Author: J. Michael Albrich, MD, FACEP, FACP, Assistant Clinical Professor of Medicine, Oregon Health Sciences University; Clinical Medical Director, Department of Emergency Medicine, Legacy Good Samaritan Hospital, Portland, OR.

Peer Reviewers: William J. Brady, MD, FACEP, Assistant Professor, Department of Emergency Medicine, University of Virginia; Clinical Director, Department of Emergency Medicine, University of Virginia Health Sciences Center, Charlottesville, VA.

Frank Ruiz, MD, Assistant Professor of Surgery, University of California-San Francisco; Department of Emergency Services, San Francisco General Hospital, San Francisco, CA.

Put simply, these patients are sick, unstable, and teetering on the cusp of clinical deterioration. They are anxious, dyspneic, diaphoretic, and in distress. Not surprisingly, there are no treatment shortcuts, and optimum outcomes require sequential administration of mortality-reducing and/or patient-stabilizing agents that range from nitrates and ACE inhibitors to morphine, diuretics, and oxygen. Other invasive procedures may also be pressed into service. In patients whose course is complicated by respiratory acidosis and persistent hypoxemia that is not rapidly reversed by venodilators or afterload reduction, endotracheal intubation can be life-saving. Finally, the differential diagnosis of congestive heart failure (CHF) includes a diverse range of precipitating factors (e.g., acute myocardial infarction, drug-induced suppression of myocardial pump function,valvular insufficiency, fluid overload, and inadequate medication therapy). Each of these requires a customized approach to patient stabilization.

In fact, short of full-blown cardiorespiratory arrest, few conditions present with a more unstable triad of hemodynamic, respiratory, and metabolic parameters, all of which require careful monitoring and normalization. In addition, appropriate choices on the clinical treatment algorithm for CHF must be made swiftly and usually under duress. Also challenging the emergency physician is the fact that patients with CHF present with many different faces. For example, the individual with CHF and pulmonary edema may have a pronounced elevation in blood pressure, whereas the patient with an acute myocardial infarction complicated by severe pump failure may present with cardiogenic shock. And, patients with CHF in the setting of renal hemodialysis require modifications in treatment protocols. Finally, to avoid iatrogenesis, the ED physician must be able to distinguish between fluid overload and volume depletion, between pulmonary and cardiac causes of dyspnea, and to gauge the risks and benefits of potent medications that can produce toxic effects.

With these issues in focus, the purpose of this two-part review is to present a systematic approach to evaluation, management, and triage of patients with mild and moderate CHF as well as patients with severe, life-threatening CHF and pulmonary edema. Part I will highlight initial evaluation, patient stabilization, and recent advances in acute drug therapy; Part II of this series will focus on special patient subgroups and ambulatory assessment of outpatient drug regimens used for CHF.

— The Editor

Introduction

Heart failure is a clinical syndrome that develops when cardiac output becomes insufficient to meet systemic metabolic demands. This syndrome can be asymptomatic or severe, as in the case of pulmonary edema and cardiogenic shock, but it most often presents as dyspnea. Characterized by impaired myocardial pump function, CHF refers to a volume overload state that develops when the left ventricle no longer empties properly. In CHF, symptoms of fatigue and dyspnea on exertion or at rest are often accompanied by signs of fluid retention.1 From a clinical perspective, pulmonary edema is a life-threatening form of CHF that produces increased pulmonary alveolar water, poor alveolar gas exchange, and hypoxia. Cardiogenic shock occurs when pulmonary edema is complicated by systemic hypotension and metabolic acidosis.

