TAILIEUCHUNG - Chapter 035. Hypoxia and Cyanosis (Part 2)

As one ascends rapidly to 3000 m (~10,000 ft), the reduction of the O 2 content of inspired air (FIO2) leads to a decrease in alveolar PO2 to about 60 mmHg, and a condition termed high-altitude illness develops (see above). At higher altitudes, arterial saturation declines rapidly and symptoms become more serious; and at 5000 m, unacclimatized individuals usually cease to be able to function normally. HYPOXIA SECONDARY TO RIGHT-TO-LEFT EXTRAPULMONARY SHUNTING From a physiologic viewpoint, this cause of hypoxia resembles intrapulmonary right-to-left shunting but is caused by congenital cardiac malformations such as tetralogy of Fallot, transposition of the great arteries, and Eisenmenger's syndrome (Chap | Chapter 035. Hypoxia and Cyanosis Part 2 HYPOXIA SECONDARY TO HIGH ALTITUDE As one ascends rapidly to 3000 m 10 000 ft the reduction of the O2 content of inspired air FIO2 leads to a decrease in alveolar PO2 to about 60 mmHg and a condition termed high-altitude illness develops see above . At higher altitudes arterial saturation declines rapidly and symptoms become more serious and at 5000 m unacclimatized individuals usually cease to be able to function normally. HYPOXIA SECONDARY TO RIGHT-TO-LEFT EXTRAPULMONARY SHUNTING From a physiologic viewpoint this cause of hypoxia resembles intrapulmonary right-to-left shunting but is caused by congenital cardiac malformations such as tetralogy of Fallot transposition of the great arteries and Eisenmenger s syndrome Chap. 229 . As in pulmonary right-to-left shunting the PaO2 cannot be restored to normal with inspiration of 100 O2. ANEMIC HYPOXIA A reduction in hemoglobin concentration of the blood is attended by a corresponding decline in the O2-carrying capacity of the blood. Although the PaO2 is normal in anemic hypoxia the absolute quantity of O2 transported per unit volume of blood is diminished. As the anemic blood passes through the capillaries and the usual quantity of O2 is removed from it the PO2 and saturation in the venous blood decline to a greater degree than normal. CARBON MONOXIDE CO INTOXICATION See also Chap. e34 Hemoglobin that is combined with CO carboxyhemoglobin COHb is unavailable for O2 transport. In addition the presence of COHb shifts the Hb-O2 dissociation curve to the left see Fig. 99-2 so that O2 is unloaded only at lower tensions contributing further to tissue hypoxia. CIRCULATORY HYPOXIA As in anemic hypoxia the PaO2 is usually normal but venous and tissue PO2 values are reduced as a consequence of reduced tissue perfusion and greater tissue O2 extraction. This pathophysiology leads to an increased arterial-mixed venous O2 difference or a -V gradient. Generalized circulatory hypoxia occurs in .

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