Congestive Heart Failure and Pulmonary Edema

Coauthored by David FM Brown, MD, Assistant Chief, Instructor, Department of Emergency Medicine, Harvard Medical School, Massachusetts General Hospital

Shamai Grossman, MD, MS, is a member of the following medical societies: Society for Academic Emergency Medicine

Edited by William Chiang, MD, Assistant Director, Assistant Professor, Department of Emergency Medicine, Bellevue Hospital Center; Francisco Talavera, PharmD, PhD, Department of Pharmacy, Creighton University; Gary Setnik, MD, Chair, Assistant Professor, Department of Emergency Medicine, Harvard Medical School; John Halamka, MD, chief Information Officer/CareGroup Healthcare System, Assistant Professor of Medicine, Department of Emergency Medicine, Beth Israel Deaconess Medical Center; and Barry Brenner, MD, PhD, Vice-Chair, Director, Associate Clinical Professor, Department of Emergency Medicine, Division of Research, Cornell University, The Brooklyn Hospital Center

Author's Email:	Shamai Grossman, MD, MS	Topic Last Updated:
Editor's Email:	William Chiang, MD	09/12/2000 16:45:27

INTRODUCTION

Background: Congestive heart failure (CHF) is an imbalance in pump function in which the heart fails to maintain the circulation of blood adequately. The most severe manifestation of CHF, pulmonary edema, develops when this imbalance causes an increase in lung fluid secondary to leakage from pulmonary capillaries into the interstitium and alveoli of the lung.

CHF can be categorized as forward or backward ventricular failure. Backward failure is secondary to elevated systemic venous pressure, while left ventricular failure is secondary to reduced forward flow into the aorta and systemic circulation. Furthermore, heart failure can be subdivided into systolic and diastolic dysfunction. Systolic dysfunction is characterized by a dilated left ventricle with impaired contractility, while diastolic dysfunction occurs in a normal or intact left ventricle with impaired ability to relax and receive as well as eject blood.

The New York Heart Association's functional classification of CHF is one of the most useful. Class I describes a patient who is not limited symptomatically by normal physical activity. Class II occurs when ordinary physical activity results in fatigue, dyspnea, or other symptoms. Class III is characterized by a marked limitation in normal physical activity. Class IV is defined by symptoms at rest or with any physical activity.

Pathophysiology: CHF is summarized best as an imbalance in Starling forces or an imbalance in the degree of end-diastolic fiber stretch proportional to the systolic mechanical work expended in an ensuing contraction. This imbalance may be characterized as a malfunction between the mechanisms that keep the interstitium and alveoli dry and the opposing forces that are responsible for fluid transfer to the interstitium.

Maintenance of plasma oncotic pressure (generally about 25 mm Hg) higher than pulmonary capillary pressure (about 7-12 mmHg), maintenance of connective tissue and cellular barriers relatively impermeable to plasma proteins, and maintenance of an extensive lymphatic system are the mechanisms that keep the interstitium and alveoli dry.

Opposing forces responsible for fluid transfer to the interstitium include pulmonary capillary pressure and plasma oncotic pressure. Under normal circumstances, when fluid is transferred into the lung interstitium with increased lymphatic flow, no increase in interstitial volume occurs. When the capacity of lymphatic drainage is exceeded, however, liquid accumulates in the interstitial spaces surrounding the bronchioles and lung vasculature, thus, creating CHF. When increased fluid and pressure cause tracking into the interstitial space around the alveoli and disruption of alveolar membrane junctions, fluid floods the alveoli and leads to pulmonary edema.

Etiologies of pulmonary edema may be placed in the following 6 categories:

1. Pulmonary edema secondary to altered capillary permeability - This category includes acute respiratory deficiency syndrome (ARDS), infectious causes, inhaled toxins, circulating exogenous toxins, vasoactive substances, disseminated intravascular coagulopathy (DIC), immunologic processes reactions, uremia, near drowning, and other aspirations.

2. Pulmonary edema secondary to increased pulmonary capillary pressure - This includes cardiac causes and noncardiac causes, including pulmonary venous thrombosis, stenosis or veno-occlusive disease, and volume overload.

3. Pulmonary edema secondary to decreased oncotic pressure found with hypoalbuminemia

4. Pulmonary edema secondary to lymphatic insufficiency

5. Pulmonary edema secondary to large negative pleural pressure with increased end expiratory volume

6. Pulmonary edema secondary to mixed or unknown mechanisms including high altitude pulmonary edema (HAPE), neurogenic pulmonary edema, heroin or other overdoses, pulmonary embolism, eclampsia, postcardioversion, postanesthetic, postextubation, and postcardiopulmonary bypass

This chapter will limit itself to cardiac causes of pulmonary edema and CHF and its relevant emergency care.

