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CHAPTER 53: Acute Heart Failure 367 monitored for a period of time in the ED or observation area and, if well, discharged with a prolonged monitoring device. 38,71,72 Monitoring is the key investigation of arrhythmia detection, whether inpatient or outpatient. Echocardiogram abnormalities are uncommon in patients with a negative cardiac history, in the setting of a normal cardiac examination and ECG. Electrophysiology testing involves invasive electrical stimulation and cardiac monitoring to uncover possible conduction abnormalities that predispose to tachydysrhythmias (both ventricular and supraventricular) or bradydysrhythmias.  OUTPATIENT EVALUATION Most low-risk patients need no workup unless symptoms are recur rent. Long-term cardiac monitoring includes many different ambulatory or event monitors, which are useful to identify dysrhythmias, especially in intermediate- to high-risk patients who are discharged after a period of hospital monitoring ( Table 52-4). The duration one should wear an ambulatory monitor has not been established with certainty. However, prolonged monitoring for patients with syn cope has now become a recommendation in the newest American Heart Association guidelines. 21 Long-term use of implantable loop recorders has a diagnostic yield of >50% in patients with recurrent syncope. 73-75 Tilt-table testing is designed to identify reflex-mediated syncope by rapidly moving the patient from a supine position on the tilt table to an upright position of 60 degrees for 45 minutes. A positive end point is reached if syncope, hypotension, or the patient’s typical symptoms are reproduced. Recurrent reflex-mediated syncope resistant to conservative therapies can be treated with a cardiac pace maker. Psychiatric referral is recommended for young patients without underlying heart disease who have frequent syncopal events. General ized anxiety and depressive disorders are the most commonly assigned diagnoses. Patients with a prolonged QT segment should be referred for genetic testing for the LQTS gene. Those who are gene negative have very little risk for fatal syncope. SPECIAL POPULATIONS  THE ELDERLY Because of both normal physiologic changes with aging and age-related disease processes, the elderly are at increased risk for adverse outcomes after syncope or near-syncope. 9,11 Syncope in the elderly is often multi factorial and difficult to establish in the ED. Twelve percent of patients over 60 years of age who sustain cardiac arrhythmia within 30 days after syncope have a completely normal ECG at the index ED visit. Various specified ages have been studied as risk factors for fatal or serious outcomes after syncope; however, there is a gradual continuum of increasing risk with increasing age. Cardiovascular risk factors appear to be better predictors than age itself. Decreased adrenergic responsiveness contributes to the diminished chronotropic response seen after orthostatic stresses in the elderly. The incidence of vasova gal syncope actually decreases with age, in part as a consequence of the decreased responsiveness of the autonomic nervous systems. The elderly also have a less sensitive thirst mechanism and a decreased endocrine response to volume depletion, exacerbating orthostatic hypotension. Postprandial hypotension is more common in the elderly, especially in nursing home patients, and is thought to be due to a rapid rate of nutrient delivery from the stomach into the small intestine.

s sensitive thirst mechanism and a decreased endocrine response to volume depletion, exacerbating orthostatic hypotension. Postprandial hypotension is more common in the elderly, especially in nursing home patients, and is thought to be due to a rapid rate of nutrient delivery from the stomach into the small intestine. Aortic stenosis is the most common obstructive cardiac lesion in the elderly, producing a fixed cardiac output. Diabetes may lead to auto nomic dysfunction and peripheral neuropathy. Finally, medication usage is much more common in the elderly population, increasing the risk of orthostasis and decreasing autonomic responsiveness to orthostatic stress. REFERENCES The complete reference list is available online at www.TintinalliEM.com. Acute Heart Failure Alan B. Storrow Brian Bales Sean P. Collins INTRODUCTION AND EPIDEMIOLOGY Acute heart failure covers a wide spectrum of illness severity, ranging from a gradual increase in leg swelling, shortness of breath, or decreased exercise tolerance to the abrupt onset of pulmonary edema. While the alternative terms decompensated heart failure, acute heart failure syn drome, or hospitalized with heart failure are often used in an overlapping manner, we refer to patients with either an acute exacerbation of chronic heart failure or a new-onset heart failure as having acute heart failure. The outdated term congestive heart failure describes patients with signs and symptoms of fluid accumulation. Most ED visits for acute heart failure result in hospital admission. ED physicians drive most disposition decisions in this setting. 2,3 With the aging population, increased survival from acute myocardial infarc tion, and outpatient treatment options, the prevalence of heart failure is expected to increase over the next decade. 4-6 Although long-term heart failure management has improved through the use of β-blockers, angiotensin-converting enzyme inhibitors, spironolactone, and car diac resynchronization therapy, 4,5 acute heart failure therapy is largely unchanged and includes nitrates, diuretics, and positive-pressure ventilation. 7 Only one new therapy, nesiritide, was recently approved for acute heart failure treatment, but it does not improve outcomes compared to standard treatment. Heart failure has a poor prognosis, with approximately 50% of patients dying within 5 years of diagnosis. 9 Hospitalization is an inflection point in this disease, with those hospitalized having higher mortal ity than a matched nonhospitalized cohort.10 PATHOPHYSIOLOGY Heart failure is a complex clinical syndrome manifested by cardinal symptoms (shortness of breath, edema, and fatigue) occurring from functional or structural cardiac damage, impairing the ability of the heart to act as an efficient pump. Symptoms may limit exercise toler ance and lead to fluid retention, driving pulmonary and/or splanchnic congestion and/or peripheral edema. 4 There are numerous responsive adaptations in the kidney, peripheral circulation, skeletal muscle, and other organs to maintain short-term circulatory function. Eventually, these responses may contribute to long-term disease progression and to acute exacerbations. As cardiac output drops from myocardial injury or stress, a neurohormonally mediated cascade including activation of the renin-angiotensinaldosterone and sympathetic nervous systems occurs. Responses include release of norepinephrine, vasopressin, endothelin (a potent vasocon strictor), and tumor necrosis factor-α. Although not measured in routine care, elevated levels of these hormones correlate with higher mortality. The clinical effects of neurohormonal activation are sodium and water retention coupled with increased systemic vascular resistance.

