Pulmonary Edema

Lymphatics course along with vessels and play a role in draining the interstitial fluid.

The lung receives 300,000 cc’s of fluid per hour. Lymph flow out of the lungs is ~ 10-20 cc’s/hr.

Normally the alveolar gas is separated from the capillary blood by the alveolar-capillary membrane. 95% of the membrane is made up of type I alveolar cells the other 5% by type II.

Alveolar epithelium consists of type I cells that are joined by Tight Junctions which are essentially impermeable to water, solutes, and protein. The Capillary endothelium is "loose" and lets in water and solute, but no protein.

Sequence of fluid formation in pulmonary edema

Movement of fluid into interstitium exceeds the lymphatics ability to clear it. First, interstitial edema is seen in the loose interstitial space around the blood vessels and small airways. CXR may reveal peribronchial cuffing and Kerley B lines (see below). The second stage of fluid accumulation is edema of the interstitial space of the alveolar wall. This stage is associated with perihilar haziness and blurring of the normally sharp hilar vessels. Finally, alveolar flooding with edema fluid occurs and the typical "ground glass" infiltrate of pulmonary edema is seen radiographically.

Pulmonary edema can result from 2 processes.

(1) High Pressure or "Cardiogenic" pulmonary edema

Attributed to increased hydrostatic pressure. Fluid accumulation can be accounted for by Starling’s law.

Causes include: Left-sided heart failure, mitral stenosis, volume overload, pulmonary vein obstruction, ß oncotic pressure, hypoalbuminemia, nephrotic syndrome, liver disease, protein-losing enteropathies, lymphatic obstruction.

Clinically Cardiogenic pulmonary edema has

Slow onset, [protein] in edema fluid < [protein] in plasma

symptoms of cough, dyspnea, wheezing, and intense anxiety.

ß gas exchange: ß PaO₂ because of V/Q mismatch (shunt if really bad), ß PaCO₂ because of vagal stimulation (C-fibers)

ß compliance, Ý airway resistance, and Ý work of breathing

spirometry reveals restrictive changes (normal to Ý FEV₁/FVC)

CXR: pulmonary venous distention, perivascular edema, Kerley B lines, alveolar edema

Kerley B lines (a.k.a. costophrenic septal lines) – fine horizontal line's a few cm above the costophrenic angle in the CXR thought to be due to distention of interlobular lymphatics with edema fluid. Corresponds to widened interlobular septa.

Treatment of Cardiogenic pulmonary edema – give O₂to maintain pO₂, ß pulmonary capillary pressure by Ý LV function (dobutamine) and ß afterload with diuretics.

(2) Increased Permeability or "non-cardiogenic" pulmonary edema

Attributed to injury to the capillaries of the alveolar septa. Hydrostatic forces play a secondary role.

Causes include: Infectious agents, Inhaled gases (O₂, SO₂, CN, smoke), Liquid aspirations (near drowning), Drugs and Chemicals (heroin, bleomycin, amphotericin B), Shock, Trauma, Sepsis, Pancreatitis, Micro-emboli, and Radiation.

Clinically non-cardiac pulmonary edema has

sudden onset with rapid accumulation of fluid, [protein] in edema fluid ~ [protein] in plasma

ß lung compliance Þ ß lung volumes

often high V/Q mismatch (patients rarely present with hypercapnia because they hyperventilate)

ARDS – Adult Respiratory Distress Syndrome

Histologically demonstrates diffuse alveolar damage with Ý in alveolar capillary permeability causing leakage of protein rich fluid into the alveoli.

Type II epithelial cells undergo proliferation in an attempt to regenerate the alveolar lining.

Marked by the formation of an intra-alveolar hyaline membrane composed of fibrin and cellular debris.

Results in severe impairment of gas exchange with consequent severe hypoxia.

The capillary defect in ARDS is believed to be produced by an interaction of leukocytes and cytokines, O₂ radicals, complement, and eicosanoids that damages the endothelium and allows fluid and proteins to leak across it.

Three phases:

(1) Exudative – days 1-7, alveolar and interstitial edema, necrosis, and hyalinization

(2) Proliferative – days 7-20, increase in type II cells

(3) Fibrotic – > day 20, infiltration of the alveolar septa with fibroblasts leading to considerable fibrosis

Treatment of ARDS – treat underlying cause and support with mechanical ventilation, support hemodynamics, and prone position (improves V/Q mismatch). 50% of patients with ARDS survive. Most survivors are asymptomatic at 6 months.

Differentiation of Cardiogenic Edema from ARDS

Right heart catheterization	Cardiogenic	ARDS
Pressure R atrium	Ý	«
Pressure R ventricle	Ý	«
Pulmonary artery pressure	Ý	«
Wedge pressure	Ý Ý	«
Systemic vascular resistance	Ý	ß