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Cardiogenic Pulmonary Edema

  • Author: Ali A Sovari, MD, FACP; Chief Editor: Henry H Ooi, MD, MRCPI  more...
Updated: Dec 28, 2015


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 as a result of cardiac dysfunction (see the image below). (See Etiology.)

Radiograph shows acute pulmonary edema in a patien Radiograph shows acute pulmonary edema in a patient who was admitted with acute anterior myocardial infarction. Findings are vascular redistribution, indistinct hila, and alveolar infiltrates.

Pulmonary edema can be caused by the following major pathophysiologic mechanisms:

  • Imbalance of Starling forces - Ie, increased pulmonary capillary pressure, decreased plasma oncotic pressure, increased negative interstitial pressure
  • Damage to the alveolar-capillary barrier
  • Lymphatic obstruction
  • Idiopathic (unknown) mechanism

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 [LA] myxoma), and LV failure secondary to systolic or diastolic dysfunction of the left ventricle. CPE leads to progressive deterioration of alveolar gas exchange and respiratory failure. Without prompt recognition and treatment, a patient's condition can deteriorate rapidly. (See Etiology, Prognosis, Presentation, Workup, Treatment, and Medication.)


The major complications associated with CPE are respiratory fatigue and failure. Prompt diagnosis and treatment usually prevent these complications, but the physician must be prepared to provide assisted ventilation if the patient begins to show signs of respiratory fatigue (eg, lethargy, fatigue, diaphoresis, worsening anxiety). (See Prognosis and Treatment.)

Sudden cardiac death secondary to cardiac arrhythmia is another concern, and continuous monitoring of heart rhythm is helpful in prompt diagnosis of dangerous arrhythmias.

Patient education

To help prevent recurrence of CPE, counsel and educate patients in whom pulmonary edema is due to dietary causes or medication noncompliance.



CPE is caused by elevated pulmonary capillary hydrostatic pressure leading to transudation of fluid into the pulmonary interstitium and alveoli. Increased LA 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(Pcap - Pis) - l(Pcap - Pis),

where Q is net fluid filtration; K is a constant called the filtration coefficient; Pcap is capillary hydrostatic pressure, which tends to force fluid out of the capillary; Pis 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; the second Pcap is the colloid osmotic pressure of plasma, which tends to pull fluid into the capillary; and the second 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 LA 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.


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 LA pressure, the rate of lymphatic removal can be as high as 200 mL/h, which protects the lungs from pulmonary edema.


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

Stage 1

In stage 1, elevated LA 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.

Stage 2

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.

Stage 3

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 500mL 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.

Cardiac disorders manifesting as CPE

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. 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

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.

Chronic LV failure is usually the result of congestive heart failure (CHF) or cardiomyopathy. Causes of acute exacerbations include the following:

  • Acute myocardial infarction (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

Ischemia and infarction may cause LV diastolic dysfunction in addition to systolic dysfunction. With a similar mechanism, myocardial contusion induces systolic or diastolic dysfunction.

Diastolic dysfunction signals a decrease in LV diastolic distensibility (compliance). Because of this decreased compliance, a heightened diastolic pressure is required to achieve a 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 constrictive pericarditis and tamponade.


New-onset rapid atrial fibrillation and ventricular tachycardia can be responsible for CPE.

LV hypertrophy and cardiomyopathies

These can increase LV stiffness and end-diastolic pressure, with pulmonary edema resulting from increased capillary hydrostatic pressure.

LV volume overload

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. 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.

Ventricular septal rupture, aortic insufficiency, and mitral regurgitation cause elevation of LV end-diastolic pressure and LA pressure, leading to pulmonary edema. LV outflow obstruction, such as that caused by aortic stenosis, produces increased end-diastolic filling pressure, increased LA pressure, and increased pulmonary capillary pressures.

Some sodium retention may occur in association with LV systolic dysfunction. However, in certain conditions, 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 a result of noncompliance with dietary restrictions or noncompliance with hemodialysis sessions.

Myocardial infarction

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 blood pressure can be considered an etiology of LV outflow obstruction because it increases systemic resistance against the pump function of the left ventricle.



In-hospital mortality rates for patients with CPE are difficult to assign because the causes and severity of the disease vary considerably. In a high-acuity setting, in-hospital death rates are as high as 15-20%.

Myocardial infarction, associated hypotension, and a history of frequent hospitalizations for CPE generally increase the mortality risk.

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 with orotracheal intubation), and barotrauma.

Contributor Information and Disclosures

Ali A Sovari, MD, FACP Fellow in Clinical Cardiac Electrophysiology, Cedars Sinai Medical Center/Heart Institute

Ali A Sovari, MD, FACP is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Physician Scientists Association, American Physiological Society, Biophysical Society, Heart Rhythm Society, Society for Cardiovascular Magnetic Resonance

Disclosure: Nothing to disclose.


Abraham G Kocheril, MD, FACC, FACP, FHRS Professor of Medicine, University of Illinois College of Medicine

Abraham G Kocheril, MD, FACC, FACP, FHRS is a member of the following medical societies: American College of Cardiology, Central Society for Clinical and Translational Research, Heart Failure Society of America, Cardiac Electrophysiology Society, American College of Physicians, American Heart Association, American Medical Association, Illinois State Medical Society

Disclosure: Nothing to disclose.

Arnold S Baas, MD, FACC, FACP Associate Professor of Medicine, Division of Cardiology, University of California, Los Angeles, David Geffen School of Medicine; Attending Physician, Ronald Reagan UCLA Medical Center

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, American Society of Echocardiography

Disclosure: Nothing to disclose.

Chief Editor

Henry H Ooi, MD, MRCPI Director, Advanced Heart Failure and Cardiac Transplant Program, Nashville Veterans Affairs Medical Center; Assistant Professor of Medicine, Vanderbilt University School of Medicine

Disclosure: Nothing to disclose.


Amal Mattu, MD, FACEP, FAAEM, Program Director, Emergency Medicine Residency, Co-Director, Emergency Medicine/Internal Medicine Combined Residency Program, Department of Surgery, Division of Emergency Medicine, University of Maryland School of Medicine

Amal Mattu, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine.

Disclosure: Nothing to disclose.

Ari M Perkins, MD, Consulting Staff, Department of Emergency Medicine, Greenwich Hospital

Disclosure: Nothing to disclose.

Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital

Sat Sharma, MD is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association

Disclosure: Nothing to disclose.

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.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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Radiograph shows acute pulmonary edema in a patient who was admitted with acute anterior myocardial infarction. Findings are vascular redistribution, indistinct hila, and alveolar infiltrates.
Radiograph shows acute pulmonary edema in a patient known to have ischemic cardiomyopathy. Findings are Kerley B lines (1mm thick and 1cm long) in the lower lobes and Kerley A lines in the upper lobes.
Radiograph demonstrates cardiomegaly, bilateral pleural effusions, and alveolar opacities in a patient with pulmonary edema.
Radiograph shows interstitial pulmonary edema, cardiomegaly, and left pleural effusion presenting at an earlier stage of pulmonary edema.
Lateral chest radiograph shows prominent interstitial edema and pleural effusions.
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