis is not clear. 4.“I just assumed he hadn’t been taking his medications.” Medication noncompliance and dietary indiscretion 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 anxious. I thought he could tolerate the 10 mg bolus of morphine!” This patient stopped breathing and had to be precipitously intubated. Injudicious use of opiates can result in excessive sedation and loss of respiratory drive.Although useful in small doses for relieving anxiety,opiates provide little hemodynamic benefit in patients with pulmonary edema. 6.“She was clearly‘wet’and needed to be aggressively diuresed. Is it my fault her creatinine doubled by the next day?” Continued on page 11
  11. 11. 11 Emergency Medicine PracticeFebruary 2002 of acutely decompensated heart failure 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 acutely decompensated heart failure.114,118 Few studies of ACE inhibitors for acutely decompen- sated heart failure have been performed in the ED setting. Small studies have demonstrated that sublingual captopril is safe and effective for ED patients with pulmonary edema.95,119 In one retrospective analysis, the use of sublin- gual captopril in the ED was associated with lower rates of mechanical ventilation and CCU admission.120 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 rela- tively prolonged duration of action, making dosage less easily titratable. Inotropes While the role of long-term inotropic therapy for chronic heart failure remains controversial, short-term therapy in acutely decompensated failure appears to benefit select patients. Classically, inotropic agents have been reserved for the treatment of cardiogenic shock. However, short-term inotropic support may also be beneficial for patients who fail to respond to (or who are not candidates for) conven- tional therapy with diuretics and vasodilators.16 While short-term inotropic therapy clearly improves hemody- namic performance, data on clinical outcomes are limited. In the absence of frank cardiogenic shock, inotropic support is typically initiated using an agent that both increases myocardial contractility and reduces afterload. This class of “vasodilator inotropes” includes beta-agonists such as dobutamine as well as the phosphodiesterase inhibitors amrinone, milrinone, and enoximone. (See Table 5 on page 9.) Small trials with each of these agents have demonstrated short-term hemodynamic improvement in patients with acutely decompensated heart failure, most commonly in the setting of MI.123-127 The addition of low- dose nitrate therapy to an inotropic regimen may confer additional hemodynamic benefits.128,129 In one head-to-head comparison in patients who sustained heart failure follow- ing an acute MI, milrinone (50 mcg/kg bolus over 10 minutes, infusion at 0.25-0.75 mcg/kg/min) appeared to confer more consistent short-term hemodynamic improve- ment than dobutamine (infusion at 2.5-15.0 mcg/kg/min).130 Other evidence suggests some advantage in milrinone over dobutamine in patients with severe heart failure even in the absence of acute MI.131 As we see more heart failure patients maintained on chronic beta-blocker therapy, the theoretical TenExcusesThatDon’tWorkInCourt(continued) Maybe.This elderly woman with acute diastolic dysfunction was not suffering from volume overload. Her pulmonary congestion may have responded better to vasodilator therapy than to aggressive diuresis that ended up impairing her renal function and prolonging her hospital stay. 7.“I always thought sublingual nitroglycerines were harmless. I didn’t expect his systolic BP to drop to single digits!” Nitrates are fast, effective,and relatively safe, but patients with preload-dependent conditions (e.g.,valvular stenosis) do not tolerate them well. Nor do patients taking Viagra! 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, CPAP can reduce the need for endotracheal intubation and decrease length of ICU stay. 9.“He was in rapid atrial fibrillation, and I figured rate- control would improve his cardiac function.” Unfortunately, you failed to consider the negative inotropic effects of verapamil, and the patient’s heart failure further decompensated.When a patient presents with decompensated heart failure in the context of rapid atrial fibrillation, it is important to address the clinical situation as a whole,which means treating for both conditions simultaneously and recognizing that the treatment of the one may impact upon the other.If the emergency physician believes that new-onset atrial fibrillation has precipitated acute pulmonary edema, emergent cardioversion is indicated. 10.“She felt a little better after the Lasix, so we sent her home 10 minutes later. Her short length of stay was impressive!” 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. v
