Keith W. Van Meter- Section of Emergency Medicine, Department of Medicine, LSU School of Medicine, New Orleans, LA, United States
For short periods, even without the presence of red blood cells, hyperbaric oxygen can safely allow plasma to meet the oxygen delivery requirements of a human at rest. By this means, hyperbaric oxygen, in special instances, may be used as a bridge to lessen blood transfusion requirements. Hyperbaric oxygen, applied intermittently, can readily avert oxygen toxicity while meeting the body's oxygen requirements. In acute injury or illness, accumulated oxygen debt is shadowed by adenosine triphosphate debt. Hyperbaric oxygen efficiently provides superior diffusion distances of oxygen in tissue compared to those provided by breathing normobaric oxygen. Intermittent application of hyperbaric oxygen can resupply adenosine triphosphate for energy for gene expression and reparative and anti-inflammatory cellular function. This advantageous effect is termed the hyperbaric oxygen paradox. Similarly, the normobaric oxygen paradox has been used to elicit erythropoietin expression. Referfusion injury after an ischemic insult can be ameliorated by hyperbaric oxygen administration. Oxygen toxicity can be averted by short hyperbaric oxygen exposure times with air breaks during treatments and also by lengthening the time between hyperbaric oxygen sessions as the treatment advances. Hyperbaric chambers can be assembled to provide everything available to a patient in modern-day intensive care units. The complication rate of hyperbaric oxygen therapy is very low. Accordingly, hyperbaric oxygen, when safely available in hospital settings, should be considered as an adjunct for the management of critically injured or ill patients with disabling anemia.
Preclinical introduction
The clinical use of hyperbaric oxygen therapy (HBOT) to address the absence of sufficient hemoglobin levels began with the work of Dutch surgeon, I. Boerema, in the late 1950s. He rapidly exsanguinated swine to hemoglobin levels as low as 1 g per deciliter and then resuscitated them by intravenous volume repletion with a Ringer's lactate–dextran 6%–dextrose water 5% solution. Next, he pressurized the unconscious, collapsed but still breathing, swine to three atmospheres of pressure in a hyperbaric chamber and made them breathe 100% oxygen. At three atmospheres of pressure, inhaled oxygen of 100% provided a surface equivalent fraction of inhaled oxygen of 300% (SEFIO2 300%). He kept the swine at three atmospheres of pressure for 15 min and then re-transfused them with their shed blood and depressurized the chamber to the surface, whereupon the swine walked off unimpaired. He published these results in an article entitled “Life Without Blood” (1).
These results were replicated in a laboratory in the United States in 2010 at the LSU Health Sciences Center in New Orleans in an Institutional Animal Care Utilization Committee (IACUC)-approved pilot study. An acutely anesthetized, exsanguinated swine was monitored by a polarographic oxygen tension probe through a cranial burr hole (2). The swine, breathing normobaric room air, had a baseline brain tissue pO2 level of 30 mmHg. After a rapid exsanguination involving the removal of 40% of the blood volume, the swine's brain tissue pO2 dropped to 0 mmHg even while the swine was being ventilated with normobaric 100% oxygen. For volume replacement, the swine received intravenous Ringers' D5W solution. Next, the animal was pressurized inside a hyperbaric chamber while being kept on 100% oxygen inhalation at three atmospheres of pressure. At this pressure, the oxygen inhalation provided SEFIO2 of 300% oxygen. The brain tissue pO2 rose back to 30 mmHg, and the animal remained pressurized for 50 min. Before ascent to the surface, the swine was transfused with its shed blood. Upon reaching the surface at ambient pressure, the animal was recovered from anesthesia, and monitoring access catheters were removed. The swine walked off unimpaired and was returned to a rescue ranch for a long life (3). Table 1 shows a summary of published animal experiments investigating the use of HBOT in severe anemia. The tabular summary includes a thumbnail of evidence-based analysis using three different criteria (AHA/NCI-PDQ/BMJ) (4).
Table 1. Summary of published animal experiments investigating the use of hyperbaric oxygen therapy in severe anemia.
The clinical use of hyperbaric oxygen
Hyperbaric oxygen (HBO) may be used as a bridging therapy in the Advanced Trauma Life Support (ATLS) and Advanced Cardiac Life Support (ACLS) resuscitation of a precariously anemic patient to prevent multiunit transfusion until damage control surgical efforts can be implemented. The initial damage control surgery aims at preventing continued blood loss to allow the patient to retain transfused blood (35).
