الفهرس 
Functional Anatomy of the Alveolar-Capillary InterfaceOnly 14 pages are availabe for public view
 |  | from | 250 |  |  |
| | | from | 250 | | |
Abstract
A
cute pulmonary edema is defined as fluid accumulation in the lungs that leads to dyspnea, respiratory failure and even death, so that it requires immediate intervention and emergency treatment.
The lung surface is formed of two types of epithelium; airway epithelium and alveolar epithelium. Airway epithelium is present in all surface epithelia of the conducting airways. It’s composed of different cell types; mainly ciliated cells, Clara cells, undifferentiated basal cells, and goblet cells. These cells are responsible for the transport of inhaled particles and the mucous layer and secrete some ions and proteins. The main function of the alveolar epithelium is efficient gas and water exchange through the thin side and thick side of the alveolar capillary membrane. It also has a role in immune defense responses in the lung by having alveolar type I (ATI) and type II (ATII) Cells.
Acute pulmonary edema is mainly classified into two types: cardiogenic and noncardiogenic pulmonary edema. Cardiogenic pulmonary edema results from increased pulmonary capillary hydrostatic pressures which occur mainly due to a cardiac problem like left ventricular dysfunction; with or without additional cardiac pathology, such as coronary artery disease or valve abnormalities. However, a variety of conditions result in cardiogenic pulmonary edema in the absence of heart disease. These include primary fluid overload; excessive blood transfusion, severe hypertension, renal artery stenosis, and severe renal disease.
Non-cardiogenic pulmonary edema or high permeability edema occurs due to injury of the alveolar-capillary barrier with leakage of protein-rich fluid into the interstitium and air spaces, in the absence of elevated pulmonary capillary wedge pressure. It usually occurs with acute respiratory distress syndrome and acute lung injury. There are other less common types of noncardiogenic pulmonary edema. The most important are: high altitude pulmonary edema, neurogenic pulmonary edema, pulmonary edema in pregnancy and negative pressure pulmonary edema.
Diagnosis of acute pulmonary edema depends on: history taking to identify any underlying cause, symptoms and signs like dyspnea, orthopnea, fatigue, hypo-or hypertension, and detection of any abnormalities in lung and heart examination. Diagnosis depends also on laboratory testing such as plasma levels of brain natriuretic peptide (BNP), arterial blood gas analysis, complete blood count and serum electrolyte measurements. Radiological examination by chest X-ray, CT scanning and echocardiography and pulmonary artery catheterization are other tools of diagnosis.
Pulmonary edema should be differentiated from other causes of dyspnea such as: pneumonia, sepsis, shock, multiple transfusions, acute pancreatitis, anaphylactic shock, myocardial ischemia, pneumothorax, pulmonary embolism, respiratory failure, acute coronary syndrome, bronchial asthma and chronic obstructive pulmonary disease.
Treatment of acute pulmonary edema includes acute management to maintain patient’s life through respiratory and cardiovascular resuscitation. Respiratory support is achieved by oxygen supply up to mechanical ventilation after assessment of breathing. The blood pressure may need to be supported with medications until respiratory status improves. When the condition of the patient is stabilized, the underlying cause is assessed and treated.
Treatment of cardiogenic pulmonary edema includes reduction of preload and afterload and inotropic support as indicated. Insertion of intra-aortic balloon pump or ultrafiltration may help in some cases. Noninvasive pressure support ventilation may be needed.
Treatment of noncardiogenic pulmonary edema is directed to the cause with proper respiratory support. In acute respiratory distress syndrome, treatment is mainly invasive mechanical ventilation with low tidal volumes, permissive hypercapnea, proper PEEP values and the use of the least FiO2 which maintains good oxygenation. Different modes of ventilation can be used in resistant patients. Extracorporeal membrane oxygenator, intravenacaval (intravascular) oxygenator and nitric oxide inhalation may be used.
Treatment of neurogenic pulmonary edema, pulmonary edema with pregnancy and high altitude pulmonary edema is mainly supportive and symptomatic. Warmth, hyperbaric oxygen with gradual descent may help in high altitude pulmonary edema.
Prognosis of the patient depends on the cause of pulmonary edema, duration of the attack and efficiency of treatment. After subsidence of the attack, changing job duties to those with less physical activities and less emotionally stressful responsibilities should occur.