Frequency:

• In the US: More than 3 million people have CHF, and over 400,000 new cases present yearly. Prevalence of CHF is 1-2% of the general population.

Mortality/Morbidity:

• Approximately 30-40% of patients with CHF are hospitalized every year. CHF is the leading diagnosis-related group (DRG) among hospitalized patients older than 65 years. The 5-year mortality after diagnosis was reported as 60% in men and 45% in women in 1971. In 1991, data from the Framingham heart study showed the 5-year mortality for CHF essentially remaining unchanged, with a median survival of 3.2 years for males and 5.4 years for females. This may be secondary to an aging US population with declining mortality due to other diseases.

• The most common cause of death is progressive heart failure, but sudden death may account for up to 45% of all deaths. After auditing data on 4606 patients hospitalized with CHF between 1992-1993, total in-hospital mortality was 19%, with 30% of deaths occurring from noncardiac causes.

• Patients with coexisting insulin-dependent diabetes mellitus have a significantly increased mortality.

Race:

• African Americans are 1.5 times more likely to die of CHF than whites. Nevertheless, African American patients appear to have similar or lower in-hospital mortality rates than white patients.

Sex:

• Male > Female for patients aged 40-75 years

• Male = Female for patients older than 75 years

Age:

• Incidence of CHF increases with increasing age and affects about 10% of the population older than 75 years.

CLINICAL

History:

• Anxiety

• Dyspnea at rest

• Dyspnea on exertion has been found to be the most sensitive complaint, yet the specificity for dyspnea is less than 60%.

• Orthopnea and paroxysmal nocturnal dyspnea (PND) are symptoms; however, sensitivity for orthopnea and PND is only 20-30%.

• Cough productive of pink, frothy sputum is highly suggestive of CHF.

• Edema

• Nonspecific complaints include the following:

• Weakness

• Lightheadedness

• Abdominal pain

• Malaise

• Wheezing

• Nausea

• Past medical history may include the following:

• Cardiomyopathy

• Valvular heart disease

• Alcohol use

• Hypertension

• Angina

• Prior myocardial infarction

• Familial heart disease

Physical:

• Findings such as peripheral edema, jugular venous distention, and tachycardia are highly predictive of CHF. Overall specificity of physical examination has been reported at 90%; however, this same study reported a sensitivity of only 10-30%.

• Tachypnea, using accessory muscles of respiration

• Hypertension

• Pulsus alternans (alternating weak and strong pulse indicative of depressed left ventricle [LV] function)

• Skin may be diaphoretic or cold, gray, and cyanotic.

• Jugular venous distention (JVD) frequently is present.

• Wheezing or rales may be heard on lung auscultation.

• Apical impulse frequently is displaced laterally.

• Cardiac auscultation may reveal aortic or mitral valvular abnormalities, S3 or S4.

• Lower extremity edema also may be noted, especially in the subacute process.

Causes:

• A variety of cardiac diseases cause CHF and pulmonary edema.

• The most common cause of heart failure is coronary artery disease, which is secondary to loss of left ventricular muscle, ongoing ischemia, or decreased diastolic ventricular compliance.

• Other disease processes include hypertension, valvular heart disease, congenital heart disease, other cardiomyopathies, myocarditis, and infectious endocarditis.

• CHF often is precipitated by cardiac ischemia or dysrhythmias, cardiac or extracardiac infection, pulmonary embolus, physical or environmental stresses, changes or noncompliance with medical therapy, dietary indiscretion, or iatrogenic volume overload.

• One also must consider systemic processes, such as pregnancy and hyperthyroidism, as precipitants of CHF.

DIFFERENTIALS

Acute Respiratory Distress Syndrome
Altitude Illness - Pulmonary Syndromes
Anaphylaxis
Anemia, Acute
Bronchitis
Chronic Obstructive Pulmonary Disease and Emphysema
Dysbarism
Hyperventilation Syndrome
Myopathies
Pericarditis and Cardiac Tamponade
Pneumonia, Aspiration
Pneumonia, Bacterial
Pneumonia, Immunocompromised
Pneumonia, Mycoplasma
Pneumonia, Viral
Pneumothorax, Iatrogenic, Spontaneous and Pneumomediastinum
Pulmonary Embolism
Shock, Septic
Venous Air Embolism

Other Problems to be Considered:

The cardiac patient with asthma or symptoms of chronic obstructive pulmonary disease (COPD) is a difficult clinical challenge.

