'Barrel chest'

|— B. Development of Barrel Chest in Emphysema

Pulmonary Edema

In pulmonary capillaries, as in systemic capillaries, filtration is determined by the effective filtration pressure, i.e., the difference between the hydrostatic and oncotic pressure gradients. An increase in effective filtration pressure in the pulmonary vessels leads to pulmonary congestion, filtration of plasma water into the e interstitial space results in interstitial pulmo-nc nary edema, and the passage of plasma water ala into alveoli causes alveolar pulmonary edema oa A, middle).

ase A rise in hydrostatic pressure in the pul-03 monary capillaries occurs when the left ventri-3 cle's forward pumping action is inadequate < (^A, right). Causes are reduced myocardial c power or excess demand on it (heart failure;

^ p. 224), mitral valve stenosis or regurgita-2 tion (^ p. 194 ff.). The resulting increase in left & atrial pressure is transmitted backward into ai the pulmonary vessels.

f The developmentof pulmonary edema is facilitated by abnormal lymphatic drainage (^ A, left). Normally, an excess of filtered fluid is removed via the lymphatics. However, the capacity of the pulmonary lymphatic system is low even under physiological conditions. If right heart failure occurs together with left heart failure, the systemic venous pressure rises and thus also the pressure at the point of drainage of the lymphatic vessels into the veins at the venous angle, so impairing lymphatic drainage.

The oncotic pressure in the capillaries is reduced by hypoproteinemia (^ A, left), favoring the development of pulmonary edema. Hypo-proteinemia is usually the result of hyperhy-dration, for example, an inappropriately high supply of fluids to patients with reduced renal excretion (e.g., due to renal failure; ^ p. 110 ff.). A reduction in plasma protein formation in the liver (liver failure; ^ p. 174) or loss of plasma proteins, for example, via the kidneys (nephrotic syndrome; ^ p. 104), also decreases plasma protein concentration.

Finally, increased capillary permeability can result in pulmonary edema (^A, right). Increased permeability of the capillary wall for proteins reduces the oncotic pressure gradient 80 and thus increases the effective filtration pressure. Capillary permeability is increased by, for example, inhalation of corrosive gases or prolonged inspiration of pure O2 (^ p. 84).

Effects of pulmonary congestion are reduced pulmonary perfusion, and thus impaired maximal O2 uptake. The distension of the congested vessels prevents enlargement of the alveoli and decreases lung compliance. In addition, the bronchi are narrowed by the distended vessels and resistance to breathing increases (^ p. 76), discernable through diminution of the maximal breathing capacity and of FEV, (^ table 2 on p. 66).

In interstitial pulmonary edema the interstitial space between capillary and alveolus is increased. As a result, diffusion is disturbed with impairment mainly of O2 uptake (^ p. 70). If, due to physical activity, O2 consumption rises, O2 concentration in blood falls (hyp-oxemia, cyanosis; ^ A, bottom).

Any further pressure increase and damage to the alveolar wall causes the passage of filtrate into the alveolar space. The fluid-filled alveoli are no longer involved in breathing (gaseous exchange) and a functional venoar-terial (pulmonary arterial to pulmonary venous) shunt occurs along with a decrease in O2 in the systemic arterial blood (central cyanosis). Fluid enters the airways and thus also increases airway resistance. Increased filtration of fluid into the pleural space (pleural effusion) also impairs breathing.

Pulmonary edemas force the patient to breathe in the upright position (orthopnea). On sitting or standing up after being recumbent (orthostasis) venous return from the lower part of the body falls (even more in the fully upright position), and thus right atrial pressure and the right cardiac output decrease. Less blood flows through the lungs, causing a fall in hydrostatic pressure in the pulmonary capillaries at the same time that pulmonary venous flow from the upper parts of the lung is increased. Moreover, the decrease of central venous pressure facilitates lymphatic drainage from the lung. As a result, pulmonary congestion as well as interstitial and alveolar edemas regress.

Capillary e.g. Hyperinfusion


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