4 Respiration, Acid-Base Balance Pulmonary Edema In pulmonary capillaries, as in systemic capil- laries, filtration is determined by the effective filtration pressure, ie., 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 interstitial space results in interstitial pulmo- nary edema, and the passage of plasma water into alveoli causes alveolar pulmonary edema (GA, middle). A rise in hydrostatic pressure in the pul- monary capillaries occurs when the left ventri- cle’s forward pumping action is inadequate (A, right), Causes are reduced myocardial power or excess demand on it (heart failure; — p.224), mitral valve stenosis or regurgita- tion (— p. 194 f.). The resulting increase in left atrial pressure is transmitted backward into the pulmonary vessels. The development of pulmonary edemais fa- cilitated 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 lym- phatic drainage. The oncotic pressure in the capillaries is re- duced 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 (eg, due to renal failure; p.110ff.). A reduction in plasma protein forma- tion in the liver (liver failure; —> p. 174) or loss of plasma proteins, for example, via the kid- neys (nephrotic syndrome; — p. 104), also de- creases plasma protein concentration. Finally, increased capillary permeability can result in pulmonary edema (>A, right). In- creased permeability of the capillary wall for proteins reduces the oncotic pressure gradient and thus increases the effective filtration pres- sure. Capillary permeability is increased by, for Silbernag/Lan Color Atlas of Pathophysiology example, inhalation of corrosive gases or pro- longed inspiration of pure O, (+p. 84). Effects of pulmonary congestion are re- duced pulmonary perfusion, and thus im- paired maximal O, 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 dim- inution of the maximal breathing capacity and of FEV, (— table 2 on p. 66). In interstitial pulmonary edema the inter- stitial space between capillary and alveolus is increased. As a result, diffusion is disturbed with impairment mainly of 0, uptake (> p.70). If, due to physical activity, 0, consump- tion rises, 0, concentration in blood falls (hyp- ‘oxemia, cyanosis; > A, bottom). Any further pressure increase and damage to the alveolar wall causes the passage of fil- trate 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 ve- nous) shunt occurs along with a decrease in , in the systemic arterial blood (central cya- nosis), Fluid enters the airways and thus also increases airway resistance. Increased filtra- tion of fluid into the pleural space (pleural ef- fusion) also impairs breathing. Pulmonary edemas force the patient to breathe in the upright position (orthopnea). On sitting or standing up after being recum- bent (orthostasis) venous return from the low- er part of the body falls (even more in the fully upright position), and thus right atrial pres- sure 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 conges- tion as well as interstitial and alveolar edemas regress. © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.A. Pulmonary Edema Ef, ¢ Capillary e.g, Hyperinfusion Hypoxemia Interstitial pulmonary edema | Abnormal diffusion Narrowing of alveoli and bronchi Reduced vital capacity Orthopnea Inhalation of corrosive gas Alveolar ea edema ct | ——> Abnormal ventilation 4 Left heart failure Plate4.8 Pulmonary Edema Interstitial space Plasma water Capillary Attempt| to lower hydrostatic pressure| Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme Allrights reserved. Usage subject to terms and conditions of license.