eMedicine Specialties > Cardiology > Myocardial Disease and Cardiomyopathies

Pulmonary Edema, Cardiogenic

Author: Ali A Sovari, MD, Research Fellow, Division of Cardiology, David Geffen School of Medicine, University of California, Los Angeles (UCLA)
Coauthor(s): Abraham G Kocheril, MD, FACC, FACP, Professor of Medicine, Director of Clinical Electrophysiology, University of Illinois at Chicago; Arnold S Baas, MD, FACC, FACP, Assistant Professor of Medicine, University of California at Los Angeles; Attending Physician, UCLA Santa Monica Hospital and UCLA Westwood Hospital
Contributor Information and Disclosures

Updated: Apr 22, 2008

Introduction

Background

Pulmonary edema refers to extravasation of fluid from the pulmonary vasculature into the interstitium and alveoli of the lung. The formation of pulmonary edema may be caused by 4 major pathophysiologic mechanisms: (1) imbalance of Starling forces (ie, increased pulmonary capillary pressure, decreased plasma oncotic pressure, increased negative interstitial pressure), (2) damage to the alveolar-capillary barrier, (3) lymphatic obstruction, and (4) idiopathic or unknown mechanism.

Cardiogenic pulmonary edema (CPE) is defined as pulmonary edema due to increased capillary hydrostatic pressure secondary to elevated pulmonary venous pressure. CPE reflects the accumulation of fluid with a low-protein content in the lung interstitium and alveoli, when pulmonary veins and left atrium venous return exceeds left ventricular (LV) output.

Increased hydrostatic pressure leading to pulmonary edema may result from many causes, including excessive intravascular volume administration, pulmonary venous outflow obstruction (eg, mitral stenosis or left atrial myxoma), or LV failure secondary to systolic or diastolic dysfunction of the LV. CPE leads to progressive deterioration of alveolar gas exchange and respiratory failure. Without prompt recognition and treatment, a patient's condition can deteriorate rapidly.


Pathophysiology

CPE is caused by elevated pulmonary capillary hydrostatic pressure leading to transudation of fluid into the pulmonary interstitium and alveoli. Increased left atrial pressure increases pulmonary venous pressure and pressure in the lung microvasculature, resulting in pulmonary edema.

Mechanism of CPE

Pulmonary capillary blood and alveolar gas are separated by the alveolar-capillary membrane, which consists of 3 anatomically different layers: (1) the capillary endothelium; (2) the interstitial space, which may contain connective tissue, fibroblasts, and macrophages; and (3) the alveolar epithelium. Exchange of fluid normally occurs between the vascular bed and the interstitium. Pulmonary edema occurs when the net flux of fluid from the vasculature into the interstitial space is increased. The Starling relationship determines the fluid balance between the alveoli and the vascular bed.

Net flow of fluid across a membrane is determined by applying the following equation:

Q = K (P cap -P is) - l(Pcap - Pis),



where Q is net fluid filtration; K is a constant called the filtration coefficient; P cap is capillary hydrostatic pressure, which tends to force fluid out of the capillary; P is is hydrostatic pressure in the interstitial fluid, which tends to force fluid into the capillary; l is the reflection coefficient, which indicates the effectiveness of the capillary wall in preventing protein filtration; Pcap is the colloid osmotic pressure of plasma, which tends to pull fluid into the capillary; and Pis is the colloid osmotic pressure in the interstitial fluid, which pulls fluid out of the capillary.



The net filtration of fluid may increase with changes in different parameters of the Starling equation. CPE predominantly occurs secondary to left atrial outflow impairment or LV dysfunction. For pulmonary edema to develop secondary to increased pulmonary capillary pressure, the pulmonary capillary pressure must rise to a level higher than the plasma colloid osmotic pressure. Pulmonary capillary pressure is normally 8-12 mm Hg, and colloid osmotic pressure is 28 mm Hg. High pulmonary capillary wedge pressure (PCWP) may not always be evident in established CPE because the capillary pressure may have returned to normal when the measurement is performed.