vasopressin, endothelin (a potent vasocon strictor), and tumor necrosis factor-α. Although not measured in routine care, elevated levels of these hormones correlate with higher mortality. The clinical effects of neurohormonal activation are sodium and water retention coupled with increased systemic vascular resistance. These maintain blood pressure and perfusion, but at the cost of increasing myocardial workload, wall tension, and myocardial oxygen demand. Although some patients are initially asymptomatic, a secondary patho logic process called cardiac remodeling begins to occur, eventually trig gering more dysfunction. Natriuretic peptides are the endogenous counterregulatory response to neurohormonal activation in heart failure. Three types exist: atrial natriuretic peptide, primarily secreted from the atria; B-type natri uretic peptide, secreted mainly from the cardiac ventricle; and C-type natriuretic peptide, localized in the endothelium. Natriuretic peptides produce vasodilation, natriuresis, decreased levels of endothelin, and inhibition of the renin-angiotensin-aldosterone system and the sym pathetic nervous systems. B-type natriuretic peptide is synthesized as CHAPTER Tintinalli_Sec07_p0329-0424.indd 367 8/2/19 6:42 PM

localized in the endothelium. Natriuretic peptides produce vasodilation, natriuresis, decreased levels of endothelin, and inhibition of the renin-angiotensin-aldosterone system and the sym pathetic nervous systems. B-type natriuretic peptide is synthesized as CHAPTER Tintinalli_Sec07_p0329-0424.indd 367 8/2/19 6:42 PM 368 SECTION 7: Cardiovascular Disease  SYSTOLIC AND DIASTOLIC HEART FAILURE Heart failure classifications also identify systolic or diastolic dysfunction based on ejection fraction, which is normally 60%. Systolic dysfunction, or heart failure with reduced ejection fraction, has an ejection fraction <50%. Mechanistically, the ventricle has difficulty ejecting blood, leading to increased intracardiac volume and afterload sensitivity. With circulatory stress (e.g., walking), failure to improve contractility despite increasing venous return results in increased cardiac pressures, pulmo nary congestion, and edema. Diastolic dysfunction, or heart failure with preserved ejection fraction, has impaired ventricular relaxation, causing an abnormal relation between diastolic pressure and volume. This results in a left ventricle that has difficulty receiving blood. Decreased left ventricular compliance necessitates higher atrial pressures to ensure adequate left ventricular diastolic fill ing, creating a preload sensitivity. The frequency of diastolic dysfunction increases with age and is more common in chronic hypertension, which leads to left ventricular hypertrophy. Coronary artery disease also con tributes, as diastolic dysfunction is an early event in the ischemic cascade. DIAGNOSIS Most hospitalized patients with heart failure receive initial care in the ED. 6 Commonly, patients present with dyspnea, which has a large differential diagnosis including acute heart failure, chronic obstructive pulmonary disease, asthma, pulmonary embolus, pneumonia, and acute coronary syndrome. Misdiagnosis increases mortality, prolongs hospital stay, and increases treatment costs. 16-20 The approach to those with dys pnea is covered in Chapter 62, “Respiratory Distress. ” There is no single diagnostic test for heart failure; it is a clinical diagnosis based on all clinical data, especially the history and physical examination.  HISTORY AND PHYSICAL EXAMINATION There is no singular historical or physical examination finding with excellent sensitivity and specificity for the diagnosis of acute heart failure.19 The initial global clinical judgment has a sensitivity of 61% and specificity of 86%. A history of heart failure is the most useful historical parameter, but has a sensitivity of only 56% and specificity of 80% (positive likeli hood ratio = 2.7; negative likelihood ratio = 0.58). 19 Risk factors for acute heart failure may be helpful, including hypertension, diabetes, valvular heart disease, old age, male sex, and obesity. The symptom with the highest sensitivity for diagnosis is dyspnea on exertion (84%). 19,20 The most specific symptoms are paroxysmal nocturnal dyspnea, orthopnea, and edema (76% to 84%). 19,20 Evaluation for precipitating factors (Table 53-2) may aid diagnosis. On exam, an S3 has the highest positive likelihood ratio for acute heart failure (4.0), but its absence is not useful (negative likelihood ratio = 0.91).19 Further, the interrater reliability of an S3 is not good,21-23 and the ambient noise in a busy ED may interfere with detection.

