Rx Pad

The Use of Drugs Under Pressure

A hyperbaric and hyperoxic environment creates numerous considerations for the use of drug therapies within it. First, the physical stress of hyperbaria impacts drug storage and has implications on which containers are most appropriate for use. Second, physiologic changes to the body from hyperbaria and hyperoxia may lead to pharmacokinetic changes in drug disposition. Lastly, hyperbaric oxygen acting as a drug can interact and enhance or ameliorate the physiologic effect of a drug.

Current knowledge indicates that there are multiple mechanisms of action of hyperbaric oxygen therapy in CO poisoning. Based on the law of mass action, elevated partial pressures of O2 will accelerate the rate of CO dissociation from hemoglobin. Thus, COHb half-life can be decreased from approximately 5 .5 hours when breathing air and to approximately 20 minutes when breathing O2 at 3 ATA. Indeed, this was the reasoning behind the first clinical implementation of hyperbaric oxygen therapy for CO poisoning. As the COHb level is not associated with clinical risk, it is hard to accept that a more rapid dissociation of CO from hemoglobin could be the central factor for the benefit of hyperbaric oxygen . A fraction of the acute mortality from CO is due to hypoxia, however, and prompt removal of CO from hemoglobin will be of benefit . HBO2 also promotes normalization of tissue hypoxia. CO binds to cytochrome oxidase, particularly when the COHb level exceeds 40% to 50% . Brown and Piantadosi demonstrated that hyperbaric oxygen at 3 ATA markedly accelerates the dissociation of CO from cytochrome oxidase. Furthermore, it was shown that HBO2 completely reversed brain mitochondrial electron transport chain inhibition by CO. Hyperbaric oxygen also has effects related to the cascade of vascular injury triggered by CO poisoning. Hyperbaric oxygen was found to be effective for preventing brain oxidative injury through increased heme oxygenase and upregulation of antioxidants. The mechanism appears to be associated with denaturation of a membrane-associated guanylate cyclase that plays a role in coordinating the elevated affinity of beta 2 integrins expressed on the cell surface. Given that vascular changes are prominent in clinical CO poisoning, it is feasible that neurological sequelae in patients may involve a perivascular injury mediated by leukocyte sequestration and activation. Moreover, HBO2 reduces neuronal apoptosis and necrosis, and it also mobilizes stem cells via a nitric oxide–dependent mechanism. Hence, timely administration of hyperbaric oxygen may ameliorate the cascade leading to brain injury via multiple mechanisms.

An Introduction to Carbon Monoxide

Carbon monoxide is a colorless, tasteless, and odorless gas. It is one of the leading causes of injury and death worldwide. Based on death certificate data, mortality from unintentional, non-fire-related carbon monoxide exposures results in an average of 439 deaths each year in the United States. However, with improved data collection through the Center for Disease Control, estimates may be closer to 2,000 deaths per year. In 2014, the National Poison Data System listed gases/fumes/vapors as the leading cause of death in children five years old or less. Furthermore, carbon monoxide poisoning results in more than 200,000 emergency department visits per year and more than 20,000 hospital admissions. 

Carbon monoxide (CO) originates from incomplete combustion of carbon-containing materials. Common external exposure sources include house fires, automobile exhaust, ice resurfacing machines, furnaces, burning of charcoal, wood, and natural gas for heating or cooking, propane-powered equipment, and methylene chloride paint stripper.

Another major source of CO is cigarette smoking. Average carboxyhemoglobin levels (COHb) of 3 .0%–7 .7% are found in heavy cigarette smokers, compared to 1 .3%–2 .0% in nonsmokers.

Carbon monoxide poisoning can occur occupationally (i.e. firefighters, ice resurfacing machine or forklift operators), unintentionally, and as a means of suicide. The incidence of carbon monoxide poisoning increases during power outages caused by natural disasters. Interestingly, since the introduction of the Clean Air Act in 1970, the mortality rate from motor vehicle–related CO poisoning has declined. Carbon monoxide is also produced endogenously through the degradation of hemoglobin by heme oxidase, resulting in detectable carboxyhemoglobin levels in nonexposed individuals.

