US Navy standard recompression protocol for decompression sickness inside a multiplace hyperbaric chamber
When a diver surfaces too quickly, dissolved inert gas (mostly nitrogen) comes out of solution and forms bubbles in blood and tissue — decompression sickness (DCS). The definitive treatment is counter-intuitive: put the patient back under pressure. Recompression in a hyperbaric chamber physically shrinks the bubbles and restores perfusion within minutes.
Boyle's Law states that at constant temperature, the volume of a gas is inversely proportional to the pressure applied to it: P₁V₁ = P₂V₂. A nitrogen bubble that forms at the surface (1 ATA) is compressed to roughly a third of its original volume the moment the patient reaches 60 fsw (2.8 ATA).
Smaller bubbles have a larger surface-area-to-volume ratio, which speeds their dissolution back into the surrounding blood and tissue. Shrinking the bubble also physically relieves the mechanical obstruction it was causing — restoring blood flow to a blocked capillary, or reducing pressure on a compressed nerve or spinal tract, often producing dramatic symptom relief within the first minutes of compression.
This is why 60 fsw was chosen as the standard initial treatment depth: it mirrors the depths at which 19th-century caisson workers and tunnel diggers were historically recompressed for "caisson disease," and it delivers enough partial pressure to meaningfully shrink bubbles without the added logistical burden and inert-gas narcosis risk of deeper excursions.
At 60 fsw a nitrogen bubble's volume falls to about 1/2.8 of its surface value — roughly 36% — while its diameter (which scales with the cube root of volume) shrinks to about 71% of the surface diameter, enough to reopen a capillary that was previously fully occluded.
Decompression sickness was first clinically described in the 1840s among compressed-air caisson workers building bridge foundations and tunnels; the term "the bends" comes from the stooped posture sufferers adopted to ease joint pain. Early physicians noticed something crucial: symptoms improved when workers went back into the pressurized caisson.
The US Navy formalized recompression treatment through the 20th century as diving operations expanded, publishing standardized "treatment tables" in the Navy Diving Manual. Table 5 handles milder, pain-only DCS; Table 6 — the subject of this simulation — is the workhorse protocol for more serious cases: neurological DCS, cardiopulmonary ("chokes") DCS, and arterial gas embolism when Table 6A is not required.
Today, Table 6 is the most frequently used recompression protocol worldwide, applied not only to divers but also to compressed-air tunnel and caisson workers and, occasionally, to high-altitude decompression events in aviation and spaceflight-adjacent testing.
Table 6 is normally run in a multiplace chamber — a steel pressure vessel large enough to hold the patient, an inside tender (a diving medical technician who accompanies the patient and helps manage the O2 mask), and sometimes a physician, all breathing chamber air while the patient breathes 100% O2 through a tight-fitting mask, hood, or built-in breathing system (BIBS).
Compression is delivered by pumping compressed air into the sealed chamber; a chamber operator outside controls depth via valves while monitoring gauges, and communicates with the inside team by intercom. Compression to 60 fsw is deliberately brisk (a few minutes) because early, aggressive recompression is strongly associated with better neurological outcomes — delay allows bubbles to organize, trigger inflammation, and cause more persistent tissue injury.
Once at treatment depth, the patient breathes 100% oxygen through a mask in timed periods, interrupted by short "air breaks" on chamber air. This O2/air cycling is the therapeutic core of Table 6: oxygen both washes inert gas out of the tissues and delivers a hyperoxic boost to injured tissue, while the air breaks keep the patient safely below the seizure threshold for CNS oxygen toxicity.
Breathing 100% O2 at 2.8 ATA drives the partial pressure of oxygen in the blood far above what tissues can consume, while simultaneously dropping the partial pressure of inspired nitrogen to essentially zero. This creates a steep diffusion gradient — sometimes called the "oxygen window" — that pulls dissolved and bubble-phase nitrogen out of tissue and into the blood for elimination via the lungs, far faster than breathing air at the same depth would.
Oxygen also directly treats the downstream injury caused by bubbles: it reduces tissue edema, counteracts the ischemia caused by an obstructed vessel, and has documented anti-inflammatory and anti-adhesion effects on white blood cells that otherwise aggravate the endothelial damage bubbles cause. This is why Table 6 uses oxygen, not just pressure, as its primary active treatment — pressure alone (as in an air-only recompression) is far less effective.
At 60 fsw on 100% O2, inspired PO2 reaches about 2.8 ATA — roughly 14 times the partial pressure of oxygen in surface air (≈0.21 ATA) — creating the steep gradient that drives accelerated nitrogen washout from injured tissue.
Prolonged breathing of high-partial-pressure oxygen carries a real risk of CNS oxygen toxicity — a syndrome that can escalate abruptly to a generalized seizure, an extremely hazardous event for a patient wearing a mask underwater-pressure inside a sealed chamber (risk of aspiration, injury, and interrupted treatment).
