HBOT vs. Normobaric Oxygen: Why Pressure Changes Everything

Many patients who’ve been on supplemental oxygen in a hospital wonder if they’ve already had something similar to HBOT. They haven’t. The difference isn’t the oxygen concentration. It’s the pressure.

Henry’s Law and What Pressure Does

Henry’s Law states that the amount of gas dissolved in a liquid is directly proportional to the partial pressure of that gas above the liquid. In practical terms: at higher pressure, more oxygen dissolves into blood plasma.

At normal atmospheric pressure (1 ATA), hemoglobin carries roughly 97% of the oxygen in your blood. Only about 0.3 mL of oxygen per 100 mL of blood travels dissolved in plasma. Breathing 100% oxygen at 1 ATA can saturate hemoglobin fully — but once saturated, hemoglobin can’t carry more oxygen. You’ve hit the ceiling.

At 2.0 ATA with 100% oxygen, the plasma-dissolved oxygen fraction increases dramatically — to roughly 4.4 mL per 100 mL of blood. At 3.0 ATA, it approaches 6 mL per 100 mL. That’s enough plasma-dissolved oxygen to meet basic tissue metabolic needs without any hemoglobin involvement at all. This is what Boerema’s 1960 “Life Without Blood” paper demonstrated in pigs at clinical HBOT pressures.

That’s the core mechanism. HBOT delivers oxygen through a pathway that hemoglobin can’t saturate — directly dissolved in plasma.

Why This Matters for Ischemic Tissue

In ischemic tissue — tissue where blood flow is reduced — red blood cells struggle to reach the injury site. Hemoglobin-bound oxygen can’t get through. Plasma-dissolved oxygen can, because it doesn’t depend on red blood cell transport. It diffuses independently through plasma and fluid to reach hypoxic cells.

For diabetic wounds, radiation-damaged tissue, and crush injuries, this independent oxygen delivery pathway is what makes HBOT effective where normobaric oxygen isn’t. The tissue oxygen levels achieved at 2.0 to 3.0 ATA are necessary to drive angiogenesis, support collagen synthesis, and produce the bactericidal effects on anaerobic organisms.

Normobaric 100% oxygen doesn’t reach these tissue oxygen levels. That’s not a limitation of oxygen concentration — it’s a limitation of pressure.

The Carbon Monoxide Case

CO poisoning is a useful example because both normobaric oxygen and HBOT are used, and the distinction matters.

CO binds hemoglobin approximately 240 times more tightly than oxygen. The resulting carboxyhemoglobin (COHb) can’t carry oxygen, causing tissue hypoxia. On room air, COHb has a half-life of about 5 hours. On normobaric 100% O2, that drops to about 60 minutes. On HBOT at 2.0-3.0 ATA, it drops to approximately 20 minutes.

But the half-life reduction isn’t the only benefit of HBOT for CO poisoning. While COHb is still present and hemoglobin is blocked, HBOT provides plasma-dissolved oxygen that can meet tissue oxygen needs independently. Normobaric O2 can displace CO more slowly but can’t provide that plasma-dissolved backup. For severe CO poisoning with neurological symptoms, the difference can be clinically significant.

See our condition page on carbon monoxide poisoning for indications and clinical criteria.

The Decompression Sickness Case

Decompression sickness (DCS) involves nitrogen gas bubbles that form in tissue and blood when ambient pressure drops too quickly. The mechanism is Boyle’s Law: as pressure decreases, gas volume expands. Bubbles that form in joints, spinal cord, or brain cause severe injury.

HBOT works for DCS through two pathways. First, elevated pressure physically compresses the bubbles — reducing their size and the mechanical damage they cause. Second, breathing 100% O2 accelerates nitrogen elimination by creating a diffusion gradient that pulls nitrogen out of tissues faster.

Normobaric oxygen accelerates nitrogen elimination to some degree, but it can’t provide the pressure needed to compress existing bubbles. This is a mechanical effect that no amount of oxygen concentration can replicate without pressure.

See our condition page on decompression sickness for more.

For Wound Care

For chronic wounds and wound healing applications, the tissue oxygen targets matter precisely. HBOT research on diabetic wounds targets a transcutaneous oxygen pressure (TcPO2) above 40 mmHg in periwound tissue. Normobaric oxygen rarely achieves these levels in hypoxic wound tissue because it depends on blood flow that’s already compromised.

Clinical HBOT raises tissue PO2 high enough to cross the threshold where angiogenesis is triggered, where bactericidal oxidative killing of anaerobic organisms occurs, and where fibroblast collagen production is restored. Normobaric oxygen supplementation doesn’t reach these thresholds in ischemic tissue.

What This Means Practically

If you’ve been on supplemental oxygen via nasal cannula or mask at a hospital, you did not receive HBOT. If a friend suggests home oxygen concentrators as a substitute for HBOT, the physics above explains why that doesn’t work.

For conditions that respond to plasma-dissolved oxygen delivery — carbon monoxide poisoning, decompression sickness, ischemic wounds — pressure is the mechanism. You can’t replicate it with higher flow rates or higher oxygen concentrations at atmospheric pressure.

See What Is HBOT and How HBOT Works for the broader clinical context.

FAQ

Why don’t hospitals just put CO poisoning patients in hyperbaric chambers immediately? Many hospitals don’t have hyperbaric chambers on-site. Transfer time and availability affect treatment decisions. Normobaric 100% O2 starts immediately while HBOT logistics are arranged. Clinical guidelines specify which CO cases warrant HBOT transfer.

Is any normobaric oxygen treatment comparable to HBOT? Normobaric 100% O2 is useful and clinically appropriate for many conditions. It’s not comparable to HBOT for the specific mechanisms that require elevated pressure: plasma oxygen dissolution, bubble compression, and ischemic tissue oxygenation beyond hemoglobin saturation limits.

Can oxygen toxicity happen with normobaric 100% O2? Prolonged normobaric 100% O2 can cause pulmonary oxygen toxicity over days. HBOT oxygen toxicity (CNS) is more acute and happens faster because of higher partial pressures. Both are managed by limiting exposure time. Clinical HBOT protocols are designed around these limits.

Does HBOT work better at 3.0 ATA than 2.0 ATA for all conditions? Not necessarily. Different conditions have optimal pressure ranges. CO poisoning and wound care typically use 2.0-2.4 ATA. DCS can require 2.8-3.0 ATA for initial treatment. More pressure isn’t universally better.

Medical Disclaimer: The content on this page is for informational purposes only. It is not medical advice and does not create a doctor-patient relationship. Consult a licensed physician for evaluation of any condition requiring oxygen therapy or hyperbaric treatment.