tors (Table 53-2) may aid diagnosis. On exam, an S3 has the highest positive likelihood ratio for acute heart failure (4.0), but its absence is not useful (negative likelihood ratio = 0.91).19 Further, the interrater reliability of an S3 is not good,21-23 and the ambient noise in a busy ED may interfere with detection. When clinicians are 80% confident of the diagnosis of acute heart failure, the “clinical gestalt” outperforms ED diagnostic tests19; however, TABLE 53-1 Classification of Acute Heart Failure Classification Characteristics Hypertensive AHF Signs and symptoms of AHF with relatively preserved left ventricular function, systolic blood pressure >140 mm Hg, typically with a chest radiograph compatible with pulmonary edema and symptom onset <48 h Pulmonary edema Respiratory distress, rales on chest auscultation, reduced oxygen saturation from baseline, verified by chest radiograph findings Cardiogenic shock (see Chapter 50) Evidence of tissue hypoperfusion (systolic blood pressure typically <90 mm Hg) Acute-on-chronic HF Signs and symptoms of AHF that are mild to moderate and do not meet criteria for hypertensive HF, pulmonary edema, or cardiogenic shock, systolic blood pressure <140 mm Hg and >90 mm Hg, typically associated with increased peripheral edema and symptom onset over several days High-output failure High cardiac output, typically with tachycardia, warm extremities, and pulmonary congestion Right heart failure Low-output syndrome with jugular venous distention, hepatomegaly, and may have hypotension Abbreviations: AHF = acute heart failure; HF = heart failure. TABLE 53-2 Common Precipitants of AHF •  Nonadherence •  Excess  salt or fluid intake •  Medication  nonadherence •  Renal  failure (especially missed dialysis) •  Substance  abuse—cocaine, methamphetamines, ethanol •  Poorly  controlled hypertension •  Iatrogenic •  Recent  addition of negative inotropic drugs (e.g., calcium channel blocker, β-blocker) •  Initiation  of salt-retaining drugs (e.g., NSAID, steroids, thiazolidinediones) •  Inappropriate  therapy reduction •  New  dysrhythmic agents Abbreviations: AHF = acute heart failure. N-terminal pre–pro-B-type natriuretic peptide, which is cleaved into two substances, inactive N-terminal pro-B-type natriuretic peptide, with a half-life of approximately 2 hours, and physiologically active B-type natriuretic peptide, with a half-life of about 20 minutes. Assays for both B-type natriuretic peptide and N-terminal pro-B-type natriuretic pep tide are available for ED use. Heart failure may also result from pump dysfunction from acute myocardial infarction. Mechanistically, loss of a critical mass of myocardium results in immediate symptoms. If there is symptomatic hypotension with inadequate perfusion, cardiogenic shock is present (see Chapter 50, “Cardiogenic Shock”). Acute pulmonary edema may be precipitous and is the clinical manifestation of a downward spiral of rapidly decreasing cardiac output and rising systemic vascular resistance on top of under lying cardiac dysfunction. Even small elevations of blood pressure can drop cardiac output, which triggers increasing systemic vascular resis tance and eventually further decreases cardiac output. Acute pulmonary edema can be abrupt, severely symptomatic, and rapidly fatal.  ACUTE HEART FAILURE CLASSIFICATION There are six phenotypes to assist with investigating the causes and precipitants for the acute presentation, as well as directing initial therapy (Table 53-1). 11 Those with acute heart failure and hyperten sion often have a precipitous presentation and may have pulmonary edema and hypoxemia. Symptoms may be due to fluid redistribution more than fluid overload, and treatment initially focuses on antihyper tensive therapy.

on, as well as directing initial therapy (Table 53-1). 11 Those with acute heart failure and hyperten sion often have a precipitous presentation and may have pulmonary edema and hypoxemia. Symptoms may be due to fluid redistribution more than fluid overload, and treatment initially focuses on antihyper tensive therapy. 12,13 Patients with pulmonary edema may benefit from noninvasive ventilation to decrease the work of breathing and avoid intubation. 14,15 Acute heart failure accompanied by hypotension or poor perfusion without another cause may be an ischemic or structural heart trigger creating cardiogenic shock. Such patients often benefit from inotropic agents and invasive hemodynamic monitoring to guide other therapies. Patients with acute decompensation of chronic heart failure tend to present with gradual symptoms (breathing changes or weakness com mon) and weight gain over days to weeks. High-output heart failure has a relatively normal ejection fraction and is often caused by anemia or thyrotoxicosis. Those with isolated right heart failure have lower extremity edema and jugular venous distension but little or no pulmo nary congestion; the cause is usually from pulmonary disease, valvular disease such as tricuspid regurgitation, or obstructive sleep apnea. Treatment approaches center on identifying and treating the underly ing cause, often without volume removal because low-output states and volume dependence may coexist. Tintinalli_Sec07_p0329-0424.indd 368 8/2/19 6:42 PM

om pulmonary disease, valvular disease such as tricuspid regurgitation, or obstructive sleep apnea. Treatment approaches center on identifying and treating the underly ing cause, often without volume removal because low-output states and volume dependence may coexist. Tintinalli_Sec07_p0329-0424.indd 368 8/2/19 6:42 PM CHAPTER 53: Acute Heart Failure 369 Yes Yes Yes ≥2 of the 8 thoracic zones with ≥3 B-lines B-line count in all 8 zones ≥10 IVC >2 cm with less than 50% collapse AHF likely LVEF >50% HFpEF likely LVEF <50% HFrEF likely Evidence of acute RV strain Obtain BNP FIGURE 53-1. Bedside US use to identify acute heart failure (AHF) in dyspneic ED patients using a curvilinear transducer or phased array probe to a depth of 15 cm. BNP = B-type natriuretic peptide; HFpEF = heart failure with preserved ejection fraction; HFrEF = heart failure with reduced ejection fraction; IVC = inferior vena cava; LVEF = left ventricular ejection fraction; RV = right ventricle. [Data adapted from Anderson KL, Jenq KY, Fields MF et al: Diagnosing heart failure among acutely dyspneic patients with cardiac, inferior vena cava, and lung ultrasonography. Am J Emerg Med 31: 1208-1214, 2013.] TABLE 53-3 Natriuretic Peptide Cut Points for Clinical Decision Making Low Cut Point (rule out HF) High Cut Point (HF likely) BNP 100 pg/mL 500 pg/mL Sensitivity 90% Sensitivity 75% Specificity 73% Specificity 90% N-terminal pro-BNP30 300 pg/mL 450 pg/mL if <50 years old 900 pg/mL if 50–75 years old 1800 pg/mL Sensitivity 93% Sensitivity 86% Sensitivity 79% Sensitivity 76% Specificity 71% Specificity 94% Specificity 84% Specificity 75% Abbreviations: BNP = B-type natriuretic peptide; HF = heart failure. clinical gestalt may be only 50% accurate in a primary care setting. 24 Data from the seminal study of B-type natriuretic peptide for the diagnosis of heart failure in the ED found that clinical judgment and a single B-type natriuretic peptide value had a similar accuracy performance.  CHEST RADIOGRAPHY Although chest radiographs showing pulmonary venous congestion, cardiomegaly, and interstitial edema are most specific for a final diag nosis of acute heart failure, 18,19 the absence of these does not exclude the diagnosis. Up to 20% of patients subsequently diagnosed with acute heart failure have chest radiographs without signs of congestion at the time of prior ED evaluation. 26 In late-stage heart failure, patients may have few radiographic signs, despite symptoms and elevated pulmonary capillary wedge pressure.  ECG AND BIOMARKERS The ECG is best used to find an underlying cause or precipitant. ECG signs of ischemia, acute myocardial infarction, or dysrhythmias (com monly atrial fibrillation) may point to the trigger. B-type natriuretic peptide and N-terminal pro-B-type natriuretic peptide may add value in the setting of undifferentiated dyspnea in the ED, improving diagnostic discrimination in a variety of settings 25,27 and correlating with cardiac filling pressures and ventricular stretch.28 As a result, B-type natriuretic peptide or N-terminal pro-B-type natriuretic peptide testing is recommended when the cause of dyspnea is unclear after standard evaluation; when the other bedside data make acute heart failure very likely, these assays add little actionable information (Table 53-3). Despite the established value of natriuretic peptide testing, there are many situations where interpretation of results is unclear. Levels can be affected by age, gender, and body mass, and may elevate later in patients who present with flash pulmonary edema. 29 Dyspnea and modest B-type natriuretic peptide elevation are evident in conditions such as pulmo nary hypertension, pulmonary embolism, pneumonia, sepsis, and renal failure.

