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 Associations (NYHAs) 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 venoocclusive 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. 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. 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.
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.