Epidemiology

Data from the Framingham Study and the National Heart, Blood, and Lung Institute indicate that CHF affects approximately 4.7 million people in the United States and results in 900,000 hospital admissions per year.2 An additional 400,000 new cases of heart failure are diagnosed annually. Once it becomes symptomatic, CHF is associated with considerable morbidity and mortality. The two-year mortality of CHF after the onset of symptoms is approximately 35%; by six years, 80% of men and 65% of women have died. Pulmonary edema has a one-year mortality rate of about 50% after the first episode.3 The mortality rate associated with cardiogenic shock is 50-85% during the week following the onset of systemic hypotension. Age is an important risk factor for CHF.4 Fewer than 1% of the population in their 50s has CHF, but almost 10% of those in their 80s are afflicted with this condition. This has profound implications for the emergency physician and for health care in general, especially in a growing nation. In fact, longitudinal studies from the 1950s to the present show no decline in the incidence of heart failure in the general population. Hypertension and coronary disease are the most common causes of heart failure, followed by cardiomyopathy and valvular disease. It should be stressed that other cardiovascular diseases as well as neurological disorders, are much more common in the presence of CHF. In this regard, stroke, sudden death, and acute myocardial infarction are 4-5 times more frequent among patients with heart failure than among the general population.5

Clinical Pathophysiology

The onset and progression of heart failure results from a complex constellation of myocardial and circulatory responses to myocardial injury and stress.6 Typically, signs and symptoms of heart failure are usually due to systolic left ventricular dysfunction, which is characterized by inadequate emptying of the left ventricle associated with reduced ejection fraction (EF). Much less frequently, pure diastolic left ventricular dysfunction, defined as elevated and end-diastolic pressure in a left ventricle of normal size, produces similar signs and symptoms.1 As a rule, both systolic and diastolic dysfunction co-exist to produce heart failure. The causes of myocardial injury or stress are presented in Table 1.

An injured left ventricle is usually remodeled to compensate for the reduction in pump efficiency associated with CHF. Functioning myocytes stretch in response to elevated filling pressure as the heart fails to adequately pump blood into the systemic circulation. This causes the ventricle to dilate. The elevated filling pressure (preload) causes the myocardium to contract more forcefully: 1) according to the Frank-Starling principle (increased filling pressure causes increased cardiac output); and, 2) under the influence of adrenergic stimulation via aortic baroreceptors responding to reduced cardiac output. Adrenergic stimulation (noradrenaline) increases the force of cardiac contraction directly and produces peripheral vasoconstriction that maintains central blood pressure at the expense of increasing cardiac work. The remaining viable myocytes expend energy at a much higher rate.

As these changes persist and become chronic, structural changes (remodeling) occur in the myocardium. Strained myocytes increase the number of their sarcomes and literally, "bulk up" the ventricular wall (hypertrophy), which reduces dilation and wall stress. The elevated filling pressure also stretches the atria. Stretch-stimulated atrial baroreceptors reduce the centrally mediated sympathetic influence on the ventricle and the atrial myocardium secretes atrial natriuretic peptide (ANP). ANP is a direct vasodilator and promotes sodium excretion in order to reduce the hemodynamic stress on the ventricle.

In spite of these compensatory mechanisms, cardiac output continues to decline. The atria are eventually depleted of ANP and sympathetic stimulation resumes. Resumption of adrenergic stimulation produces progressively less increase in cardiac output as myocardial norepinephrine is depleted.7 Signs of fluid retention develop, and treatment with diuretics stimulates activation of the renin-angiotensin system. Angiotensin II, the product of the renin-angiotensin system, acts systemically to directly stimulate the kidney to retain salt, increase salt retention by stimulating the production of aldosterone, and decrease water excretion in late heart failure by stimulating vasopressin release from the pituitary.

As ventricular wall stress persists and increases in the face of systemic vasoconstriction, myocytes become energy depleted and die. In the majority of CHF patients, the ventricle becomes thin, dilated, and fibrosed. The failing ventricle can no longer respond to elevated preload with significant increases in cardiac output (loss of Frank-Starling mechanism).

An intrinsic renal sympathetic system conserves salt and water early in heart failure, and reduced renal blood flow continues this conservation in the later stages of heart failure.8 Reduced renal blood flow stimulates secretion of intrarenal prostaglandins capable of vasodilation and diuresis, but this is overwhelmed late in heart failure by an array of vasoconstrictors that support blood pressure at the expense of the myocardium.