In industry, the major factor for carbon monoxide exposure is inadequate ventilation where propane-powered vehicles are used. Exposures from forklifts and ice resurfacing machines have been reported. Other work environments that produce large amounts of CO, and therefore heighten the risk of poisoning, are the steel industry, due to coke ovens, and the paint industry, in which inhaled methylene chloride (dichloromethane) is metabolized to CO by the liver. Firefighters and other first responders are also at increased risk for CO poisoning from smoke inhalation and from entering environments with elevated CO levels unknowingly. 

Men have higher rates of death from carbon monoxide poisoning, presumably due to higher risk behaviors and environments. The elderly (age ≥ 65) are also at increased risk for death from CO poisoning as they are more likely to dismiss symptoms as being caused by underlying medical conditions more prevalent in this population.

Women and children, however, are more likely to be exposed to carbon monoxide, and most exposures occur in the winter months (November to February).

Source Reference: Excerpted from Hyperbaric Medicine Practice 4th Edition with permission from the publisher. Reference Chapter 13, Carbon Monoxide by Jillian Theobald

Learn More

Are you seeking basic training in hyperbaric medicine? Our UHMS and NBDHMT approved 40-hour Introduction to Hyperbaric Medicine training course will teach you and your team the key fundamental elements and concepts in practicing hyperbaric medicine safely and effectively. Find your course today! https://www.woundeducationpartners.com/live-courses/hbo-courses.html

Part 2.2 How Accidents Happen: Personnel & Management as Contributing Factors in Hyperbaric Facility Accidents

In this installment of How Accidents Happen we continue looking at personnel & management as contributing factors in hyperbaric facility accidents.

In the past several years, there has been rapid growth in the number of clinical hyperbaric facilities, due in part to the availability of the monoplace, or single-person, hyperbaric chamber and the proliferation of outpatient wound care centers. Monoplace chambers are relatively inexpensive, require fewer personnel, and require less space to operate and maintain than multiplace (walk-in) chambers. Another advantage of the monoplace over the multiplace chamber is that attendants need not enter the hyperbaric chamber with the patient. However, some hyperbaric physicians express concerns about treating unstable or critically ill patients in the monoplace chamber, because of the lack of “hands-on” care during hyperbaric exposure, the lack of suitable equipment for optimal patient care, and the limitations of treatment pressures to 3 atmospheres absolute pressure (ATA). We have found that with a well-trained staff and the availability of appropriate equipment, critically ill patients can be treated safely in the monoplace chamber. We, and others, have presented monoplace chamber use in critically ill patients. Anyone who anticipates treating critically ill patients in a monoplace chamber should be familiar with this work.

Adequate wound perfusion and its delivery of oxygen to the healing tissues is fundamental to wound healing as just explained. Revascularization invariably is the first intervention considered to achieve this goal. Hyperbaric oxygen all too often is not considered in the management. In addition, other interventions can improve perfusion-oxygenation. These include edema reduction, improvement in cardiac function through medical management, and enhanced blood rheology using pharmacological methods. In contrast to the other four treatment strategies where typically a single technique is utilized, the methods to improve the perfusion-oxygenation strategy are complimentary, and typically two or more techniques are employed simultaneously.

The second source of information regarding perfusion-oxygen needs for wound healing arises from indirect information . It is obvious that markedly increased blood flow and oxygen availability are required to heal a wound and control infection.⁽¹⁹⁾ Perfusion and oxygen requirements are minimal for noncritical tissues that do not have wounds or infections because they are in a steady-state, resting status. An example of this would be the feet of the patient with advanced peripheral artery disease. If a relatively minor wound occurs in one foot, healing may not occur, and a lower limb amputation becomes necessary. In contrast, in the opposite limb that does not have a wound, but perfusion is equally poor, the foot is not immediately at risk for an amputation.

