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 (NYHA'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.
CHF is best summarized 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 25mmHg) higher than pulmonary capillary pressure (about 7-12mmHg), 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. The etiologies of pulmonary edema can be placed in the following categories.
- 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.
- Pulmonary edema secondary to increased pulmonary capillary pressure - this comprises cardiac causes and noncardiac causes, including pulmonary venous thrombosis, stenosis or veno-occlusive disease, and volume overload. Pulmonary edema may be secondary to decreased oncotic pressure found with hypoalbuminemia, and can be secondary to lymphatic insufficiency. It can also occur secondary to large negative pleural pressure with increased end expiratory volume.
- 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.
In the US,more than three million people have CHF, and more than 400,000 new cases present yearly. The prevalence of CHF is 1% to 2% of the general population.
Approximately 30% to 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 five-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 five-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 4,606 patients hospitalized with CHF between 1992 and 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.
African-American patients are 1.5 times more likely to die of CHF than white patients. Nevertheless, African-American patients appear to have similar or lower in-hospital mortality rates than white patients. The incidence is greater in males than in females for patients aged 40-75 years. No sex predilection exists for patients older than 75 years. The overall incidence of CHF increases with increasing age and effects about 10% of the population older than 75 years.
History of presenting illness is crucial in the evaluation of patients with acute CHF exacerbations and pulmonary edema.
A variety of cardiac diseases cause CHF and pulmonary edema and initial evaluation questions should reflect these processes.The most common cause of heart failure is coronary artery disease, which is secondary to loss of left ventricular muscle, on-going 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. Systemic processes such as pregnancy and hyperthyroidism as precipitants of CHF should also be considered.
The differential diagnosis for acute CHF exacerbation and pulmonary edema is broad and should include acute respiratory distress syndrome (ARDS), altitude illness, anaphalaxsis, anemia, bronchitis, chronic obstructive pulmonary disease and non cardiac asthma, dysbarism, hyperventilation syndrome, pericarditis and cardiac tamponade, pneumonia, pneumthorax and pneumomediastinum, septic shock, and venous air embolism.
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 relativly common symptoms; however, the sensitivity for orthopnea and PND is only 20% to 30%.A cough producing pink, frothy sputum is highly suggestive of CHF.
Other common presenting complaints include dyspnea at rest, edema, often localized to the lower extremities, and anxiety. Less specific complaints may include weakness, lightheadedness, abdominal pain, malaise, wheezing, and nausea. Past medical history will often include cardiomyopathy, valvular heart disease, alcohol use, hypertension, angina, prior myocardial infarction, and familial heart disease.
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% to 30%. Initial physical findings may include:
- utlization of accessory muscles of respiration;
- hypertension; and
- pulsus alternans (alternating weak and strong pulse indicative of depressed left ventricle function).
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. The apical impulse is often displaced laterally. Cardiac auscultation may reveal aortic or mitral valvular abnormalities, S3 or S4. Lower extremity edema may also be noted, especially in the subacute process.
Until recently, differentiating asthma and other pulmonary disease has been difficult in the acute setting, particularly due to 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 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 naturietic peptide (BNP) and the BNP precursor, Pro-BNP can help identify CHF as the origin of acute dyspnea.This study found sensitivities of 90% with specificities of 76%. Positive predictive value was 79% with a negative predictive value of 89%.
Mueller found a reduction in hospital length of stay of three days when BNP levels were utilized. However, this study assumed an average length of stay of 11 days.18 The average length of stay in the US for CHF exacerbations is approximately four days. In addition, although the time to initiation of therapy was reduced in this study from 90 to 60 minutes, the general practice in the US is immediate initiation of shotgun therapy.
In the primary care setting, Wright identified 305 patients with heart failure and revaluated them with or without the Pro-BNP result.20 Diagnostic accuracy improved from 52% to 60% without Pro-BNP, and from 49% to 70% with Pro-BNP. Maisel 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.17
BNP is available as a point-of-care test, with results available within 15 minutes. However, only Pro-BNP can be utilized concomitantly with Nesiritide.
Serum levels of BNP of <100pg/ml are unlikely to be from CHF. In the Breathing Not Properly Study, BNP of 50pg/ml increased sensitivity from 90% to 97% at a cost of reducing specificity. Levels of 100-500pg/ml may be CHF. However, other conditions that also elevate right filling pressures such as pulmonary embolus, primary pulmonary hypertension, end stage renal failure, cirrhosis and hormone replacement therapy may also cause elevated BNP levels in this range. BNP levels of >500pg/ml are most consistent with CHF.
Other serum laboratory values may identify prerenal azotemia or elevated alanine aminotransferase (ALT), aspartate aminotransferase (AST), or bilirubin, suggestive of a congestive hepatopathy. 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.
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.