At this stage, the heart is unable to augment cardiac output, fluid retention and filling pressure increase, and vasoconstriction is unopposed. The vasomotor balance is shifted to the side of vasoconstriction as production of endogenous vasodilator diminishes. (See Table 2.)Ultimately, a spiral of progressive ventricular dilation and declining cardiac output ensues in the face of high systemic vascular resistance, and this produces the clinical hallmarks of terminal heart failure: marked fatigue, cachexia, dyspnea at rest, intractable fluid retention, and hypotension.

Clinical Signs and Symptoms

Initial Presentation. he clinical diagnosis of CHF in the ED can be difficult when dyspnea, the most common symptom, is the sole presenting complaint. One study found that the diagnosis was falsely positive in up to half of patients in the primary care setting.9 Obesity, unrecognized cardiac ischemia, and pulmonary disease (COPD, pulmonary hypertension) were the most common causes of misdiagnosis. Although the symptoms of progressive dyspnea on exertion, orthopnea, and paroxysmal nocturnal dyspnea are more specific for heart failure than edema, fatigue, and exercise intolerance, the latter are more sensitive.10 Other less-specific symptoms include: cough, sputum production, wheezing, palpitations, dizziness, lightheadedness, syncope, upper abdominal pain (liver capsular distention due to passive congestion), and abdominal distension (ascites).11 Unfortunately, symptoms of heart failure do not necessarily correlate with the severity of myocardial dysfunction.1 The symptoms of cardiogenic pulmonary edema are well-known to the emergency physician: anxiety, marked dyspnea, chest tightness, infrequent cough, and clear, or even pink, foamy sputum production.12

History. previous medical history of hypertension, cardiac disease (ischemic or valvular), malignancy, endocrinopathy, or recent viral illness should be elicited to aid in the differential diagnosis. In particular, a history of heart disease, diabetes, and alcoholism in immediate family members may suggest risk factors in asymptomatic patients.

Personal habits, including alcohol, tobacco, and IV drug use, particularly cocaine, may suggest risk factors for causes of heart failure (alcohol, cocaine, ischemic heart disease, valvular heart disease, and endocarditis.)

If time permits, reviewing the old chart for such pertinent information as a history of cardiac and pulmonary disease, or procedures such as echocardiogram or angiography, which may help define the current presentation.

Physical Examination. hysical findings are also non-specific for heart failure.10 Tachycardia and tachypnea may be present, particularly in the latter stages of heart failure. Hypertension is frequently present due to adrenergic stimulation. Hypotension is an ominous finding in heart failure. Cheynes-Stokes respiration (alternating hyperventilation and apnea) may be noted in late heart failure as is pulsus alternans, which is due to alternating strong and weak myocardial contractions.13 A third heart sound (S3) suggests left ventricular dysfunction. Unfortunately, intraobserver error in detection of an S3 approaches 50%.14

A systolic murmur may indicate aortic stenosis or mitral regurgitations, both of which can cause heart failure. A diastolic murmur may indicate aortic insufficiency or mitral stenosis, also causes of heart failure. A laterally displaced or broadened point of maximal impulse (PMI) suggests ventricular hypertrophy. Rales are often present in heart failure, but they may indicate other processes, such as pneumonia. Airway edema in heart failure may produce wheezing. Barrel chests, pulmonary hyperinflation, and obesity make auscultation difficult. Generally speaking, edema that develops with increasing symptoms of dyspnea and accompanying jugular venous distension is likely due to heart failure. Isolated peripheral edema is almost always unrelated to heart failure. In pulmonary edema, the patient appears more acutely ill; in addition to the auscultatory findings of rales and wheezes, the skin is diaphoretic, cyanotic, or mottled, indicating poor peripheral perfusion.

The New York Heart Association (NYHA) classification for heart failure is a useful clinical assessment tool for evaluation of severity of disease and, in the outpatient setting, helps predict response to treatment. (See Table 3.)

Diagnostic Studies in the ED

The diagnosis of cardiogenic pulmonary edema is usually straightforward and is less problematic than deciphering the multiple causes of dyspnea associated with chronic CHF.12Cardiogenic pulmonary edema is usually associated with a progressive history of CHF or ischemic chest pain. In contrast, non-cardiogenic pulmonary edema caused by adult respiratory distress syndrome (ARDS) or neurologic injury usually develops unheralded over 24-72 hours.