ults is unclear. Levels can be affected by age, gender, and body mass, and may elevate later in patients who present with flash pulmonary edema. 29 Dyspnea and modest B-type natriuretic peptide elevation are evident in conditions such as pulmo nary hypertension, pulmonary embolism, pneumonia, sepsis, and renal failure. As many as 25% of patients will fall into the diagnostic “gray zone” (100 to 500 pg/mL for B-type natriuretic peptide), complicating test interpretation. Heart failure can largely be excluded in patients presenting with acute dyspnea and N-terminal pro-B-type natriuretic peptide <300 pg/mL or B-type natriuretic peptide <100 pg/mL. In addition, N-terminal pro-B-type natriuretic peptide has age-specific cutoffs to further increase accuracy, with cutoff levels of 450, 900, and 1800 pg/mL in patients <50, 50 to 75, and >75 years old, respectively. 30 B-type natriuretic peptide/N-terminal pro-b-type natriuretic peptide testing is best used when diagnostic uncertainty exists and as an addition to the physician assessment, rather than as a routine measurement. 27 Similarly, although marked natriuretic peptide elevations are associated with worse short-term outcomes, even low elevations have increased mortality risk, limiting usefulness in bedside prognostication in the ED. 31,32  POCUS Point-of-care cardiopulmonary US can help to determine the cause of dyspnea, including cardiac tamponade, and can determine left ven tricular function and volume status, but is not a substitute for compre hensive echocardiography. 31,32 Bedside cardiopulmonary US can also address three questions (Figure 53-1): (1) Are there signs of pulmonary Tintinalli_Sec07_p0329-0424.indd 369 8/2/19 6:42 PM

including cardiac tamponade, and can determine left ven tricular function and volume status, but is not a substitute for compre hensive echocardiography. 31,32 Bedside cardiopulmonary US can also address three questions (Figure 53-1): (1) Are there signs of pulmonary Tintinalli_Sec07_p0329-0424.indd 369 8/2/19 6:42 PM 370 SECTION 7: Cardiovascular Disease congestion? (2) Are there signs of volume overload by measuring the size of the inferior vena cava and its collapsibility? (3) Is the left ventricular ejection fraction low or normal? Pulmonary US is used first to determine if pulmonary congestion is present by looking for B-lines. Sonographic B-lines (Figure 53-2) are ring-down artifacts that arise from the interface of the visceral and parietal pleura when there is swelling of the lung’s interlobular septa due to lymphatic congestion, as is seen in pulmonary edema. 33 They are the sonographic equivalent of Kerley B-lines seen on chest radiography. 34 The presence of more than two B-lines in any one sonographic window along the anterior and anterolateral chest is pathologic and highly spe cific for alveolar and interstitial edema. Because bilateral B-lines can be present in other conditions not caused by pulmonary edema (e.g., pulmonary fibrosis, pulmonary contusion, bilateral pneumonia), rapid assessment for elevated central venous pressure follows. 36 An inferior vena cava size >2 cm or collaps ibility index of <50% is indicative of elevated central venous pressure. In the absence of significant pulmonary disease, these measures are highly correlated with pulmonary capillary wedge pressure and are specific for acute heart failure. Use US to look for other clinical conditions that cause an elevation in right heart pressure, including pulmonary embo lism or tricuspid regurgitation, both of which could cause inferior vena cava changes consistent with heart failure. Determining the crude left ventricular ejection fraction is the final piece of ED-based bedside US. With focused training, emergency physicians have reasonable agreement with expert cardiology interpretations by classifying a visual US estimation of left ventricular ejection fraction into broad categories of normal, moderately reduced, and severely reduced. 37,38 Other markers, such as E-point septal separation and fractional shortening, are less reliable markers and may be more time consuming in the ED setting. TREATMENT The initial approach is driven by the presentation acuity, hemodynamics, and volume status. In critically ill patients, airway management is the first priority to ensure adequate oxygenation and ventilation. In those who are less acutely ill, a focused evaluation ensues next, followed by treatment. Use pulse oximetry and supplemental oxygen to keep oxygen saturation at or above 95%. Because hypoxemia is a greater risk than hypercarbia, do not withhold oxygen if saturations are depressed or unknown, even when there is concern about carbon dioxide retention. FIGURE 53-2. B-lines representing thickened interalveolar/interlobular septa. R = rib; arrow = B-line. [Reproduced with permission from Ma OJ, Mateer JR, Reardon RF, Joing SA (eds): Emergency Ultrasound, 3rd ed. New York, NY: McGraw-Hill, Inc.; 2014. Fig. 7-5, Part C only.] Capnometry and blood gas measurements can later help titrate therapy in the critically ill. In those with extreme findings, use endotracheal intubation. Noninvasive positive-pressure ventilation often improves the symptoms in patients with heart failure or pulmonary edema. 14,40 Successful noninvasive ventilation requires close monitoring, hemodynamic stability, facial anatomy allowing an adequate facemask seal, and patient cooperation (see Chapter 28, “Noninvasive Airway Management and Supraglottic Airways”).

