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==Overview==
Pulmonary [[edema]] is fluid accumulation in the [[lung]]s. This fluid accumulation leads to impaired gas exchange and [[hypoxia]].


==Pathophysiology==
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").<ref name=Ware>Ware LB, Matthay MA. Acute pulmonary edema. ''N Engl J Med'' 2005;353:2788-96. PMID 16382065.</ref>
===Cardiogenic===
* Severe [[cardiac arrhythmia|arrhythmias]] ([[tachycardia]]/fast heartbeat or [[bradycardia]]/slow heartbeat)
* [[Arteriovenous malformation]]
* [[Anomalous pulmonary venous return]]
* [[Aortic Regurgitation]]
* [[Aortic Stenosis]]
* [[Arrhythmia]]
* [[Cardiomyopathy]]
* [[Congestive heart failure]]
* [[Coronary Heart Disease]]
* [[Hypertensive crisis]]
* [[Left Heart Failure]]
* Left-to-Right Shunt
* [[Mitral Regurgitation]]
* [[Mitral Stenosis]]
* [[Myocarditis]]
* [[Pericardial Disease]]. [[Pericardial effusion]] with tamponade
* ST elevation [[MI]] with [[left ventricular failure]]
===Non-cardiogenic===
This form is contiguous with ARDS ([[acute respiratory distress syndrome]]):
* Acute Bronchial [[Asthma]]
* [[Acute Renal Failure]]
* Bacterial toxins
* Blood [[Transfusions]]
* [[Burns]]
* Chronic [[mediastinitis]]
* Decompression sickness
* [[Disseminated Intravascular Coagulation]]
* [[Drowning]]
* [[Drugs]]
* Fibrotic/inflammatory disease
* Fluid overload, e.g. from [[renal failure|kidney failure]]
* Gastric content [[aspiration]]
* [[Goodpasture's Syndrome]]
* [[High altitude sickness]]. Ascent to high altitude occasionally causes [[high altitude pulmonary edema]] (HAPE)<ref>{{cite web | author=M Bates | title=High altitude pulmonary edema| url=http://www.altitude.org/hape_altitude.htm| publisher=Apex (Altitude Physiology Expeditions) | accessdate=2007-03-06}}</ref>
* [[Hyperhydration]]
* [[Hypoalbuminemia]] / Albumin deficiency
* [[Idiopathic Venoocclusive Disease]]
* Inhalation of toxic gases
* [[Infection]]
* [[Leukemia]]
* [[Malaria]]
* Miliary [[Tuberculosis]]
* Neurogenic, e.g. [[subarachnoid hemorrhage]]
* [[Pheochromocytoma]]
* [[Pneumonia]]
* Pulmonary contusion, i.e. high-energy trauma
* [[Pulmonary Embolism]]
* Reexpansion, i.e. post [[pneumonectomy]] or large volume [[thoracentesis]]
* Reperfusion injury, i.e. postpulmonary thromboendartectomy or [[lung transplantation]]
* [[Sepsis]]
* [[Shock]]
* [[Toxic Shock Syndrome]]
* Multi[[trauma]], e.g. motor vehicle accident
* Upper airway obstruction
* [[Uremia]]
==Natural History, Complications and Prognosis==
If left untreated, acute pulmonary edema can lead to [[coma]] and even death, generally due to its main complication of [[Hypoxia (medical)|hypoxia]].
==Diagnosis==
===Symptoms===
====Acute Pulmonary Edema====
*[[Anxiety]]
*[[Cough]], particularly [[coughing up blood]] or bloody froth
*Difficulty [[breathing]]
*Excessive [[sweating]] or [[diaphoresis]]
*Feeling of "air hunger" or "[[drowning]]" (if this occurs suddenly, awakening the patient from [[sleep]] and causing the patient to sit up and catch their [[breath]], it's called "[[paroxysmal nocturnal dyspnea]]")
*Grunting or gurgling sounds with [[breathing]]
*Pale or blue skin
*Blue or [[cyanotic]] lips
*[[Restlessness]]
*[[Shortness of breath]]
*[[Shortness of breath]] when lying down ([[orthopnea]])
*[[Wheezing]]
====Chronic Pulmonary Edema====
If [[pulmonary edema]] develops gradually, there may be symptoms of fluid overload:
*Ankle or [[pedal edema]] (swelling of the legs, generally of the "pitting" variety, where the skin is slow to return to normal when pressed upon)
*[[Nocturia]] (frequent urination at night)
*[[Orthopnea]] (inability to lie down flat due to breathlessness)
*[[Paroxysmal nocturnal dyspnea]] (episodes of severe sudden breathlessness at night)
===Physical Examination===
====General Appearance of the Patient====
*Anxious
*Decrease in level of [[alertness]] ([[consciousness]])
*Inability to speak in full sentences
====HEENT====
*Nasal flaring
====Lungs====
*End-inspiratory [[crackles]] (sounds heard at the end of a deep breath)
====Cardiovascular====
*A [[third heart sound]] ([[S3]]) may be present<ref name=Ware/>
==Laboratory Studies==
===Brain Natriuretic Peptide===
[[Brain natriuretic peptide|B-type natriuretic peptide]] (BNP) is elevated in the patient with cardiogenic pulmonary edema. A low BNP (<100 pg/ml) makes a cardiac cause very unlikely and is associated with non-cardiogenic pulmonary edema.<ref name=Ware/>