Hepatojugular Reflux and Valsalva Maneuver.Hepatojugular reflux and the Valsalva maneuver are useful ED tools for evaluating patients with heart failure.15 The hepatojugular reflux maneuver is performed with the patient recumbent at 45°. A partially inflated pressure cuff is placed on the upper abdomen and the physician presses the cuff against the abdomen to develop a pressure of 33 mmHg. Pressure is maintained for 10 seconds; a rise in jugular venous distension of 3 cm of H2O is called a positive test. The hepatojugular reflux test has a sensitivity of 0.24 and 0.96.16

The Valsalva maneuver can be obtained in about two-thirds of patients with CHF. A blood pressure cuff is inflated to 15 mmHg over the systolic pressure and auscultation is performed at the antecubital fossa. The patient then bears down for about 15 seconds to increase intraabdominal pressure. At least two beats are required for an interpretable test. In the normal response, several beats are heard at the beginning of the maneuver followed by disappearance of sounds during the sustained maneuver. When the maneuver is terminated, the sounds reappear briefly. In the abnormal response associated with CHF, the sounds persist through the duration of the maneuver and then disappear when the maneuver is terminated. In CHF, the left ventricular volume remains high and unchanged during the sustained maneuver unlike the normal heart. It is thought that this gives rise to the persistently elevated blood pressure during Valsalva in heart failure, whereas the normal heart demonstrates a rise then fall in blood pressure with Valsalva.17 The Valsalva maneuver has a sensitivity of 0.73 and a specificity of 0.65. 15

The Electrocardiogram.Twelve-lead electrocardiography is indicated in all patients suspected of having heart failure. The electrocardiogram (ECG) is almost always abnormal in heart failure; in fact, a normal ECG is strong evidence against left ventricular dysfunction.18 ECG abnormalities in heart failure include chamber enlargement (most often left atrial and left ventricular) and conduction abnormalities (interventricular conduction delays, left bundle branch block). These ECG changes portend the clinical manifestations of heart failure at 17 times the rate of the general population.5 Important information from the ECG includes the presence of myocardial ischemia or infarction and the detection of tachycardias, atrial fibrillation, and ventricular tachycardia that may precipitate heart failure. An extremely broad QRS complex, especially when it is associated with bradycardia and/or hypotension, suggests critical hyperkalemia. This is most often seen in dialysis patients, patients on angiotensin-converting enzyme inhibitors (ACEIs), and/or a combination of ACEIs and potassium-sparing diuretics.

Chest X-Ray.The abnormalities of the chest radiograph in heart failure are the manifestations of left ventricular dysfunction and cardiac enlargement. Cardiomegaly is defined as a cardiac shadow greater than 0.5 of the chest width as seen in the chest x-ray in the anterioposterior view. Lung parenchymal abnormalities are loosely related to pulmonary capillary wedge (POW) pressure.19 (See Table 4.)Pleural effusions, which are located at the lung bases, may be unilateral or bilateral and are preceded by evidence of increased pulmonary fluid retention. The development of radiographic changes of CHF may lag behind the clinical presentation.

Pulse Oximetry. ontinuous pulse oximetry is useful for monitoring therapy. Severe or persistent hypoxemia in a normally responsive patient is evaluated with arterial blood gas (ABG) analysis, which may detect early respiratory acidosis that requires acute respiratory intervention.

Echocardiography.Doppler echocardiography is essential for in-hospital evaluation of all non-emergent dyspneic patients thought to have heart failure,14 but it is rarely useful in the ED. Exceptions to this statement include emergent Doppler echocardiography in the evaluation of cardiogenic shock or intractable pulmonary edema—thought to be caused by pericardial effusion— acute mitral or aortic insufficiency, or ischemic ventriculoseptal defect.2

Initial Stabilization of Patients With Severe Pulmonary Edema/CHF

Treatment of pulmonary edema12 and CHF has been the focus of a number of recent reviews.1,10,11,20,21 Practice guidelines have been published by the American College of Cardiology/American Heart Association (ACC/AHA) Task Force on Practice Guidelines (Committee on Evaluation and Management of Heart Failure.)2 The following recommendations for the treatment of these entities and cardiogenic shock draw heavily on ACC/AHA task force guidelines that reflect the recent literature.

