Pulmonary edema pathophysiology

Jump to navigation Jump to search

Pulmonary edema Microchapters


Patient Information


Historical Perspective




Differentiating Pulmonary Edema from other Diseases

Epidemiology and Demographics

Risk Factors


Natural History, Complications and Prognosis


Diagnostic study of choice

History and Symptoms

Physical Examination

Laboratory Findings

X Ray




Echocardiography or Ultrasound

Other Imaging Findings

Other Diagnostic Studies


Medical Therapy

Interventional Therapy


Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Pulmonary edema pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides


Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Pulmonary edema pathophysiology

CDC on Pulmonary edema pathophysiology

Pulmonary edema pathophysiology in the news

Blogs on Pulmonary edema pathophysiology

Directions to Hospitals Treating Pulmonary edema

Risk calculators and risk factors for Pulmonary edema pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Farnaz Khalighinejad, MD [2]


Pulmonary edema is due to either failure of the heart to remove fluid from the lung circulation ("cardiogenic pulmonary edema"), or due to a direct injury to the lung parenchyma or increased permeability or leakiness of the capillaries ("noncardiogenic pulmonary edema").


It is understood that pulmonary edema is the abnormal increase in extravascular lung water (EVLW). This condition may be caused by the following underlying physiologic changes:[1][2][3]

  • Imbalance of staling force
  • Altered valvular capillary membrane permeability
  • Lymphatic insufficiency
  • Other factors

These factors have been described bellow:

Imbalance of starling force

The flux of fluid across the capillary wall is controlled by a balance between hydrostatic pressure and osmotic pressure gradients between the capillaries and interstitial space that can be calculated via Starling equation:

JV = K.S.([Pmv-Ppmv]-σd[πmv-πpmv])


JV = volume flow across the capillary bed
K = filtration coefficient of the capillary wall
S = surface area of the capillary bed
Pmv = microvascular hydrostatic pressure
Ppmv = perimicrovascular (interstitial) hydrostatic pressure
πmv = plasma colloid osmotic pressure
πpmv = perimicrovascular (interstitial) colloid osmotic pressure
σd = protein reflection coefficient
  • Increase negative interstitial pressure
    • Negative-pressure pulmonary edema (NPPE) or postobstructive pulmonary edema[4]
      • It is understood that postobstructive pulmonary edema is caused by highly negative intrathoracic pressure that create by forceful attempts to inhale against an obstruction, this causes elevated venous return, declined cardiac output and fluid transudation into the alveolar space.
Altered alveolar-capillary membrane permeability (acute respiratory distress syndrome)

Following are a few important aspects about altered alveolar capillary membrane permeability leading to pulmonary edema:

  • In noncardiogenic pulmonary edema, the most common mechanism for a rise in transcapillary filtration is an increase in capillary permeability.
  • This increase in permeability damages the alveolar-capillary membrane, causing increased movement of water and proteins from the intravascular space to the interstitial space.
  • In most cases of noncardiogenic pulmonary edema, the concentration of protein in the interstitium exceeds 60 percent of the plasma value, compared to less than 45 percent in cardiogenic pulmonary edema.

ARDS can be seen in a number of disorders:

Lymphatic insufficiency

Lymphatic insufficiency may follow:

Other factors

Various other factors contributing to the development of pulmonary edema include:

  • High-altitude pulmonary edema
    • It is understood that high-altitude pulmonary edema is caused by hypoxic pulmonary vasoconstriction at altitudes above 12,000 to 13,000 feet (3600 to 3900 m).[5]
  • Neurogenic pulmonary edema
    • It is understood that neurogenic pulmonary edema is caused by sympathetic overreactivity with massive catecholamine surges that shifts blood from the systemic to the pulmonary circulation.[6]
  • Narcotic overdose
    • The exact pathogenesis of narcotic overdose pulmonary edema is not fully understood. Proposed mechanisms include combination of direct toxicity of the drug, hypoxia, and acidosis secondary to hypoventilation and/or cerebral edema.[7]
  • Pulmonary embolism 
    • It is understood that pulmonary embolism can cause pulmonary edema by damaging the pulmonary and nearby pleural systemic circulations, increasing hydrostatic pressures in pulmonary and/or systemic veins, and decreasing pleural pressure due to atelectasis.[8]
  • Re-expansion pulmonary edema
    • The exact pathogenesis of re-expansion pulmonary edema is not fully understood. Direct injury from surfactant dysfunction in chronic atelectatic lung, elevated transpleural pressures, or indirect injury from reperfusion has been proposed.[9]

Gross Pathology

Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

Microscopic Pathology


  1. Sibbald WJ, Cunningham DR, Chin DN (1983). "Non-cardiac or cardiac pulmonary edema? A practical approach to clinical differentiation in critically ill patients". Chest. 84 (4): 452–61. PMID 6617283.
  2. Ware LB, Matthay MA (2005). "Clinical practice. Acute pulmonary edema". N. Engl. J. Med. 353 (26): 2788–96. doi:10.1056/NEJMcp052699. PMID 16382065.
  3. Pena-Gil C, Figueras J, Soler-Soler J (2005). "Acute cardiogenic pulmonary edema--relevance of multivessel disease, conduction abnormalities and silent ischemia". Int. J. Cardiol. 103 (1): 59–66. doi:10.1016/j.ijcard.2004.08.029. PMID 16061125.
  4. Bhattacharya M, Kallet RH, Ware LB, Matthay MA (2016). "Negative-Pressure Pulmonary Edema". Chest. 150 (4): 927–933. doi:10.1016/j.chest.2016.03.043. PMID 27063348.
  5. Dunham-Snary KJ, Wu D, Sykes EA, Thakrar A, Parlow LR, Mewburn JD, Parlow JL, Archer SL (2017). "Hypoxic Pulmonary Vasoconstriction: From Molecular Mechanisms to Medicine". Chest. 151 (1): 181–192. doi:10.1016/j.chest.2016.09.001. PMC 5310129. PMID 27645688.
  6. Busl KM, Bleck TP (2015). "Neurogenic Pulmonary Edema". Crit. Care Med. 43 (8): 1710–5. doi:10.1097/CCM.0000000000001101. PMID 26066018.
  7. Radke JB, Owen KP, Sutter ME, Ford JB, Albertson TE (2014). "The effects of opioids on the lung". Clin Rev Allergy Immunol. 46 (1): 54–64. doi:10.1007/s12016-013-8373-z. PMID 23636734.
  8. Porcel JM, Light RW (2008). "Pleural effusions due to pulmonary embolism". Curr Opin Pulm Med. 14 (4): 337–42. doi:10.1097/MCP.0b013e3282fcea3c. PMID 18520269.
  9. Feller-Kopman D, Berkowitz D, Boiselle P, Ernst A (2007). "Large-volume thoracentesis and the risk of reexpansion pulmonary edema". Ann. Thorac. Surg. 84 (5): 1656–61. doi:10.1016/j.athoracsur.2007.06.038. PMID 17954079.

Template:WikiDoc Sources