Rx Pad

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 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.

Below you'll find some of the questions we get asked about the Introductory Course in Hyperbaric Medicine (ICHM) - along with our honest answers. We'll tell you everything about the program and what it takes so you can make the best enrollment decision for you.

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

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?