Pitfalls in the Management of Pulmonary Edema and CHF

• Jugular venous distention, hypotension, and absence of gross pulmonary and peripheral edema should suggest right ventricular infarction or pericardial tamponade. Fluid challenge may help.

• Failure to rapidly detect and treat acute respiratory acidosis in pulmonary edema with the appropriate ventilatory support.

• Failure to rapidly administer aspirin and a thrombolytic to acute myocardial infarction (AMI) patients with mild CHF, particularly the elderly who can least afford the injury.

• Failure to consider early PTCA (where available) for AMI patients in pulmonary edema or cardiogenic shock.

• Failure to consider the diagnosis of heart failure because radiographic heart size is normal.

• Aggressive diuresis of cor pulmonale, right ventricular infarction, and pericardial tamponade may produce hypotension.

• In chronic congestive heart failure, for patients not treated with ACEI or combination hydralazine and isosorbide dinitrate: 1) the ED physician should discuss the patient’s care with his or her private physician, if possible; or, 2) the patients should be encouraged to see their private physician so that life-extending therapy may be started.

• Subtherapeutic dose of vasodilator or diuretic may be responsible for symptom exacerbation and may not confer the survival benefits of the higher doses used in clinical trials to establish their efficacy.

• Failure to suspect and treat hyperkalemia in dialysis patients in CHF.

Airway and Breathing

Mild CHF may be evaluated non-emergently, but the patient who is severely dyspneic requires immediate evaluation and treatment. As with all potentially life-threatening disorders in emergency medicine, the ABCs are primary.

The dyspneic patient who does not need immediate airway management is placed in the upright position and given supplemental oxygen (4 L/min by nasal cannula). The patient is placed on an ECG monitor, should have IV access established, and their blood is sent to the laboratory for a complete blood count (CBC), electrolytes, blood urea nitrogen (BUN), creatinine, glucose, and cardiac enzyme levels. In dialysis patients with pulmonary edema, the potassium level is extremely important. In some institutions, the potassium levels may be available most rapidly from a blood gas analyzer.

Vital signs should be obtained concurrently. Continuous pulse oximetry establishes baseline oxygen saturation, which should be at least 94-95%. This parameter should be followed for patient response to therapy.

Intermittent automatic blood pressure monitoring is also useful. Once calibrated by mercury sphygmomanometer, it frees nursing staff to perform other tasks and maintain the critical care record.

If oxygen saturation cannot be maintained at 95% with nasal cannula, the patient should be placed on 100% oxygen by face mask. For persistent hypoxemia in spite of high F102 or progressive respiratory acidosis and fatigue, continuous positive airway pressure (CPAP) applied by face mask has been shown to reduce the need for endotracheal intubation (ETI) in patients who would otherwise have required it.22 CPAP rapidly improved oxygenation, reduced tachypnea, and corrected respiratory acidemia by reducing the work of breathing, increasing lung volume, and recruiting alveoli. CPAP redistributes fluid within the lung, reduces afterload, and increases cardiac output by increasing intrathoracic pressure by compressing the heart and increasing ejection fraction. CPAP also reduced the vasoconstrictor, endothelin-1 (elevated in pulmonary edema and CHF) more rapidly than face-mask oxygen.23

Unfortunately, current studies do not confirm a mortality benefit with the use of CPAP.24 More recently, a modification of positive airway pressure called bi-level PAP has been introduced to control both inspiratory (IPAP) and expiratory (EPAP) pressures. The reduced EPAP allows patients to adapt more readily to the PAP technique by reducing the pressure against which they have to exhale. One study reported the use of bi-level PAP in 22 patients suffering acute respiratory failure warranting ETI due to cardiogenic pulmonary edema. Only two patients (9%) required ETI due to failure of bi-level PAP.25 In a small study comparing BiPAP and CPAP, BiPAP appeared to improve ventilation and vital signs more rapidly than CPAP.26 ETI provides definitive management of the airway, and delivers the highest F1O2. It assumes the work of breathing in all patients who do not respond to less aggressive forms of assisted ventilation. Rapid sequence intubation provides the most successful and and least stressful approach to ETI for both patient and physician. It should be stressed that the patient should not be allowed to develop complete respiratory failure before initiating ETI. Finally, the patient’s subjective sense of improvement or worsening condition is a valuable monitoring parameter.