Although imaging tests are of limited benefit in acute CHF, chest X-ray (CXR) is the most useful tool. Cardiomegaly may be observed with a cardiothoracic ratio greater than 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 12-18mmHg.As the interstitial fluid accumulates, more advanced CHF may be demonstrated by Kerley B lines (PCWP: 18-25mmHg). Pulmonary edema is observed as perihilar infiltrates often in the classic butterfly pattern reflecting a PCWP greater than 25mmHg.
Several limitations exist in the use of chest X-rays when attempting to diagnose CHF. 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) 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. Electrocardiogram (ECG) is a non-specific 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.
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, treatment and assessment of prognosis.
In patients refractory to medical therapy or with evidence of cardiogenic shock, cardiac catheterization, angioplasty, coronary bypass, or intra-aortic balloon pump (IABP) may be helpful.
Management of a patient presenting with signs and symptoms of CHF and pulmonary edema with the ABCs should begin with administration of supplemental oxygen, initially 100% non-rebreather facemask. Cardiac monitoring and continuous pulse oximetry must also be utilized, and intravenous (IV) access obtained. To reduce venous return, the head of the bed should be elevated. 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, the underlying cause should be treated as well. 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. Contributing factors must be eliminated where possible, and fluid and sodium restricted.
Recent data comparing nasal CPAP therapy with facemask ventilation therapy has demonstrated a 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.
The goal of pharmacotherapy is to achieve a PCWP of 15-18mmHg and a cardiac index >2.2L/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 is limited to acute use in patients with diastolic dysfunction and heart failure, a condition not easily determined in the emergency department (ED).
First-line therapy generally includes a loop diuretic such as furosemide, which will inhibit sodium chloride reabsorption in the ascending loop of Henle. Loop diuretics should be administere IV, since this allows for both superior potency and higher peak concentration despite increased incidence of side-effects, particularly ototoxicity. Higher doses and more rapid redosing may be appropriate for the patient in severe distress. Metolazone and chlorothiazide have been used as adjunctive therapy in patients initially refractory to furosemide.
Nitrates reduce myocardial oxygen demand by lowering preload and afterload.Nitoglycerin is particularly useful in the patient who presents with acute pulmonary edema with a systolic blood pressure of at least 100mmHg. However, oral nitrates, due to delayed absorption, have little role in the acute presentations of CHF.
Morphine IV 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. Morphine 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.
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 25mg of SL captopril with 0.8mg 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 1mg of IV enalapril to 20 patients presenting with acute class III and class IV CHF over two hours and demonstrated rapid hemodynamic improvement with no significant adverse effects 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, is currently unclear - use should be limited 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.
Roles of theophyline and aminophylline in the acute setting must be limited. 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 by increasing cardiac work.
Steroids, IV or oral (PO), have been shown to worsen pre-existing 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. Steroids, IV or oral (PO), have been shown to worsen pre-existing 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.
Human B-type natriuretic peptides such as Nesiritide may decrease hospital length of stay by up to four days. BNP binds to particulate guanylate cyclase receptor of vascular smooth muscle and endothelial cells. Binding to the receptor causes increase in cyclic GMP, which serves as second messenger to dilate veins and arteries. BNP reduces pulmonary capillary wedge pressure and improves dyspnea in patients with acutely decompensated CHF. Contraindications include systolic blood pressure <90mmHg - patients suspected of having, or known to have, low cardiac filling pressures, significant valvular stenosis, restrictive or obstructive cardiomyopathy, constrictive pericarditis, pericardial tamponade, and conditions in which cardiac output is dependent upon venous return.
Nesirtitide may affect renal function in patients whose renal function may depend on activity of renin-angiotensin-aldosterone system; it may cause hypotension, ventricular tachycardia, non-sustained VT, headache, abdominal pain, back pain, insomnia, anxiety, angina pectoris, nausea, and vomiting. BNP in the emergency setting should likely be reserved at this time, for those patients with pulmonary edema refractory to initial diuretics, CPAP or BiPaP.
Digoxin has no role in the emergency management of CHF due to delayed absorption and diminished efficacy at times of increased sympathetic tone. Thus, it has little, if any, benefit in the patient presenting concomitantly with atrial fibrillation and rapid ventricular response. Digoxin should be limited to chronic CHF in which its role has been well established.
Dopamine 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. Dobutamine produces vasodilation and increases inotropic state. At higher dosages it may cause an increased heart rate, exacerbating myocardial ischemia.
With few exceptions, patients presenting with acute symptoms of CHF or pulmonary edema require hospital admission. Many patients who respond rapidly to early therapy may require only an observation unit admission with telemetry monitoring if ischemic etiologies are being considered. Criteria for discharge from the ED 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 units (ICU) or cardiac care units (CCU) admission.
Based on data from 4,606 patients hospitalized with CHF between 1992 and 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 are usually 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.