  12. 12. EmergencyMedicinePractice 12 February 2002 advantages to phosphodiesterase inhibitors over beta- agonists increase.132 It is important to understand the expected hemody- namic effects of inotropic agents and set clear goals for therapy. Most inotropic agents have multiple pharmacologic actions, some of which may be deleterious. Undesirable chronotropic effects, arrhythmogenesis, or ischemia resulting from increased myocardial oxygen consumption may curtail the use of any particular drug. Digoxin has a very limited role in the ED management of heart failure. The inotropic effects of digoxin are modest, unpredictable, and delayed for at least 90 minutes after IV loading.123 For patients with acutely decompensated heart failure, the only reasonable use for digoxin is to help control the ventricular response to atrial fibrillation (as described later in the text). Morphine Morphine is one of the oldest drugs still in use for the treatment of acute heart failure and remains an important adjunct for treating the anxiety and discomfort associated with pulmonary edema. With high doses of morphine, direct vasodilation may result from histamine release, but the predominant hemodynamic effects of morphine appear to be mediated through the central nervous system.133 Morphine can be administered safely to most patients. However, because of its sedative properties and potential to depress respirations, exercise caution when administering morphine in the setting of chronic pulmonary insufficiency or suspected acidosis. One retrospective study found that ED administration of morphine to patients with pulmonary edema was associated with an increased rate of endotra- cheal intubation and CCU admission.120 Respiratory Therapy The majority of patients with respiratory distress respond to supplemental oxygen and standard pharmacologic 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.”) Mask-applied continuous positive airway pressure (CPAP) of 5-10cm H2O has been shown in several random- ized, controlled clinical trials to reduce the need for endotra- cheal intubation in patients with severe cardiogenic pulmonary edema.134-136 Pooled data also suggest that the use of CPAP in this setting may be associated with de- creased mortality.137 CPAP improves lung mechanics by recruiting atelectatic alveoli, improving pulmonary compli- ance, and reducing the work of breathing.138 At the same time, particularly in patients with CHF, CPAP improves hemodynamics by reducing preload and afterload, thereby enhancing left ventricular performance.139-142 BiPAP—or noninvasive positive pressure ventilation (NPPV)—provides the physiological advantages of CPAP during expiration but provides additional assistance with the inspiratory work of breathing. Evidence from several case series and a recent randomized trial supports the use of this therapy in patients with acute cardiogenic pulmonary edema.143-147 A small, randomized trial comparing BiPAP with CPAP demonstrated a more rapid clinical improve- ment with BiPAP but no difference in the rates of intuba- tion.148 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 of similar safety concerns.149 At present, it seems prudent to employ CPAP rather than BiPAP for patients with cardiogenic pulmonary edema and hypoxemic respiratory failure.150 The success of noninvasive respiratory support depends on appropriate patient selection. For patients with compromised upper airway function or significantly altered level of consciousness, intubation and mechanical ventila- tion 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 noninvasive 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 respiratory effort. Although the decision to initiate noninvasive respira- tory support is dependent on a variety of factors, the presumption is that the earlier therapy is instituted, the greater the likelihood of averting intubation. Recent studies suggest that the use of noninvasive ventilatory support in the prehospital setting is feasible and potentially beneficial for patients with presumed cardiogenic pulmonary edema.38,151 If there is progressive respiratory failure in spite of noninvasive support, the patient requires intubation and mechanical ventilation. Special Circumstances “But his flawed heart / (Alack, too weak the conflict to support!) / ‘Twixt two extremes of passion, joy and grief, / Burst smilingly.” —William Shakespeare (1564–1616), in King Lear, act 5, sc. 3, l. 197-200. Cardiogenic Shock Hypotension in the setting of decompensated heart failure is presumed to be due to cardiogenic shock and requires aggressive management. Regardless of blood pressure, patients who present with evidence of inadequate tissue perfusion (i.e., cool skin, altered mental status) should be approached in the same manner. Mortality rates for patients with frank cardiogenic shock remain alarmingly high, ranging from 50% to 80%.152 Although there is a lack of data from controlled trials regarding the optimal management of these patients, consensus guidelines offer some direction.16 Cardiogenic shock is most often seen in the setting of acute ST-segment elevation MI, but it occurs in other acute coronary syndromes as well.153 In the context of acute MI, emergent cardiac catheterization and revascularization improves outcome and should be strongly considered.154 In the absence of Continued on page 19