Severe, Life-Threatening CHFThe Pharmacotherapeutic Arsenal Circulatory support and symptomatic management of acute, life-threatening CHF are dedicated to correction of fundamental abnormalities in CHF, pump function, and pulmonary edema. These include increased afterload and hypertension associated with marked vasoconstriction mediated by norepinephrine and other vasoconstrictors, fluid retention in the lungs and peripheral tissues, and hypotension due to cardiogenic shock.

Nitrates

Nitroglycerin 0.4-0.6 mg sublingual or buccal spray every 5-10 minutes as needed.

IV Nitroglycerin 10 mcg/min initially, and then advance to 5-130 mcg/min in 5-10 mcg/min increments.

IV Nitroprusside 0.1-5 mcg/kg/min.

No other group of agents improves the symptoms of acute CHF as rapidly or as effectively as nitrates.27 Nitrates reduce systemic vasoconstriction, increase cardiac output, and lower left ventricular filling pressures.28 In patients with normal cardiac function, venodilation predominates. But, in left ventricular dysfunction, nitrates primarily induce afterload reduction.29 Sublingual and intravenous nitroglycerin are rapidly vasoactive. Topical nitrates (patches or paste) are typically discouraged in acute CHF because of their delayed onset of action.

Because of their short half lives, intravenous nitrates have the added benefit of rapid dose adjustment. Patients with a blood pressure as low as 95 mmHg benefit from intravenous nitroglycerin as long as there is close observation.

Adverse reactions include headache, vagal response, and hypotension. The vagal response is manifested by a slow pulse rate and transient hypotension lasting minutes. If hypotension develops and the pulse is rapid, consider a right ventricular myocardial infarction. Obtain right-sided ECG leads V3R, V4R and begin vigorous fluid challenge. Both nitrates and loop diuretics can produce marked hypotension in right ventricular infarction.

ACE Inhibitors

Captopril for BP greater than or equal to 110 mmHg: Two 12.5 mg capsules (25 mg) opened and powder placed sublingually.

Captopril for BP 90-110 mmHg: one 12.5 mg capsule as above.

aptopril plus nitroglycerin, alone or in combination, given in a well-tolerated sublingual regimen, and dosed as 25 mg and 0.8 mg respectively, has been shown to substantially improve cardiac index (40% vs. 25%, respectively, for captopril and nitroglycerin) when given for severe CHF (NYHA III and IV).30 In this study, the onset of action was earlier for nitroglycerin, but captopril had a more pronounced and prolonged beneficial effect. Another study found that patients in acute pulmonary edema (APE) who were given sublingual captopril in addition to the standard regiment of O2, nitrates, morphine, and furosemide, improve more rapidly than patients treated with just the standard regimen as measured by an APE distress score (APEX).31 There was a trend toward fewer patients requiring intubation in the captopril group. Administration of 25 mg of sublingual captopril is also effective in the management of APE in dialysis patients.32

Loop Diuretics

Furosemide (Lasix) 40-80 mg IV

Bumetinide (Bumex) 1-2 mg IV

Torsemide (Demedex) 10-20 mg IV

he potent loop diuretics such as furosemide, bumetanide, and torsemide reduce the volume overload that commonly accompanies pulmonary edema and CHF. Unlike the nitrates, the loop diuretics activate the neurohumoral axis, which results in peripheral vasoconstriction. In fact, 20 minutes after injection with a loop diuretic, heart rate, systemic vascular resistance, norepinephrine, renin, arginine vasopressin, and systemic vascular resistance increased and stroke-volume index is decreased.33 This significantly increases left ventricular dysfunction for about two hours. By four hours, intravascular volume, left ventricular filling pressure, and neurohumoral vasocontrictors return to control levels, which greatly improves symptoms, but left ventricular function has not fully returned to normal.

