House of Hyperbaric

Day: August 10, 2026

  • Physiology of Oxygen Under Pressure

    Physiology of Oxygen Under Pressure

    How Increased Ambient Pressure Changes Oxygen Transport, Tissue Diffusion, Vascular Function, and Cellular Metabolism

    Oxygen is essential for aerobic metabolism, but its physiologic effects depend on more than the percentage present in the breathing gas. Pressure determines the partial pressure of oxygen, the quantity that dissolves in plasma, the distance it can diffuse through tissue, and the cellular responses produced by hyperoxia.

    During hyperbaric oxygen therapy, a patient breathes near 100 percent oxygen while the surrounding pressure is increased above normal atmospheric pressure. This creates a physiologic state that cannot be achieved by breathing supplemental oxygen at sea level alone.

    The result is a temporary but substantial increase in arterial and tissue oxygen tension. Understanding how the body responds requires looking at several connected principles, including gas behavior, oxygen carriage, microvascular regulation, cellular respiration, and oxidative signaling.

    What Pressure Means in Hyperbaric Medicine

    At sea level, the pressure exerted by the atmosphere is approximately 1 atmosphere absolute, or 1 ATA. Hyperbaric treatment increases the total pressure surrounding the patient, commonly to a prescribed range of approximately 2.0 to 3.0 ATA for many established clinical protocols.

    The word absolute is important. Hyperbaric treatment pressures are measured relative to a complete vacuum, not simply as the additional pressure shown on a gauge. A chamber operating at 2 ATA exposes the patient to twice the total atmospheric pressure present at sea level.

    Pressure affects every gas within the treatment environment and every gas-containing space in the body. It influences:

    • The partial pressure of inspired oxygen
    • The amount of oxygen dissolved in blood and tissue fluids
    • The volume of enclosed gas spaces
    • The movement of gases between the lungs, bloodstream, and tissues
    • The elimination of inert or toxic gases

    Pressure is therefore not merely a method for delivering more oxygen. It is part of the therapeutic dose.

    Dalton’s Law and Oxygen Partial Pressure

    Dalton’s law states that the total pressure of a gas mixture is equal to the sum of the partial pressures of its individual gases. Each gas contributes to the total pressure in proportion to its concentration.

    At sea level, oxygen makes up approximately 21 percent of air. Its partial pressure is therefore only a fraction of the total atmospheric pressure. When a patient breathes 100 percent oxygen, the inspired oxygen partial pressure increases because the nitrogen normally present in air has been largely removed from the breathing gas.

    When the surrounding pressure is also increased, the partial pressure of oxygen rises further. Breathing oxygen at 2 ATA produces a much higher inspired oxygen partial pressure than breathing oxygen at 1 ATA, even though the oxygen concentration remains 100 percent in both settings.

    Inspired oxygen pressure is not identical to arterial oxygen pressure. Water vapor, carbon dioxide, ventilation, diffusion across the alveolar membrane, and normal physiologic shunting all influence the final arterial value. Even after accounting for these variables, arterial oxygen tension during hyperbaric exposure can rise well above the levels achievable with normobaric oxygen. (PubMed Central (PMC))

    This distinction between oxygen concentration and oxygen partial pressure is central to hyperbaric physiology. The body responds to the pressure exerted by oxygen, not simply to the percentage printed on the oxygen delivery system.

    Henry’s Law and Dissolved Oxygen in Plasma

    Henry’s law describes the relationship between gas pressure and gas solubility. At a constant temperature, the amount of a gas that dissolves in a liquid is proportional to the partial pressure of that gas above the liquid.

    In practical terms, increasing arterial oxygen partial pressure allows more oxygen to dissolve physically in plasma.

    Under normal conditions, dissolved oxygen represents only a small portion of total blood oxygen content. Most oxygen is carried by hemoglobin within red blood cells. Because hemoglobin is already close to fully saturated in healthy arterial blood, increasing inspired oxygen at sea level produces only a modest increase in hemoglobin-bound oxygen.

    The dissolved component behaves differently. It continues to increase as arterial oxygen pressure rises.