WORKUP

Lab Studies:

• Serum lab values may identify prerenal azotemia or elevated alanine aminotransferase (ALT), aspartate aminotransferase (AST), or bilirubin, suggestive of a congestive hepatopathy. Cardiac enzymes and other serum markers for ischemia or infarction may be useful as well.

• Arterial blood gas (ABG) may be of benefit in evaluation of hypoxemia, ventilation/perfusion (V/Q) mismatch, hypercapnia, and acidosis.

• Mild azotemia, decreased erythrocyte sedimentation rate (ESR), and proteinuria are observed in early and mild-to-moderate disease.

• Increased creatinine, hyperbilirubinemia, and dilutional hyponatremia are observed in severe cases.

Imaging Studies:

• Chest x-ray (CXR)

• Although diagnostic tests are of limited benefit in acute CHF, CXR is the most useful tool.

• Cardiomegaly may be observed with a cardiothoracic ratio > 50%. Pleural effusions may be present bilaterally, or if they are unilateral, are more commonly observed on the right.

• Early CHF may manifest as cephalization of pulmonary vessels, generally reflecting a pulmonary capillary wedge pressure (PCWP) of 12-18 mm Hg. As the interstitial fluid accumulates, more advanced CHF may be demonstrated by Kerley B lines (PCWP: 18-25 mm Hg).

• Pulmonary edema is observed as perihilar infiltrates often in the classic butterfly pattern reflecting a PCWP > than 25 mm Hg.

• Several limitations to the use of chest x-rays when attempting to diagnose CHF exist. Classic radiographic progression often is not found, and as much as a 12-hour radiographic lag from onset of symptoms may occur. In addition, radiographic findings frequently persist for several days despite clinical recovery.

• Emergency transthoracic echocardiography (ECHO)

• ECHO may help identify regional wall motion abnormalities as well as globally depressed or myopathic left ventricular function.

• ECHO may help identify cardiac tamponade, pericardial constriction, and pulmonary embolus.

• ECHO also is useful in identifying valvular heart disease, such as mitral or aortic stenosis, or regurgitation.

Other Tests:

• Electrocardiogram (ECG) is a nonspecific tool but may be useful in diagnosing concomitant cardiac ischemia, prior myocardial infarction (MI), cardiac dysrhythmias, chronic hypertension, and other causes of left ventricular hypertrophy.

Procedures:

• No defined role exists for invasive monitoring devices such as central venous placement (CVP) lines. Time-consuming placement of pulmonary artery catheters has not been shown to prolong survival, even in the coronary care unit and, thus far, has not been well studied in the ED setting.

• Cardiac catheterization may be necessary for a complete evaluation and assessment of prognosis.

TREATMENT

Prehospital Care:

• Prehospital notification by EMS personnel should alert ED staff of a patient presenting with signs and symptoms of CHF and pulmonary edema. They should receive on-line medical advice for patients with high-risk presentations.

• Treatment should begin with the ABCs. Supplemental oxygen, initially 100% nonrebreather facemask should be administered.

• Cardiac monitoring and continuous pulse oximetry should be utilized.

• IV access should be obtained, as well as a prehospital ECG, if available.

• Nitroglycerin sublingual (SL) or spray for active chest pain in the patient without severe hypotension and IV furosemide should be given.

Emergency Department Care:

• ED management of a patient presenting with signs and symptoms of CHF and pulmonary edema should begin with the ABCs. Administer supplemental oxygen, initially 100% nonrebreather facemask. Utilize cardiac monitoring and continuous pulse oximetry. Obtain IV access.

• To reduce venous return, elevate the head of the bed. Patients may be most comfortable in a sitting position with their legs dangling over the side of the bed, which allows for reduced venous return and decreased preload.

• Therapy generally starts with nitrates and diuretics, if patients are hemodynamically stable. Many other treatment modalities may play some role in acute management.

• If possible, treat the underlying cause as well, if identified. This is particularly true for patients with known diastolic dysfunction who respond best to reductions in blood pressure, rather than to diuretics, nitrates, and inotropic agents.

• Eliminate contributing factors when possible.

• Restrict fluid and sodium.

• Consider other treatment modalities.

• Continuous positive airway pressure (CPAP) and bilevel positive airway pressure (BiPAP) - Recent data comparing nasal CPAP therapy and facemask ventilation therapy has demonstrated decreased need for intubation rates when these modalities are used. In patients with severe CHF treated with CPAP, however, no significant difference was found in short-term mortality and hospital stay. Although BiPAP therapy may improve ventilation and vital signs more rapidly then CPAP, a higher incidence of MI associated with BiPAP has been reported. BiPAP and CPAP are contraindicated in the presence of acute facial trauma, the absence of an intact airway, and in patients with an altered mental status or who are uncooperative.