This emphasizes the central importance of nitrates and ACEIs early during the acute diuresis phase of pulmonary edema and decompensated CHF. Both agents support the failing ventricle during diuresis at a time when the diuretic alone would actually worsen ventricular dysfunction. Indeed, 12.5 mg of oral captopril has been shown to augment the diuretic effects of furosemide when given to patients in decompensated CHF who are already on an ACEI.34 Furosemide may have some direct effect on pulmonary shunting based on the observation that anuric or severely oliguric patients in CHF who were treated with IV furosemide improved oxygenation over controls in 0.5 through two hours without significant hemodynamic changes and no significant diuresis.35

Adverse reactions include hypotension, hypokalemia, and, rarely, allergy. Hypotension occurs especially in the presence of hypovolemia, tamponade, and right ventricular infarction.

Morphine.

Morphine 2-3 mg IV, q 3-5 min.

orphine has been used for decades to relieve the anxiety associated with the breathlessness of acute pulmonary edema. Whether morphine contributes a beneficial hemodynamic effect is controversial. One study found that at 45 minutes after injection, blood pressure and heart rate fell, but so did cardiac index.36 They conclude that the salutary effect of morphine must be its central action. More recently, another investigation, found that morphine injection in healthy volunteers doubled the blood level of the important endogenous vasodilator, atrial naturetic hormone (ANP) five minutes after injection.37 Currently, the ANP response to morphine in patients with pulmonary edema (where it is known to be depleted) is unknown.

Adverse reactions include nausea and vomiting, which can be controlled by a small dose of IV anti-emetic, hypotension; allergy; and hypoventilation.

Summary

The evolution of heart failure to advanced stages is a complex process that is incompletely understood. It is clear, however, that the process has both hemodynamic and neuroendocrine precipitants. A myocardial insult reduces the functioning myocardium below a "critical mass," and this becomes a long, slow myocardial decline. The emergency physician provides acute care to both life-threatening cases and to individuals with mild to moderate CHF.

References

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2. Guidelines for the evaluation and management of heart failure: Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee of Evaluation and Management of Heart Failure). Circulation 995;92:2764-2784.

3. Goldberger JJ, Peled HB, Stroh JA, et al. Prognostic factors in acute pulmonary edema. Arch Intern Med 986;146:489-493.

4. Kannel WB, Ho K, Thom T. Changing epidemiological features of cardiac failure. Br Heart J 994;72:S3-S9.

5. Kannel WB, Belanger AJ. Epidemiology of heart failure. Am Heart J 991;121:951-957.

6. Packer M. Pathophysiology of chronic heart failure. Lancet 992;340:88-92.

7. Sigurdsson A, Swedberg K. Neurohormonal activation and congestive heart failure: Today's experience with ACE inhibitors and rationale for their use. Eur Heart J1995;16 Suppl N:65-72.

8. Riley DJ, Weir M, Bakris GL. Renal adaptation to the failing heart. Understanding the cascade of responses. Postgrad Med 994;95:141-146, 149-150.

9. Remes J, Miettinen H, Reunanen A, et al. Validity of clinical diagnosis of heart failure in primary health care. Eur Heart J1991;12:315-321.

10. Karon BL. Diagnosis and outpatient management of congestive heart failure. Mayo Clin Proc 995;70:1080-1085.

11. Fromm RE, Jr., Varon J, Gibbs LR. Congestive heart failure and pulmonary edema for the emergency physician. J Emerg Med 995;13:71-87.

12. Colice GL. Detecting the presence and cause of pulmonary edema. Postgrad Med 993;93:161-6, 169-70.

13. Surawicz B, Fisch C. Cardiac alternans: Diverse mechanisms and clinical manifestations. J Am Coll Cardiol 992;20:483-499.