In general, fire prevention is described in terms of the Fire Triangle model. For a fire to occur, a fuel, an oxidizer, and an ignition source must be present. Fire prevention in a hyperbaric chamber must account for an increase in the oxygen component of the atmosphere in terms of both oxygen fraction and partial pressure. The resultant increase in oxygen renders what might be inactive fuels and ignition sources in a “normal” air environment active, which increases the risk of a fire.

Wound oxygenation is an essential strategy for the management of wounds regardless of their severity. Fortunately, in most wound healing situations, autoregulatory mechanisms ensure that oxygen is adequate to meet metabolic requirements. When not adequate, wound healing may be impeded or even totally interrupted, infection may not be controlled, and tissues may die, leading to limb amputations . Wound oxygenation is a function of perfusion. This part of the three-part series discusses oxygen requirements for wound healing and control of infection and methods (and their rationale) for augmenting wound perfusion-oxygenation and introduces the subject of hyperbaric oxygen (HBO₂) as a tactic for mitigating hypoxia in wounds in particular and in other conditions where HBO₂ is useful in general.

Safety in a hyperbaric chamber begins with design and specifications that are incorporated in construction codes such as the ASME Boiler and Pressure Vessel Code. ASME and related codes establish minimum standards for materials utilized in the construction of a chamber and how those materials are fabricated.^₂ Subcodes address specific requirements for pressure vessels intended for human occupancy and the viewports utilized in the chamber.³ ASME codes focus on maintenance of the structural integrity of the chamber during routine operations as well as providing safety components such as pressure relief valves to reduce the potential for catastrophic failure of the chamber in the event of overpressure resulting from fire or other mishap. A chamber will undergo inspection, testing, and be stamped to indicate that it has been manufactured in compliance with the applicable pressure vessel code. In many locales, only stamped pressure vessels are allowed to be utilized.

For some accidents there is a clear “smoking gun.” However, most accidents are caused by a combination of factors, each of which contributes in some manner. Often these factors accumulate over some period of time preceding the accident. This chapter addresses the factors that foster conditions under which accidents are more likely to happen and discusses some of the steps to be taken to avoid them. Also included is a case history illustrating several of the factors.

Determing the best interventions, including dressing selection, for patients and their wounds requires looking at the situation holistically. Creating the treatment plan for a chronic wound is dependent upon many diverse patient, wound, economic, and social considerations. The dressing selection goes beyond simply choosing a product to cover the wound. Details assessments of the patient and wound should drive the components of goal-directed wound care. The health-care provider must determine the etiology of the wound, patient comorbidities that may impair the wound healing process (e.g. diabetes and blood glucose levels), nutrition/hydration status, systemic and local tissue oxygenation, and patient/familiy concerns such as pain and odor issues. Each of these factors contribute to creating an individualized plan for care for choosing the most appropriate products and interventions. 

We are pleased to announce Michael White, MD, UHM, MMM, CWS as the incoming Medical Director for Wound Care Education Partners. Dr. White is assuming the role from the outgoing Medical Director, Helen Gelly, MD, FUHM, FACCWS, UHM/ABPM.

In this 3 - Part series, we're looking at the most commonly used classification scales currently in use to classify diabetic foot ulcers, including: 

There are many scales that attempt to classify diabetic foot ulcers, but few have been validated and none have demonstarated prognistic reliabilty or accuracy with regard to healing a DFU. Some scales focus on anatomy (depth of ulcer), some include vasular assessment, and others include the presence or absence of infection.

Diabetes mellitus is an epidemic of global proportion with a steadily rising prealence of disease. There were an estimated 28.9 million (21 million diagnosed, 8.1 million undiagnosed) adults with diabetes mellitus in the United States in 2012. The prevalence of diabetes mellitus among adults has quadrupled from 1980 to 2014. This rate continues to rise, with 1.7 million new cases reported in 2012. Globally, it is estimated that there are 422 million adults with diabetes mellitus. 