    This relationship can be seen in the standard arterial oxygen content equation:

    Arterial oxygen content = hemoglobin-bound oxygen + dissolved oxygen

    Clinically, it is often expressed as:

    CaO₂ = (1.34 × Hb × SaO₂) + (0.0031 × PaO₂)

    In this equation:

    • CaO₂ is arterial oxygen content
    • Hb is hemoglobin concentration
    • SaO₂ is arterial hemoglobin oxygen saturation
    • PaO₂ is arterial oxygen partial pressure
    • 0.0031 represents the approximate solubility coefficient of oxygen in plasma

    At a PaO₂ near 100 mmHg, the dissolved contribution is approximately 0.3 mL of oxygen per deciliter of blood. At a PaO₂ approaching 2,000 mmHg, the dissolved contribution can approach approximately 6 mL per deciliter. Experimental and clinical reviews have noted that this amount may be sufficient to approach the resting oxygen requirements of tissues even without relying entirely on hemoglobin-bound oxygen. (PubMed Central (PMC))

    This does not mean hemoglobin becomes unnecessary during routine HBOT. It demonstrates that hyperbaric pressure creates an additional, immediately available oxygen reservoir within the liquid portion of the blood.

    Hemoglobin Saturation Versus Oxygen Availability

    Pulse oximetry can create an incomplete picture of oxygen physiology under pressure.

    A patient with normal lungs may have a peripheral oxygen saturation of 97 to 100 percent while breathing room air. When that patient begins breathing oxygen, the saturation reading may increase only slightly because hemoglobin was already near the plateau of the oxyhemoglobin dissociation curve.

    The small change in saturation does not reflect the much larger change in oxygen partial pressure.

    During HBOT, hemoglobin remains highly saturated, but plasma oxygen content and arterial oxygen tension rise substantially. These changes increase the amount of oxygen that can move out of the circulation and into surrounding tissue.

    This is why pulse oximetry is not a useful measure of the oxygen dose delivered during hyperbaric treatment. It shows the percentage of available hemoglobin binding sites occupied by oxygen, but it does not measure the large increase in dissolved plasma oxygen or tissue oxygen tension.

    The distinction is particularly important in compromised tissue. Oxygen delivery depends not only on arterial saturation but also on:

    • Hemoglobin concentration
    • Cardiac output
    • Regional blood flow
    • Microvascular patency
    • Arterial oxygen tension
    • Diffusion distance between capillaries and cells
    • Cellular ability to use delivered oxygen

    A normal saturation value therefore does not establish that every tissue is adequately oxygenated.

    Oxygen Diffusion into Hypoxic Tissue

    Oxygen moves from areas of higher partial pressure to areas of lower partial pressure. In healthy tissue, oxygen leaves the capillary, crosses the interstitial space, and enters cells where it is used primarily within mitochondria.

    The effectiveness of this process depends on the oxygen pressure gradient and the distance oxygen must travel.

    Edema, capillary loss, fibrosis, vascular injury, and increased metabolic demand can widen the gap between oxygen supply and tissue need. Cells located farther from a functioning capillary may become hypoxic even when arterial oxygen saturation appears normal.

    Hyperbaric oxygen markedly increases the pressure gradient between capillary blood and surrounding tissue. This allows oxygen to diffuse farther from the perfused microcirculation than it can under normal atmospheric conditions. (PubMed Central (PMC))

    The distinction between perfusion and diffusion remains important. HBOT does not force blood through a completely obstructed vessel. Instead, it increases the amount of oxygen carried by the plasma that reaches functioning vessels and enhances oxygen movement from those vessels into adjacent tissue.

    This can temporarily support cells at the margins of ischemia, where blood flow is impaired but not entirely absent. It can also improve oxygen availability in tissues affected by edema, small-vessel injury, radiation-associated vascular damage, or other barriers to normal diffusion.

    Boyle’s Law and Gas Volume Under Pressure

    Boyle’s law describes the inverse relationship between pressure and gas volume at a constant temperature. As surrounding pressure increases, the volume of a gas decreases. As pressure decreases, gas volume expands.

    This principle is most clinically apparent in decompression sickness and arterial gas embolism. Increasing chamber pressure reduces bubble volume, which may decrease mechanical obstruction and improve local blood flow. Breathing oxygen also increases the gradient for nitrogen removal, promoting the transfer of inert gas from bubbles and tissues into the bloodstream for elimination through the lungs. (PubMed)

    Boyle’s law also explains why pressure equalization is necessary during compression and decompression. Gas in the middle ear, sinuses, lungs, dental spaces, and medical devices changes volume as chamber pressure changes.

    During compression, enclosed gas spaces become smaller unless additional gas can enter. During decompression, trapped gas expands. A patient who cannot equalize pressure across the tympanic membrane may develop middle-ear barotrauma. A patient with an untreated pneumothorax may be at risk of expanding pleural gas during decompression, potentially producing a tension pneumothorax.

