Page 90 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Pulmonary Edema
In pulmonary capillaries, as in systemic capil- example, inhalation of corrosive gases or pro-
laries, filtration is determined by the effective longed inspiration of pure O 2 (→ p. 84).
filtration pressure, i.e., the difference between Effects of pulmonary congestion are re-
the hydrostatic and oncotic pressure gradients. duced pulmonary perfusion, and thus im-
An increase in effective filtration pressure in paired maximal O 2 uptake. The distension of
the pulmonary vessels leads to pulmonary the congested vessels prevents enlargement
congestion, filtration of plasma water into the of the alveoli and decreases lung compliance.
interstitial space results in interstitial pulmo- In addition, the bronchi are narrowed by the
Acid–Base Balance into alveoli causes alveolar pulmonary edema increases (→ p. 76), discernable through dim-
nary edema, and the passage of plasma water
distended vessels and resistance to breathing
(→ A, middle).
inution of the maximal breathing capacity
and of FEV 1 (→ table 2 on p. 66).
A rise in hydrostatic pressure in the pul-
In interstitial pulmonary edema the inter-
monary capillaries occurs when the left ventri-
cle’s forward pumping action is inadequate
stitial space between capillary and alveolus is
increased. As a result, diffusion is disturbed
(→ A, right). Causes are reduced myocardial
Respiration, power or excess demand on it (heart failure; with impairment mainly of O 2 uptake (→
p. 70). If, due to physical activity, O 2 consump-
→ p. 224), mitral valve stenosis or regurgita-
tion rises, O 2 concentration in blood falls (hyp-
tion (→ p.194ff.). The resulting increase in left
oxemia, cyanosis; → A, bottom).
atrial pressure is transmitted backward into
Any further pressure increase and damage
The development of pulmonary edema is fa-
4 the pulmonary vessels. to the alveolar wall causes the passage of fil-
cilitated by abnormal lymphatic drainage trate into the alveolar space. The fluid-filled
(→ A, left). Normally, an excess of filtered fluid alveoli are no longer involved in breathing
is removed via the lymphatics. However, the (gaseous exchange) and a functional venoar-
capacity of the pulmonary lymphatic system terial (pulmonary arterial to pulmonary ve-
is low even under physiological conditions. If nous) shunt occurs along with a decrease in
right heart failure occurs together with left O 2 in the systemic arterial blood (central cya-
heart failure, the systemic venous pressure nosis). Fluid enters the airways and thus also
rises and thus also the pressure at the point of increases airway resistance. Increased filtra-
drainage of the lymphatic vessels into the tion of fluid into the pleural space (pleural ef-
veins at the venous angle, so impairing lym- fusion) also impairs breathing.
phatic drainage. Pulmonary edemas force the patient to
The oncotic pressure in the capillaries is re- breathe in the upright position (orthopnea).
duced by hypoproteinemia (→ A, left), favoring On sitting or standing up after being recum-
the development of pulmonary edema. Hypo- bent (orthostasis) venous return from the low-
proteinemia is usually the result of hyperhy- er part of the body falls (even more in the fully
dration, for example, an inappropriately high upright position), and thus right atrial pres-
supply of fluids to patients with reduced renal sure and the right cardiac output decrease.
excretion (e.g., due to renal failure; → Less blood flows through the lungs, causing a
p.110ff.). A reduction in plasma protein forma- fall in hydrostatic pressure in the pulmonary
tion in the liver (liver failure; → p.174) or loss capillaries at the same time that pulmonary
of plasma proteins, for example, via the kid- venous flow from the upper parts of the lung
neys (nephrotic syndrome; → p.104), also de- is increased. Moreover, the decrease of central
creases plasma protein concentration. venous pressure facilitates lymphatic drainage
Finally, increased capillary permeability can from the lung. As a result, pulmonary conges-
result in pulmonary edema (→ A, right). In- tion as well as interstitial and alveolar edemas
creased permeability of the capillary wall for regress.
proteins reduces the oncotic pressure gradient
80 and thus increases the effective filtration pres-
sure. Capillary permeability is increased by, for
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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