Lymphatics

The lymphatics play an important role in maintaining an adequate fluid balance in the lungs by removing solutes, colloid, and liquid from the interstitial space at a rate of approximately 10-20 mL/h. An acute rise in pulmonary arterial capillary pressure (ie, to >18 mm Hg) may increase filtration of fluid into the lung interstitium, but the lymphatic removal does not increase correspondingly. In contrast, in the presence of chronically elevated left atrial pressure, the rate of lymphatic removal can be as high as 200 mL/h, which protects the lungs from pulmonary edema.

Stages

The progression of fluid accumulation in CPE can be identified as 3 distinct physiologic stages.

In stage 1, elevated left atrial pressure causes distention and opening of small pulmonary vessels. At this stage, blood gas exchange does not deteriorate, or it may even be slightly improved.

In stage 2, fluid and colloid shift into the lung interstitium from the pulmonary capillaries, but an initial increase in lymphatic outflow efficiently removes the fluid. The continuing filtration of liquid and solutes may overpower the drainage capacity of the lymphatics. In this case, the fluid initially collects in the relatively compliant interstitial compartment, which is generally the perivascular tissue of the large vessels, especially in the dependent zones. The accumulation of liquid in the interstitium may compromise the small airways, leading to mild hypoxemia. Hypoxemia at this stage is rarely of sufficient magnitude to stimulate tachypnea. Tachypnea at this stage is mainly the result of the stimulation of juxtapulmonary capillary (J-type) receptors, which are nonmyelinated nerve endings located near the alveoli. J-type receptors are involved in reflexes modulating respiration and heart rates.

In stage 3, as fluid filtration continues to increase and the filling of loose interstitial space occurs, fluid accumulates in the relatively noncompliant interstitial space. The interstitial space can contain up to 500 mL of fluid. With further accumulations, the fluid crosses the alveolar epithelium in to the alveoli, leading to alveolar flooding. At this stage, abnormalities in gas exchange are noticeable, vital capacity and other respiratory volumes are substantially reduced, and hypoxemia becomes more severe.

Pathophysiologic considerations

CPE usually occurs secondary to left atrial outflow impairment or LV dysfunction. Left atrial outflow impairment may be acute or chronic. Causes of chronic impairment include mitral stenosis or left atrial tumors. Increased heart rate, which may occur secondary to atrial fibrillation, leads to pulmonary edema because of reduced LV filling. Acute mitral-valve regurgitation secondary to papillary muscle dysfunction or ruptured chordae tendineae increases LV end-diastolic pressure and is another cause of pulmonary edema.

LV dysfunction can be systolic or diastolic or combined. It can also be associated with LV volume overload or LV outflow obstruction. Systolic dysfunction, a common cause of CPE, is defined as decreased myocardial contractility that reduces cardiac output. The fall in cardiac output stimulates sympathetic activity and blood volume expansion by activating the renin-angiotensin-aldosterone system, which causes deterioration by decreasing LV filling time and increasing capillary hydrostatic pressure, respectively.

Diastolic dysfunction signals a decrease in LV diastolic distensibility (compliance). Therefore, a heightened diastolic pressure is required to achieve the similar stroke volume. Despite normal LV contractility, the reduced cardiac output in conjunction with excessive end-diastolic pressure generates hydrostatic pulmonary edema. Diastolic abnormalities can also be caused by constriction and restriction.

LV volume overload occurs in a variety of cardiac or noncardiac conditions. Cardiac conditions are ventricular septal rupture, acute or chronic aortic insufficiency, and acute or chronic mitral regurgitation. The noncardiac condition is volume overload. These conditions cause elevation of LV end-diastolic pressure and left atrial pressure, leading to pulmonary edema. LV outflow obstruction, such as aortic stenosis, produces increased end-diastolic filling pressure, increased left atrial pressure, and increased pulmonary capillary pressures. Cardiac tamponade results in elevation of left atrial (pulmonary capillary pressure), and right atrial pressure resulting in pulmonary and peripheral edema, respectively.

