Congestive Heart Failure and Pulmonary Edema

Introduction

Background

Congestive heart failure (CHF) is an imbalance in pump function in which the heart fails to adequately maintain the circulation of blood. 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, whereas 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, whereas diastolic dysfunction occurs in a normal or intact left ventricle with impaired ability to relax and receive as well as eject blood.

Chest radiograph shows signs of congestive heart failure (CHF).

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 with normal physical activity by symptoms. 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

Congestive heart failure (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 mm Hg), 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. However, when the capacity of lymphatic drainage is exceeded, 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: Acute respiratory distress 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: 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 post–cardiopulmonary bypass

This article is limited to cardiac causes of pulmonary edema and congestive heart failure (CHF) and its relevant emergency care.

Frequency

United States

More than 3 million people have congestive heart failure (CHF), and more than 400,000 new patients present yearly. The prevalence rate of CHF is 1-2%.

Mortality/Morbidity

• Approximately 30-40% of patients with congestive heart failure (CHF) are hospitalized every year. CHF is the leading diagnosis-related group (DRG) among hospitalized patients older than 65 years. The 5-year mortality rate after diagnosis was reported in 1971 as 60% in men and 45% in women. In 1991, data from the Framingham heart study showed the 5-year mortality rate 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, the total in-hospital mortality rate was 19%, with 30% of deaths occurring from noncardiac causes.
• Patients with coexisting insulin-dependent diabetes mellitus have a significantly increased mortality rate.

Race

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

Sex

• Prevalence is greater in males than in females in patients aged 40-75 years.
• No sex predilection is noted among patients older than 75 years.

Age

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

Clinical

History

• Anxiety
• Dyspnea at rest
• Dyspnea upon exertion: This has been found to be the most sensitive symptom reported, yet the specificity for dyspnea is less than 60%.
• Orthopnea and paroxysmal nocturnal dyspnea (PND): These symptoms are observed; however, the sensitivity for orthopnea and PND is only 20-30%.
• Cough: Cough that produces pink, frothy sputum is highly suggestive of congestive heart failure (CHF).
• Edema
• Nonspecific symptoms
  • Weakness
  • Lightheadedness
  • Abdominal pain
  • Malaise
  • Wheezing
  • Nausea
• Past medical history
  • 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 congestive heart failure (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, has been observed.
• Hypertension may be present.
• Pulsus alternans (alternating weak and strong pulse indicative of depressed left ventricle [LV] function) may be observed.
• The skin may be diaphoretic or cold, gray, and cyanotic.
• Jugular venous distention (JVD) is frequently present.
• Wheezing or rales may be heard on lung auscultation.
• Apical impulse is frequently laterally displaced.
• Cardiac auscultation may reveal aortic or mitral valvular abnormalities (S₃ or S₄).
• Lower extremity edema may also be noted, especially in the subacute process.

Causes

• Various cardiac diseases cause congestive heart failure (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 is often 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.

Differential Diagnoses

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

Other Problems to Be Considered

The cardiac conditions combined with asthma or symptoms of chronic obstructive pulmonary disease (COPD) are difficult clinical challenges.

Workup

Laboratory Studies

• Until recently, differentiating asthma and other pulmonary disease has been difficult in the acute setting, particularly because of the poor sensitivities and specificities of most elements of history and physical examination. The standard of care has been shotgun therapy, namely treating patients for both congestive heart failure (CHF) and an acute pulmonary process such as asthma, with both diuretics and beta-agonists.
• The Breathing Not Properly Study has suggested that serum levels of beta-natriuretic peptide (BNP) and the BNP precursor, Pro-BNP, can help identify CHF as the origin of acute dyspnea.¹ This study found sensitivities of 90% with specificities of 76%. Positive predictive value was 79%, with a negative predictive value of 89%. Mueller et al found a reduction in hospital length of stay of 3 days when BNP levels were used.² This study assumed an average length of stay of 11 days; however, the average length of stay in the United States for CHF exacerbations is approximately 4 days. Also, although the time to initiation of therapy was reduced in this study from 90 to 60 minutes, the general practice in the United States is immediate initiation of shotgun therapy.
• In the primary care setting, Wright et al identified 305 patients with heart failure and then reevaluated them with or without the Pro-BNP result.³ Diagnostic accuracy improved from 52% to 60% without Pro-BNP and from 49% to 70% with Pro-BNP.
• Maisel et al identified in the Breathing Not Properly Study a 20% increase in patients with CHF who presented with dyspnea and a history of asthma or COPD but no prior history of CHF.⁴
• Mueller et al found that BNP reduced time to discharge from 12 to 3 days and reduced costs of hospitalization by 15%.²
• BNP is available as a point-of-care test, with results available within 15 minutes; however, only Pro-BNP can be concomitantly used with nesiritide.
• Serum levels of BNP lower than 100 pg/mL are unlikely to be from CHF. In the Breathing Not Properly Study, a BNP level of 50 pg/mL increased sensitivity from 90% to 97%, although specificity was reduced.¹ Levels of 100-500 pg/mL may be CHF. However, other conditions that also elevate right filling pressures (eg, pulmonary embolus, primary pulmonary hypertension, end-stage renal failure, cirrhosis, hormone replacement therapy) may also cause elevated BNP levels in this range. BNP levels more than 500 pg/mL are most consistent with CHF.
• Serum laboratory values may reveal prerenal azotemia or elevated alanine aminotransferase (ALT), aspartate aminotransferase (AST), or bilirubin levels, which is suggestive of a congestive hepatopathy. Cardiac enzymes and other serum markers for ischemia or infarction may also be useful.
• ABG levels 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 levels, hyperbilirubinemia, and dilutional hyponatremia are observed in severe cases.