===Oxygen Saturation===
Low [[oxygen saturation]] or hypoxia may be present on [[arterial blood gas]] readings.
==Chest X Ray==
[[Image:Pulmonary edema.gif|right|Pulmonary edema|250px]]The diagnosis is confirmed on [[X-ray]] of the lungs, which shows increased fluid in the alveolar walls. [[Kerley B lines]], increased vascular filling, [[pleural effusion]]s, upper lobe diversion (increased blood flow to the higher parts of the lung) may be indicative of cardiogenic pulmonary edema, while patchy alveolar infiltrates with air bronchograms are more indicative of noncardiogenic edema<ref name=Ware/>
==Echocardiography==
[[Echocardiography]] is useful in confirming a cardiac or no-cardiac cause of pulmonary edema.  Among cardiac causes, echocardiography can identify if systolic or [[diastolic dysfunction]] is present.  Echocardiography is useful in identify if focal segment wall motion abnormalities are present which would suggest ischemia or [[myocardial infarction]] as an underlying cause. If there is a global impairment of left ventricular function, then this suggests a [[cardiomyopathy]] may be present. Echocardiography may identify the presence and severity of valvular causes of pulmonary edema including [[aortic stenosis]], [[aortic insufficiency]], [[mitral stenosis]]. [[mitral insufficiency]], and [[hypertrophic cardiomyopathy]].
==Cardiac Catheterization==
Insertion of a [[pulmonary arterial catheter]] (a.k.a. a [[Swan-Ganz catheter]]) may be required to distinguish between the two main forms of pulmonary edema and to help guide management<ref name=Ware/>.  In patients with cardiogenic pulmonary edema the pulmonary artery pressure will be elevated. Among patients with non-cardiogenic pulmonary edema the wedge pressure will not be elevated.
==Treatment==
''See also the chapter on [[congestive heart failure]]''.
===Acute Pulmonary Edema===
In patients with acute pulmonary edema, the goal is to reduce both [[preload]] and [[afterload]] and to [[diurese]] the patient. Intravenous  nitroglycerin can be used to reduce both the preload and afterload. Diuretics such as [[furosemide]] or [[bumetanide]] can be used to reduce volume overload. The dose that the patient is on chronically should be doubled and administered intravenously in the setting of flash pulmonary edema.  [[Morphine sulfate]] may be helpful in reducing the drive to breathe, improving patient comfort, and reducing the [[preload]].
Oxygen therapy is required to minimize [[cyanosis]] and to maintain adequate oxygenation. High-flow oxygen, noninvasive ventilation (either [[continuous positive airway pressure]] (CPAP) or variable positive airway pressure (VPAP) may be effective<ref>Masip J, Roque M, Sanchez B, Fernandez R, Subirana M, Exposito JA. Noninvasive ventilation in acute cardiogenic pulmonary edema: systematic review and meta-analysis. ''JAMA'' 2005;294:3124-30. PMID 16380593.</ref><ref>Peter JV, Moran JL, Phillips-Hughes J, Graham P, Bersten AD. Effect of non-invasive positive pressure ventilation (NIPPV) on mortality in patients with acute cardiogenic pulmonary oedema: a meta-analysis. ''Lancet'' 2006;367(9517):1155-63. PMID 16616558.</ref>).  If the simple measures are not effective then [[mechanical ventilation]] may be required.
Treatment should also be directed at managing the underlying cause of an episode of acute pulmonary edema.  This would include managing as [[acute myocardial infarction]], [[mitral regurgitation]], [[aortic regurgitation]], or any other condition that causes an increase in left ventricular filling pressures.
===Chronic Pulmonary Edema===
Reoccurrence of FPE is thought to be associated with [[hypertension]]<ref>Kramer K, Kirkman P, Kitzman D, Little WC. Flash pulmonary edema: association with hypertension and reoccurrence despite coronary revascularization. Am Heart J. 2000 Sep;140(3):451-5. PMID 10966547.</ref> and may signify [[renal artery stenosis]].<ref>Pickering TG, Herman L, Devereux RB, Sotelo JE, James GD, Sos TA, Silane MF, Laragh JH. Recurrent pulmonary oedema in hypertension due to bilateral renal artery stenosis: treatment by angioplasty or surgical revascularisation. ''Lancet'' 1988;2(8610):551-2. PMID 2900930.</ref> Prevention of reoccurrence is based on managing hypertension, coronary artery disease, renovascular hypertension, and heart failure.


