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Pulmonary Vascular Diseases

Pulmonary Edema

Pulmonary edema is swelling and/or fluid accumulation in the lungs. It leads to impaired gas exchange and may cause respiratory failure. It is due to either failure of the heart to remove fluid from the lung circulation, or due to a direct insult to the lung parenchyma. Treatment depends on the cause, but focuses on maximizing respiratory function and removing the cause.


Signs and symptoms

Symptoms of pulmonary edema include difficulty breathing, coughing up blood, excessive sweating, anxiety and pale skin. If left untreated, it can lead to coma and even death, generally due to its main complication of hypoxia.

If pulmonary edema has been developing gradually, symptoms of fluid overload may be elicited. These include nocturia (frequent urination at night), ankle edema (swelling of the legs, generally of the “pitting” variety), orthopnea (inability to lie down flat due to breathlessness) and paroxysmal nocturnal dyspnea (episodes of severe sudden breathlessness at night).



Pulmonary edema is generally suspected due to findings in the medical history of a patient, such as previous cardiovascular disease, and physical examination: end-inspiratory crackles (sounds heard at the end of a deep breath) on auscultation (listening to the breathing through a stethoscope) are characteristic for pulmonary edema. The presence of a third heart sound (S3) is predictive of cardiogenic pulmonary edema.


Blood tests are generally performed for electrolytes (sodium, potassium) and markers of renal function (creatinine, urea). Liver enzymes, inflammatory markers (usually C-reactive protein) and a complete blood count, as well as coagulation studies (PT, aPTT) are typically requested. B-type natriuretic peptide (BNP) is available in many hospitals, especially in the US, sometimes even as a point-of-care test. Low levels of BNP (<100 pg/ml) make a cardiac cause very unlikely.


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.


Low oxygen saturation and disturbed arterial blood gas readings may strengthen the diagnosis and provide grounds for various forms of treatment. If urgent echocardiography is available, this may strengthen the diagnosis, as well as identify valvular heart disease. In rare occasions, insertion of a Swan-Ganz catheter may be required to distinguish between the two main forms of pulmonary edema.



Pulmonary edema is either due to direct damage to the tissue or as a result of inadequate functioning of the heart or circulatory system.



• Congestive heart failure
• Severe heart attack with left ventricular failure
• Severe arrhythmias (tachycardia/fast heartbeat or bradycardia/slow heartbeat)
• Hypertensive crisis
• Pericardial effusion with tamponade
• Fluid overload, e.g. from kidney failure



This form is contiguous with ARDS (acute respiratory distress syndrome):
• Inhalation of toxic gases
• Multiple blood transfusions
• Severe infection
• Pulmonary contusion, i.e. high-energy trauma
• Multitrauma, e.g. severe car accident
• Neurogenic, e.g. subarachnoid hemorrhage
• Aspiration, e.g. gastric fluid or in case of drowning
• Certain types of medication
• Upper airway obstruction
• Reexpansion, i.e. postpneumonectomy or large volume thoracentesis
• Reperfusion injury, i.e. postpulmonary thromboendartectomy or lung transplantation
• Ascent to high altitude occasionally causes high altitude pulmonary edema (HAPE)



Focus is initially on maintaining adequate oxygenation. This may happen with high-flow oxygen, noninvasive ventilation (either continuous positive airway pressure (CPAP) or variable positive airway pressure (VPAP) or mechanical ventilation in extreme cases.


When circulatory causes have led to pulmonary edema, treatment with intravenous nitrates (glyceryl trinitrate), and loop diuretics, such as furosemide or bumetanide, is the mainstay of therapy. These improve both preload and afterload, and aid in improving cardiac function.


There are no causal therapies for direct tissue damage; removal of the causes (e.g. treating an infection) is the most important measure.

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