often improves the symptoms in patients with heart failure or pulmonary edema. 14,40 Successful noninvasive ventilation requires close monitoring, hemodynamic stability, facial anatomy allowing an adequate facemask seal, and patient cooperation (see Chapter 28, “Noninvasive Airway Management and Supraglottic Airways”). Noninvasive ventilation plus standard medical therapy reduces the need for intubation and improves respiratory dis tress and metabolic disturbance versus standard therapy alone. 14,15 The effect on hospital mortality remains unclear.14 Alternatively, high-velocity nasal insufflation of oxygen via nasal cannula (flow rates between 20 and 35 L/min) may be superior to stan dard oxygen delivered by nasal cannula and noninferior to noninvasive positive-pressure ventilation in treatment of undifferentiated respira tory failure in adult patients presenting to the ED. However, in the only randomized trial of high-velocity/flow oxygen, its benefit relative to noninvasive positive-pressure ventilation was unclear. High-velocity nasal insufflation provides high concentrations of oxygen and a mild distending pressure, and it may improve ventilatory efficiency by way of dead-space washout. High-velocity nasal insufflation is easier to use and better tolerated by many patients compared with noninvasive positivepressure ventilation. Acute heart failure with hypotension occurs in approximately 3% of patients, often in conjunction with acute coronary syndrome. Man agement may require reperfusion therapy or vasomotor support (see Chapter 49, “ Acute Coronary Syndromes, ” and Chapter 50, “Cardiogenic Shock”). Other standard initial care measures include cardiac monitoring, IV access, and frequent vital sign assessments. A urinary drainage catheter may aid in monitoring fluid status in the severely ill or incontinent, but this is best reserved for those with extreme illness or an inability to void (to avoid catheter-related complications later). HYPERTENSIVE ACUTE HEART FAILURE The failing heart is sensitive to increases in afterload, with some patients developing pulmonary edema with a systolic blood pressure as low as 150 mm Hg. Prompt recognition and afterload reduction with vasodilators can avoid the need for intubation. Nitroglycerin A short-acting, rapid-onset, systemic venous and arterial dilator, nitroglycerin decreases mean arterial pressure by reducing preload; at high doses initially, it reduces afterload. Nitro glycerin may have coronary vasodilatory effects, decreasing myocar dial ischemia and improving cardiac function. Choose the routes—IV , sublingual, or transdermal—based on symptom severity. Sublingual nitroglycerin spray is easily administered, rapidly bioavailable, and titratable to reach a desired clinical end point provided there is ade quate blood pressure. An initial approach is sublingual administration of nitroglycerin, 0.4 milligrams (400 micrograms), 1-2 sprays or tablets every 5 minutes until relief or replacement with IV nitroglycerin. A starting dose of 0.5 to 0.7 microgram/kg/min IV is common and titrated every few minutes up to 200 micrograms/min based on the blood pressure tolerance and symptoms ( Table 53-4). High doses aid in the acute setting, and adverse events are uncommon. 43 Apply transdermal nitroglycerin (0.5–2 inches to the chest wall based on blood pressure) only after initial therapy has improved conditions or if the symptoms are minor, because transdermal medication has a slow onset of action. The most important nitroglycerin complication is hypotension, often lasting only transiently and, at times, even seen with overall clinical improvement. Hypotension usually resolves after cessation of nitroglycerin (Table 53-5).

ns or if the symptoms are minor, because transdermal medication has a slow onset of action. The most important nitroglycerin complication is hypotension, often lasting only transiently and, at times, even seen with overall clinical improvement. Hypotension usually resolves after cessation of nitroglycerin (Table 53-5). If persistent, think of concomitant volume depletion or right ventricular infarct, and deliver a normal saline fluid bolus (250 to 1000 mL). Headache is frequent, but acetaminophen usually is adequate therapy. Methemoglobinemia is a theoretic possibility, but not a concern unless high doses are used for extended intervals. Despite Tintinalli_Sec07_p0329-0424.indd 370 8/2/19 6:42 PM CHAPTER 53: Acute Heart Failure 371 TABLE 53-4 Management of Hypertensive Acute Heart Failure* Stepwise Approach Comments Administer oxygen as needed for saturation ≥95%; give sublingual nitroglycerin. Sublingual nitroglycerin may be repeated 1-2 sprays or tablets every 5 minutes. If severe dyspnea, consider NIV or intubation. If BP >150/100 mm Hg, add IV nitroglyc erin or nitroprusside; if BP falls below 100 mm Hg, stop nitrates, and monitor for persistent hypotension or symptoms (see Chapter 50, “Cardiogenic Shock”). If BP <150/100 mm Hg after sublingual administration and if improved, consider transdermal nitroglycerin. See Chapter 58, “Pulmonary Hypertension”; see text for discussion of these agents. Start IV loop diuretic (furosemide or bumetanide) in the setting of volume overload. Initiate nitrates before diuretics. Assess for severity of illness/high risk: altered mental status persistent, hypoxia despite NIV, hypotension, troponin elevation, ischemic ECG changes, tachycardia, tachypnea, or inadequate urine output. See Chapter 49, “Acute Coronary Syndromes,” for ECG criteria. Admit to intensive care unit if high severity of illness or risk of decompensation.