==References==
==References==
{{Reflist|2}}
{{reflist|2}}


==See also==
*[[High Altitude Pulmonary Edema]]
*[[Myocardial infarction]]
{{Respiratory pathology}}
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Revision as of 19:37, 18 August 2011

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Pulmonary edema is fluid accumulation in the lungs. This fluid accumulation leads to impaired gas exchange and hypoxia.

Pathophysiology

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").[1]

Cardiogenic

Non-cardiogenic

This form is contiguous with ARDS (acute respiratory distress syndrome):

Natural History, Complications and Prognosis

If left untreated, acute pulmonary edema can lead to coma and even death, generally due to its main complication of hypoxia.

Diagnosis

Symptoms

Acute Pulmonary Edema

Chronic Pulmonary Edema

If pulmonary edema develops gradually, there may be symptoms of fluid overload:

  • Ankle or pedal edema (swelling of the legs, generally of the "pitting" variety, where the skin is slow to return to normal when pressed upon)
  • Nocturia (frequent urination at night)
  • Orthopnea (inability to lie down flat due to breathlessness)
  • Paroxysmal nocturnal dyspnea (episodes of severe sudden breathlessness at night)

Physical Examination

General Appearance of the Patient

HEENT

  • Nasal flaring

Lungs

  • End-inspiratory crackles (sounds heard at the end of a deep breath)

Cardiovascular

Laboratory Studies

Brain Natriuretic Peptide

B-type natriuretic peptide (BNP) is elevated in the patient with cardiogenic pulmonary edema. A low BNP (<100 pg/ml) makes a cardiac cause very unlikely and is associated with non-cardiogenic pulmonary edema.[1]

Oxygen Saturation

Low oxygen saturation or hypoxia may be present on arterial blood gas readings.