    The rate and profile of pressure change must therefore be managed as carefully as the oxygen exposure itself.

    Cardiovascular Effects of Hyperbaric Hyperoxia

    Hyperbaric oxygen produces several acute cardiovascular responses. Systemic hyperoxia commonly causes arteriolar vasoconstriction, particularly in tissues that normally regulate blood flow according to oxygen availability.

    At first, vasoconstriction may appear inconsistent with the goal of improving oxygenation. Reduced vessel diameter can decrease regional blood flow. However, the oxygen content and partial pressure of blood are substantially elevated during treatment, allowing tissue oxygen delivery to remain high despite the reduction in flow.

    This response may provide an additional benefit in edematous tissue. Reduced arteriolar inflow and capillary hydrostatic pressure can limit fluid filtration into the interstitial space while venous and lymphatic outflow continue. Lower tissue edema can reduce microvascular compression and shorten the effective diffusion distance between capillaries and cells. (UHMS)

    Hyperbaric hyperoxia can also produce:

    • Increased systemic vascular resistance
    • Reflex bradycardia
    • Reduced cardiac output
    • Relatively preserved stroke volume in many patients
    • Changes in ventricular loading conditions

    These effects are usually tolerated by appropriately screened patients, but they are clinically relevant in individuals with impaired ventricular function, significant pulmonary disease, or limited cardiovascular reserve. (PubMed)

    The cardiovascular response reinforces an important principle: oxygen delivery is not determined by blood flow alone. It reflects the interaction of blood flow, hemoglobin, dissolved oxygen content, partial pressure gradients, and tissue demand.

    Oxygen, Mitochondria, and Cellular Energy Production

    Within the mitochondria, oxygen serves as the terminal electron acceptor in the electron transport chain. This allows oxidative phosphorylation to proceed and supports the production of adenosine triphosphate, or ATP.

    When oxygen availability falls below a critical level, mitochondrial ATP production becomes limited. Cells increasingly depend on anaerobic metabolism, which is less efficient and contributes to lactate production, ion-pump dysfunction, cellular swelling, and eventual loss of membrane integrity.

    By increasing oxygen availability, HBOT can temporarily support aerobic metabolism in hypoxic but viable tissue. This may help preserve cellular function while definitive treatment addresses the underlying cause of ischemia or impaired perfusion.

    There is still a limit to this effect. Oxygen cannot restore metabolism in tissue that is irreversibly necrotic, and it cannot independently correct a major arterial obstruction. The clinical opportunity exists in threatened tissue that remains biologically viable and accessible to at least some functioning microcirculation.

    Reactive Oxygen Species and Redox Signaling

    Hyperbaric oxygen increases the formation of reactive oxygen species and reactive nitrogen species. These molecules include superoxide, hydrogen peroxide, hydroxyl radicals, nitric oxide-related intermediates, and other chemically reactive products of oxygen metabolism.

    Excessive production can damage lipids, proteins, DNA, cellular membranes, and pulmonary or neurologic tissue. At controlled levels, however, reactive species also function as signaling molecules.

    Intermittent hyperoxia can influence redox-sensitive pathways involved in:

    • Inflammatory regulation
    • Endothelial function
    • Antioxidant enzyme activity
    • Growth-factor expression
    • Leukocyte adhesion
    • Stem and progenitor cell mobilization
    • Angiogenic signaling
    • Cellular responses to hypoxia and oxidative stress

    The physiologic response is therefore not adequately described as simply placing more oxygen into tissue. HBOT creates a controlled oxidative stimulus that can alter cellular behavior during and between treatments. (PubMed)

    This helps explain why the effects of a treatment series may extend beyond the period when tissue oxygen tension is directly elevated. The immediate oxygen exposure is temporary, but the signaling events it initiates may contribute to longer-term vascular and tissue responses.

    Oxygen Dose, Exposure Time, and Toxicity

    Oxygen behaves pharmacologically. Its effects depend on concentration, pressure, exposure time, treatment frequency, and the susceptibility of the individual patient.

    A therapeutic dose can support metabolism and activate adaptive signaling. An excessive dose can overwhelm antioxidant defenses and cause oxygen toxicity.

