Pathomechanism
The main issue in hemic hypoxia is the inability of the blood to carry a sufficient amount of oxygen. This occurs due to a reduced hemoglobin concentration or an alteration in its functional properties. It is important to understand that the lungs function properly in this condition, so arterial blood remains saturated with oxygen (PaO2 is normal), but the total oxygen content (CaO2) drops critically.
Pathological forms of hemoglobin
The transport function of the blood is impaired when pathological forms of hemoglobin appear:
- Methemoglobin (MetHb): occurs when the heme iron is oxidized from the Fe2+ form to the Fe3+ form. Causes can include nitrates, sulfonamides, or anesthetics. The process is reversible once the toxic factor is eliminated.
- Carboxyhemoglobin (COHb): formed when hemoglobin binds to carbon monoxide (CO). In addition to blocking oxygen transport, CO inhibits cytochrome c oxidase, which further triggers mechanisms of tissue hypoxia.
Main parameters in methemoglobinemia
| Parameter | Parameter |
|---|---|
| PaO2 | N |
| SaO2 | N |
| OTC | ↓ |
| CaO2 | ↓ |
| CvO2 | ↓ |
| pH | ↓ (acidosis) |
Briefly: answers to topical questions
What pathological conditions and diseases lead to the development of hemic hypoxia?
Hemic hypoxia is caused by anemias and conditions associated with the accumulation of pathological forms of hemoglobin.
- Anemia — a decrease in the number of red blood cells and hemoglobin, including in hemolytic disease of the fetus.
- Hemoglobinopathies — congenital and acquired pathological forms of hemoglobin that impair its transport function.
- Methemoglobinemia — a condition in which heme iron transitions from the ferrous to the ferric form under the influence of nitrates, nitrites, and drugs.
- Carboxyhemoglobinemia — accumulation of a pathological form of hemoglobin upon interaction with carbon monoxide.
Which groups of chemicals and medicinal products are capable of causing methemoglobin formation?
Methemoglobin formation is caused by methemoglobin-inducing agents, which include nitrates, nitrites, and medications.
- Nitrates and nitrites — contaminated spring or well water; vegetables with a high nitrate content.
- Medications — inorganic nitrites (vasodilators), sulfonamides, NSAIDs (nonsteroidal anti-inflammatory drugs), local anesthetics.
What acute and long-term compensatory mechanisms are triggered in the body during hemic hypoxia?
In response to hemic hypoxia, respiratory, cardiovascular, and bone marrow compensatory mechanisms are triggered.
- Compensatory hyperventilation — develops in response to metabolic acidosis, bringing the carbon dioxide level to normal or lower.
- Cardiovascular compensatory reactions — include the development of tachycardia.
- Bone marrow phase of compensation — a long-term mechanism developing within 4–5 days, consisting of the stimulation of erythropoiesis under the influence of erythropoietins, which manifests as reticulocytosis.
Hemic = "Blood-related." Remember: "Blood is not empty, but capacity is low." In hemic hypoxia, the lungs "breathe" normally (PaO2 is normal), but the "delivery truck" (hemoglobin) is broken or there is too little of it.
Class and exam questions
Why does PaO2 remain normal in hemic hypoxia?
Because the partial pressure of oxygen depends on lung function and gas diffusion, which are not impaired in hemic hypoxia. The problem is not plasma saturation, but the reduced capacity of hemoglobin to carry oxygen.
What is the difference between hemic and tissue hypoxia in carbon monoxide poisoning?
Hemic hypoxia occurs due to CO binding to hemoglobin, while tissue hypoxia occurs due to the direct blocking of the cytochrome c oxidase enzyme in the mitochondria by carbon monoxide.
Is methemoglobinemia an irreversible condition?
No, this is a reversible process. When the source of nitrates or medicinal substances that caused iron oxidation is removed, hemoglobin gradually returns to its active form.
What else to study on this topic
- The role of compensatory hyperventilation in metabolic acidosis.
- Mechanisms of carboxyhemoglobin dissociation during treatment.
- Differences between anemic and hemic hypoxia.
- The effect of blood pH on the affinity of hemoglobin for oxygen.
- Biochemical basis of the blockade of complex IV of the electron transport chain.
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