s/high risk: altered mental status persistent, hypoxia despite NIV, hypotension, troponin elevation, ischemic ECG changes, tachycardia, tachypnea, or inadequate urine output. See Chapter 49, “Acute Coronary Syndromes,” for ECG criteria. Admit to intensive care unit if high severity of illness or risk of decompensation. Choose discharge or ED observation unit admission if good response to therapy, no high-risk features, and good social support. Admit the rest. Admit to intensive care unit if any ongoing cardiorespiratory compromise or acute ischemia. Scoring systems may not reliably identify all patients at risk. *Inclusion: SBP >140 mm Hg. Abbreviations: BP = blood pressure; NIV = noninvasive ventilation; SBP = systolic blood pressure. TABLE 53-5 Causes of Hypotension After Vasodilator Use •  Excessive  vasodilation •  Hypertrophic  obstructive cardiomyopathy •  Intravascular  volume depletion •  Right  ventricular infarction •  Cardiogenic  shock/myocardial infarction •  Aortic  stenosis •  Anaphylaxis •  Unsuspected  sepsis broad uptake into regular clinical practice, nitroglycerin use has little supporting prospective data. Nitroprusside If requiring further afterload reduction (i.e., contin ued high systemic vascular resistance usually manifested by persistent elevated blood pressure and continued symptoms despite nitroglycerin doses >200 micrograms/min), use IV nitroprusside. This is a potent arterial vasodilator; its hemodynamic effects include decreased blood pressure, left ventricular filling pressure reduction, and increased car diac output. The initial dose of nitroprusside is 0.3 microgram/kg/min, titrated upward every 5 to 10 minutes based on blood pressure and clinical response (maximum 10 micrograms/kg/min). The major complication is hypotension. It is also associated with thiocyanate toxicity, especially with high doses, prolonged (>3 days) use, and hepatic or renal impairment. The critical end point is rapidly lowering filling pressure to prevent the need for endotracheal intubation. Give or titrate up IV vasodilators as soon as possible when the blood pressure remains elevated. Loop Diuretics After vasodilator therapy (or with near-normal blood pressure and symptoms; see next section), patients may require diuresis (see Table 53-6 and next section) based on continued symptoms after blood pressure is controlled. Loop diuretics (furosemide is the most commonly used) administered alone without vasodilators for hypertensive heart failure may increase mortality 44 and worsen renal dysfunction. Ultimately, successful management of blood pressure and cardiac filling pressure creates marked improvement in respiratory status long before any diuresis. Contraindications and Alternatives to Vasodilation in Select Settings Because all vasodilators exert hypotensive effects, do not use if there are signs of hypoperfusion or existing hypotension. Flowlimiting, preload-dependent states such as right ventricular infarc tion, aortic stenosis, hypertrophic obstructive cardiomyopathy, or volume depletion increase the risk of vasodilator-associated hypotension (Table 53-5). Combined with acute pulmonary edema, the latter preload-dependent states are very difficult to manage. In these settings, aim therapy at decreasing the outflow gradient by slowing heart rate and cardiac contractility. Although this can be accomplished with IV β-blockers, it is best done with invasive hemodynamic guidance. If there is coexistent shock in the setting of hypertrophic obstructive cardiomy opathy, phenylephrine (40 to 100 micrograms/min IV) is a good choice because it creates peripheral vasoconstriction without increasing cardiac contractility.

omplished with IV β-blockers, it is best done with invasive hemodynamic guidance. If there is coexistent shock in the setting of hypertrophic obstructive cardiomy opathy, phenylephrine (40 to 100 micrograms/min IV) is a good choice because it creates peripheral vasoconstriction without increasing cardiac contractility. NORMOTENSIVE HEART FAILURE Shortness of breath, orthopnea, jugular venous distention, rales, and an S3 may exist in the presence of normal vital signs, oxygenation, and ventilation. In this situation, diuresis should occur first, with further treatment based on response to therapy (Table 53-6). Loop diuretics provide rapid symptomatic relief of congestive symptoms and improve the effects of angiotensin-converting enzyme inhibitors by decreasing intravascular volume. Most ED patients with anything but modest symptoms should receive IV dosing because bowel wall edema may prevent proper GI absorption. Choose the dose based on symptoms and prior usage (Table 53-6). In general, dose loop diuretics at the lowest possible dose that relieves congestion. After initial relief, a fixed maintenance dose helps prevent recurrence. Loop diuretics promote water and sodium excretion; they are effec tive except in severe renal dysfunction or diuretic resistance (failure to achieve the therapeutically desired reduction in congestion despite a full dose of diuretic). Furosemide is inexpensive and effective. Alternatives are bumetanide (1 milligram equivalent to 40 milligrams of furosemide) or torsemide (20 milligrams equivalent to 40 milligrams of furosemide). All usually trigger rapid diuresis after an IV dose, often within 10 to 15 minutes. The DOSE trial suggests that a reasonable starting point for IV diuretic dosing is 1 to 2.5 times the patient’s previous total daily oral dose, divided in half and administered by IV bolus every 12 hours. 45 For example, if the patient is on furosemide 80 milligrams PO twice a day, then an initial ED dose is 80 to 200 milligrams IV bolus. Higher doses create more rapid symptom improvement but also a slight decrease in renal function. For patients who are loop diuretic naive, a reasonable starting dose is furosemide 40 milligrams IV bolus. Ethacrynic acid (0.5 to 1 milligram/kg; maximum 100 milligrams) is another option. Sulfa allergy is generally not a concern with nonantibiotic drugs such as diuretics that contain a sulfa moiety. Diuretics may worsen renal function and create hypokalemia. If a prolonging QT interval exists, look for hypocalcemia, hypokalemia, or hypomagnesemia. Ototoxicity is rare but may occur if using diuretics with aminoglycoside antibiotics. Potassium-sparing diuretics, such as spironolactone (25 to 50 milligrams PO), are common in care of those with advanced chronic heart failure; these are used more for their mor tality benefit than diuretic effect. Urinary diuretic response requires monitoring. With greater symp toms or less response to initial IV diuretics, double the dose and repeat in 30 to 60 minutes or as needed based on urine output. Ongoing con gestion or dyspnea after a loop diuretic may signal the need for another therapy, such as a vasodilator. Several studies have evaluated the relationship of timing of diuretic therapy in relationship to patient outcomes in the setting of acute Tintinalli_Sec07_p0329-0424.indd 371 8/2/19 6:42 PM