Likewise, HBO may be used as a bridging therapy for patients who refuse blood transfusions due to religious or philosophical reasons. Tincture of time could then allow the provision of hematinic nutrients and pharmaceuticals to support hematopoiesis to endogenously provide red blood cell replacement (36). If hemoglobin's ability to transport oxygen by carbon monoxide, cyanide, or hydrogen sulfide is impaired, HBO can be used acutely to treat these conditions to assist in patient recovery from the chemical hypoxia imposed by the poisoning (37–41).
In yet another clinical instance, HBO may be used if an anticipated complication of a blood transfusion precludes further transfusion (42):
1. Blood group incompatibility.
2. Febrile non-hemolytic transfusion reaction (FNHTR).
3. Both delayed amnestic and primary hemolytic anemia.
4. Allergy from urticaria to anaphylaxis.
5. Transfusion-associated graft-versus-host disease (TAGVHD).
6. Acute radiation-induced anemia in disasters with a supply shortage.
7. Transfusion-transmitted infections (TTI).
8. Both red blood cell and human leukocyte antigen (HLA) allosensitization.
9. Confounding severe congestive heart failure with profound anemia until stabilization, providing the safety of transfusion.
10. Stacking hemosiderosis from multiple transfusions by lessening the number of transfusions.
11. The prevention of long-term transfusion immunomodulation by lessening the number of transfusions.
12. The prevention of short-term induction of multiorgan failure by red blood cell-associated lipids and cytokines.
13. Transfusion-related lung injury (TRALI).
HBOT has been documented to ameliorate the adult respiratory syndrome induced by trauma or infection in severely anemic patients (43–46). This effect of HBOT may also be found to be an additional advantage of HBO as a bridging treatment until safe transfusions are possible in a patient with TRALI or acute respiratory distress (ARDS) in SARS-CoV2 patients with severe anemia (47). Research into this area is necessary. A randomized, controlled study has been published evidencing the use of HBOT to perform this (44). Table 2 shows human case studies and series for use in the treatment of severe anemia. The tabular summary includes a thumbnail, evidence-based analysis of the published papers using three different criteria (AHA/NCI-PDQ/BMJ) (4). More recently, a randomized, controlled trial of HBOT used in severe anemia has been published (57).
Table 2. Human case reports and series for use of hyperbaric oxygen therapy in treatment of severe anemia.
When considering the use of HBOT in cases of severe anemia, the clinician should consult a hyperbaric physician specialist to determine whether HBOT would be helpful for the individual patient. Figure 1 demonstrates the treatment course recommended by the UHMS in their 2023 edition of the Hyperbaric Medicine Indications Manual. The patient would undergo HBOT at two–three ATA for 60–90 min with one–two intermittent 5-min air breaks (4).
Figure 1. Flowchart of Severe Anemia.
Discussion
The operational practicality of using HBO as a bridging therapy in a remote non-medical setting was reported in a case of severe exsanguination of a commercial diver while in saturation offshore in the Gulf of Mexico. The patient bled out hemoglobin of 2 g per deciliter acutely when his duodenal artery was eroded by a duodenal ulcer. The requisite decompression to the surface required 3 days. During his recompression, he was kept alive without transfusion by Ringers' D5 solution administered by hypodermoclysis and intermittent HBO breathing periods. At the surface, he was then transfused with intravenous packed red blood cells (58). Many years before, three cases of patients with severe blood loss who each refused transfusion for religious belief were reported in the medical literature. The cases were successfully treated with intermittently administered HBO in the same way at a naval dock in a hyperbaric chamber (50).
High concentrations of continuously administered oxygen have been reported to be deleterious when used in patient's resuscitative management (59, 60). This observation has remained consistent regardless of whether the patients enrolled in clinical trials have had high, normal, or low hemoglobin levels, whether acute or chronic (61). How could HBO provided by ventilation with SEFIO2 of inhaled oxygen of 150%−300% not be deleterious? For one, the inhaled oxygen under these conditions is not continuous but is intermittent, with administered air breaks incorporated during HBOT sessions (62). Additionally, as the series of HBO treatment sessions progresses and the patient's condition improves, the patient becomes increasingly tolerant of the off-oxygen periods. This allows the HBOT to be spread out with longer periods between treatments (49). During the HBO breathing periods, enough oxygen is dissolved in plasma to allow plasma to deliver oxygen to tissue mitochondria to reduce the previously accumulating oxygen debt, which, in effect, is an adenosine triphosphate (ATP) debt (63–66).