14. Anonymous. linical signs in heart failure. Lancet 989;2:309-.

15. Marantz PR, Kaplan MC, Alderman MH. Clinical diagnosis of congestive heart failure in patients with acute dyspnea [see comments]. Chest 990;97:776-781.

16. Zema MJ. Heart failure and the bedside Valsalva maneuver [editorial, comment]. Chest1990;97:772-773.

17. Little WC, Barr WK, Crawford MH. Altered effect of the Valsalva maneuver on left ventricular volume in patients with cardiomyopathy. Circulation 985;71:227-233.

18. Rihal CS, Davis KB, Kennedy JW, et al. The utility of clinical, electrocardiographic, and roentgenographic variables in the prediction of left ventricular function. Am J Cardiol1995;75:220-223.

19. Hodgkinson DW, O'Driscoll BR, Driscoll PA, et al. ABC of emergency radiology. Chest radiographs II [comments]. Br Med J1993;307:1273-1277.

20. Goldman L. Internal medicine update: Seven important advances in medical diagnosis and management for the general internist. J Gen Intern Med1995;10:331-341.

21. Packer M. Treatment of chronic heart failure. [see comments.] Lancet 992;340:92-95.

22. Bersten AD, Holt AW, Vedig AE, et al. Treatment of severe cardiogenic pulmonary edema with continuous positive airway pressure delivered by face mask. N Engl J Med1991;325:1825-1830.

23. Takeda S, Takano T, Ogawa R. The effect of nasal continuous positive airway pressure on plasma endothelin-1 concentrations in patients with severe cardiogenic pulmonary edema. Anesth Analg 997;84:1091-1096.

24. Lin M, Yang YF, Chiang HT, et al. Reappraisal of continuous positive airway pressure therapy in acute cardiogenic pulmonary edema. Short-term results and long-term follow-up. Chest1995;107:1379-1386.

25. Sacchetti AD, Harris RH, Paston C, et al. Bi-level positive airway pressure support system use in acute congestive heart failure: Preliminary case series. Acad Emerg Med1995;2:414-718.

26. Mehta S, Jay GD, Woolard RH, et al. Randomized, prospective trial of bi-level vs. continuous positive airway pressure in acute pulmonary edema. Crit Care Med 997;25:620-628.

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28. Leier CV, Bambach D, Thompson MJ, et al. Central and regional hemodynamic effects of intravenous isosorbide dinitrate, nitroglycerin, and nitroprusside in patients with congestive heart failure. Am J Cardiol 981;48:1115-1123.

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Physician CME Questions

The most common presenting complaint in CHF is:

A. cough.

B. dizziness.

C. dyspnea.

D. upper abdominal pain. 

18. A 12-lead ECG:

A. is almost always abnormal in heart failure.

B. can show abnormalities like chamber enlargement and conduction delays that are associated with heart failure.

C. is indicated in all patients suspected of having heart failure.

D. All of the above. 

19. Which of the following is true regarding use of continuous positive airway pressure (CPAP)?

A. A study comparing CPAP and a bi-level PAP found that CPAP improved ventilation faster.

B. CPAP has been shown to reduce the incidence of endotracheal intubation.

C. Current studies confirm a mortality benefit in using CPAP vs. ETI.

D. None of the above 

. A common adverse reaction to the use of nitrates in CHF patients is:

A. headache.

B. emesis.

C. hypertension.

D. All of the above 

21. Which of the following physical findings suggests ventricular hypertrophy?

A. systolic murmur

B. wheezing

C. laterally displaced or broadened point of maximal impulse

D. rales 

22. In CHF, pulse oximetry is useful for:

A. diagnosing problem areas of the heart.

B. monitoring therapy.

C. detecting respiratory acidosis.

D. None of the above

23. What is the mortality rate associated with cardiogenic shock during the week following onset of systemic hypotension?

A. 35%

B. 50-85%

C. 65%

D. 10% 

24. Which of the following is effective in the management of acute pulmonary edema in dialysis patients?

A. 0.4 mg sublingual nitroglycerin

B. 3 mg of morphine

C. 25 mg of sublingual captopril

D. All of the above