This is the third and final installment in the series about how to prepare your patient for wound care treatment.

COVID-19 Information as related to wound care and hyperbaric medicine

We have aggregrated information and resources for you that answer many questions and offer the latest knowledge, research, and treaments of COVID-19 as related to wound care and hyperbaric medicine.

Question: I am interested in the CHT classes. Can you guide me as to what I need? I just finished an EMT course. Do I need to be certified EMT to take the CHT classes?

First, a huge and heartfelt thank you to all providers who have been called into action on the front lines of the COVID-19 response. Thank you. 

Question: I am interested in adding hyperbaric oxygen therapy to my clinic. What are your recommendations for staff education and management of hyperbaric medicine in my clinic?

Answer: The first step we recommend is that you attend a 40-hour UHMS and NBDHMT approved basic training in hyperbaric medicine course, Introduction to Hyperbaric Medicine. Wound Care Education Partners offers the course many times per year across the U.S., and we could also do onsite training at your facility.

Upcoming course dates and locations can be found at the following link https://www.woundeducationpartners.com/live-courses/upcoming-courses.html

As for management, we recommend that you attend our Business of Wound Care and Hyperbaric Medicine course. This 16-hour CME/CEU course guides you through the administration of operating and managing a profitable wound care/hyperbaric clinic. This course is offered a few times per year at various locations across the U.S. 

Find upcoming courses at the following link: https://www.woundeducationpartners.com/live-courses/the-business-of-wound-care-and-hyperbaric-medicine.html

For more information on any of our courses please contact us at This email address is being protected from spambots. You need JavaScript enabled to view it. or call 5

Although the incidence of clostridial myonecrosis infections has dropped precipitously in recent decades, it always remains a threat in injuries where contamination and severe tissue disruption have occurred.

We often get the question, "Are there pre-requisites for taking the CHT course?"

PHYSICIAN - WOUND CARE (FT)

A question that we get frequent phone calls about is regarding physician supervision of Hyperbaric Oxygen Therapy (HBO). Here are the answers to some of the most frequently asked questions . . .

We receive a number of phone calls each week from folks inquiring how to become a Certified Hyperbaric Technologist (CHT).  The added qualification of CHT is administrated by the National Board of Diving and Hyperbaric Medical Technology (NBDHMT).

Clinic and Hospital Administrators: Do you need to get your staff trained in hyperbaric medicine but have a limited budget?

Sinus and internal and external ear disorders are the most common side effects of hyperbaric oxygen therapy (HBO₂).¹ These spaces are the cranium’s pneumatic sockets and, particularly those of the middle and inner ear, are most frequently involved in the pressure stress caused by compression and decompression maneuvers during exposure to altered pressures in the hyperbaric chamber. Barotrauma is the mechanical tissue damage produced by environmental pressure variation, and the middle ear is the most frequently involved structure in this kind of damage. According to Boyle’s law (the product of pressure and volume is a constant for a given mass of confined gas) it is easy to understand why all enclosed air cavities are more susceptible to this kind of lesion. Barotraumas can occur due to an increase or decrease of gas volume. To avoid gas volume decrease during the compression phase, the patient must perform some compensatory maneuvers aimed at inhaling and forcing gas (air or oxygen) into the nasal and sinus cavities. During decompression in the chamber or even underwater, the body’s gas expands and is expelled from cavities to the outside, usually without any active maneuver. It is essential to teach the patient about the functions of the hyperbaric chamber and the correct maneuvers of baro compensation. In this article, we will describe the main barotraumas that can occur during hyperbaric oxygen therapy.

We conduct and announce a lot of courses in hyperbaric medicine throughout the year. Each course is a little different, with unique aspects we would like to highlight to help you decide which course might be a good fit for you to attend.