• Alternating tourniquets, formerly a mainstay of therapy, have been used to decrease preload. Their use has been supplanted by newer therapies such as IV nitroglycerin and nitroprusside.

• Phlebotomy with removal of 500 cc of blood or via plasmapheresis is another former mainstay of therapy used to decrease preload. Its use has been supplanted by newer therapies such as IV nitroglycerin and nitroprusside.

Consultations:

• Cardiology

• Critical care services

• Cardiothoracic surgery for possible heart valve surgery or transplantation

MEDICATION

The goal of pharmacotherapy is to achieve a PCWP of 15-18 mm Hg and a cardiac index > 2.2 L/min/m², while maintaining adequate blood pressure and perfusion to essential organs. These goals may need to be modified for some patients.

Use of diuretics, nitrates, analgesics, and inotropic agents are indicated for the treatment of CHF and pulmonary edema. Calcium channel blockers, such as nifedipine and nondihydropyridines, increase mortality and increase incidence of recurrent CHF with chronic use. Conflicting evidence currently exists in favor, as well as against, the use of calcium channel blockers in the acute setting; at this time limit their acute use to patients with diastolic dysfunction and heart failure, a condition not easily determined in the ED.

Angiotensin converting enzyme (ACE) inhibitors, such as SL captopril or IV enalapril, may rapidly reverse hemodynamic instability and symptoms, possibly avoiding an otherwise imminent intubation. Haude compared 25 mg of SL captopril with 0.8 mg of sublingual nitroglycerin in 24 patients with class III and class IV CHF and found that captopril induces a more sustained and more pronounced improvement in hemodynamics. Annane gave 1 mg of IV enalapril to 20 patients presenting with acute class III and class IV CHF over 2 hours and demonstrated rapid hemodynamic improvement with no significant adverse affects on cardiac output or hepatosplanchnic measurements. Captopril may play a unique role in sustaining patients with renal failure and concomitant acute CHF while awaiting definitive therapy with dialysis. Since the information on this subject is still controversial and limited to small studies, their routine use cannot be recommended at this time. ACE inhibitors remain a promising area in need of further study.

Beta-blockers, possibly by restoring beta-1 receptor activity or via prevention of catecholamine activity, appear to be cardioprotective in patients with depressed left ventricular function. The US Carvedilol Heart Failure study group demonstrated a two-thirds decrease in mortality in patients taking carvedilol with left ventricular ejection fractions of 35% or less. Beta-blockers, particularly carvedilol, have been shown to improve symptoms in patients with moderate-to-severe heart failure. The role of beta-blockers in the acute setting, however, currently is unclear; limit use until hemodynamic studies indicate that further deterioration will not occur.

Because differentiating CHF and asthma exacerbations is often difficult, treating both with the shotgun approach often is employed, particularly as both may cause bronchospasm. Aerosolized beta-2 agonists, which are the more selective of beta agonists, decrease tachycardia, dysrhythmias, and cardiac work while transiently enhancing cardiac function. Terbutaline has been shown to be successful in this setting, as well as albuterol, isoetharine, and bitolterol.

Limit roles of theophyline and aminophylline in the acute setting. They are positive inotropic agents mediated by an increase in catecholamines, and they dilate coronaries and exert mild diuretic effects. Nevertheless, they can exacerbate dysrhythmias (eg, multifocal atrial tachycardia [MAT], ischemia) by increasing cardiac work.

Steroids, IV or PO, have been shown to worsen preexisting heart failure due to systemic sodium retention and volume expansion, hypokalemia, and occasional hypertension. Inhaled steroids, due to their lack of systemic side effects, may be a reasonable option in this confusing patient presentation; however, given their delayed onset of action, they remain an area in need of further study.

Please see the chapter on Asthma for dosing schedules.

Drug Category: Diuretics - First-line therapy generally includes a loop diuretic such as furosemide, which will inhibit sodium chloride reabsorption in the ascending loop of Henle.