  13. 13. 13 Emergency Medicine PracticeFebruary 2002 The evidence for recommendations is graded using the following scale.For complete definitions,see back page.Class I:Definitely recommended. Definitive,excellent evidence provides support.Class II:Acceptable and useful.Good evidence provides support.Class III:May be acceptable, possibly useful.Fair-to-good evidence provides support.Indeterminate:Continuing area of research. This clinical pathway is intended to supplement,rather than substitute, professional judgment and may be changed depending upon a patient’s individual needs. Failure to comply with this pathway does not represent a breach of the standard of care. Copyright  2002 EB Practice, LLC. EB Practice, LLC (1-800-249-5770) grants each subscriber limited copying privileges for educational distribution within your facility or program. Commercial distribution to promote any product or service is strictly prohibited. ClinicalPathway:PrehospitalTherapy ForAcutelyDecompensatedHeartFailure Impending respiratory failure? • Upright sitting position (Class indeterminate) • Oxygen therapy (Class I) • Cardiac monitor (12-lead ECG if available;Class indeterminate) • IV access (Class I) • Endotracheal intubation (Class I) or CPAP if available and no contraindications (see text) (Class II) • Alert ED regarding patient status Expedite transport to the ED • SL TNG/Nitro-Spray (Class II) • IV furosemide* (Class III) • IV morphine* (Class III) * These drugs can cause complica- tions if patient is misdiagnosed as pulmonary edema in the field • ASA (Class I) • SL TNG/Nitro-Spray (Class II) • IV morphine (Class II) • ACLS interventions (Class I-III; use caution with calcium- channel blockers and beta- blockers) → → Pulmonary edema? Chest pain? Arrhythmia? → → → →→ → → →→
  14. 14. EmergencyMedicinePractice 14 February 2002 The evidence for recommendations is graded using the following scale.For complete definitions,see back page.Class I:Definitely recommended. Definitive,excellent evidence provides support.Class II:Acceptable and useful.Good evidence provides support.Class III:May be acceptable, possibly useful.Fair-to-good evidence provides support.Indeterminate:Continuing area of research. This clinical pathway is intended to supplement,rather than substitute,professional judgment and may be changed depending upon a patient’s individual needs.Failure to comply with this pathway does not represent a breach of the standard of care. Copyright  2002 EB Practice, LLC. EB Practice, LLC (1-800-249-5770) grants each subscriber limited copying privileges for educational distribution within your facility or program. Commercial distribution to promote any product or service is strictly prohibited. ClinicalPathway:EmergencyDepartmentTherapy ForAcutelyDecompensatedHeartFailure • Upright sitting position (Class indeterminate) • Oxygen therapy (Class I) • Chest x-ray (Class I) • Cardiac monitor and 12-lead ECG (Class I) • Pulse oximetry (Class I-II) • IV access (Class I) • Foley catheter if significant distress (Class indeterminate) → → • Acute MI, persistent cardiac ischemia? Yes → • ASA (Class I) • percutaneous transluminal coronary angioplasty (PTCA) (Class I) • Thrombolytics (Class I-II for ST-elevation MI) → No → • Unstable tachycardia? Yes → Go to top of next page • Determine if patient is a candidate for cardioversion (ventricular tachycardia or acute-onset atrial fibrilla- tion,atrial flutter) (Class II) • Antiarrhythmic therapy* (Class II) *Special caution needed with beta-blockers and calcium- channel blockers due to negative inotropy No → • Cardiogenic shock? No → • Pressors/inotropes (Class II) • Inra-aortic balloon counterpulsation (IABC) if potentially reversible etiology (Class II) • Cardiology consult (Class indeterminate) Yes → → • Compromised upper airway function? • Altered level of consciousness? • Hemodynamic instability/cardiogenic shock? • Myocardial infarction or severe ischemia? Consider CPAP (Class II) Endotracheal intubation (Class I) • Persistent respiratory distress? Yes → → → Yes No No →