We get a lot of questions from hospital administrators and clinic directors asking what makes our Introductory Course in Hyperbaric Medicine unique. While there are many benefits to hosting hyperbaric team training through Wound Care Education Partners (WCEP), we have broken out the four most valuable reasons why hosting a live, classroom-based Introductory Course in Hyperbaric Medicine with WCEP may be right for your facility. Watch this short, insightful video to find answers before you book hyperbaric team training with any organization.

Many refer to Dr. Eric Kindwall at the "Father of Hyperbaric Medicine," and his contributions to hyperbaric medicine are legendary. Dr. Kindwall was born on January 17, 1934 and passed away on January 18, 2012. For this reason, we find it fitting to highlight his contributions to the field of hyperbaric medicine during the month of January.

We all learn about barotrauma in the Introductory Course in Hyperbaric Medicine. The question we have for you today is whether or not you remember the mechanisms of what causes barotrauma and how to properly pre-screen HBOT patients.

Question: "I would be interested in the current perspective regarding supervision of hyperbaric dives by Nurse Practitioners.

Question. Is myocardial irritability a complication frequently experienced by patients with clostridial myonecrosis?

Cardiac arrest is a rarity in the chamber, as most arrhythmias seem to improve under hyperbaric conditions. Anecdotally, it can be noted that one patient with a myocardial infarction, who was being treated with hyperbaric oxygen as part of a research study, suffered 30 cardiac arrests during the 48 hours he was being treated with the chamber. The schedule being followed called for two hours at pressure in the chamber followed by one hour on the surface. This cycle was repeated for two days. It can be seen that the patient spent only 1/3 of his time breathing air on the surface. During the study, the patient suffered 28 cardiac arrests while breathing air on the surface, but only two arrests while at pressure in the chamber. The patient eventually recovered and returned to work. (Thurston, J. Westminster Hosp, London, Personal Communication, 1973.)

The cardiovascular assessment of a critical care patient receiving hyperbaric oxygen therapy is similar to any cardiovascular assessment of a critical care patient. Cardiac rhythm should be assessed and monitored during the treatment. If the patient would experience a cardiac emergency during HBO treatment, the staff should be trained to handle such an emergency. It is important to remember that a patient at depth is well oxygenated and will remain so for 5 to 8 minutes. The safest way to bring a patient that has had a cardiac arrest to the surface is to bring them up at 5 psig (fastest rate on a monoplace chamber), while the staff prepares to deliver emergency care. Performing a rapid ascent using the emergency ascent button on monoplace chambers places the person at grave risk for air embolism due to expansion injuries. Once the patient has surfaced, move them to the point farthest away from the open chamber, remove the hyperoxygenated clothing, and if appropriate, defibrillate. Cold oxygen will fall to the floor and dissipate in 30 seconds, so do not place the area at an increased fire risk with the use of a defibrillator. The staff needs to be able to respond quickly and appropriately to such an emergency, so it is our recommendation that the staff be Advanced Cardiac Life Support (ACLS) certified.

Hyperbaric oxygen exposure can produce significant hemodynamic changes. An increase in systemic afterload due to hyperoxic vasoconstriction in well perfused tissues can lead to a decrease in left ventricular function and a decrease in ejection fraction in some patients. When this decrease in left ventricular function occurs in the setting of pulmonary arterial vasodilatation due to improved alveolar oxygenation with increased left atrial and left ventricular filling, acute left ventricular dysfunction and pulmonary edema can result. Cases have been reported in patients with a history of pulmonary edema or low left ventricular ejection fractions or in patients with sudden fluid shifts from volume overload. Acute pulmonary edema appears to be more common in monoplace than multiplace treatment settings, perhaps because of the requirement for patients to be in a more supine position in the monoplace chamber rather than the sitting position with legs dependent available in the multiplace chamber.

Question. What sparked the dawn of the modern hyperbaric era?

Question: Each winter many hyperbaric oxygen therapy patients have difficulty getting to their scheduled treatments due to inclement weather. What recommendations do you have for helping keep patients' treatment schedules on track when the weather is a barrier to treatment?