Drug Name	Furosemide (Lasix)- Administer loop diuretics IV, since this allows for both superior potency and a higher peak concentration despite increased incidence of side effects, particularly ototoxicity.
Adult Dose	A reasonable approach for furosemide might be as follows: 10-20 mg IV for patients symptomatic with CHF not already using diuretics 40-80 mg IV for patients already using diuretics 80-120 mg IV for patients whose symptoms are refractory to the initial dose after 1 h of its administration Higher doses and more rapid redosing may be appropriate for the patient in severe distress.
Contraindications	Documented hypersensitivity; hepatic coma; anuria; state of severe electrolyte depletion
Interactions	Metformin decreases furosemide concentrations. Conversely, furosemide interferes with the hypoglycemic effect of antidiabetic agents. It also antagonizes the muscle relaxing effect of tubocurarine. Auditory toxicity appears to be increased with concurrent use of aminoglycoside and furosemide. Hearing loss of varying degrees may occur. Anticoagulant activity of warfarin may be enhanced when taken concurrently with this medication. Increased plasma lithium levels and toxicity are possible when taken concurrently with this medication.
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Monitor for electrolyte imbalance. Exercise caution with coadministration of nephrotoxic drugs.

Drug Name	Metolazone (Mykrox, Zaroxolyn)- Both chlorothiazide and metolazone have been used as adjunctive therapy in patients initially refractory to furosemide. Chlorothiazide, however, at doses of 250-500 mg IV, has been shown to decrease GFR with CHF and, thus, is less potent and causes a greater loss of potassium. Metolazone, on the other hand, repeatedly has been demonstrated to be synergistic with loop diuretics in treating refractory patients.
Adult Dose	5-10 mg PO before redosing with furosemide
Contraindications	Documented hypersensitivity; hepatic coma; encephalopathy; anuria
Interactions	Thiazides may decrease effect of anticoagulants, sulfonylureas, and gout medications. Anticholinergics and amphotericin B may increase toxicity of thiazides. Effects of thiazides may decrease when used concurrently with bile acid sequestrants, NSAIDs, and methenamine. When coadministered, thiazides increase toxicity of anesthetics, diazoxide, digitoxin, lithium, loop diuretics, antineoplastics, allopurinol, calcium salts, vitamin D, and nondepolarizing muscle relaxants.
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Exercise caution with hepatic and renal disease, diabetes mellitus, gout, and lupus erythematosus.

Drug Name	Nitroglycerin (Nitro-Bid, Nitrol)- SL nitroglycerin and Nitrospray are particularly useful in the patient who presents with acute pulmonary edema with a systolic blood pressure of at least 100 mmHg. Similar to SL, Nitrospray’s onset is 1-3 min with a half-life of 5 min. The applicability of Nitrospray may be easier, and storage is up to 4 y. One study demonstrated significant and rapid hemodynamic improvement in 20 patients given Nitrospray with pulmonary edema in an ICU setting. Topical nitrate therapy is reasonable in a patient presenting with class I to II CHF. However, in patients with more severe signs of heart failure or pulmonary edema, IV nitroglycerin is preferred since it is easier to monitor hemodynamics and absorption, particularly in the diaphoretic patient. Oral nitrates, due to delayed absorption, have little role in the acute presentations of CHF.
Adult Dose	Nitrospray: single spray (0.4 mg) equivalent to a single 1/150 SL; may repeat q3-5min as hemodynamics permit, up to a maximum of 1.2 mg Ointment: Apply 1-2 inches of nitropaste to the chest wall Injection: start at 20 mcg/min IV and titrate to effect in 5-10 mcg increments q3-5min
Contraindications	Documented hypersensitivity; severe anemia; shock; postural hypotension; head trauma; closed-angle glaucoma; cerebral hemorrhage
Interactions	Aspirin may increase nitrate serum concentrations. Marked symptomatic orthostatic hypotension may occur when coadministered with calcium channel blockers, and an adjustment in the dose of either agent may be necessary.
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Exercise caution with coronary artery disease and low systolic blood pressure.

Drug Name	Nitroprusside sodium (Nitropress)- Produces vasodilation and increases inotropic activity of the heart. At higher dosages it may exacerbate myocardial ischemia by increasing heart rate. It is easily titratable.
Adult Dose	10-15 mcg/min and titrate to effective dose range of 30-50 mcg/min and a systolic blood pressure of at least 90 mmHg
Contraindications	Documented hypersensitivity; subaortic stenosis; optic atrophy; tobacco amblyopia; idiopathic hypertrophic; atrial fibrillation or flutter
Interactions	Patients receiving other hypertensive therapy may be more sensitive to sodium nitroprusside.
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Exercise caution with increased intracranial pressure, hepatic failure, severe renal impairment, and hypothyroidism. In renal or hepatic insufficiency, nitroprusside levels may increase and can cause cyanide toxicity. Sodium nitroprusside has the ability to lower blood pressure; thus, use only in those patients with mean arterial pressures > 70 mm Hg.

