Effect of hyperbaric oxygen therapy on blood pressure in patients undergoing treatment

Abstract

Introduction: Hyperbaric oxygen (HBO2) therapy is generally safe and well tolerated. However, known side effects do exist. Elevation in the blood pressure of patients undergoing HBO2 therapy is a less defined potential side effect. We sought to better quantify effects of HBO2 on blood pressure (BP) in patients undergoing HBO2. Methods: A retrospective chart review was performed on quality assurance data captured on all patients undergoing HBO2 between March 2012 and October 2015 at a large tertiary referral university hospital hyperbaric center. Results: We identified 155 patients who received 3,147 hyperbaric oxygen treatments. For all treatments there was an overall increase in the median systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) following treatment (Table 2). No statistically significant difference was found when comparing patients with and without hypertension. Calcium channel blockers (CCB) and beta-blockers (BB) were found to have an agonizing effect while ACE inhibitors (ACEI) were found to have a protective effect (Table 4). The change in SBP was less with each additional treatment in patients undergoing more than one treatment. Discussion: The current study demonstrates that absolute rises in blood pressure do occur as a result of HBO2 therapy. However, the extent of this effect is not large. BB and CCB had agonizing effects while ACEI had a protective effect. Finally, there was a protective effect with more treatments.

Magnitude and Clinical Predictors of Blood Pressure Changes in Patients Undergoing Hyperbaric Oxygen Therapy: A Retrospective Study

“…Lower baseline ABP presumably predisposed patients to a greater increase in ABP after HBOT, thus future work is warranted to determine reproducibility of this effect. Interestingly, in contrast to Heyboer et al [ 8 ], the current study showed an exponential increase in ABP after each HBOT treatment ( Figure 1 ). This trend was more evident between patients with a history of hypertension compared to normotensive patients ( Figure 2 ); it is likely that the vasoconstrictive response becomes more pronounced after treatment, and it may either represent an improved arteriolar smooth muscle activity or a lack of vasorelaxation.…”

“…It is suspected that such hemodynamic changes observed during and after HBOT can be ascribed to a protective vasoconstriction response [ 6 ]; however, the magnitude of this response is not well described, and conflicting scientific evidence is found in the literature. In a recent report, Heyboer et al (2017) [ 8 ] evaluated 155 elective patients, for a total of 3147 HBOT sessions, and showed an increase in ABP after treatment in the range of 4–7 mmHg [ 8 ]. These findings were in accordance with several additional studies that found no significant changes in ABP following HBOT [ 15 , 19 , 20 ].…”

“…The mechanism triggering vasoconstriction is related to the loss of vasorelaxation that is generated by hyperoxia-induced oxidation of nitric oxide radicals produced by the endothelium [ 6 ]. Additional contributors to vasoconstriction include a decrease of vasodilatory prostaglandins, an increase of vasoconstrictor endothelin-1 [ 8 ], and potentially a direct stimulation of the sympathetic nervous system producing an increase in plasmatic epinephrine and norepinephrine [ 7 ], even though the latter has been recently questioned suggesting a direct inhibition of the sympathetic outflow [ 9 ]. Overall, the arteriolar vasoconstriction leads to increased systemic vascular resistance causing arterial hypertension [ 6 , 10 , 11 , 12 ], which results in stimulation of baroreceptors [ 9 ] and cardio-inhibitory center [ 13 , 14 ] with subsequent increase in parasympathetic activity and decreased heart rate.…”

“…Despite these clinical findings, there are conflicting results about the incidence and magnitude of HBOT induced hemodynamic changes. Several studies have shown only mild fluctuations in ABP during HBOT [ 8 , 15 , 16 ], while one study showed a significant increase in ABP, particularly in patients with chronic hypertension and diabetes [ 17 ]. Medical therapy with beta-blockers and calcium-channel antagonists [ 8 , 17 ], as well as the different levels of barometric pressure utilized during HBOT [ 8 ] may account for the differences in the reported proportional rise of ABP.…”

Mechanistic Rationale and Clinical Efficacy of Hyperbaric Oxygen Therapy in Chronic Neuropathic Pain: An Evidence-Based Narrative Review

“…It is well described that HBOT causes vasoconstriction and decreases edema [13,33]. It is suggested that the hyperoxic environment leads to increased oxidation of NO radicals produced by the endothelium and a loss of the vasorelaxant effect [51], alterations in other vasodilator compounds (i.e., prostaglandins) [52], and stimulation of central vasoregulation via the sympathetic nervous system [53]. Indeed, an RCT of patients with CRPS [33] demonstrated improved range of motion and decreased edema following HBOT.…”