One might say that HBOT, as bridge therapy, serves to resuscitate patients much like the bridging function of veno-venous extracorporeal membrane oxygenation (VV-ECMO) during resuscitative support of critically anemic patients with restrictions on red blood cell transfusion. In the instance of intermittent non-invasive HBOT, the patient can similarly be successfully supported (67). By simile, one might compare VV-ECMO to a continuous weld and short-interval intermittent HBOT to a spot weld (in effect, intermittent HBOT is VV-ECMO-like or “ECMoid” in function). Both therapeutic modalities attempt to hold the metabolic structure of the patient together. ECMO has up to a 30% serious adverse side effect incidence (68). Hyperbaric oxygen has, on average, one in 10,000 incidences of serious side effects including pneumothorax, oxygen toxicity seizure, fire or explosion, and arterial gas embolism (69–71). The ECMO hospital facility support fee is often US $50,000 per day (72) and a hospital-based HBOT series of 30 treatments includes a facility charge of US $7,500 (73, 74). In almost all instances, 30 HBOT treatments would be more than enough to bridge a patient through an anemic crisis. In the United States, the cost of a unit of packed red blood cells, along with its administration, is comparable to the cost of one HBOT treatment (4).
The tolerance to high-dose oxygen administration by intermittent application has been well-documented with oxygen administered at one atmosphere pressure as well as at increased atmospheric pressure (62, 75). There is more than just oxygen tolerance provided by the intermittency of use; this is the effect of intermittency itself. ATP resupply occurs when the mitochondrial intermembrane space minimally attains 1.5–2.0 mmHg of oxygen, which is a requisite for the unimpaired production of ATP by the mitochondrial respiratory chain of enzymes (76). In a severely anemic patient, equally important is the return of tissue hypoxia after the completion of an HBOT treatment. It is hypoxia that incites ATP-dependent reparative cytokine tissue release and antioxidant production. For the reparative and anti-inflammatory cytokines to work at cellular receptor sites, ATP is needed. The anteceding HBOT would have supplied the needed ATP for this to occur. The ensuing tissue hypoxia between treatments induces the following energy-dependent or ATP-dependent activity:
1. Antioxidant productions and functions to include catalase and peroxidase (77), glutathione (78), superoxide dismutase (79), and ATP itself as an antioxidant (80).
2. Support of genomic activity (81).
3. Support of epigenomic activity (82).
4. Support of proteomic activity (83) and protein folding (84).
5. Support of lipidomic activity (85).
6. Support of anti-inflammatory and reparative cytokines/chemokines (86).
7. Leukocyte function (87, 88).
8. Adaptive function in hypoxia: (erythropoietin) (89, 90) (heat shock protein) (91) (nitric oxide) (92) (hypoxia-inducible factor) (93).
This oscillation between hyperoxia and hypoxia may be graphically depiected as a sinusoidal timeline by Figure 2 and is the crux of the oxygen paradox.
Figure 2. The sinusoidal horizontal timeline depicted by the thick wavy lines in the diagram represents an intermittent hyperbaric oxygen treatment course. The wave peaks represent a hyperbaric oxygen treatment producing ATP resupply (93). Post treatment when the tissue oxygen tension drops, energy requiring cytokine and antioxidant release occurs (85).
To provide ATP resupply in the instance of an acute hypoxic state, pulsed high-dose HBO inhalation can be used to diffuse minimally 1.5–2.0 mmHg of oxygen into the mitochondrial intermembrane space (94). At best, when a red blood cell gets to its destination in capillaries, it must offload a portion of its remaining oxygen content back into the plasma. As the patient inhales 100% oxygen at one atmosphere of pressure, the plasma can maximally contain only 2.3 volumes% of dissolved oxygen. In contrast, the patient in a hyperbaric chamber at three atmospheres of pressure would inhale a SEFIO2 of 300%, thereby delivering to the capillaries 6.6 volume% of dissolved oxygen with a five-fold diffusion distance outside of the capillary over that of a subject inhaling an FIO2 of 100% oxygen at one atmosphere of pressure (95–97). This concept was reported over 60 years ago by W. Brummelkamp when he reported that during an HBOT treatment, “drenching of the tissue with dissolved oxygen” occurred by way of immersing plasma with oxygen (98).
HBOT inhalation can only be accomplished safely when the entire patient is pressurized above ambient pressure in an enclosure (i.e., a hyperbaric chamber). The spectrum of potential treatment doses of oxygen using HBO pressure incorporates the pharmacologic effect of the gases at increased pressure and the physiologic effect of pressure itself (99).