Drug Name	Morphine sulfate (Duramorph, Astramorph, MS Contin)- DOC for narcotic analgesia due to reliable and predictable effects, safety profile, and ease of reversibility with naloxone. Morphine sulfate administered IV may be dosed in a number of ways and commonly is titrated until desired effect is obtained.
Adult Dose	2-5 mg and repeated q10-15min unless respiratory rate is < 20 breaths/min or systolic blood pressure is < 100 mmHg
Contraindications	Documented hypersensitivity; hypotension; potentially compromised airway with uncertain rapid airway control; respiratory depression; nausea; emesis; constipation; urinary retention
Interactions	Phenothiazine may antagonize analgesic effects of opiate agonists. Tricyclic antidepressants, MAO inhibitors, altered mental status, and other CNS depressants may potentiate adverse effects of morphine when used concurrently.
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Exercise caution with atrial flutter and other supraventricular tachycardias. Morphine has vagolytic action and may increase the ventricular response rate. Due to the addictive nature of this drug, abuse is also a concern.

Drug Name	Dopamine (Intropin)- Stimulates both adrenergic and dopaminergic receptors. Its hemodynamic effects depend on the dose. Lower doses stimulate mainly dopaminergic receptors that produce renal and mesenteric vasodilation. Cardiac stimulation and renal vasodilation is produced by higher doses. It is a positive inotropic agent at 2-10 mcg that can lead to tachycardia, ischemia, and dysrhythmias. Doses > 10 mcg cause vasoconstriction, which increases afterload.
Adult Dose	5 mcg/kg/min and increase at 5 mcg/kg/min increments to a 20 mcg/kg/min dose
Contraindications	Documented hypersensitivity; pheochromocytoma; ventricular fibrillation
Interactions	Phenytoin, alpha- and beta-adrenergic blockers, general anesthesia, and MAO inhibitors increase and prolong effects of this medication; thus, lower the dosage.
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Monitor closely urine flow, cardiac output, pulmonary wedge pressure, and blood pressure during infusion. Prior to infusion, correct hypovolemia with either whole blood or plasma, as indicated. Monitoring of central venous pressure or left ventricular filling pressure may be helpful in detecting and treating hypovolemia.

Drug Name	Dobutamine (Dobutrex)- Produces vasodilation and increases inotropic state. At higher dosages it may cause increased heart rate, thus exacerbating myocardial ischemia. Strong inotropic agent with minimal chronotropic effect and no vasoconstriction.
Adult Dose	Starting dose: 2.5 mcg/kg/min; generally therapeutic in the range of 10-40 mcg/kg/min
Contraindications	Documented hypersensitivity; idiopathic hypertrophic subaortic stenosis; atrial fibrillation or flutter
Interactions	Beta-adrenergic blockers antagonize effects of nitroprusside. Conversely, general anesthetics may increase its toxicity.
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Following an MI use dobutamine with extreme caution. Correct a hypovolemic state before using this drug.

FOLLOW-UP

Further Inpatient Care:

• Depending on the response to initial ED therapy, disposition decisions will vary.

• With few exceptions, patients presenting with acute symptoms of CHF or pulmonary edema will require hospital admission. Many patients, however, who respond rapidly to early therapy may require only standard hospital ward admission with telemetry monitoring if ischemic etiologies are being considered.

• Some criteria for discharge from the ED would include gradual onset of shortness of breath, rapid response to therapy, oxygen saturation greater than 90%, and acute coronary syndromes and MI unlikely as the precipitating event.

• Those patients who require intubation or remain with significant respiratory, hemodynamic, and/or cardiovascular compromise often will require ICU or CCU admission.

• If left ventricular function has not been well established previously, obtain either a multigated nuclear imaging (MUGA) scan or an echocardiogram, which enables assessment of valvular function and wall motion abnormalities as well as ejection fraction.

• In patients refractory to medical therapy or with evidence of cardiogenic shock, cardiac catheterization, angioplasty, coronary bypass, or intraaortic balloon pump (IABP) may be helpful.

Further Outpatient Care:

• Center outpatient care around patient education with specific instructions regarding dietary restrictions and compliance with medical therapy.

In/Out Patient Meds:

• ACE inhibitors are indicated in patients with ejection fractions of 35% or less.

• Digoxin also may be helpful in patients with ejection fractions of 35% or less.

• Diuretics, such as furosemide, may be helpful regardless of ejection fraction.

• Beta-blockers appear to be cardioprotective in patients with depressed left ventricular function. The US carvedilol heart failure study group demonstrated a two-thirds decrease in mortality in patients taking carvedilol with left ventricular ejection fractions of 35%. Beta-blockers are indicated as therapy for patients with diastolic dysfunction or for patients with coronary insufficiency.