After pulmonary edema begins to develop, a self-perpetuating cycle of events occurs in the cardiopulmonary system. The cycle begins when LV systolic dysfunction decreases myocardial contractility and cardiac output, activating the renin-angiotensin-aldosterone system and stimulating catecholamine production. As a result, systemic vascular resistance increases leading to increased myocardial wall tension, myocardial ischemia, and worsening LV function and cardiac output, all of which perpetuate the cycle. The increase in myocardial wall tension also leads to concurrent diastolic dysfunction, which increases pulmonary artery and pulmonary capillary pressures. When the pulmonary capillary hydrostatic pressure exceeds the pulmonary interstitial pressure, transudation of fluid in the pulmonary interstitium and alveoli occurs. If the cycle is not aborted promptly with appropriate treatment, pulmonary edema rapidly develops.

Mortality/Morbidity

  • In-hospital mortality rates are difficult to assign because the causes and the severity vary considerably. In a high-acuity setting, in-hospital death rates are as high as 15-20%.
  • Severe hypoxia may result in myocardial ischemia or infarction. Mechanical ventilation may be required if medical therapy is delayed or unsuccessful. Endotracheal intubation and mechanical ventilation are associated with their own risks, including aspiration (during intubation), mucosal trauma (more common with nasotracheal intubation than orotracheal intubation), and barotrauma.

Clinical

History

Patients with CPE present with the dramatic clinical features of left heart failure. Patients develop a sudden onset of extreme breathlessness, anxiety, and feelings of drowning.

  • Clinical manifestations of acute CPE reflect evidence of hypoxia and increased sympathetic tone (increased catecholamine outflow).
  • Patients most commonly complain of shortness of breath and profuse diaphoresis.
  • Patients with symptoms of gradual onset (eg, over 24 h) often report dyspnea on exertion, orthopnea, and paroxysmal nocturnal dyspnea.
  • Cough is a frequent complaint that may provide an early clue to worsening pulmonary edema in patients with chronic LV dysfunction. Pink, frothy sputum may be present in patients with severe disease. Occasionally, hoarseness may be present as a result of recurrent laryngeal nerve palsy from mitral stenosis or pulmonary hypertension (Ortner sign).
  • Chest pain should alert the physician to the possibility of acute myocardial ischemia/infarction, or aortic dissection with acute aortic regurgitation as the precipitant of pulmonary edema.

Physical

  • Physical findings in patients with CPE are notable for tachypnea and tachycardia.
  • Patients may be sitting upright, they may demonstrate air hunger, and they may become agitated and confused.
  • Patients usually appear anxious and diaphoretic.
  • Hypertension is often present because of the hyperadrenergic state. Hypotension indicates severe LV systolic dysfunction and the possibility of cardiogenic shock. Cool extremities may indicate low cardiac output and poor perfusion.
  • Auscultation of the lungs usually reveals fine crepitant rales, but rhonchi or wheezes may also be present. Rales are usually heard at the bases first; as the condition worsens, they progress to the apices.
  • Cardiovascular findings are usually notable for S 3 , accentuation of pulmonic component of S 2 and jugular venous distension.
    • Auscultation of murmurs can help in the diagnosis of acute valvular disorders manifesting with pulmonary edema.
    • Aortic stenosis is associated with a harsh crescendo-decrescendo systolic murmur, which is heard best at the upper sternal border and radiating to the carotid arteries.
    • In contrast, acute aortic regurgitation is associated with a short, soft diastolic murmur.
    • Acute mitral regurgitation produces a loud systolic murmur heard best at the apex or lower sternal border. In the setting of ischemic heart disease, this may be a sign of acute myocardial infarction (MI) with rupture of mitral valve chordae.
    • Mitral stenosis typically produces a loud S 1 , opening snap, and diastolic rumble at the cardiac apex.
  • Another notable physical finding is skin pallor or mottling resulting from peripheral vasoconstriction, low cardiac output, and shunting of blood to the central circulation in patients with poor LV function and substantially increased sympathetic tone. Skin mottling at presentation is an independent predictor of an increased risk of in-hospital mortality.
  • Patients with concurrent right ventricular (RV) failure may present with hepatomegaly, hepatojugular reflux, and peripheral edema.
  • Severe CPE may be associated with a change in mental status, which may be the result of hypoxia or hypercapnia. Although CPE is usually associated with hypocapnia, hypercapnia with respiratory acidosis may be seen in patients with severe CPE or underlying COPD.