Risk of CNS toxicity rises steeply with both PO2 and continuous exposure duration. Interrupting O2 breathing every 20 minutes with a 5-minute air break drops the PO2 back toward normal, allowing partial clearance of the physiological changes that predispose to a seizure, and resets the toxicity "clock" before it approaches a dangerous threshold. Early warning signs tenders watch for during O2 periods — grouped under the mnemonic "VENTID" (visual disturbance, ears ringing, nausea, twitching/tingling, irritability, dizziness) — prompt an immediate switch to air if noticed.
The 20-min-on/5-min-off ratio (4:1) was empirically derived from decades of Navy diving experience and is deliberately conservative: it allows long total O2 exposure across a multi-hour table while keeping the seizure rate very low.
The inside tender performs a focused neurological and symptom check at the end of each O2 period and air break — motor strength, sensation, coordination, joint pain, and any respiratory or vestibular ("staggers") symptoms are reassessed and compared against the baseline exam taken before compression.
Complete or near-complete relief of symptoms after the initial O2 periods is a good prognostic sign and allows the table to proceed on its standard schedule. Incomplete relief signals that bubble load or secondary tissue injury is more severe, and is the clinical trigger for extending the table — either with additional O2 periods at 60 fsw or, more commonly in current practice, extensions applied later at 30 fsw (Stage 4).
After the initial oxygen periods at 60 fsw, the chamber is slowly decompressed to 30 fsw. The ascent rate is tightly controlled — fast enough to keep the table moving, slow enough that it does not itself provoke new bubble formation from gas still dissolved in the patient's tissues.
Every foot of ascent reduces ambient pressure and therefore re-expands any remaining bubbles slightly and reduces the diffusion gradient driving inert gas out of tissue. An overly fast ascent risks two things: mechanical re-expansion of bubbles that had shrunk (potentially re-obstructing a vessel that had just reopened), and a reversal of the favorable outward diffusion gradient established during the 60 fsw oxygen periods.
A rate of 1 foot per minute — some six times slower than typical working-dive ascent rates — keeps the pressure change gradual enough that gas continues to leave tissue faster than any bubble can meaningfully re-expand. The patient continues breathing 100% O2 throughout the ascent (with one scheduled air break near the midpoint) so that the oxygen window keeps working even as ambient pressure falls.
30 fsw (1.9 ATA) is chosen as the next plateau rather than continuing straight to the surface because it still delivers a clinically meaningful inspired PO2 on 100% O2 (about 1.9 ATA) while allowing longer, more sustainable O2 breathing periods than are safe at 60 fsw.
The lower ambient pressure at 30 fsw reduces the CNS oxygen toxicity risk per minute of O2 breathing compared with 60 fsw, which is precisely why Table 6 shifts to longer 60-minute O2 periods once the patient reaches this depth (Stage 4) — the therapeutic oxygen dose can be extended safely at the shallower plateau even as the mechanical, Boyle's-Law bubble-shrinking effect of pressure itself is smaller here than it was at 60 fsw.
Going from 60 fsw to 30 fsw drops ambient pressure from 2.8 ATA to 1.9 ATA — a meaningful fall in the mechanical bubble-shrinking effect, which is why the protocol compensates by extending total oxygen breathing time at the shallower depth rather than relying on pressure alone.
Ascent is one of the higher-risk windows of the table: any recurrence or worsening of neurological symptoms during or shortly after ascent is taken seriously and can prompt the chamber operator to pause the ascent or even return briefly to 60 fsw before resuming, at the treating physician's direction.
The inside tender continues symptom checks through the ascent, and vital signs (heart rate, respiratory rate, and — where equipped — pulse oximetry adapted for chamber pressure) are tracked continuously. This transition period is also when equipment checks for the 30 fsw oxygen delivery system (masks, BIBS overboard dump valves, chamber CO2 scrubbing) are re-verified before the longer oxygen periods of Stage 4 begin.
The bulk of Table 6's treatment time is spent at 30 fsw, cycling through longer oxygen periods than were used at depth. This is also where the protocol's built-in flexibility matters most: if neurological or joint symptoms have not fully resolved, the table can be extended with additional oxygen segments before the final ascent is permitted.
The 60-minute-on/15-minute-off cycle at 30 fsw follows the same logic as the 60 fsw periods — sustained hyperoxia to drive inert-gas washout and tissue-level anti-inflammatory effects, interrupted before CNS oxygen toxicity risk accumulates too far — but the lower ambient PO2 at this shallower depth allows each O2 segment to run three times longer before an air break is needed.
Across two full cycles, the patient accumulates roughly two hours of oxygen breathing at 30 fsw on top of the O2 already delivered at 60 fsw and during the ascent — the single largest block of therapeutic oxygen exposure in the entire table.
Table 6 was designed with built-in flexibility for cases where symptoms are not fully resolved after the standard oxygen periods. The treating physician can order up to two extension segments, each adding roughly 25 minutes of additional oxygen breathing plus a 5-minute air break, before allowing the final ascent to proceed.