    Central nervous system oxygen toxicity may present with visual changes, auditory symptoms, nausea, facial twitching, irritability, dizziness, or a generalized seizure. Pulmonary oxygen toxicity is associated with longer cumulative exposures and may cause substernal discomfort, cough, irritation, or measurable changes in pulmonary function.

    Clinical treatment protocols control oxygen exposure through:

    • Selection of treatment pressure
    • Defined oxygen-breathing periods
    • Limits on treatment duration
    • Scheduled air breaks when appropriate
    • Assessment of medications and comorbidities
    • Monitoring for neurologic, pulmonary, and glucose-related risk factors

    Air breaks temporarily replace oxygen breathing with air breathing while the patient remains at treatment pressure. They are commonly incorporated into certain protocols to reduce uninterrupted oxygen exposure, although their precise protective effects vary with the pressure, duration, and treatment context. (PubMed Central (PMC))

    More oxygen is not automatically more therapeutic. The objective is to produce a sufficient physiologic response while remaining within established safety limits.

    Why Oxygen Physiology Matters Clinically

    The physiologic effect of HBOT varies by diagnosis because different conditions depend on different aspects of pressure and hyperoxia.

    For intravascular gas, the central effects include bubble compression and inert-gas elimination. For carbon monoxide poisoning, the treatment increases oxygen availability while accelerating carbon monoxide displacement and elimination. For hypoxic wounds and radiation-damaged tissue, the emphasis shifts toward repeated tissue oxygenation, oxygen-dependent repair, inflammatory modulation, and vascular remodeling.

    A treatment protocol should therefore be selected according to the intended physiologic target, not simply according to chamber availability or a general desire to increase oxygen.

    The most clinically useful way to understand hyperbaric oxygen is as a controlled combination of:

    • Increased ambient pressure
    • Increased oxygen partial pressure
    • Increased dissolved plasma oxygen
    • Enhanced tissue diffusion
    • Altered vascular tone
    • Supported aerobic metabolism
    • Dose-dependent redox signaling

    These effects occur together, but their relative importance changes with the condition being treated.

    HBOT does not create permanent hyperoxygenation. It produces a defined period of markedly elevated oxygen availability and a series of physiologic signals that may help stabilize threatened tissue, support oxygen-dependent repair, and complement definitive medical or surgical care.

  • How Hyperbaric Oxygen Therapy Works

    How Hyperbaric Oxygen Therapy Works

    A Clinical Look at Pressure, Oxygen Transport, Cellular Signaling, and Tissue Repair

    Hyperbaric oxygen therapy, commonly abbreviated as HBOT, is a medical treatment in which a patient breathes 100 percent oxygen while exposed to an ambient pressure greater than normal atmospheric pressure. Depending on the chamber design, oxygen may be delivered directly within a monoplace chamber or through a mask or hood inside a pressurized multiplace chamber.

    The therapeutic effect is not produced by oxygen or pressure alone. HBOT works through the interaction of increased ambient pressure, elevated oxygen partial pressure, altered gas behavior, improved oxygen diffusion, and a series of cellular responses to controlled hyperoxia. These mechanisms can be used to address markedly different clinical problems, from intravascular gas bubbles to hypoxic wounds and delayed radiation injury.

    Hyperbaric Oxygen Increases Dissolved Oxygen in Plasma

    Under normal conditions, most oxygen in the blood is carried by hemoglobin. Only a small amount is physically dissolved in the plasma. Because hemoglobin is already close to fully saturated in healthy arterial blood, simply increasing the inspired oxygen concentration has a limited effect on hemoglobin-bound oxygen.

    HBOT changes this relationship by substantially increasing the partial pressure of oxygen in the lungs and arterial circulation. According to Henry’s law, the amount of a gas that dissolves in a liquid is proportional to that gas’s partial pressure. As oxygen pressure rises inside the chamber, considerably more oxygen dissolves directly into the plasma and other body fluids.

    This oxygen-rich plasma can travel through the circulation and establish a stronger diffusion gradient between functioning capillaries and nearby tissues. That gradient is clinically important in areas where oxygen delivery has been impaired by edema, vascular injury, radiation damage, infection, or compromised microcirculation. It allows oxygen to diffuse farther from the capillary and reach viable but hypoxic tissue that may not be adequately supported under normal atmospheric conditions.

    HBOT does not restore blood flow through an obstructed artery or revive irreversibly necrotic tissue. Instead, it can temporarily increase the oxygen available to threatened tissue while the underlying cause is addressed through surgery, revascularization, infection control, wound care, or other appropriate interventions. 