Causes

  • Atrial outflow obstruction: This can be due to mitral stenosis or, in rare cases, atrial myxoma, thrombosis of a prosthetic valve, or a congenital membrane in the left atrium (eg, cor triatriatum). Mitral stenosis is usually a result of rheumatic fever, after which it may gradually cause pulmonary edema. Therefore, other causes of CPE often accompany mitral stenosis in acute CPE; an example is decreased LV filling because of tachycardia in arrhythmia (eg, atrial fibrillation) or fever.
  • LV systolic dysfunction: Chronic LV failure is usually the result of congestive heart failure (CHF) or cardiomyopathy. Causes of acute exacerbations include the following:
    • Acute MI or ischemia
    • Patient noncompliance with dietary restrictions (eg, dietary salt restrictions)
    • Patient noncompliance with medications (eg, diuretics)
    • Severe anemia
    • Sepsis
    • Thyrotoxicosis
    • Myocarditis
    • Myocardial toxins (eg, alcohol, cocaine, chemotherapeutic agents such as doxorubicin [Adriamycin], trastuzumab [Herceptin])
    • Chronic valvular disease, aortic stenosis, aortic regurgitation, and mitral regurgitation
  • LV diastolic dysfunction, nonischemic acute mitral regurgitation (ruptured chordae tendineae), and acute aortic insufficiency (endocarditis, aortic dissection): This can cause acute, severe systemic hypertension (diastolic dysfunction), resulting in CPE.
    • Constrictive pericarditis and pericardial tamponade are other etiologies that mainly compromise LV diastolic function.
    • Ischemia and infarction may cause LV diastolic dysfunction in addition to systolic dysfunction. With a similar mechanism, myocardial contusion induces systolic or diastolic dysfunction.
  • Dysrhythmias: New-onset rapid atrial fibrillation and ventricular tachycardia can be responsible for CPE.
  • LVH and cardiomyopathies: These can increase LV stiffness and end-diastolic pressure, leading to pulmonary edema by increasing capillary hydrostatic pressure.
  • LV volume overload
    • Some sodium retention may occur in association with LV systolic dysfunction. However, in some situations, such as primary renal disorders, sodium retention and volume overload may play a primary role. CPE can occur in patients with hemodialysis-dependent renal failure, often as the result of noncompliance with dietary restrictions or noncompliance with hemodialysis sessions.
    • Valvular diseases, especially aortic regurgitation and mitral regurgitation, may be associated with volume overload. Endocarditis, aortic dissection, traumatic rupture, rupture of a congenital valve fenestration and iatrogenic causes are the most important etiologies of acute aortic regurgitation that may lead to pulmonary edema.
  • MI: One of the mechanical complications of MI can be the rupture of ventricular septum or papillary muscle. These mechanical complications substantially increase volume load in the acute setting and therefore may cause pulmonary edema.
  • LV outflow obstruction
    • Acute stenosis of the aortic valve can cause pulmonary edema. However, aortic stenosis due to a congenital disorder, calcification, prosthetic valve dysfunction, or rheumatic disease usually has a chronic course and is associated with hemodynamic adaptation of the heart. This adaptation may include concentric LV hypertrophy, which itself can cause pulmonary edema by way of LV diastolic dysfunction.
    • Hypertrophic cardiomyopathy is a cause of dynamic LV outflow obstruction.
    • Elevated systemic BP can be considered an etiology of LV outflow obstruction because it increases systemic resistance against the pump function of the LV.

