Pulmonary edema overview
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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
- Severe 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 kidney failure
- Gastric content aspiration
- Goodpasture's Syndrome
- High altitude sickness. Ascent to high altitude occasionally causes high altitude pulmonary edema (HAPE)[2]
- 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
- Multitrauma, 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.
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[1]
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
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.
References
- ↑ 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.
- ↑ M Bates. "High altitude pulmonary edema". Apex (Altitude Physiology Expeditions). Retrieved 2007-03-06.
- ↑ 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.
- ↑ 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.