Imaging Studies

• Chest radiography
  • Although diagnostic tests are of limited benefit in acute congestive heart failure (CHF), chest radiography is the most useful tool. A recent study showed that 1 out 5 patients admitted to the hospital with CHF lacked signs of congestion on chest radiograph.⁵
  • Cardiomegaly may be observed with a cardiothoracic ratio greater than 50%. Pleural effusions may be present bilaterally or if they are unilateral 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 is 18-25 mm Hg).
  • Pulmonary edema is observed as perihilar infiltrates often in the classic butterfly pattern, reflecting a PCWP of more than 25 mm Hg.
  • Several limitations to chest radiography are observed when attempting to diagnose CHF. Classic radiographic progression is often 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
  • Emergency transthoracic echocardiography (ECHO) may help identify regional wall motion abnormalities as well as globally depressed or myopathic left ventricular function.
  • ECHO may help reveal cardiac tamponade, pericardial constriction, and pulmonary embolus.
  • ECHO is also useful in revealing valvular heart disease, such as mitral or aortic stenosis or regurgitation.

Other Tests

• 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 is recognized 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 emergency department (ED) setting.
• Cardiac catheterization may be necessary for a complete evaluation and assessment of prognosis.

Treatment

Prehospital Care

• Prehospital notification by emergency medical services (EMS) personnel should alert ED staff of a patient presenting with signs and symptoms of congestive heart failure (CHF) and pulmonary edema. They should receive online medical advice for patients with high-risk presentations.
• Begin treatment with the ABCs. Administer supplemental oxygen, initially 100% nonrebreather facemask.
• Use cardiac monitoring and continuous pulse oximetry.
• Obtain intravenous access, as well as a prehospital ECG, if available.
• Provide nitroglycerin sublingual or spray for active chest pain in the patient without severe hypotension and intravenous furosemide.

Emergency Department Care

• Begin ED treatment of a patient presenting with signs and symptoms of congestive heart failure (CHF) and pulmonary edema with the ABCs. Administer supplemental oxygen, initially 100% nonrebreather facemask. Use cardiac monitoring and continuous pulse oximetry. Obtain intravenous 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 necessary for patients with known diastolic dysfunction who respond best to reductions in blood pressure, rather than to diuretics, nitrates, and inotropic agents. Serum BNP levels may be very useful in the setting of undifferentiated dyspnea, or in the future may be useful to gauge therapeutic success.
• Eliminate contributing factors when possible.
• Restrict fluid and sodium.
• Consider other treatment modalities, including nesiritide. Nesiritide may be useful in lieu of nitroglycerin in patients with moderate respiratory distress, particularly if the patient will not tolerate noninvasive ventilation or in the patient who cannot have nitroglycerin by protocol (ie, in an observation unit).
  • Data comparing nasal CPAP therapy and facemask ventilation therapy have demonstrated decreased need for intubation rates when these modalities are used.⁶ However, in patients with severe CHF treated with CPAP, no significant difference was found in short-term mortality rates and length of 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 intravenous nitroglycerin and nitroprusside.
  • Phlebotomy with removal of 500 mL 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 intravenous nitroglycerin and nitroprusside.