A measure of the safety of HBO can best be described by Pascal's Law, where in a confined space, any contained fluid will transmit the pressure evenly throughout the fluid non-destructively. The human skin envelope contains the fluid of all the body's tissue (gas is not a problem in sinus spaces if vented by an open ostia and in the middle ear if vented by a patient's functioning Eustachian tube) (100). By virtue of the principle of Pascal's law, a patient may be ventilated without barotrauma by pressurized gas at the same pressure as that of hyperbaric chamber pressurization. Ventilators have been developed to do this safely, and chambers can be fitted with all the functions of critical care hospital units (101, 102).
Henry's Gas Law states that the concentration of a solute gas in a solution is directly proportional to the partial pressure of the gas over the solution. Inhalation of HBO at three atmospheres of pressure allows enough dissolved oxygen (6.6 volumes%) in plasma to supply the metabolic extraction rate of most of the tissue in a human body at rest (103).
The operational safety of hyperbaric medicine units has evolved through adherence to developing safety guidelines. This has allowed a remarkable safety record for hospital-based units for equipment, patients, and healthcare providers for both multiplace and monoplace chamber facilities (104, 105).
At the 21% oxygen content of air in one atmosphere, hemoglobin makes up for plasma's inability to deliver adequate oxygen to tissue. This is because a subject breathing air would have, at maximum, a 0.48 volume% of plasma dissolved oxygen, which clearly would not be enough to support human life (0.003 ml × 21% × 760 mmHg, where 0.003 ml is the amount at one atmosphere of oxygen dissolved in plasma for each mmHg of pressure, 21% is the oxygen content of air, and 760 mmHg is the pressure for each mmHg of pressure in the atmosphere at sea level) (106). Using the same equation for breathing 100% oxygen at one atmosphere, the maximum amount of dissolved oxygen in plasma would be 2.3 volume%. As mentioned, this would be far below the average oxygen extraction rate of most human tissue with the body at rest. To get around this problem, hemoglobin serves as a powerful gas clathrate, especially for oxygen. When a red blood cell picks up oxygen in the lung and discharges it in the periphery, the maximum oxygen conceivably dissolved in plasma would be 2.3 volume% at both ends of the line.
Plasma delivers the oxygen from the red blood cells to the endothelium, where it diffuses into the interstitial fluid, then diffuses through cellular membranes into the cytosol, and finally passes into the intermembrane space (IMS) of mitochondria. HBO administered at three atmospheres of pressure (SEFIO2 300%) allows 6.6 volume% of oxygen to be dissolved in plasma. It is this concentration that begins its journey by diffusion through the capillary endothelium, ultimately filling the IMS of mitochondria minimally with the 1.5–2.0 mmHg of dissolved oxygen requisite for the electron transport chain along with ATP synthase to produce ATP (107). Figures 3, 4 demonstrate this process.
Figure 3. The most oxygen that can conceivably be dissolved in plasma by a subject who breathes 100% oxygen is 2.3 volume%, and the plasma level enters the red blood cells in the lung capillary, where the blood content can be boosted as high as 20 volume% by the presence of the gas-clathrate-like function of hemoglobin. When the red blood cell gets to its destination in a capillary of distant tissue, the highest possible concentration as the oxygen unloads from the red blood cell into the plasma possible at normobaric pressure is again at the very highest, 2.3 volume%. Under hyperbaric conditions at three atmospheres of pressure, the equivalent amount of oxygen possible in plasma during the circulatory route all the way to distal capillaries at the very highest would be 6.6 volume% (108).
Figure 4. The increased ability of hyperbaric oxygen allows for an increased quantity of dissolved oxygen in body fluids. The facilitated delivery of oxygen thereby to the IMS of mitochondria throughout the body provides for necessary oxidative phosphorylation. Oxygen, by attaching to the cytochrome 3 oxidase enzyme of the mitochondrial electron transport chain, produces the necessary supply of hydronium ions for ATP.
The increased diffusivity of oxygen in tissue afforded by hyperbaric pressure is important. Krogh has described the diffusion distance of oxygen from plasma through the capillary endothelium (95, 97). This has been further expounded upon to include the added effect of the diffusivity of oxygen in the hyperbaric environment (99) as demonstrated in Figure 5.
Figure 5. Krogh calculated the diffusion distance of oxygen outside of capillaries into tissue when a human breathed normobaric air. Extrapolation incorporating three atmospheres of pressure provided by hyperbaric treatment would provide a fivefold improvement in diffusion distance (94, 110).
Tissue oxygen capacitance increases during and after an HBOT treatment. The oxygen that is onloaded into the tissue during HBOT is, in part, slowly off-gassed, much like an inert gas with tissue elimination half-lives supplemented by the additional elimination of oxygen by metabolic consumption (109). Furthermore, some oxygen is retained in tissue by attaching to cellular gas clathrates [i.e., neuroglobin (110), cytoglobin (111), and myoglobin (112)]. With serial HBOT treatment, tissue oxygen capacitance increases (113).
