Pulmonary Edema

The pulmonary edema is the accumulation of excess fluid in the extravascular space of the lungs. This accumulation can slowly occur in patients with renal insufficiency or abruptly on patients with heart insufficiency to myocardial infarction. The pulmonary edema presents itself usually as dyspnea. In severe cases the pulmonary edema may present also edema liquid on the phlegm, leading to acute respiratory insufficiency.

Etiology

Causes of pulmonary edema:

Transmural increased pulmonary capilary wedge pressure (increased hydrostatic pressure): Increased left atrial pressure, pulmonary venous hypertension, increased capillary blood volume, decreased interstitial pressure, reduced colloid osmotic pressure (hypoalbuminemia due to nephrotic syndrome and liver failure).

Permeability of increased pulmonary capillary endothelium: Circulatin toxins, infectious pneumonia, pulmonary edema due to the high altitude after pulmonary bypass.

Increased permeability of the alveolar epithelium: Inhaled toxins, aspiration of gastric contents, drowning or near drowning, decreased surfactant.

Decreased lymphatic drainage.

Phatophysiology

A problem in one or more of the following factors: The capillary or alveolar endothelial permeability and the colloid osmotic and hydrostatic pressure are related to almost every clinic presentations of pulmonary edema.

In clinical practice these four factors are grouped into two types of pulmonary edema:

 - Cardiogenic pulmonary edema related to edema resulting from increased hydrostatic or osmotic pressure.

 - Noncardiogenic pulmonary edema  related to edema resulting from changes in the endothelium and alveolar capillary permeability. This edema it’s often known as Adult Respiratory Distress Syndrome (ARDS). The alveolar liquid that accumulates as result of lost of integrity of alveolar epithelium allows that solutes and large molecules (as albumin) entering the alveolar spaces. These changes can result from the injury of the alveolar epithelium by inhaled toxins or by pulmonary infection or even by changes that occur after a primary injury of the endothelium by circulating toxins. The circulating factors may act directly on capillary endothelium or may affect it by immune mediators. For example in infections by Gram bacteria the bacterial endotoxins cause the adherence of neutrophils and macrophages to endothelial surfaces that also cause the release of prostaglandins, thromboxanes and leukotrienes as oxygen radicals that cause oxidative injury. Both neutrophils and macrophages can release proteolytic enzymes that cause more damage.

Clinical manifestations

There are two types of pulmonary edema that cause an increase of the extravascular liquid in the lung and both can lead to respiratory insufficiency.