Chronic hypoxia in an infant with a cyanotic congenital heart defect most likely results in which condition?

Chronic hypoxia in an infant with a cyanotic congenital heart defect leads to polycythemia as a compensatory mechanism. When the body senses low levels of oxygen (hypoxia), it strives to increase the oxygen-carrying capacity of the blood. This is primarily achieved by stimulating the production of red blood cells in the bone marrow. The increase in red blood cells is an adaptation intended to enhance oxygen delivery to tissues that are not receiving sufficient oxygen due to the heart defect.

In the context of cyanotic congenital heart defects, where there's a right-to-left shunt, deoxygenated blood mixes with oxygenated blood, resulting in a reduced oxygen saturation in the systemic circulation. As a consequence of ongoing hypoxia, erythropoietin (a hormone produced by the kidneys) is secreted in greater amounts, promoting the production of more red blood cells, which leads to increased hematocrit levels.

Understanding the physiological response to chronic hypoxia clarifies why polycythemia is the most likely outcome in these infants. This condition can contribute to increased blood viscosity and may have further implications for the child's health, but it fundamentally stems from the body’s compensatory response to sustained low oxygen levels.