urine output. Ongoing con gestion or dyspnea after a loop diuretic may signal the need for another therapy, such as a vasodilator. Several studies have evaluated the relationship of timing of diuretic therapy in relationship to patient outcomes in the setting of acute Tintinalli_Sec07_p0329-0424.indd 371 8/2/19 6:42 PM 372 SECTION 7: Cardiovascular Disease heart failure. One trial noted a hospital mortality benefit (2.3% vs. 6%) for patients receiving diuretics within 60 minutes of ED arrival. 46 Conversely, another trial found no significant difference in in-hospital mortality or mortality 1 month after hospital discharge between those who received IV diuretics early compared to those who received them later. 47 Such confounding results may be related to the heterogeneity of presentation of acute heart failure leading to variations in the timing of diagnosis (and thus associated therapy). Morphine is not a good choice for acute heart failure due to the potential for adverse events, including the need for mechanical ventilation, prolonged hospitalization, intensive care unit admission, and mortality. If desired for its venodilation properties or pain control, use morphine in small, titrated doses (2 to 4 milligrams IV) and with monitoring. Oral angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are given for hypertension and chronic heart fail ure, but there are no solid data to recommend use in the ED for acute heart failure. 49 Ongoing oral angiotensin-converting enzyme inhibitors decrease mortality and hospitalizations in patients with reduced ejection fraction. 4 Consider these after observation care if no contraindications exist and with coordination together with the follow-up physician. Oral angiotensin receptor blockers are alternatives or can be added to angiotensin-converting enzyme inhibitors in select heart failure patients with reduced ejection fraction. 4 IV enalaprilat appears safe and perhaps efficacious in patients with acute heart failure, but further data are required to define an ED role. β-Blockers are not usually initiated in the acute setting except to control rate-related heart failure. Norepinephrine levels are elevated in heart failure, contribute to myocardial hypertrophy, increase afterload and coronary vasoconstriction, and are associated with mortality. β-Blockers reduce sympathetic nervous system activity and are used for mortality reduction and symptom relief. Oral calcium channel blockers have myocardial depressant activity and are not routine treatment for acute heart failure; trials demonstrate either no benefit or worse outcomes. Avoid selective or nonselective NSAIDs in patients with acute heart failure. They can cause sodium and water retention and blunt the effects of diuretics 4 and may increase morbidity and mortality. DISPOSITION DECISIONS Emergency physicians serve as major decision makers for approximately one half of all inpatient admissions for acute heart failure in the United States. A lack of national guideline disposition recommendations, the absence of robustly validated decision tools, and the high rates of relapse and mortality after an ED discharge lead to ED admission for >80% of patients treated in the ED for acute heart failure. 6,12 Consensus guidelines have addressed acute heart failure risk stratification, but they provide little objective instruction for ED disposition decision making. Thus, disposition decisions are often based on physician judgment, a physiologic risk evaluation, and an assessment of barriers to success ful outpatient care such as caregiver support, medication access, and timely follow-up ( Figure 53-3).

they provide little objective instruction for ED disposition decision making. Thus, disposition decisions are often based on physician judgment, a physiologic risk evaluation, and an assessment of barriers to success ful outpatient care such as caregiver support, medication access, and timely follow-up ( Figure 53-3). 3 There have been many investigations of high-risk physiologic markers in ED patients with acute heart fail ure (Table 53-7), but most were retrospective, involved hospitalized patients, lacked a measurement of additive value to clinical assessment, and did not use a rigorous acute heart failure diagnostic standard. 12,50 These limitations notwithstanding, renal dysfunction, low blood pressure, low serum sodium, and elevated cardiac biomarkers (troponin or natriuretic peptides) are consistently associated with an increased risk of morbidity and mortality. Unfortunately, high-risk markers are not present in up to 50% of ED patients, limiting the impact in disposition decisions. Admit patients with high-risk features to the hospital ( Table 53-8).51 Those who require invasive monitoring or procedures require intensive care unit admission. Others may be appropriate for non–intensive care unit level care. Observation unit management is an option in those who lack higher-risk features. Many patients do not have high-risk features at initial evaluation and experience improvement in dyspnea during their ED stay after treatment with standard therapy. 52 Many have complete symptom resolution within 12 to 24 hours of initial therapy, a typical time period of observation. The monitoring of blood pressure, heart rate, urine output, and body weight is easily accomplished in the obser vation unit, and additional diagnostic testing (labs, echocardiography) needed can occur. Finally, an extended observation interval allows patients to receive heart failure education, confirm outpatient medica tions, assess self-care barriers, and arrange follow-up prior to discharge. If discharged directly or after an observation stay, outpatient follow-up within 5 days can decrease readmissions. Prior studies suggest 75% of patients will respond to therapy, will have no identifiable high-risk features, and will be discharged home. Their rates of readmission are similar to or better than those who are managed in an inpatient setting. 54,55 Patients with an inadequate response to initial therapy or with high-risk features identified during observation should be admitted to the hospital for further management. An observation unit strategy can help reduce costs while delivering quality care for select lower-risk ED patients with acute heart failure.