    Increased Pressure Changes the Behavior of Gas

    Pressure itself has a direct therapeutic role, particularly when abnormal gas bubbles are present in the bloodstream or tissues.

    Boyle’s law describes the inverse relationship between pressure and gas volume. When ambient pressure increases inside a hyperbaric chamber, the volume of a gas bubble decreases. This effect is central to the treatment of decompression sickness and arterial gas embolism, where bubbles can obstruct blood flow, damage the endothelium, and initiate inflammatory responses.

    Breathing oxygen at increased pressure also creates concentration gradients that promote the elimination of inert gases such as nitrogen. In carbon monoxide poisoning, high oxygen partial pressures accelerate the displacement and elimination of carbon monoxide while improving oxygen availability to tissues. HBOT may also influence inflammatory and oxidative processes that continue after carboxyhemoglobin levels begin to fall.

    For these acute conditions, HBOT is therefore doing more than increasing oxygen delivery. It is also changing gas volume, gas solubility, and the rate at which unwanted gases leave the body.

    Hyperoxic Vasoconstriction Can Reduce Tissue Edema

    One of the more counterintuitive effects of hyperbaric oxygen is vasoconstriction. High oxygen tensions can cause arterioles in certain tissues to constrict, reducing regional blood flow.

    Under ordinary circumstances, reduced blood flow could worsen tissue hypoxia. During HBOT, however, the oxygen content of plasma is markedly elevated. This allows oxygen delivery to remain high despite a decrease in blood flow.

    The resulting vasoconstriction can help limit fluid leakage and reduce tissue edema. As swelling decreases, the distance oxygen must travel between the capillary and the cell may also decrease. This can be particularly relevant in crush injury, compromised grafts and flaps, burns, and other conditions in which edema contributes to microvascular compression and progressive tissue ischemia.

    HBOT may also reduce neutrophil adhesion to injured endothelium. Excessive leukocyte-endothelial interaction is an important component of ischemia-reperfusion injury and can contribute to capillary obstruction, endothelial damage, and secondary inflammation. By modifying this response, HBOT may help preserve the microcirculation after an ischemic event.

    Controlled Hyperoxia Influences Cellular Signaling

    Oxygen is not only a metabolic substrate. It also participates in cellular signaling.

    Exposure to hyperbaric oxygen temporarily increases the production of reactive oxygen species and reactive nitrogen species. Although these molecules are often discussed exclusively as sources of oxidative damage, they also function as signaling intermediates. In controlled amounts, they can influence gene expression, inflammatory activity, endothelial function, antioxidant defenses, and growth-factor pathways.

    This is why HBOT is delivered intermittently rather than continuously. A prescribed oxygen dose is followed by a return to normal atmospheric oxygen levels, allowing therapeutic signaling to occur while limiting oxygen toxicity. Some protocols also incorporate scheduled air breaks to reduce cumulative central nervous system oxygen exposure.

    Research suggests that these controlled oxidative signals contribute to several effects associated with HBOT:

    • Modulation of inflammatory pathways 
    • Reduced neutrophil adhesion and endothelial injury
    • Increased activity of selected growth factors
    • Mobilization of endothelial progenitor cells
    • Changes in cellular antioxidant defenses
    • Support for vascular remodeling and tissue repair

    These responses are dose dependent. More pressure, more oxygen, or longer exposure does not automatically produce a better therapeutic result. The clinical objective is to deliver an appropriate oxygen dose for the diagnosis while remaining within established safety parameters.

    Hyperbaric Oxygen Supports Angiogenesis and Wound Healing

    Many chronic or complex wounds remain hypoxic because of impaired perfusion, edema, inflammation, infection, or damage to small blood vessels. Hypoxia can interfere with several oxygen-dependent steps required for normal tissue repair.

    Fibroblast activity, collagen formation, leukocyte function, and extracellular matrix development all depend to varying degrees on adequate tissue oxygenation. By repeatedly raising tissue oxygen tension, HBOT can create periods during which these processes function more effectively.

    The immediate effect of a treatment is temporary hyperoxygenation. The longer-term objective of a treatment course is different. Repeated exposures may stimulate angiogenic signaling and support the formation of new capillary networks in selected hypoxic tissues. As vascular density improves, tissue may become better able to maintain oxygenation between treatments and after the treatment course has ended.

