Hyperbaric Physiology
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Direct answer
Breathing 100% oxygen at 3 atmospheres absolute dissolves enough oxygen in plasma — roughly 6 mL per dL — to meet the entire resting tissue consumption without any contribution from haemoglobin; that single consequence of Dalton's and Henry's laws is the whole basis of hyperbaric oxygen therapy. At 2.5-3 atmospheres absolute (ATA), used in standard chamber protocols, carbon monoxide is displaced from haemoglobin far faster — the carboxyhaemoglobin half-life falls from about 4-5 hours on room air to roughly 60-90 minutes on normobaric 100% oxygen and about 20-30 minutes under hyperbaric oxygen (commonly quoted figures). The same physics cuts both ways: nitrogen dissolves in tissue during compressed-air diving and comes out of solution as bubbles on too-rapid ascent — decompression sickness — treated by recompression (US Navy Table 6), while oxygen becomes toxic to the brain above about 2 ATA (Paul Bert effect, seizures) and to lung tissue on prolonged exposure (Lorrain Smith effect).
What you must remember
- Governing laws: Dalton's law (total pressure equals the sum of partial pressures, so inspired PO2 scales with depth) and Henry's law (gas dissolves in proportion to its partial pressure, so tissue nitrogen loads during compression).
- Dissolved oxygen arithmetic: plasma carries about 0.003 mL O2 per dL per mmHg PO2; at 3 ATA with 100% oxygen the alveolar PO2 approaches 2,200 mmHg and dissolved oxygen approaches 6 vol% — enough for resting needs.
- Carbon monoxide protocol: hyperbaric oxygen is indicated for coma, seizures, carboxyhaemoglobin above roughly 25-30%, pregnancy and persistent neurological deficit; it also dissociates CO from cytochrome oxidase, a benefit beyond the half-life effect.
- Decompression sickness types: type I — joint bends and skin lymphatic manifestations; type II — neurological, vestibular and pulmonary ("chokes"); the bubbles are nitrogen, and recompression plus oxygen is definitive.
- Other accepted indications: clostridial myonecrosis (oxygen inhibits clostridial alpha-toxin production and growth), arterial gas embolism from diving or iatrogenic air, refractory osteomyelitis, radiation tissue injury and compromised grafts — the standard list worth memorising in pairs.
- Oxygen toxicity ceilings: CNS toxicity with tremor and convulsions above about 2 ATA (divers limit PO2 to about 1.4-1.6 ATA while working); pulmonary toxicity with absorption atelectasis, substernal burning and falls in vital capacity on prolonged 100% oxygen even at 1 ATA.
- Practical chamber hazards: middle-ear barotrauma on compression (myringotomy for patients who cannot equalise), and fire risk in oxygen-rich atmospheres.
A worked case: the winter geyser poisoning
A family is brought in from a closed bathroom with a malfunctioning gas geyser: one member comatose with cherry-red lips, another dizzy with headache. Carboxyhaemoglobin returns 42% in the comatose patient. Immediate high-flow oxygen via non-rebreather starts the clock — the half-life of roughly 4-5 hours on room air shrinks to about an hour — and coma, carboxyhaemoglobin above 25-30% and any pregnancy trigger transfer for hyperbaric therapy, where elimination approaches 20-30 minutes and dissolved oxygen sustains delivery meanwhile. The Indian setting is the teaching hook: winter carbon monoxide poisoning from geysers, angeethi braziers and indoor generators is under-recognised, and the physiology explains why whole families are affected simultaneously while pulse oximetry reads spuriously normal (standard devices cannot distinguish carboxyhaemoglobin). Contrast the diver surfacing with shoulder pain and a confusing spinal deficit: same physics, opposite direction — nitrogen bubbles formed on ascent, and the treatment is recompression on Table 6, not oxygen alone.
Where students slip
The first slip is quoting the room-air carboxyhaemoglobin half-life as minutes; it is hours, and every escalation of oxygen therapy is measured against that slow baseline. Second, students explain hyperbaric benefit purely as "more oxygen dissolved" and omit the cytochrome oxidase displacement and the lipid-soluble bubble resolution — the exam wants both delivery and mechanism-level effects. Third, the two toxicity syndromes get swapped: central nervous system toxicity (seizures) belongs to high partial pressure, short exposure; pulmonary toxicity belongs to lower partial pressure, long exposure. If a patient seizes inside a chamber, remove the oxygen, not the patient — the seizure stops as PO2 falls. Finally, do not confuse decompression sickness with pulmonary barotrauma causing arterial gas embolism: both are treated with recompression, but the embolism arises from breath-holding expansion during ascent (Boyle's law), not dissolved nitrogen.
Frequently asked questions
Why does hyperbaric oxygen work when haemoglobin is saturated?
Because dissolved plasma oxygen rises linearly with alveolar PO2 — approaching 6 mL per dL at 3 ATA on 100% oxygen — enough to meet resting tissue demand irrespective of haemoglobin-bound oxygen.
How does hyperbaric therapy change carboxyhaemoglobin half-life?
From about 4-5 hours on room air to roughly an hour on normobaric 100% oxygen and 20-30 minutes at 2.5-3 ATA, while also displacing carbon monoxide from cytochrome oxidase.
What causes decompression sickness and which gas forms the bubbles?
Nitrogen, dissolved in tissue during compression per Henry's law, comes out of solution as bubbles on too-rapid ascent; treatment is recompression with oxygen.
What is the Paul Bert effect?
Central nervous system oxygen toxicity — tremor followed by generalised seizures at partial pressures above roughly 2 ATA — the reason divers cap working PO2 near 1.4-1.6 ATA.
Which infection is a classical hyperbaric oxygen indication and why?
Clostridial myonecrosis, because high tissue oxygen tensions halt clostridial growth and alpha-toxin production, supplementing surgery and antibiotics.