  15. 15. 15 Emergency Medicine PracticeFebruary 2002 The evidence for recommendations is graded using the following scale.For complete definitions,see back page.Class I:Definitely recommended. Definitive,excellent evidence provides support.Class II:Acceptable and useful.Good evidence provides support.Class III:May be acceptable, possibly useful.Fair-to-good evidence provides support.Indeterminate:Continuing area of research. This clinical pathway is intended to supplement,rather than substitute, professional judgment and may be changed depending upon a patient’s individual needs. Failure to comply with this pathway does not represent a breach of the standard of care. Copyright  2002 EB Practice, LLC. EB Practice, LLC (1-800-249-5770) grants each subscriber limited copying privileges for educational distribution within your facility or program. Commercial distribution to promote any product or service is strictly prohibited. ClinicalPathway:EmergencyDepartmentTherapy ForAcutelyDecompensatedHeartFailure(continued) If inadequate clinical improvement Nitrates* • Sublingual while starting IV or if moderate symptoms (Class II) • Transdermal if good skin perfusion no significant diaphoresis (Class III) • Intravenous nitroglycerin if severe distress or significant hypertension (Class I-II): start at 0.3-0.5 mcg/kg/min and titrate to blood pressure and symptoms *Do not use if patient taking sildenafil (Viagra) → Add diuretics* • Furosemide twice daily dose intravenously or start with 40-80 mg IV (Class II) • If inadequate urinary output, consider one or more of the following: • Double furosemide dose (Class II) • Add different loop diuretic (torsemide [Demadex] or bumetanide [Bumex]) (Class III) • Add thiazide diuretic (Chlorothiazide [Diuril] or other) (Class II) • Begin furosemide infusion:start at 20-40 mg/h, titrate to achieve urine output of 100 cc/h (Class II) *Avoid diuretics in case of acute diastolic dysfunction (flash pulmonary edema with presumed ischemia) and in case of hypotension→→ Add ACE inhibitors* • Enalapril 1.25 mg IV given over 5 minutes (Class II-III) • Captopril 12.5-25.0 mg PO or SL (Class II-III) *Avoid in hypotension,pregnancy, hyperkalemia, or a history of ACE-inhibitor-induced angioedema Add inotropes • Milrinone (50-mcg/kg bolus over 10 minutes, infusion at 0.25-0.75 mcg/kg/min) (Class I-II) • Dobutamine (infusion at 2.5-15.0 mcg/kg/min) (Class I-II) → Go to top of next page Consider morphine sulfate (2-3 mg boluses) for anxiety as needed (Class II-III) If inadequate clinical improvement →→ If inadequate clinical improvement →→
  16. 16. EmergencyMedicinePractice 16 February 2002 • New murmur? • Unexplained etiology for pulmonary edema? • Clinical exam suspicious for tamponade? • Shock? Pericardial tamponade? Valve/septal rupture? The evidence for recommendations is graded using the following scale.For complete definitions,see back page.Class I:Definitely recommended. Definitive,excellent evidence provides support.Class II:Acceptable and useful.Good evidence provides support.Class III:May be acceptable, possibly useful.Fair-to-good evidence provides support.Indeterminate:Continuing area of research. This clinical pathway is intended to supplement,rather than substitute,professional judgment and may be changed depending upon a patient’s individual needs.Failure to comply with this pathway does not represent a breach of the standard of care. Copyright  2002 EB Practice, LLC. EB Practice, LLC (1-800-249-5770) grants each subscriber limited copying privileges for educational distribution within your facility or program. Commercial distribution to promote any product or service is strictly prohibited. ClinicalPathway:EmergencyDepartmentTherapy ForAcutelyDecompensatedHeartFailure(continued) → Diagnostic studies • Cardiac enzymes: Sudden/rapid onset,anginal pain, ischemic changes on ECG, or significant risk factors for coronary artery disease (Class II) • B-natriuretic peptide: Possible competing diagnosis or unclear clinical picture (Class II) • Electrolytes (Class II) • CBC or hemoglobin (Class II-III) Emergent or urgent transthoracic echocardiography depending on clinical stability (Class II) → Yes Disposition according to clinical status → → → → Pericardiocentesis (Class II) Cardiothoracic consult (Class II) → → →
  17. 17. 17 Emergency Medicine PracticeFebruary 2002 • Atrial fibrillation/atrial flutter? • Fluid overload in renal failure? • Uncontrolled hypertension? • Infection/sepsis? The evidence for recommendations is graded using the following scale.For complete definitions,see back page.Class I:Definitely recommended. Definitive,excellent evidence provides support.Class II:Acceptable and useful.Good evidence provides support.Class III:May be acceptable, possibly useful.Fair-to-good evidence provides support.Indeterminate:Continuing area of research. This clinical pathway is intended to supplement,rather than substitute, professional judgment and may be changed depending upon a patient’s individual needs. Failure to comply with this pathway does not represent a breach of the standard of care. Copyright  2002 EB Practice, LLC. EB Practice, LLC (1-800-249-5770) grants each subscriber limited copying privileges for educational distribution within your facility or program. Commercial distribution to promote any product or service is strictly prohibited. ClinicalPathway:EmergencyDepartmentTherapy ForAcutelyDecompensatedHeartFailure—SpecialCircumstances Yes → No → • Consider cardioversion for new-onset atrial fibrillation (Class II; Class I if unstable patient with new-onset atrial fibrillation) • Rate control: • IV/PO diltiazem (Class II) • IV amiodarone (Class II) • IV/PO digoxin (Class II) Yes → No → • Dialysis (Class I) • IV nitroglycerin (Class II) • IV nitroprusside (Class II) • IV/PO ACE inhibitor (Class II) • IV furosemide (Class II) Yes → No → • IV nitroglycerin (Class I-II) • IV nitroprusside (Class I-II) • IV/PO ACE inhibitor (Class II) • IV furosemide (Class II) Yes → • Antibiotics (Class I) • Pressors (Class I-II) • Fluids (Class II)