• Calcium channel blockers, such as nifedipine and nondihydropyridines, increase mortality and incidence of recurrent CHF with chronic use in patients with depressed LV function. Amlodipine is the exception to this rule. Calcium channel blockers are useful in patients with diastolic dysfunction and heart failure.

Transfer:

• Consider transfer for unstable patients being evaluated in a center without access to cardiac catheterization or IABP. These patients might include the following:

• Those who are refractory to medical therapy

• Those in cardiogenic shock

• Those with significant aortic stenosis or other valvular abnormalities possibly requiring surgical intervention or valvuloplasty

Deterrence/Prevention:

• Emphasize patient education with intense instruction regarding compliance with dietary restrictions and medical therapy.

• Emphasize close monitoring of blood pressure, particularly in patients with diastolic dysfunction.

• Patient should modify diet as follows:

• Sodium restriction (initially 4 gm qd)

• Weight reduction (if appropriate)

• Appropriate fluid restriction

• Patient should modify activity as follows:

• During severe stage, bed rest with elevation of head of bed and anti-embolism stockings to help control leg edema

• Gradual increase in activity with walking to help increase strength

Complications:

• Acute MI

• Cardiogenic shock

• Arrhythmias (most commonly atrial fibrillation)

• Ventricular arrhythmias, such as ventricular tachycardia, often are seen in patients with significantly depressed left ventricular function.

• Electrolyte disturbances

• Mesenteric insufficiency

• Protein enteropathy

• Digitalis intoxication

Prognosis:

• Based on data from 4606 patients hospitalized with CHF between 1992-1993, total in-hospital mortality was 19%, with 30% of deaths occurring from noncardiac causes. These patients, however, were noted to have had suboptimal use of proven efficacious therapy, compared with those who survived hospitalizations, particularly among women and the elderly. Thirty-year data from the Framingham heart study demonstrated a median survival of 3.2 years for males and 5.4 years for females.

• Results of initial treatment usually are good, regardless of cause.

• Long-term prognosis is variable. Mortality rates range from 10% in patients with mild symptoms to 50% with advanced, progressive symptoms.

Patient Education:

• Provide instructions to patients discharged home to return to the ED for recurrence or changes in severity of symptoms.

• Provide specific instructions to patients discharged regarding dietary restrictions and compliance with medical therapy.

• Require patients to promptly follow up with their primary care physician or cardiologist.

• Advise patients that printed information is available from the following organizations:

• American Heart Association, 7320 Greenville Ave, Dallas, TX 75231, (214) 373-5300

• American College of Cardiology, 911 Old Georgetown Rd, Bethesda, MD 20814, (301) 897-5400

MISCELLANEOUS

Medical/Legal Pitfalls:

• Failure to recognize and initiate early management of a patient presenting with signs and symptoms of CHF and pulmonary edema is a pitfall because therapy must begin with the ABCs, and early treatment should include nitrates and diuretics, if hemodynamics are stable.

• Failure to obtain an ECG early is a pitfall because this may be useful in diagnosing dysrhythmias, concomitant cardiac ischemia, or prior MI; early ECG also is helpful in differentiating CHF from other etiologies. Remember, the most common cause of CHF is coronary artery disease.

• Failure to consider use of both CPAP and BiPAP early in therapy as a means to decrease need for intubation and improve acute respiratory status

• Failure to consider and evaluate for diseases with similar presentations

• Failure to educate patients concerning changes or noncompliance with medical therapy and dietary restrictions to help prevent further recurrence

• Discharging patients who may have had acute MI as a cause of CHF

TEST QUESTIONS

CME Question 1: A 45-year-old male with a history of chronic obstructive pulmonary disease (COPD) and an anterior myocardial infarction 1 year ago presents with complaints of sudden onset of cough, wheezing, and dyspnea. Physical exam is difficult, secondary to obesity but is significant for an oxygen saturation of 90%; a rapid, irregular heartbeat; and scattered wheezing and rhonchi in all lung fields. Symptoms persist despite 160 mg of IV furosemide. Which of the following would not be included in management of this patient?

A: Nasal continuous positive airway pressure (CPAP)
B: IV digoxin
C: IV morphine
D: Oral metolazone
E: Nebulized albuterol

The correct answer is B: Digoxin has no role in the ED management of CHF due to its delayed absorption and diminished efficacy at times of increased sympathetic tone. It has little, if any, benefit in use in the patient presenting concomitantly with atrial fibrillation and rapid ventricular response. The use of digoxin should be limited to chronic CHF, where its role has been well established.

