The term Stagnant Tissue Hypoxia is preferred over Stagnant Hypoxia to avoid ambiguity when the tissue but not the arterial blood is hypoxic. This occurs when the flow of blood to the tissue is low or stagnant. Some people will also refer to this condition as hypoxia ignoring the distinction between arterial blood and the tissue or capillaries. Some people might consider it a given assumption that Stagnant Hypoxia applies to the tissue but the term Stagnant Tissue Hypoxia makes it clear and is better. Some authors use terms such as Hypoxic Hypoxia which a strange way to describe whatever it describes. In some cases, hypoxia of the tissue is due to hypoxia of the arterial blood. This is probably what hypoxic hypoxia refers to most of the time.
When the capillary blood becomes stagnant as in having poor flow below the resistance arterioles the tissue can become hypoxic even when the arterial blood is not. This can happen in some vascular beds but not others. It occurs more in tissues where the metabolic requirements are high such as the muscle. In such tissues, flow is required to replenish the oxygen being consumed. When the flow is low the oxygen can become depleted. In some tissues such as skin and bone metabolic requirements are low and hypoxia of these tissues will be less dependent on the flow of blood to them.
Stagnant tissue hypoxia causes anaerobic metabolism leading to the accumulation of lactic acid. That is in a practical sense the only way we know that this hypoxic condition of stagnant blood exists. Measuring blood flow showing that it is impaired at the capillary or even arteriolar level is essentially impossible, at least in vivo in humans. This is theoretically what Stagnant Tissue Hypoxia implies but as this cannot be measured, we identify stagnate tissue hypoxia because of anaerobic metabolism and the accumulation of lactic acid. This is a diagnosis made by exclusion. If the arterial blood is not hypoxic and there is no poisoning such as cyanide then anaerobic metabolism is likely due to stagnant tissue hypoxia. Sepsis is an example of this.
Anaerobic metabolism frequently develops as a result of intense physical exertion which occurs commonly in athletes. This creates a metabolic acidosis the same as does stagnant tissue hypoxia from illness. This is a demand versus supply problem. When aerobic metabolism does not keep up with the demand for oxygen and energy is needed in the short term anaerobic metabolism supplements the need while producing lactic acid in the process. With intense physical exertion the balance is shifted by the high demand. With Stagnant Tissue Hypoxia the limited delivery of oxygen shifts the balance and the result is the same. There is accumulation of lactic acid and the development of an acidemia.
Supplemental energy is provided when the need for energy exceeds that which the aerobic metabolism of the mitochondria can supply. This anaerobic metabolism adds to but does not replace the energy from aerobic metabolism. Exercise physiologists like to refer to anaerobic metabolism and anaerobic exercise and aerobic metabolism and aerobic exercise as if it were one or the other but this is never the case. Both mechanisms exist all the time. With intense exertion there is the production of lactic acid but we do not shift into anaerobic exercise as if anaerobic metabolism were the only process of energy production.
1. Arterial Hypoxemia – The blood coming from the aorta has a low PaO2*. Arterial Hypoxia results from disease in the lungs or the airways. Stagnant tissue hypoxia is not a disease of the lungs and not it a problem of airway obstruction. It is a vascular or circulatory problem affecting the flow and distribution of blood to the tissues.
2. Anemia – The blood has an inadequate amount of hemoglobin which lowers the oxygen content of the blood. Both Arterial Hypoxemia (low PaO2) and Anemia (low hemoglobin) result in arterial blood that is lacking in oxygen content. This limits the distribution of oxygen and can result in tissue hypoxia even with normal blood flow.
3. Shock – Shock is often stated as inadequate perfusion of the tissues but the term shock is thoroughly ingrained in the concept of low blood pressure measured in a peripheral location such as the brachial artery. Hypotension is almost always labeled shock when the peripheral blood pressure is low enough. In theory shock is perfusion, not just blood pressure but the use of the term in this way is so common that shock strictly in terms of blood pressure is the de facto use of the term. Blood pressure beyond the resistance arterioles could be used to determine flow to the tissues but is impossible to measure blood flow at this level. The resistance to flow is equally important to flow as is the pressure driving flow. It is common to assume that the resistance between the brachial artery and capillary bed is is normal but we cannot actually know. It is unknown. The presence of lactic acidosis means that tissue perfusion is inadequate but the peripheral blood pressure could well be normal even elevated. Many people consciously or subconsciously believe that perfusion depends on a blood pressure that they can measure in the brachial artery and not on a blood pressure they can’t measure in the capillary bed. This ignores the effect of resistance. It is extremely difficult for the first providers in emergency situations doing the best they can with limited information in difficult situations to not operate with anything but the erroneous assumption that peripheral blood pressure equals perfusion. It is understandable how this technically erroneous concept must be used in emergency situations particularly outside the hospital. Stagnant tissue hypoxia is useful as a different term because shock in not blood pressure but so frequently used that way.
4 Histotoxic hypoxia – This is when the cellular utilization of oxygen is poisoned by a substance such as cyanide. This causes aerobic metabolism to fail and leads to anaerobic metabolism and the accumulation of lactic acid. This is very difficult to distinguish histotoxic hypoxia from stagnate tissue hypoxia except when a tissue toxin like cyanide is identified. In most clinical situations it is safe to assume that cyanide toxicity is not likely and we don’t usually need to test for the presence of cyanide. Forensic investigators might have to consider the possibly of cyanide poisoning. There are other toxins that could be mentioned as poisoning the use of oxygen by mitochondria but cyanide toxicity is the purest example.
Stagnant Tissue Hypoxia is caused by the impaired circulation of blood in the terminal arterioles and capillaries. It is important to understand that this can happen when the peripheral blood pressure in normal or high or even very high. Some clinicians believe that if the blood pressure is extremely high, blood flow to tissues cannot be impaired. This is not true. When blood pressure is extremely high and perfusion is impaired because resistance is also extremely high the situation is usually labeled flash pulmonary edema. This is a situation where a cardiovascular disease has a pulmonary name.
Even though this is a cardiovascular disease, it is most often thought of and treated as a pulmonary disease. The word pulmonary edema in the syndrome known as flash “pulmonary” edema is misleading. This is a disease of circulation and flow, a cardiovascular disease. The word edema in the syndrome known as flash pulmonary “edema” is also misleading. The tachypnea of flash pulmonary edema is mostly due to compensatory hyperventilation due to metabolic acidosis and not the edema of the lungs. Both edema of the lungs and metabolic acidosis are typically present but the metabolic acidosis is primary and the edema is secondary. Most clinicians recognize edema of the lungs as contributing to tachypnea but do not suspect it as secondary and compensatory to the metabolic acidosis. Besides hypoxia and metabolic acidosis, sluggish flow in the capillaries causes edema in the lungs. The edema is the result of the disease and not the cause of the disease. The word “pulmonary” and the word “edema” in this syndrome is misleading.
The content of oxygen in arterial blood may change little with modest increases in altitude because the oxyhemoglobin dissociation curve is relatively flat at the top. Oxygen saturation changes little at the start when atmospheric pressure begins to drop. This preserves the oxygen content and hemoglobin saturation of arterial blood to a certain extent. Barometric pressure however affects the entire oxygen cascade down to the mitochondria. When oxygen is released from hemoglobin it is released into the same barometric pressure as in the lung it was when it was bound to hemoglobin. This would be reduced at altitude. Although the PaO2 of the capillary blood cannot be measured the physics of blood gases determines that barometric pressure affects it. The blood in the capillaries could have a low PaO2 because of a low barometric pressure.