  18. 18. EmergencyMedicinePractice 18 February 2002 Tool 1.Sample Discharge Instructions For ED Heart Failure Patients. You have been evaluated and treated for symptoms of heart failure in the emergency department. Your condition has sufficiently improved or stabilized so that you will be discharged from the emergency department for outpatient follow-up. However, your heart failure may deteriorate once again, in which case you should return to the emergency department. If you experience any of the following, please return to the emergency department immediately: 1.Chest pain or discomfort 2.Progressive shortness of breath 3.Fainting or lightheadedness 4.Persistent palpitations or (new) irregular pulse 5.Significantly reduced amount of urine 6.Persistent cough 7.Wheezing 8.High fever or shaking chills 9.Any new, different, or worsening problem Follow-up Instructions • Return to emergency department for re-evaluation in _______ hours/days. • Check in with your doctor (Primary Care Provider or Cardiologist) if not improved in _______ days. • Check in with your doctor (Primary Care Provider or Cardiologist) in _______ days. • You will need to have the following (x-rays/tests) checked in _______ days: ________________ • You may need to have an outpatient (stress test/echocardiogram). This (has/has not) been discussed with your regular doctor. Medications Take the following medicines as prescribed: __________________________________________________________________________________ __________________________________________________________________________________ __________________________________________________________________________________ __________________________________________________________________________________ Additional Instructions 1.Avoid salty foods. 2.Limit fluid/water intake as instructed (daily fluid restriction: _______ ). 3.Keep a daily measurement of your weight in a logbook for your doctor to see. 4.Visiting Nurse/Home Health Aide/Social Work/Outpatient Heart Failure Team has been arranged. They will contact and check on you within _______ days. 5.Read through the provided heart failure materials, and contact your regular doctor if you have any questions. Copyright  2002 EB Practice, LLC. EB Practice, LLC (1-800-249-5770) grants each subscriber limited copying privileges for educational distribution within your facility or program. Commercial distribution to promote any product or service is strictly prohibited.
  19. 19. 19 Emergency Medicine PracticeFebruary 2002 emergent catheterization, thrombolysis may be useful, especially when given in combination with intra-aortic balloon counterpulsation (IABC).155 Other potentially reversible causes of cardiogenic shock, such as acute valvular dysfunction, septal rupture, and pericardial tamponade, need to be excluded or addressed promptly. Non-cardiac etiologies of shock, such as hypovolemia, sepsis, poisoning, and massive pulmonary embolism, must also be entertained. As mentioned previously, the use of a fluid bolus to treat cardiogenic shock is not well-studied. While conven- tional wisdom holds that hypotension due to a right ventricular infarction generally responds well to fluid infusion, some data call this notion into question.156,157 Patients who present in shock with a normal blood pressure or with mild hypotension often respond favorably to dobutamine (starting at 2-3 mcg/kg/min). Compared with dopamine, dobutamine is associated with a lower incidence of arrhythmias, less peripheral vasoconstriction, and more consistent reduction in left ventricular filling pressure for a comparable rise in cardiac output.158 Dopamine is required for patients who have severe or persistent hypotension (systolic blood pressure < 70-80 mmHg) in the presence of volume overload or after bolus administration of saline. At moderate doses (4-5 mcg/kg/ min), dopamine improves cardiac output without causing excessive systemic vasoconstriction. 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. If hypotension or clinical shock persists at dopamine doses of 15 mcg/kg/min or greater, IABC should be considered, presuming the patient has a potentially reversible condition. For example, IABC can be an effective temporiz- ing measure in anticipation of coronary revascularization or cardiac valve repair. Likewise, a patient with massive beta- blocker overdose can be maintained on IABC until the drug is metabolized or otherwise removed from the body.159 The patients least likely to benefit from the IABC are those with multiple previous infarctions, massive irreversible myocar- dial necrosis, 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 levels (≥ 80 mmHg). 