Chest X Ray

Pulmonary edema
Pulmonary edema

The diagnosis is confirmed on X-ray of the lungs, which shows increased fluid in the alveolar walls. Kerley B lines, increased vascular filling, pleural effusions, upper lobe diversion (increased blood flow to the higher parts of the lung) may be indicative of cardiogenic pulmonary edema, while patchy alveolar infiltrates with air bronchograms are more indicative of noncardiogenic edema[1]

Echocardiography

Echocardiography is useful in confirming a cardiac or no-cardiac cause of pulmonary edema. Among cardiac causes, echocardiography can identify if systolic or diastolic dysfunction is present. Echocardiography is useful in identify if focal segment wall motion abnormalities are present which would suggest ischemia or myocardial infarction as an underlying cause. If there is a global impairment of left ventricular function, then this suggests a cardiomyopathy may be present. Echocardiography may identify the presence and severity of valvular causes of pulmonary edema including aortic stenosis, aortic insufficiency, mitral stenosis. mitral insufficiency, and hypertrophic cardiomyopathy.

Cardiac Catheterization

Insertion of a pulmonary arterial catheter (a.k.a. a Swan-Ganz catheter) may be required to distinguish between the two main forms of pulmonary edema and to help guide management[1]. In patients with cardiogenic pulmonary edema the pulmonary artery pressure will be elevated. Among patients with non-cardiogenic pulmonary edema the wedge pressure will not be elevated.

Treatment

See also the chapter on congestive heart failure.

Acute Pulmonary Edema

In patients with acute pulmonary edema, the goal is to reduce both preload and afterload and to diurese the patient. Intravenous nitroglycerin can be used to reduce both the preload and afterload. Diuretics such as furosemide or bumetanide can be used to reduce volume overload. The dose that the patient is on chronically should be doubled and administered intravenously in the setting of flash pulmonary edema. Morphine sulfate may be helpful in reducing the drive to breathe, improving patient comfort, and reducing the preload.

Oxygen therapy is required to minimize cyanosis and to maintain adequate oxygenation. High-flow oxygen, noninvasive ventilation (either continuous positive airway pressure (CPAP) or variable positive airway pressure (VPAP) may be effective[3][4]). If the simple measures are not effective then mechanical ventilation may be required.

Treatment should also be directed at managing the underlying cause of an episode of acute pulmonary edema. This would include managing as acute myocardial infarction, mitral regurgitation, aortic regurgitation, or any other condition that causes an increase in left ventricular filling pressures.

Chronic Pulmonary Edema

Reoccurrence of FPE is thought to be associated with hypertension[5] and may signify renal artery stenosis.[6] Prevention of reoccurrence is based on managing hypertension, coronary artery disease, renovascular hypertension, and heart failure.

References

  1. 1.0 1.1 1.2 1.3 1.4 Ware LB, Matthay MA. Acute pulmonary edema. N Engl J Med 2005;353:2788-96. PMID 16382065.
  2. M Bates. "High altitude pulmonary edema". Apex (Altitude Physiology Expeditions). Retrieved 2007-03-06.
  3. Masip J, Roque M, Sanchez B, Fernandez R, Subirana M, Exposito JA. Noninvasive ventilation in acute cardiogenic pulmonary edema: systematic review and meta-analysis. JAMA 2005;294:3124-30. PMID 16380593.
  4. Peter JV, Moran JL, Phillips-Hughes J, Graham P, Bersten AD. Effect of non-invasive positive pressure ventilation (NIPPV) on mortality in patients with acute cardiogenic pulmonary oedema: a meta-analysis. Lancet 2006;367(9517):1155-63. PMID 16616558.
  5. Kramer K, Kirkman P, Kitzman D, Little WC. Flash pulmonary edema: association with hypertension and reoccurrence despite coronary revascularization. Am Heart J. 2000 Sep;140(3):451-5. PMID 10966547.
  6. Pickering TG, Herman L, Devereux RB, Sotelo JE, James GD, Sos TA, Silane MF, Laragh JH. Recurrent pulmonary oedema in hypertension due to bilateral renal artery stenosis: treatment by angioplasty or surgical revascularisation. Lancet 1988;2(8610):551-2. PMID 2900930.

See also

Template:Respiratory pathology

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