CME Question 2: A 25-year-old alcoholic male is brought to the ED complaining that he just doesn't feel right. Which one of the following would not lead to the diagnosis of congestive heart failure (CHF)?

A: Cough productive of pink, frothy sputum
B: Pulsus alternans
C: A mid-to-late systolic murmur
D: A musical wheeze
E: Pleuritic chest pain

The correct answer is E: ED patients with CHF generally complain of dyspnea but often have nonspecific complaints. Cough productive of pink, frothy sputum is highly suggestive of CHF. On physical examination, patients often will be hypertensive with pulsus alternans (alternating weak and strong pulse indicative of depressed left ventricular [LV] function). Wheezing or rales may be heard on lung auscultation. The apical impulse frequently is displaced, while cardiac auscultation may reveal aortic or mitral valvular abnormalities, an S3 or S4. Cardiac asthma is characterized by a high pitched or musical wheeze; however, this is neither specific nor sensitive. This patient`s history of alcoholism raises concerns of alcoholic cardiomyopathy, while his physical exam is worrisome for critical aortic stenosis with CHF.

Pearl Question 1 (T/F): A 50-year-old male presents with shortness of breath, BP 200/110, and a heart rate of 100. His physical exam and chest x-ray are consistent with congestive heart failure (CHF) while the echocardiogram demonstrates normal left ventricular (LV) and valvular function. A beta-blocker may be helpful in this case.

The correct answer is True: Patients with diastolic dysfunction benefit most from beta-blockers and calcium channel blockers; diuretics are of more limited benefit.

Pearl Question 2 (T/F): An 80-year-old female from a third-world country just arrived in the US and presents with complaints of increasing difficulty of breathing over the past 2 weeks with minimal or no urine output. Her evaluation is consistent with severe congestive heart failure (CHF) and her creatinine is noted to be 10. One of the medical students suggests giving her a blocker or inhibitor or something to tide her over until dialysis can be arranged. No other additional treatment options are available.

The correct answer is False: Promising data exist suggesting that the use of SL captopril or IV enalapril may reverse hemodynamic instability and symptoms rapidly, possibly avoiding an otherwise imminent intubation. Recent data suggest that captopril may play a unique role in sustaining patients with renal failure and concomitant acute congestive heart failure while awaiting definitive therapy with dialysis. ACE inhibitors remain a promising area in need of further study.

Pearl Question 3 (T/F): A 75-year-old female presents with acute shortness of breath. Physical exam reveals jugular venous distention (JVD), an S3, and rales in all lung fields. Chest x-ray is clear. She is treated with diuretics, nitrates, and morphine with brisk diuresis and rapid improvement. Two days later, all symptoms have resolved and her physical exam is normal. Chest x-ray is repeated and read as consistent with pulmonary edema. These chest x-ray findings are not commonly seen in CHF.

The correct answer is False: Early congestive heart failure (CHF) may be manifest as cephalization of the pulmonary vessels. As the interstitial fluid accumulates, more advanced CHF may be demonstrated by Kerley B line, while pulmonary edema is seen as perihilar infiltrates, often in the classic butterfly pattern. However, several limitations to the use of chest x-ray in CHF exist. This classic radiographic progression often is not seen. As much as a 12-hour radiographic lag may occur from onset of symptoms, and radiographic findings frequently persist for several days despite clinical recovery.

Pearl Question 4 (T/F): A 95-year-old otherwise healthy male from Framingham, MA presents with his first episode of congestive heart failure (CHF). Median survival will be between 3-6 years.

The correct answer is True: Based on data from 4606 patients hospitalized with CHF between 1992-1993, total in-hospital mortality was 19%, with 30% of deaths occurring from noncardiac causes. These patients, however, were noted to have had suboptimal use of proven efficacious therapy, compared with those who survived hospitalizations, particularly among women and the elderly. Thirty-year data from the Framingham heart study demonstrated a median 5-year survival of 3.2 years for males and 5.4 years for females.

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NOTE:

Medicine is a constantly changing science and not all therapies are clearly established. New research changes drug and treatment therapies daily. The authors, editors, and publisher of this textbook have used their best efforts to provide information that is up-to-date and accurate and is generally accepted within medical standards at the time of publication. However, as medical science is constantly changing and human error is always possible, the authors, editors, and publisher or any other party involved with the publication of this text do not warrant the information in this text is accurate or complete, nor are they responsible for omissions or errors in the text or for the results of using this information. The reader should confirm the information in this text from other sources prior to use. In particular, all drug doses, indications, and contraindications should be confirmed in the package insert. FULL DISCLAIMER

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