It is our red blood cells that are responsible for carrying oxygen to our tissues. We constantly use this oxygen as our main source of energy. A molecule within the erythrocytes (red blood cells) called hemoglobin, causes oxygen molecules to adhere to it, which are then carried throughout our bodies and distributed by the circulating blood. Therefore, when there is shortage of blood or shortage of hemoglobin (anemia) structures to ‘capture’ the surrounding oxygen, we are deprived of the ability to distribute oxygen inhaled by our lungs, to all our tissues. This occurs for instance in atherosclerotic processes in the coronary artery, where due to buildup of plaque within the artery lumen, there is insufficient blood being supplied to the cardiac muscle, resulting in infarction. This scenario, where a particular organ is not receiving adequate amounts of blood/oxygen, is called ischemia. When our organs are denied oxygen, they are said to be in a hypoxic state.

Our bodies have mechanisms to attempt to normalize oxygen levels. We have all experienced some of these forms of compensation: deep breaths for greater oxygen intake, an increase in inhalation/exhalation frequency, a rise in systolic pressure to pump more oxygen carrying erythrocytes into circulation.  Vasodilation helps make the ‘highways’ through which blood circulates broader for more blood cells to fit as it passes through and into tissue. These changes occur within the body quite rapidly and are a very important defense mechanism against hypoxia.

If oxygen is manageably low, brain stem chemoreceptors send a signal to the brain causing a reflexive reaction that causes a rise in the number of breaths we take. This action becomes even more dramatic when carbon dioxide levels rise as oxygen levels diminish, if breathing becomes too rapid it is known as hyperventilation. The important takeaway here is how chemoreceptors located in the brain measure levels of oxygen versus carbon dioxide and how they signal to our brain to make necessary adjustments to ensure proper breathing, adequate oxygen saturation along with the synchronized expulsion of carbon dioxide as we exhale.

If mild hypoxia persists chronically, the body will compensate via hematopoiesis in the bone marrow. Hematopoiesis is the process by which we produce more blood elements. Therefore, it is not uncommon for chronically hypoxic patients to have polycythemia which is an increase in the number of red blood cells and a higher concentration of hemoglobin, resulting in a   denser or thicker blood. The drawback of this reaction to hypoxia is that it forces the cardiac muscle to pump harder since thick blood is more difficult to circulate.

All self-activating mechanisms are obviously extremely important to maintain proper gas saturation levels. In extreme or poorly managed hypoxia however, the body is unable to adequately compensate and blood pressure dips, respiratory failure ensues and cardiac arrest is imminent.

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