The decision to extend is clinical, not automatic: it weighs residual neurological deficit, joint pain, and any objective findings against the cumulative oxygen exposure already delivered (to avoid excessive pulmonary or CNS oxygen toxicity risk) and the practical limits of how long a patient and tending staff can safely remain in the chamber. More severe presentations — spinal cord DCS, cardiopulmonary DCS ("the chokes"), or arterial gas embolism — are more likely to require the full extension allowance, and some protocols call for a follow-up Table 5 or Table 6 the next day if deficits persist.
Each extension segment adds roughly 25 minutes of oxygen breathing plus a 5-minute air break at 30 fsw. With both extensions used, total table time rises from about 4 h 45 min to roughly 5 h 45 min — a deliberate trade-off of chamber time for a better chance of full symptom resolution.
Oxygen toxicity is tracked two ways during a long table: acute CNS toxicity risk (managed by the air-break schedule) and cumulative pulmonary oxygen toxicity, often tracked using Oxygen Tolerance Units (OTUs), which weight exposure by both PO2 and duration. A full Table 6 without extensions already delivers several hundred OTUs; each extension segment adds a further, non-trivial dose.
Because of this, extensions are not applied casually — they are reserved for cases with objective, incompletely resolved findings, and the treatment team continues to weigh incremental benefit against toxicity risk after each additional segment, exactly the trade-off reflected by adjusting the Symptom Severity control in this simulation.
The last phase brings the patient from 30 fsw back to surface pressure, still breathing oxygen for most of the ascent. Reaching the surface does not end the episode of care — patients are observed for hours afterward for symptom recurrence, and HBOT itself is used far beyond DCS, across a range of conditions where a hyperoxic, hyperbaric environment promotes healing.
The final leg to the surface mirrors the 60→30 fsw ascent: a controlled 1 fsw/min rate, continued oxygen breathing (with a scheduled air break), and continuous symptom monitoring. Reaching surface pressure (1 ATA) does not mean the treatment episode is complete — decompression sickness symptoms can recur ("relapse") in the hours after a treatment, particularly if the initial bubble load was large or if the patient is exposed to further altitude change (such as flying) too soon.
Standard practice keeps the patient under direct observation for at least a couple of hours after the table, with a low threshold to recompress again — typically with a shorter Table 5 — if any symptom returns. Patients are also advised to avoid flying or further altitude exposure for a defined period afterward, since reduced cabin pressure can provoke recurrent bubble formation in a patient who has not fully off-gassed.
While Table 6 exists specifically for decompression sickness and arterial gas embolism, the underlying physiology of hyperbaric oxygen — dramatically increased dissolved-oxygen delivery to tissue, independent of hemoglobin — makes HBOT useful across a range of other approved indications:
• Carbon monoxide poisoning: hyperbaric O2 accelerates dissociation of CO from hemoglobin and cytochrome oxidase far faster than normobaric oxygen, reducing delayed neurological sequelae • Gas gangrene / necrotizing soft-tissue infection: hyperoxia is directly toxic to the anaerobic Clostridium species that cause gas gangrene and boosts neutrophil bactericidal function • Problem wounds (diabetic foot ulcers, radiation injury): elevated tissue oxygen tension stimulates angiogenesis and collagen deposition in poorly perfused, hypoxic wound beds • Air or gas embolism from any cause (not just diving): mechanical bubble compression plus accelerated gas resorption • Crush injury and compartment syndrome, select skin grafts and flaps, and severe blood loss anemia when transfusion is not possible or accepted
Not every recompression uses Table 6. The Navy Diving Manual defines a family of tables matched to presentation severity and available gas mixtures, summarized below. Table 5 is reserved for pain-only DCS with prompt, complete relief on the first oxygen period; Table 6 is the default for anything more serious; Table 6A adds an initial deeper excursion to 60 fsw on air (with a brief spike to a deeper stop if needed) for suspected arterial gas embolism; and Table 4, run on a heliox or nitrox mixture at much greater depth over many hours to days, is reserved for the most severe, refractory cases as a saturation-style treatment.
| Product | Indication | Trial Design | Key Result |
|---|---|---|---|
| Table 5 | Pain-only DCS, prompt relief | Compress to 60 fsw, short 100% O2 periods, no extensions typically needed | ≈2 h 15 min — fastest standard table |
| Table 6 | Serious / neurological DCS | Compress to 60 fsw, O2/air cycling at 60 & 30 fsw, up to 2 extensions | ≈4 h 45 min, extendable to ~5 h 45 min |
| Table 6A | Arterial gas embolism (AGE) | Initial brief excursion toward 165 fsw on air/mixed gas, then converts into a Table 6 profile | Deeper initial mechanical bubble compression |
| Table 4 | Severe, refractory DCS/AGE | Saturation-style treatment on heliox/nitrox at depth for many hours to days | Reserved for cases unresponsive to Table 6/6A |