. 54,55 Patients with an inadequate response to initial therapy or with high-risk features identified during observation should be admitted to the hospital for further management. An observation unit strategy can help reduce costs while delivering quality care for select lower-risk ED patients with acute heart failure. TABLE 53-6 Medications for Acute Heart Failure Vasodilators for Acute Heart Failure Vasodilator Dose Titration End Point Complications Sublingual NTG 0.4 milligram every 1–5 min Blood pressure Hypotension IV NTG 0.5–0.7 microgram/kg/min (starting dose if blood pressure okay) Symptoms Headache, hypotension Nitroprusside 0.3 microgram/kg/min (starting dose), 10 micrograms/kg/min (maximum) Blood pressure Symptoms Hypotension, cyanide/thiocyanate toxicity, coronary steal Diuretics for Heart Failure Diuretic Dose (IV) Effect Complications Furosemide No prior use: 20–40 milligrams IVP Diuresis starts within 15–20 min ↓ K +, ↓ Mg2+, hyperuricemia, hypovolemia If prior use: total daily IV dose 1–2.5 times the patient’s previous total daily oral dose, divided in half and given IV bolus every 12 h If no effect by 20–30 min, increase subsequent dose Duration of action is 4–6 h Ototoxicity, prerenal azotemia Bumetanide 1–3 milligrams IV (40:1 furosemide) Diuresis starts within 10 min Peak action at 60 min Same as above Torsemide 10–20 milligrams IV (2:1 furosemide) Diuresis starts within 10 min Peak action in 1–2 h Same as above Abbreviations: IVP = IV push; NTG = nitroglycerin; ↓ = decreased. Tintinalli_Sec07_p0329-0424.indd 372 8/2/19 6:42 PM

ams IV (40:1 furosemide) Diuresis starts within 10 min Peak action at 60 min Same as above Torsemide 10–20 milligrams IV (2:1 furosemide) Diuresis starts within 10 min Peak action in 1–2 h Same as above Abbreviations: IVP = IV push; NTG = nitroglycerin; ↓ = decreased. Tintinalli_Sec07_p0329-0424.indd 372 8/2/19 6:42 PM CHAPTER 53: Acute Heart Failure 373 Comprehensive AHF Evaluation for Disposition ACUTE HEART FAILURE Provider Risk Determination Patient-Centric Self-Care Evaluation Clinical Gestalt Physiologic Risk Profile Facilitators or Barriers Ideal Self-Care May include consideration of some physiologic or selfcare measures Vital signs Examination Laboratory testing Radiography Past cardiac measures Caregiver support Hospitalization history Symptom monitoring Level education Medication/healthcare provider access Geospatial environment Disease knowledge Medication adherence Highly variable Risk models Severity scores Interviews Past medical history Established measures of activation, education, disease knowledge, literacy, numeracy & adherence GIS measures Level of care needs Morbidity Mortality Readmission risk Components Quantification Ideal Disposition Plan Shared Decision Making FIGURE 53-3. Factors impacting disposition decisions in ED patients with acute heart failure (AHF). [Reproduced with permission from Collins SP, Storrow AB: Moving toward comprehensive acute heart failure risk assessment in the emergency department: the importance of self-care and shared decision making, JACC Heart Fail. 2013 Aug;1(4):273-280.] TABLE 53-7 Selected ED-Based Risk-Stratification Studies That Examine Events Within 30 Days or Less of Index ED Presentation Author/Year No.

ard comprehensive acute heart failure risk assessment in the emergency department: the importance of self-care and shared decision making, JACC Heart Fail. 2013 Aug;1(4):273-280.] TABLE 53-7 Selected ED-Based Risk-Stratification Studies That Examine Events Within 30 Days or Less of Index ED Presentation Author/Year No. of Patients Predicted Outcome Variables in Final Model Low-Risk Markers Miro 2017 4867/3229 30-day mortality Barthel index of activities of daily living, SBP, age, NT-proBNP, potassium level, Tn, NYHA classification, RR, low-output symptoms, saO2, ACS, hypertrophy on ECG, creatinine level Collins 2015 1033 ACS, coronary revascularization, emergent dialysis, intubation, mechanical cardiac support, cardiopulmonary resuscitation, death Age, BMI, BNP, BUN, dialysis, DBP, sodium, supplemental oxygen, outpatient ACEI, QRS duration, RR, O 2 saturation, Tn Lassus 2013 441–4450 (pooled analysis, total number varied by biomarker evaluated) 30-d and 1-y mortality ST2, MR-proADM, CRP, NT-proBNP, BNP, and MR-proANP in addition to clinical model (age, gender, BP on admission, estimated glomerular filtration rate <60 mL/min/1.73 m 2, sodium and hemoglobin levels, and heart rate) Stiell 2013 559 30-d death and 14-d serious nonfatal events History of TIA/CVA, vital signs, ECG and lab findings No Lee 2012 15,164 7-d mortality Creatinine, BP, O2 saturation, Tn, history of cancer, home metolazone, EMS transport Yes Hsieh 2008 8384 Inpatient mortality or serious medical complications, 30-d mortality pH, pulse, renal function, WBC, glucose, sodium Yes Lee 2003 2624/1407 30-d mortality Age, RR, BP, BUN, sodium, cerebrovascular disease, dementia, COPD, cirrhosis, cancer, hemoglobin Yes Auble 2005 33,533 Inpatient mortality or serious medical complications, 30-d mortality, and AHF readmission pH, pulse, renal function, WBC, glucose, sodium Yes Fonarow 2005 65,275 In-hospital mortality BUN, systolic BP, creatinine No Abbreviations: ACEI = angiotensin-converting enzyme inhibitor; ACS = acute coronary syndrome; ADM = adrenomedullin; AHF = acute heart failure; ANP = atrial natriuretic peptide; BMI = body mass index; BNP = B-type natriuretic peptide; BP = blood pressure; COPD = chronic obstructive pulmonary disease; CRP = C-reactive protein; CVA = cerebrovascular accident; DBP = diastolic blood pressure; MR = midregional; NT = N-terminal; NYHA = New York Heart Association; RR = respiratory rate; saO 2 = arterial oxygen saturation; SBP = systolic blood pressure; TIA = transient ischemic attack; Tn = troponin. Tintinalli_Sec07_p0329-0424.indd 373 8/2/19 6:42 PM