Rx Pad

Did you know there are ways to:
Manage revenue cycle to meet (and exceed) budget goals
Discover patient revenue left on the table due to incorrect medical coding 
Increase patient load Become a profit center for the hospital 

Five years ago Wound Care Education Partners wrote a blog "How to Become Certified in Hyperbaric Medicine". In those years since the original post the field Hyperbaric Medicine has grown significantly. According to hyperbaric oxygen therapy market insights the CAGR (Compound Annual Growth Rate) for hperbaric medicine s expected to increase by 5.8% over the next four years. (TechNavo; Jan 2025, "Hyperbaric Oxygen Therapy Market Size 2025-2029" ) 

WOUND CARE CERTIFICATION BASIC TRAINING & REFRESHER COURSE  will be held this Saturday, February 1st , 2025. If you or your co-workers need this course sign up today before the cut off. (Next class is not till April)

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.

If you've been thinking of taking a training course to become certified in wound care (or need a refresher) - now is a great time to take action!

Learn Hyperbaric Facility Safety

There are two distinct aspects to the field of hyperbaric medicine that influence safety: 

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. 

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?"

"Before anything else, preparation is the key to success." - Alexandar Graham Bell

It's time to start planning now to earn your 2019 CME/CNE/CEU credits. Don't know how to start? Below are five questions to help you start the planning process, and watch the short video to get all the details.

PHYSICIAN - WOUND CARE (FT)

By providing community education to potential patients you are building awareness, and with that awareness we’re able to impact healing outcomes for patients in our community.

Have you thought about the impact of the front office operations in the success, health, and growth of your wound care and hyperbaric medicine clinic?

Question: Patients present to the wound care practitioner in a myriad of ways, how does the practitioner decide how to manage the wound?

These texts provide you with the most up-to-date, cutting-edge information for your wound care practice.  

This Tuesday, December 5 at 10am EDT we are hosting a live free webinar information session to discuss affordable solutions for hyperbaric staff training in 2018.

Even though millions are affected by various forms of lymphedema worldwide, the existing literature fails to fully define the population-based prevalence, health outcomes, and treatment costs of this disorder.

We get a lot of questions from students as to how they can prepare for their attendance at one of our live courses. Read below how to prepare. 

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.