The term Stagnant Tissue Hypoxia is more descriptive than simply Stagnate Hypoxia. The word hypoxia without a modifier commonly refers to arterial hypoxia. When the arterial blood is hypoxic the cascade of oxygen tension demonstrates that the tissue will also be hypoxic. When the capillary blood becomes stagnant as in having poor flow below the resistance arterioles the tissue can become hypoxic. To be clear the term Stagnant Tissue Hypoxia is preferred to avoid ambiguity when the tissue but not the arterial blood is hypoxic. This only happens when the resistance in the arterioles isolates the flow of blood between the arteries and the capillaries. Some authors use terms such as Hypoxic Hypoxia which is confusing and best avoided.
Stagnant Tissue Hypoxia is where the tissues are lacking oxygen not due to a low oxygen content of the arterial blood but instead because the flow of the blood to the tissues is impaired. Stagnant tissue hypoxia is a frequent cause of anaerobic metabolism leading to the accumulation of lactic acid. That is in a practical sense the only way we know that it is present. There are other causes of the tissue becoming hypoxic besides the blood becoming stagnant below the resistance arterioles. 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 as a cause of anerobic metabolism by excluding other causes.
Anaerobic metabolism frequently develops as a result of intense physical exertion. This occurs commonly in athletes. This creates a metabolic acidosis the same as does stagnant tissue hypoxia. There is no method to exclude the possibility that the metabolic capacity of the mitochondria are overwhelmed in the presence of adequate or normal oxygen tension. The effect is the same.
The cells switch to anaerobic metabolism when the need for energy exceeds that which the aerobic metabolism of the mitochondria can supply. There may be other factors that limit aerobic metabolism other than reduced mitochondrial oxygen tension. Presumably with high demand the delivery of oxygen is limited and oxygen tension is reduced by the increased consumption.
1. Arterial Hypoxemia – The blood coming from the aorta has a low PaO2.
It could be that a low PaO2 could be due to a low barometric pressure. 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. This preserves the PaO2 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 it was when it was bound to hemoglobin. When the oxygen at the tissue level is released from its binding to hemoglobin into whatever barometric pressure exists, 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.
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 so thoroughly ingrained in the concept of inadequate perfusion due to low blood pressure measured in the brachial artery that stagnant tissue hypoxia is useful as a different term. Hypotension is almost always labeled shock when the peripheral blood pressure is low enough. In theory shock is 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. It is important to move away from the idea that the peripheral blood pressure as in that measured in the brachial artery can determine tissue perfusion. This is the concept of stagnant tissue hypoxia. 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. The resistance between the brachial artery and capillary bed is unknown. We can assume that it is normal but we could be wrong. It is unknown. The presence of lactic acidosis means that tissue perfusion is inadequate and 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 clinicians, physicians, nurses, firefighters, etc to not practice with the erroneous assumption that peripheral blood pressure equals perfusion. This is an unfortunate situation that will not be remedied anytime soon.
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 essentially impossible to distinguish histotoxic hypoxia from stagnate tissue hypoxia except when a tissue toxin like cyanide is identified. Forensic investigators might have to consider the possibly of cyanide poisoning. Lactic acidosis is the key to knowing that stagnant tissue hypoxia is present. Cyanide poisoning could mimic it convincingly. There are other toxins that could be mentioned as poisoning the use of oxygen by mitochondria but cyanide toxicity is the purest example. Carbon Monoxide impairs the mitochondria but more significantly it prevents the binding of oxygen to hemoglobin.
Stagnant Tissue Hypoxia or Stagnant 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. When blood pressure is extremely high and perfusion is impaired because resistance is also extremely high the situation is usually labeled flash pulmonary edema.
Flash Pulmonary Edema as a result of Stagnant Tissue Hypoxia
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 completely misleading.