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. Dialysis Patients Heart failure is present in about one-third of patients who begin dialysis and will develop over time in an additional 25%.160 Among anuric hemodialysis patients, heart failure is the most common cause of ED visits.161 In these patients, acutely decompensated failure is most often due to volume overload between dialysis treatments. Although hemodialy- sis is the treatment of choice for these patients, it may not be immediately available. ED treatment is directed at stabiliz- ing these patients until hemodialysis can be performed. Because of their direct vascular effects, diuretics may still have a role in managing anuric patients with volume overload.162 Vasodilator therapy with nitrates and ACE inhibitors has been shown to be particularly effective.95 In any dialysis patient with an unstable cardiac rhythm, hyperkalemia and digoxin toxicity must be considered. An older therapy that is sometimes considered when dialysis is unavailable and other interventions fail is the administration of oral sorbitol (100 mg PO). This interven- tion draws intravascular fluid into the gut, which is then excreted in the diarrheal stool.163 Atrial Fibrillation Atrial arrhythmias, and atrial fibrillation in particular, are commonly seen in patients with chronic heart failure. In fact, it is frequently the same underlying condition—e.g., hypertension, coronary artery disease, or valvular disease— that predisposes the patient to both atrial fibrillation and heart failure. 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 consequences. Moreover, when atrial fibrillation is accompanied by a rapid ventricular response, the tachycardia itself is problematic because it means reduced filling time and increased myocardial oxygen demand. When assessing the patient with rapid atrial fibrillation and acutely decompensated heart failure, it is often difficult to attribute cause and effect. Was the onset of rapid atrial fibrillation a response to worsening heart failure (e.g., via neurohormonal activation and/or increased atrial stretch)? Alternatively, did ventricular function deteriorate because of the onset of rapid atrial fibrillation? Rather than risk getting caught up in a “chicken-and-egg” debate, the important point is to address the patient’s clinical status as a whole. Often this means treating for both conditions simultaneously, recognizing that the treatment of the one may impact upon the other. For example, use of a beta- blocker or calcium-channel blocker for rate control may have negative inotropic effects that worsen existing systolic dysfunction. On the other hand, use of an inotropic agent like dobutamine to enhance myocardial contractility may result in a faster ventricular rate. In general, diltiazem and amiodarone (and, to a lesser extent, digoxin) are considered first-line therapies for rate control in patients with left ventricular dysfunction.166-168 Electrical cardioversion may be life-saving for the unstable patient who has acute atrial fibrillation. However, maintaining sinus rhythm may not be possible if the underlying heart failure is not addressed. Controversies/Cutting Edge Impedance Cardiography Impedance cardiography (IC) is a noninvasive means of Continued from page 12
  20. 20. EmergencyMedicinePractice 20 February 2002 hemodynamic monitoring, capable of providing real-time estimates of cardiac output and pulmonary capillary wedge pressure by employing principles of thoracic bioimpedance. Over the past three decades, IC has been investigated in a variety of clinical settings and has been found to compare moderately well with other modalities for assessing hemodynamics (e.g., echocardiography, Swan-Ganz catheterization).169,170 Because the technique is noninvasive, portable, and capable of providing beat-to-beat information, potential applications in the ED are numerous.171 IC is less accurate in patients with underlying heart disease, but serial measurements may still provide useful information—for example, for monitoring response to therapy.170 Also, there may be a distinct role for IC in helping to differentiate between systolic and diastolic dysfunction.171 Beta-blockers Large randomized, controlled trials have demonstrated clear benefits for long-term beta-blocker therapy in patients with systolic heart failure.172-174 In contrast, short-term administration of beta-blockers to patients with severe systolic dysfunction can cause life-threatening clinical deterioration.175 Therefore, beta-blockers are not routinely recommended for treatment of acutely decompensated heart failure. In the setting of an acute decompensation, chronic beta-blocker therapy should either be temporarily discontinued or administered cautiously at a reduced dose. When decompensated heart failure occurs in the context of an acute coronary syndrome, the risk of worsen- ing heart failure must be weighed