Hypoxia is decreased oxygen supply to tissues. It can be caused by:
Ischemia is decreased blood flow to or from an organ. Ischemia can be caused by obstruction of arterial blood flow the most common cause, or by decreased perfusion of tissues by oxygen-carrying blood as occurs in cardiac failure, hypotension, and shock.
Anemia: Anemia is a reduction in the number of oxygen-carrying red blood cells.
Carbon monoxide poisoning: CO decreases the oxygen-capacity of red blood cells by chemical alteration of hemoglobin.
Poor oxygenation of blood due to pulmonary disease.
The cell injury that results following hypoxia can be divided into the following stages
1. Early (reversible) stages of hypoxic cell injury
At this stage, hypoxia results in decreased oxidative phosphorylation and ATP synthesis. Decreased ATP leads to: Failure of the cell membrane Na – K pump, which leads to increased intracellular Na and water, which cause cellular and organelle swelling. Cellular swelling (hydropic change) is characterized by the presence of large vacuoles in the cytoplasm.
The endoplasmic reticulum also swells. The mitochondria show a low amplitude swelling. All of the above changes are reversible if the hypoxia is corrected. This stage also can cause disaggregation of ribosomes and failure of protein synthesis.
2. Late (irreversible) stages of hypoxic cell injury.
This is caused by severe or prolonged injury. It is caused by massive calcium influx and very low pH, which lead to activation of enzymes, which damage the cell membrane and organelle membranes. Irreversible damage to the mitochondria, cell membranes, and the nucleus mark the point of no return for the cell, that is after this stage, the cell is destined to die.
Release of aspartate aminotransferase (AST), creatine phosphokinase (CPK), and lactate dehydrogenase (LDH) into the blood is an important indicator of irreversible injury to heart muscle following myocardial infarction.