Consultations

• Cardiologist
• Critical care specialist
• Cardiothoracic surgeon, 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 of more than 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 congestive heart failure (CHF) and pulmonary edema. Calcium channel blockers, such as nifedipine and nondihydropyridines, increase mortality and increase prevalence of recurrent CHF with chronic use. Conflicting evidence currently argues both in favor of and 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 emergency department.

ACE inhibitors, such as sublingual (SL) captopril or intravenous enalapril, may rapidly reverse hemodynamic instability and symptoms, possibly avoiding an otherwise imminent intubation. Haude et al 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.⁷ Annane et al gave 1 mg of intravenous enalapril to 20 patients presenting with acute class III and class IV CHF over 2 hours and reported rapid hemodynamic improvement with no significant adverse effects on cardiac output or hepatosplanchnic measurements.⁸

Captopril may play a unique role in sustaining patients with renal failure and concomitant acute CHF while awaiting definitive therapy with dialysis. Because the information on this subject is still controversial and is limited to small studies, the routine use of ACE inhibitors 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. However, the role of beta-blockers in the acute setting is currently unclear; limit use until hemodynamic studies indicate that further deterioration is not possible.

Because differentiating CHF and asthma exacerbations is often difficult, treating both with the shotgun approach is often used, 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 theophylline 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, intravenous or orally administered, have been shown to worsen preexisting heart failure due to systemic sodium retention and volume expansion, hypokalemia, and occasional hypertension. Inhaled steroids, because of 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 article on Asthma for dosing schedules.

Diuretics

First-line therapy generally includes a loop diuretic such as furosemide, which inhibits sodium chloride reabsorption in the ascending loop of Henle.

Furosemide (Lasix)

Administer loop diuretics IV because this allows for both superior potency and higher peak concentration despite increased incidence of side effects, particularly ototoxicity.

Dosing

Adult

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

Pediatric

Not established

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, decreases GFR with CHF and, thus, is less potent and causes a greater loss of potassium. Conversely, metolazone has been demonstrated to be synergistic with loop diuretics in treating refractory patients.

Dosing

Adult

5-10 mg PO before redosing with furosemide

Pediatric

Not established

Nitrates

These agents reduce myocardial oxygen demand by lowering preload and afterload.

In patients with severe hypertension, nitroprusside causes more arterial dilatation than nitroglycerin. Nevertheless, due to thiocyanate toxicity and the coronary steal phenomenon associated with nitroprusside, intravenous nitroglycerin is still the therapy of choice for afterload reduction.

Nitroglycerin (Nitro-Bid, Nitrol, Nitrostat)

SL nitroglycerin and nitrospray are particularly useful in patients who present with acute pulmonary edema with a systolic blood pressure of at least 100 mm Hg.
Similar to SL, nitrospray's onset is 1-3 min with a half-life of 5 min. Applicability of nitrospray may be easier, and storage is up to 4 y. One study reported 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 because it is easier to monitor hemodynamics and absorption, particularly in the patients with diaphoresis.
Because of delayed absorption, PO nitrates have little role in the acute presentations of CHF.

Dosing

Adult

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 chest wall
Injection: Start at 20 mcg/min IV and rate to effect in 5-10 mcg increments q3-5min

Pediatric

Not established

Nitroprusside sodium (Nitropress)

Produces vasodilation and increases inotropic activity of the heart. At higher dosages, may exacerbate myocardial ischemia by increasing heart rate. Easily titratable.

Dosing

Adult

10-15 mcg/min IV and titrate to effective dose range of 30-50 mcg/min and a systolic blood pressure of at least 90 mm Hg

Pediatric

Not established

Analgesics

Intravenous morphine is an excellent adjunct in acute therapy. In addition to being both an anxiolytic and an analgesic, its most important effect is venodilation, which reduces preload. This agent also causes arterial dilatation, which reduces systemic vascular resistance (SVR) and increases cardiac output. Narcan can also reverse the effects of morphine. However, some evidence indicates that morphine use in acute pulmonary edema may increase the intubation rate.

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 numerous ways and is commonly titrated until desired effect is obtained.

Dosing

Adult

2-5 mg IV and repeated q10-15min unless respiratory rate is <20>

Pediatric

Not established

Inotropic agents

Principal inotropic agents include dopamine, dobutamine, inamrinone (formerly amrinone), milrinone, dopexamine, and digoxin. In patients with hypotension presenting with CHF, dopamine and dobutamine are usually used. Inamrinone or milrinone inhibits phosphodiesterase, resulting in an increase of intracellular cyclic adenosine monophosphate (AMP) and alteration in calcium transport. As a result, they increase cardiac contractility and reduce vascular tone by vasodilatation.