against the known benefits of beta-blockade.176-178 Less is known about the safety and efficacy of beta- blocker therapy for patients with acute diastolic dysfunc- tion. In theory, the value of reducing hypertension and tachycardia would outweigh any concern about negative inotropy in these patients. Anecdotal experience with beta- blockers—for example, in the management of hypertensive crises—has been positive. Further studies are needed to clarify the role of beta-blockers in the treatment of acute diastolic dysfunction. B-Natriuretic Peptide As a naturally occurring counter-regulatory hormone, BNP also has therapeutic potential. Like the other natriuretic peptides in its class, BNP exerts favorable hemodynamic, natriuretic, and neurohormonal effects when administered in supraphysiologic doses.179-182 Studies show that nesiritide (Natrecor), a recombinant form of BNP, improves short-term hemodynamic function and clinical status in patients hospitalized with decompensated heart failure.183 The FDA has recently approved this drug for the treatment of heart failure. Like other vasodilator agents, the major adverse effect of nesiritide is hypotension. Whether or not there is a role for nesiritide in the ED remains unclear. A multicenter, randomized clinical trial of nesiritide in an ED-based heart-failure observation-unit setting is currently under way (PROACTION). Calcium Sensitizers Calcium sensitizers (levosimendan, pimobendan) are a novel class of agents that modify the configuration of troponin C to promote myofilament sensitivity to calcium, enhancing contractility without impeding diastolic relax- ation.184 In small studies of patients with severe decompen- sated heart failure, these agents have been shown to be as effective as dobutamine and milrinone in increasing cardiac output and reducing pulmonary capillary wedge pressure, but without increasing myocardial oxygen demand as conventional inotropes do.185,186 Implications for ED utiliza- tion await additional clinical trials. Disposition Even in this era of cost containment, the vast majority of patients who present with decompensated heart failure are admitted to the hospital.18 Meanwhile, hospital costs for inpatient care of decompensated heart failure are continuing to rise. In 1996, an average of over $5000 was paid on behalf of Medicare beneficiaries per hospital discharge for heart failure.2 However, while the realities of modern healthcare economics may not favor routine hospitalization, premature release of inadequately treated patients is likely to increase short-term morbidity and mortality.187 Alarmingly, a recent outcome study of 112 patients discharged from the ED with a primary diagnosis of CHF showed that within three months of the initial visit, more than 60% experienced a recurrent ED visit, hospitalization, or death.13 In general, clinicians have great difficulty judging the prognosis of patients with exacerbations of heart failure.188 Acutely decompensated heart failure is a dynamic entity, and the ED physician is with the patient for only a short time. Some patients are dramatically ill at presentation but respond rapidly to treatment, while others deteriorate after a period of relative stability. Previous studies have found that certain patient characteristics predict in-hospital morbidity and mortality. Multivariate analyses have found several independent correlates of major complications or death during hospital- ization.6,9,189,190 These include hypotension, tachypnea, jugular venous distention, electrocardiographic abnormali- ties, hyponatremia, and poor initial diuresis. A number of other characteristics have also been correlated with in-hospital mortality.6,8-11,15,189,191-195 (See Table 6.) Disturbingly, even patients without any independent risk Table 6.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 • Digoxin use • Advanced renal dysfunction • Poor response to initial therapy
  21. 21. 21 Emergency Medicine PracticeFebruary 2002 factors appear to have substantial rates (6%) of in-hospital morbidity and mortality.6 The AHCPR has established criteria for hospitalization of patients with heart failure.17 (See Table 7.) However, in one study, these criteria failed to identify up to one-third of the patients who die within 30 days.18 In this same study, the ED physician’s clinical judgment appeared to be a better predictor of 30-day mortality. ACC/AHA guidelines state that in the absence of specific criteria (e.g., recent MI, symptom- atic arrhythmias, marked hypokalemia), patients with “mild-to- moderate symptoms” are generally at low risk and do not require hospital admission. Using ACC/AHA definitions, over half of the patients admitted for heart failure may be “low risk,” yet up to 5% of these “low-risk” admissions are associated with an adverse cardiovascular event.196 Thus, while published criteria and guidelines can help with triage, the significant rate of morbidity even among “low-risk” patients mandates that