    This is particularly relevant in tissues affected by radiation. Radiation injury can cause progressive endarteritis, fibrosis, reduced capillary density, and chronic tissue hypoxia. In this setting, HBOT is generally used as a series of treatments intended to support vascular and tissue remodeling rather than as a single oxygen exposure.

    HBOT should not be viewed as a replacement for comprehensive wound management. Appropriate care may still require:

    • Surgical debridement
    • Revascularization or vascular assessment
    • Infection control and antimicrobial therapy
    • Pressure offloading
    • Glycemic management
    • Nutritional support
    • Moisture and edema management
    • Correction of other barriers to healing

    The best outcomes occur when HBOT is integrated into a coordinated treatment plan that addresses the cause of tissue injury, not merely the visible wound.

    Hyperbaric Oxygen Can Strengthen Antimicrobial Defenses

    The relationship between oxygen and infection is complex. HBOT is not a general-purpose antibiotic and should not be presented as a stand-alone treatment for infection. Its antimicrobial effects depend on the organism, the tissue environment, the host response, and the accompanying surgical and medical care.

    Elevated oxygen tensions can directly inhibit or damage certain anaerobic organisms. HBOT may also improve oxygen-dependent microbial killing by neutrophils, which can become impaired in severely hypoxic tissue.

    For selected serious infections, HBOT may be used as an adjunct to surgical source control and appropriate antimicrobial therapy. It may also influence edema, toxin activity, inflammatory injury, and antibiotic effectiveness in specific clinical settings. These mechanisms do not eliminate the need for urgent debridement, culture-directed antibiotics, hemodynamic support, or other established standards of care.

    Different Conditions Rely on Different HBOT Mechanisms

    There is no single mechanism that explains every clinical use of hyperbaric oxygen therapy. The relative importance of pressure, oxygen delivery, inflammation control, antimicrobial activity, and tissue remodeling varies by diagnosis.

    For example:

    • In decompression sickness and arterial gas embolism, bubble compression and inert-gas elimination are central.
    • In carbon monoxide poisoning, accelerated carbon monoxide elimination and restoration of tissue oxygenation are important.
    • In selected hypoxic wounds and delayed radiation injury, repeated oxygenation, angiogenic signaling, fibroblast function, and tissue remodeling are emphasized.
    • In compromised grafts, flaps, or acutely injured tissue, temporary oxygen support and edema reduction may help preserve viable tissue.
    • In selected infections, improved leukocyte function, inhibition of susceptible organisms, and support of damaged tissue may complement surgery and antibiotics.

    These differences explain why HBOT protocols are not interchangeable. Treatment pressure, oxygen exposure time, air breaks, treatment frequency, and the total number of sessions should be selected according to the condition, clinical urgency, treatment response, and patient-specific risk factors.

    Clinical Screening and Hyperbaric Safety Matter

    HBOT is a prescription medical treatment that requires appropriate patient selection, equipment, monitoring, and trained personnel.

    Pressure changes can affect air-containing spaces in the ears, sinuses, lungs, and gastrointestinal tract. Middle-ear barotrauma is among the most frequently encountered adverse effects. Other potential complications include sinus discomfort, temporary changes in vision, pulmonary oxygen toxicity, and oxygen-induced seizure. An untreated pneumothorax is generally considered an absolute contraindication because pressure changes can expand trapped pleural gas during decompression.

    The oxygen-rich treatment environment also requires strict fire-safety controls. Clothing, dressings, medical equipment, personal items, chamber maintenance, electrical grounding, and staff training must follow established hyperbaric safety requirements. In an August 25, 2025 safety communication, the FDA emphasized manufacturer instructions, fire prevention, patient supervision, equipment maintenance, and staff training following reports of serious hyperbaric chamber incidents.

    Patients should be evaluated for pulmonary disease, difficulty equalizing ear pressure, seizure risk, medication interactions, implanted devices, glucose-management needs, and other factors that may influence treatment. The purpose of screening is not merely to determine whether a patient can enter the chamber. It is to ensure that the anticipated benefit, treatment protocol, and safety plan are appropriate for that individual.

    Hyperbaric oxygen therapy works by temporarily changing the physical and biochemical environment of the body. Increased pressure compresses gas, elevated oxygen partial pressure increases plasma oxygen content, hyperoxia alters vascular behavior, and controlled oxidative signaling influences inflammation and tissue repair. When applied to an evidence-supported condition as part of a coordinated medical plan, these mechanisms can help protect threatened tissue and support healing processes that are limited by hypoxia.