Dopexamine is a new synthetic catecholamine with beta-2 and dopaminergic properties that cause vasodilation and increased inotropism but with tachycardia as well. Dopexamine may ultimately have a role as an emergent inotropic agent; however, dobutamine is probably the current agent of choice.

Digoxin has no role in the emergency management of CHF due to delayed absorption and diminished efficacy at times of increased sympathetic tone. Thus, digoxin has little, if any, benefit in patients who present with atrial fibrillation and rapid ventricular response. Limit use of digoxin to chronic CHF, in which its role has been well established.

These agents augment both coronary and renal blood flow.

Dopamine (Intropin)

Stimulates both adrenergic and dopaminergic receptors. 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.
Positive inotropic agent at 2-10 mcg that can lead to tachycardia, ischemia, and dysrhythmias. Doses >10 mcg cause vasoconstriction, which increases afterload.

Dosing

Adult

5 mcg/kg/min IV and increase at 5 mcg/kg/min increments to a 20 mcg/kg/min dose

Pediatric

Not established

Dobutamine (Dobutrex)

Produces vasodilation and increases inotropic state. At higher dosages may cause increased heart rate, thus exacerbating myocardial ischemia. Strong inotropic agent with minimal chronotropic effect and no vasoconstriction.

Dosing

Adult

Starting dose: 2.5 mcg/kg/min IV; generally therapeutic in the range of 10-40 mcg/kg/min

Pediatric

Not established

Human B-type natriuretic peptides

Growing data suggest that Human B-type natriuretic peptides such as Nesiritide may be effective in reducing PCWP and improving dyspnea in patients with acutely decompensated congestive heart failure. Nesiritide serves as a second messenger to dilate veins and arteries.

Nesiritide (Natrecor)

Recombinant DNA form of human B-type natriuretic peptides (hBNP), which dilate veins and arteries.
Human BNP binds to particulate guanylate cyclase receptor of vascular smooth muscle and endothelial cells. Binding to receptor causes an increase in cyclic GMP, which serves as second messenger to dilate veins and arteries. Reduces PCWP and improves dyspnea in patients with acutely decompensated CHF.

Dosing

Adult

2 mcg/kg IV bolus over 60 seconds; follow by 0.01 mcg/kg/min continuous infusion; bolus volume (mL) = 0.33 X patient weight (kg); infusion flow rate of bolus (mL/h) = 0.1 X patient wt (kg)

Pediatric

Not established

Follow-up

Further Inpatient Care

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

• With few exceptions, patients presenting with acute symptoms of congestive heart failure (CHF) or pulmonary edema require hospital admission. However, many patients who rapidly respond 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 require intensive care unit or critical care unit admission.
• If left ventricular function has not been previously well established, perform either multigated nuclear imaging (MUGA) scanning or echocardiography, which enable 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.

Inpatient & Outpatient Medications

• ACE inhibitors are indicated in patients with ejection fractions of 35% or less.
• Digoxin may also 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 rates 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 may 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 g/d)
  • 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

Complications of congestive heart failure (CHF) and pulmonary edema may include the following:

• 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 congestive heart failure (CHF) between 1992-1993, the total in-hospital mortality rate was 19%, with 30% of deaths occurring from noncardiac causes.⁹ However, these patients 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.¹⁰
• Results of initial treatment are usually good, regardless of cause.
• Long-term prognosis varies. 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
    1615 Stemmons Freeway
    Dallas, TX 75207
    (214) 748-7212
  • American College of Cardiology
    9111 Old Georgetown Rd
    Bethesda, MD 20814
    (301) 897-5400
• For excellent patient education resources, visit eMedicine's Heart Center. Also, see eMedicine's patient education article Congestive Heart Failure.

Miscellaneous

Medicolegal Pitfalls

• Failure to recognize and initiate early management of a patient who presents with signs and symptoms of congestive heart failure (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 is a pitfall.
• Failure to consider and evaluate for diseases with similar presentations is also a pitfall.
• Failure to educate patients concerning changes or noncompliance with medical therapy and dietary restrictions to help prevent further recurrence is a concern.
• Discharging patients who may have had acute MI as a cause of CHF is a pitfall.

Source : http://emedicine.medscape.com/article/757999