clinical judgment be incorporated into the decision- making process. ACC/AHA guidelines explicitly allow for an observa- tion period prior to determining a patient’s disposition.16 During this period of time, patients can be monitored for their response to therapy and for the development of any potentially serious adverse events. Theoretically, an ED- based observation unit or other subacute care setting can accomplish this at substantial cost savings. Observation units have been advanced as a safe and effective means of reducing hospital admissions in general and heart failure admissions in particular.197,198 Appropriate patient selection is critical for the functioning of such units. (See Table 8.) For patients who are ultimately discharged home, consultation with the patient’s primary care physician and/ or cardiologist is imperative. Patients and their families need to understand that there is a substantial chance of outpatient failure necessitating a repeat ED visit or hospital- ization within the next 30 days.13 Depending on what precipitated the decompensation, the patient’s outpatient drug regimen may require some adjustment. Intensive outpatient follow-up has been shown to be successful in preventing repeat visits to the ED.199,200 Referral to an outpatient heart failure program where available can reduce the frequency of ED visits and hospitalizations.201 Sample discharge instructions are shown on page 18. v 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, randomized, and blinded trial should carry more weight than a case report. To help the reader judge the strength of each reference, 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. In addition, the most informative references cited in the paper, as determined by the authors, will be noted by an asterisk (*) next to the number of the reference. 1.* Kannel WB, Belanger AJ. Epidemiology of heart failure. Am Heart J 1991;121:951-7. (Review) 2. American Heart Association. 2000 Heart and Stroke Statistical Update. Washington, DC: American Heart Association; 2000. (Review) 3. McCaig LF, Burt CW. National Hospital Ambulatory Medical Care Survey (NHAMCS): 1999 Emergency Department Summary. Adv Data 2001;320:1-36. (Epidemiologic survey) 4. Allegra JR. Monthly, weekly, and daily patterns in the incidence of congestive heart failure. Acad Emerg Med 2001;8:682-685. (Retrospective chart review; 26,224 patients) 5. Daley J, Jencks S, Draper D, et al. Predicting hospital-associated mortality for Medicare patients. A method for patients with stroke, pneumonia, acute myocardial infarction, and congestive heart failure. JAMA 1988;260:3617-3624. (Retrospective, cohort; 5888 patients) 6.* Chin MH, Goldman L. Correlates of major complications or death in patients admitted to the hospital with congestive heart failure. Arch Intern Med 1996;156:1814-1820. (Prospective, cohort; 435 patients) 7. Jaagosild P, Dawson NV, Thomas C, et al. Outcomes of acute exacerbation of severe congestive heart failure: quality of life, resource use, and survival. Arch Intern Med 1998;158:1081-1089. (Prospective, cohort, multi-center; 1390 patients) 8. Plotnick GD, Kelemen MH, Garrett RB, et al. Acute cardiogenic pulmonary edema in the elderly: factors predicting in-hospital and one-year mortality. South Med J 1982;75:565-569. (Prospective, observational; 55 patients) 9. Katz MH, Nicholson BW, Singer DE, et al. The triage decision in pulmonary edema. J Gen Intern Med 1988;3:533-539. (Prospective, observational; 216 patients) 10. Le Conte P, Coutant V, Nguyen JM, et al. Prognostic factors in acute cardiogenic pulmonary edema. Am J Emerg Med 1999;17:329- 332. (Prospective, cohort; 186 patients) 11. Edoute Y, Roguin A, Behar D, et al. Prospective evaluation of pulmonary edema. Crit Care Med 2000;28:330-335. (Prospective, observational; 150 patients) 12. Barron HV, Every NR, Parsons LS, et al. Investigators in the National Registry of Myocardial Infarction 2. Am Heart J 2001 Table 7.AHCPR Criteria For Hospital Admission. • Myocardial ischemia • Pulmonary edema/severe respiratory distress • Hypoxia (oxyhemoglobin saturation < 90%) • Anasarca • Severe complicating medical disease • Symptomatic hypotension or syncope • Heart failure refractory to outpatient management • Inadequate social support for safe outpatient management Table 8.Observation Unit Heart Failure Protocol— Exclusion Criteria. • Alternative diagnosis primarily responsible for acute symptoms (e.g.,chronic obstructive pulmonary disease, pneumonia,arrhythmia) • Acute myocardial infarction or persistent anginal chest pain • New persistent oxygen requirement • Requirement for mechanical ventilation (including noninvasive ventilatory support) • Requirement for vasopressor/inotropic agents to support hypotension • Requirement for nitroprusside to control hypertension • Requirement for emergent hemodialysis • Severe complicating medical disease • Inadequate social support for expected disposition to safe outpatient management