THE ACID-BASE STATUS IN CYANOTIC CONGENITAL HEART DISEASE.
The relation between oxygen consumption, metabolic status and prognosis was studied in two infants with identically low arterial oxygen tensions (20 mm. Hg) due to cyanotic congenital heart disease. The first patient had low oxygen consumption, arterial blood acidosis and increased arterial lactate, and died at the age of 36 hours. The second had normal oxygen consumption, arterial acid-base balance, lactate and pyruvate, and survived. Since arterial oxygen tensions were similar in both, it was concluded that compensatory factors, such as cardiac output, pulmonary and systemic blood flow and increased oxygen saturation at normal pH levels (Bohr effect), are important in maintaining tissue oxidation and preventing anaerobiosis and lactate production. The importance of a knowledge of acid-base status in the immediate prognosis of cyanotic congenital heart disease is stressed. The treatment of acidosis by buffer therapy may be an important palliative, improving cardiac output and tissue oxidation, and should be undertaken as soon as possible before irreversible cellular damage has occurred.
D000136:Acid-Base Equilibrium; D000138:Acidosis; D001784:Blood Gas Analysis; D002302:Cardiac Output; D006330:Heart Defects, Congenital; D006801:Humans; D000860:Hypoxia; D007223:Infant; D007231:Infant, Newborn; D007773:Lactates; D019344:Lactic Acid; D008660:Metabolism; D010101:Oxygen Consumption; D011379:Prognosis; D011773:Pyruvates; D019289:Pyruvic Acid
D007773:Lactates; D011773:Pyruvates; D019344:Lactic Acid; D019289:Pyruvic Acid
ACID-BASE EQUILIBRIUM; ACIDOSIS; HEART DEFECTS, CONGENITAL; INFANT, NEWBORN; LACTATES; METABOLISM; PROGNOSIS; PYRUVATES