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References
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Further Reading

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Keywords

PE, pulmonary edema, cardiogenic pulmonary edema, pulmonary edema cardiogenic, CPE, congestive heart failure, CHF, decompensated heart failure, heart failure, increased capillary hydrostatic pressure, increased capillary permeability, decreased plasma oncotic pressure, lymphatic obstruction, noncardiogenic pulmonary edema, NCPE

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Contributor Information and Disclosures

Author

Ali A Sovari, MD, Research Fellow, Division of Cardiology, David Geffen School of Medicine, University of California, Los Angeles (UCLA)
Ali A Sovari, MD is a member of the following medical societies: American College of Physicians, American Heart Association, and American Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

Abraham G Kocheril, MD, FACC, FACP, Professor of Medicine, Director of Clinical Electrophysiology, University of Illinois at Chicago
Abraham G Kocheril, MD, FACC, FACP is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, Cardiac Electrophysiology Society, Central Society for Clinical Research, Heart Failure Society of America, Heart Rhythm Society, and Illinois State Medical Society
Disclosure: Nothing to disclose.

Arnold S Baas, MD, FACC, FACP, Assistant Professor of Medicine, University of California at Los Angeles; Attending Physician, UCLA Santa Monica Hospital and UCLA Westwood Hospital
Arnold S Baas, MD, FACC, FACP is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Federation for Medical Research, and American Society of Echocardiography
Disclosure: Pfizer Honoraria Speaking and teaching

Medical Editor

George A Stouffer III, MD, Henry A Foscue Distinguished Professor of Medicine and Cardiology, Director of Interventional Cardiology, Cardiac Catheterization Laboratory, Chief of Clinical Cardiology, Division of Cardiology, University of North Carolina Medical Center
George A Stouffer III, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Heart Association, Phi Beta Kappa, and Society for Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Marschall S Runge, MD, PhD, Charles and Anne Sanders Distinguished Professor of Medicine, Chairman, Department of Medicine, Vice Dean for Clinical Affairs, University of North Carolina at Chapel Hill School of Medicine
Marschall S Runge, MD, PhD is a member of the following medical societies: American Association for the Advancement of Science, American College of Cardiology, American College of Physicians-American Society of Internal Medicine, American Federation for Clinical Research, American Federation for Medical Research, American Heart Association, American Physiological Society, American Society for Clinical Investigation, American Society for Investigative Pathology, Association of American Physicians, Association of Professors of Cardiology, Association of Professors of Medicine, Southern Society for Clinical Investigation, and Texas Medical Association
Disclosure: Pfizer Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching; Orthoclinica Diagnostica Consulting fee Consulting

CME Editor

Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Chief Editor

Patrice Delafontaine, MD, FACC, FAHA, FACP, FESC, Sidney W and Marilyn S Lassen Professor of Cardiovascular Medicine, Chief, Section of Cardiology, Director, Cardiovascular Center of Excellence, Tulane University; Professor of Physiology, Chair, Department of Medicine, Tulane University School of Medicine
Patrice Delafontaine, MD, FACC, FAHA, FACP, FESC is a member of the following medical societies: Alpha Omega Alpha, American Association for the Advancement of Science, American College of Cardiology, American College of Physicians, American Diabetes Association, American Federation for Clinical Research, American Federation for Medical Research, American Heart Association, American Medical Association, American Society for Clinical Investigation, Association of American Physicians, Association of Professors of Cardiology, Association of Professors of Medicine, Endocrine Society, European Society of Cardiology, Louisiana State Medical Society, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.

 
 
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