Hemic hypoxia is a condition caused by a decrease in the oxygen-carrying capacity (OCC) of the blood, impairing oxygen transport from the lungs to the tissues. Unlike other types of hypoxia, the partial pressure of oxygen in arterial blood remains within normal limits.
Oxygen-Carrying CapacityThe maximum volume of O2 bound by hemoglobin in 100 ml of blood.
Normal OCC1 gram of hemoglobin is capable of binding 1.34 ml of oxygen.
Critical COHb LevelAn increase in carboxyhemoglobin to 70–75% leads to a fatal outcome.
Key FeatureReduced OCC with normal PaO2 and SaO2 values.
Mechanism of Development
The primary issue in hemic hypoxia is the blood's inability to transport a sufficient amount of hemoglobin-bound oxygen. This occurs due to a reduced hemoglobin concentration or altered functional properties. It is important to note that the lungs function properly, so arterial blood remains well-oxygenated (PaO2 is normal), but the total oxygen content (CaO2) drops critically.
Pathological Hemoglobin Variants
Blood transport function is impaired when pathological forms of hemoglobin appear:
Methemoglobin (MetHb): Occurs when heme iron is oxidized from the Fe2+ form to Fe3+. Causes include nitrates, sulfonamides, or anesthetics. The process is reversible once the toxic factor is removed.
Carboxyhemoglobin (COHb): Forms when hemoglobin binds to carbon monoxide (CO). In addition to blocking oxygen transport, CO inhibits cytochrome c oxidase, which further triggers tissue hypoxia mechanisms.
Key Parameters in Methemoglobinemia
Parameter
Change
PaO2
N
SaO2
N
OCC
↓
CaO2
↓
CvO2
↓
pH
↓ (acidosis)
Mnemonic
Hemic = «Blood-related». Remember: «The blood vessels aren't empty, but capacity is small.» In hemic hypoxia, the lungs «breathe» normally (normal PaO2), but the «delivery truck» (hemoglobin) is broken or in too low supply.
Frequently asked 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 hemoglobin variants.
Anemia — a decrease in red blood cell count 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 where heme iron transitions from the ferrous to the ferric state under the influence of nitrates, nitrites, and drugs.
Carboxyhemoglobinemia — the accumulation of a pathological form of hemoglobin resulting from interaction with carbon monoxide.
What groups of chemicals and medications can cause methemoglobin formation?
Methemoglobin is induced by methemoglobin-forming agents, which include nitrates, nitrites, and certain medications.
Nitrates and nitrites — contaminated spring or well water; vegetables with elevated nitrate content.
Medications — inorganic nitrites (vasodilators), sulfonamides, NSAIDs (nonsteroidal anti-inflammatory drugs), and 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 activated.
Compensatory hyperventilation — develops in response to metabolic acidosis, bringing carbon dioxide levels to normal or lowering them.
Cardiovascular compensatory reactions — include the development of tachycardia.
Bone marrow phase of compensation — a long-term mechanism developing within 4–5 days, consisting of erythropoiesis stimulation driven by erythropoietins, manifesting as reticulocytosis.
Why does PaO2 remain normal in hemic hypoxia?
Because the partial pressure of oxygen depends on lung function and gas diffusion, which are unimpaired in hemic hypoxia. The problem lies not in plasma oxygen saturation, but in the reduced ability of hemoglobin to carry oxygen.
What is the difference between hemic and tissue hypoxia during CO poisoning?
Hemic hypoxia arises from CO binding to hemoglobin, whereas tissue hypoxia results from carbon monoxide directly blocking the enzyme cytochrome c oxidase in the mitochondria.
Is methemoglobinemia an irreversible condition?
No, it is a reversible process. Upon removing the source of nitrates or drugs that caused iron oxidation, hemoglobin gradually returns to its active form.
Go deeper
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 hemoglobin affinity for oxygen.
Biochemical basis of complex IV blockade in the electron transport chain.