Oxygen at the tissue level: interstitial and cellular PO₂
- Mechanism
- Exam priority: medium
Oxygen steps down from blood to tissue fluid to cells. Mitochondria need very little, so cells usually burn O₂ as fast as they need energy.
Also called: Tissue PO₂, Critical mitochondrial PO₂, Supply-dependent O₂ consumption
What it is
Oxygen leaves capillaries by diffusion, down a pressure gradient from blood (about 95 mmHg arterial) to interstitial fluid (about 40 mmHg) to cell interior (about 5–40 mmHg). Tissue PO₂ is a balance between delivery by blood flow and use by metabolism. Because mitochondria work at a PO₂ of only a few mmHg, O₂ use is normally set by energy demand (ADP), and only becomes limited by supply when delivery falls very low.
How it works, step by step
- Arterial blood enters capillaries at PO₂ ≈ 95 mmHg; O₂ diffuses out toward the lower interstitial PO₂.
- By the venous end, capillary PO₂ has fallen to about 40 mmHg, close to interstitial PO₂.
- From interstitial fluid O₂ diffuses into cells, where its PO₂ falls further with distance from the capillary.
- Inside the cell, cytochrome c oxidase binds O₂ so avidly that the reaction runs at full speed above about 1 mmHg.
- So, with enough O₂, the rate of use depends on ADP: work makes ADP, ADP speeds oxidative phosphorylation.
- As tissue PO₂ falls, hemoglobin unloads more O₂ for a small drop in PO₂, which holds tissue PO₂ up.
- If delivery keeps falling (shock, severe anemia), extraction reaches its limit; mitochondrial PO₂ drops below critical and anaerobic glycolysis makes lactate.
Oxygen–hemoglobin dissociation curve
P50 26.8 mmHgArterial blood 97 %Mixed venous blood 75 %O₂ given up to the tissues 23 %
Normal curve. Tap a point (arterial, venous or P50) or move a control.
- Current curve
- Normal curve (pH 7.40 · 37 °C)
- Arterial blood (PO₂ 100)
- Mixed venous blood (PO₂ 40)
- O₂ given up to the tissues
Equations
- VO2
- O₂ consumption, mL/min
- Q
- blood flow
- CaO2 − CvO2
- arteriovenous O₂ content difference
Whole body at rest ≈ 250 mL/min; flow and extraction trade off.
- DO2
- O₂ delivery = Q × CaO₂
≈ 25% at rest; when it nears its maximum, use becomes supply-dependent.
O₂ partial pressures along the path (approximate, at rest)
| Parameter | Value | Note |
|---|---|---|
| Arterial blood | ≈ 95 mmHg | |
| Venous end of capillary | ≈ 40 mmHg | |
| Interstitial fluid | ≈ 40 mmHg | lower in active tissue |
| Inside cells | ≈ 5–40 mmHg | average ≈ 23 mmHg |
| Critical mitochondrial PO₂ | ≈ 1–3 mmHg | |
| Resting extraction ratio | ≈ 25% |
Approximate values for a healthy adult at rest; each laboratory sets its own ranges.
Regulation
- +Higher blood flow: Raises tissue PO₂, up to the arterial value.
- −Higher metabolic rate: Lowers tissue PO₂ and raises extraction.
- +Right shift of the O₂–Hb curve (acid, CO₂, heat, 2,3-BPG): More O₂ unloaded at the same PO₂.
- −Edema and longer diffusion distance: Lowers PO₂ in cells far from capillaries.
Clinical notes
- Rising lactate in sepsis or shock signals that some tissues have passed from ADP-limited to supply-limited O₂ use (or have impaired O₂ use).
- A low mixed venous saturation means tissues are extracting more because delivery is falling behind demand.
- Edema lengthens diffusion distance, one reason swollen tissue heals poorly.
Test yourself
Think of the answer, then tap the question to see it.
What normally limits the rate of O₂ use by cells when intracellular PO₂ is above a few mmHg?
The concentration of ADP: cells use O₂ in proportion to the energy they spend (ADP-limited), not in proportion to supply.
What happens to tissue PO₂ when blood flow to a muscle doubles at constant metabolism?
It rises toward, but never above, arterial PO₂, because more O₂ arrives per minute than the same metabolism removes.
How does hemoglobin act as a tissue O₂ buffer?
On the steep part of its curve, a small fall in tissue PO₂ releases a large amount of O₂, so tissue PO₂ stays in a narrow range even when supply or demand changes.
Why does lactate rise when O₂ delivery falls below a critical level?
Extraction is already maximal, so mitochondrial PO₂ falls below the critical level, oxidative phosphorylation slows and cells turn to anaerobic glycolysis, making lactate.
Connections
In Biochemistry2
Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.
Sources: Lactic acidosis: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2025); Lactate Test: MedlinePlus Medical Test (MedlinePlus, US National Library of Medicine, 2025); Hypovolemia and Hypovolemic Shock (StatPearls (NCBI Bookshelf), 2025).
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Representative model, for educational purposes only.