The red blood cell, as a biconcave disk, has a shape that maximizes its surface area. As a short-lived bag of hemoglobin, the mature red blood cell does not have mitochondria or a nucleus. An important mission of the red blood cell is to overcome the poor solubility of oxygen in plasma at one atmosphere in order to adequately get a supply of oxygen to mitochondria. The use of HBOT, especially in remote settings, has compelled some tertiary urban trauma medical staff to consider the development of a hyperbaric ambulance to mimic the success of the deck decompression chambers on operational sites to address injury of commercial divers (114). Figure 6 demonstrates this point.
Figure 6. Having a hyperbaric ambulance to bring immediate hyperbaric oxygen treatment to severely anemic, injured, or ill patients in transit to a hospital emergency department increases the chance of having the same success rate as commercial diving operations, which require a hyperbaric chamber on site for accidents.
A consideration of the potential toxic properties of a prolonged administration of O2 in almost all cases under normobaric, hyperbaric, or hypobaric exposures is a certainty (115–117). A judicious use of short-tie exposures of 60–90 min with intermittency of 5 min air breaks during administration and with gradual spreading of time intervals between treatments has thoroughly been documented to be safe, allowing the “hyperoxic–hypoxic paradox” prevail to the patient's benefit (118–120).
Conclusion
Red blood cells play an important role in the chain of oxygen delivery to the mitochondrial IMS. Finally, in the IMS, oxygen attaches to cytochrome c oxidase in the electron transport chain of enzymes embedded in the inner IMS (121). Reacting with the oxygen and hydrogen ions, cytochrome c oxidase expels the by-product of water. The hydrogen ions in the IMS fall down the molecular shoot of the ATP synthase nanomachine, and by rotary catalysis, Pi ions join with ADP to form ATP. It is an evolutionary wonder that the red blood cell without mitochondria carts oxygen to mitochondria in all the body's cells to provide the energy for the homeostasis of life.
HBOT, if used promptly, can serve as a bridge therapy to alleviate illness and injury when transfusion of red blood cells is necessary, otherwise requiring massive transfusion protocols. In other instances, HBOT could address severely anemic patients burdened with complicating comorbidities that otherwise would preclude the desirability of transfusion of red blood cells in any amount or by transfusion altogether. Hypoxic stress simulates recovery, and recovery requires energy provided by ATP.
Emerging ways that HBOT can safely and quickly be available are currently in existence (122). Hyperbaric units can be parts of emergency departments (123), intensive care units (124), and ambulances (114). Figure 7 shows schematics for a designed hyperbaric ambulance. The cost of an HBOT treatment is equal to the cost of a unit of blood and its administration (4). HBOT does not need type and crossing, or IV access, as the systemic dose of oxygen is administered via breathing or through a patient ventilator.
Figure 7. The best of all possibilities would be to have a hyperbaric ambulance system that deploys to the street to transport a severely anemic, ill, or injured patient under pressure with oxygen administration. Upon arrival at the hospital, the pressurized patient compartment would hydraulically depart the ambulance chaise and roll into the hospital emergency department to continue conventional normobaric resuscitation. The option could be for the detached patient compartment of the ambulance to mate with a hyperbaric intensive care multiplace chamber for continued hyperbaric resuscitation (113).
Author contributions
KV: Writing – original draft, Writing – review & editing.
Funding
The author(s) declare that no financial support was received for the research, authorship, and/or publication of this article.
Conflict of interest
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Keywords: anemia, normobaric oxygen, hyperbaric oxygen, adenosine triphosphate, advanced cardiac life support, advanced trauma life support, oxygen debt, normobaric oxygen paradox
Citation: Van Meter KW (2024) Hyperbaric oxygen therapy in the ATLS/ACLS resuscitative management of acutely ill or severely injured patients with severe anemia: a review. Front. Med. 11:1408816. doi: 10.3389/fmed.2024.1408816
Received: 28 March 2024; Accepted: 19 August 2024;
Published: 08 October 2024.
Edited by:
Carmine Siniscalchi, University of Parma, ItalyReviewed by:
Lucia Prezioso, University Hospital of Parma, ItalyAlfredo Caturano, University of Campania Luigi Vanvitelli, Italy
Costantino Balestra, Haute École Bruxelles-Brabant (HE2B), Belgium
Copyright © 2024 Van Meter. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Keith W. Van Meter, a3Zhbm1lJiN4MDAwNDA7bHN1aHNjLmVkdQ==