Can hyperoxia and hyperbaric conditions induce a increase in systemic pressures (SBP, DBP, MAP) to the breathing of 100 percent oxygen at normal and hyperbaric barometric pressure?
Authors: Duvallet Alain Louis , Duvallet Emilie , Lhuissier François , Constantin Pascal , Beaudry Michele 
Published: November 2023

The objectives of this study were to assess systolic, diastolic and mean blood pressure (BP) levels with large increases of systemic oxygen while breathing hyperoxic gas.

The survey consisted of a repetitive measure of arterial pressure during a standardized compressions in a hyperbaric chamber (absolute pression : 2.8 bars, 41 psi), for 90 minutes while the breathing pure oxygen, with air breaks every 25 minutes to reduce oxygen toxicity, during a hyperbaric oxygen therapy (HBOT).

Methods

(see Fig1)

Systolic and diastolic blood pressure (SBP and DBP) were measured by auscultatory method, with calculated mean blood pressure (MBP). 57 volunteer subjects were recruited (mean age : 60.6 years +/− 15.8)

Result

(see Fig2)

In normoxia compared with the surface, outside and in the hyperbaric chamber (opened door), all pressures increase (SBP : 7.8%, MBP : 7% and DBP: 10.6%). Theses variations are significant.

Effects of depth: In normoxia, compared with the surface, at depth all pressures decreases (SBP : −2%, MBP : −2.2% and DBP : −22%). These variations are not significant.

Effects of hyperoxia (75 minutes: 3 × 25 minutes): all pressures increases gradually (SBP :17.3%, MBP :2.2% and DBP : 11%). These variations are significant.

Discussion

In this investigation of hyperoxia and hyperbaric conditions over the range of oxygen percent from 21 to 100% and the range of pressure from 1 to 2.8 atm absolue (ATA), we found that SBP, DBP and MAP were increased by stress, hyperoxia and pressure.

With a constant Pio2 (percentage FiO2= 21%) at outside and in hyperbaric chamber (opened door, ATA = 1), all blood pressures increase significantly; the stress before compression is the main increasing factor.

Constant percentage (FiO2 = 21%) and increasing PiO2 with the pressure (from 160 to 450 mmHg and from 1 to 2.8 respectively) have little effect with only a non‐significant decrease.

With constant hyperbaric pressure (P = 2.8 ATA) and increased percentage (FiO2= 100%) blood pressure are gradually increased, with significant differences after 75 minutes.

Hyperoxia increased the systemic vascular resistances with a rise of arterial pressure. The change is not major eventhough still increased over the normal clinical value for hypertension. This observation is in agreement with a cardio‐vascular regulation. Hyperbaric oxygen causes a reduction of 10–20% of cardiac flow, with a bradycardia and a reduction of the cardiac output. Arterial pressure is not noticeably changed, notwithstanding the generalized vascular constriction. If the vascular constriction can be interpreted as a defense mechanism against possible hyperoxic damage, it is evident that a parasympathetic response, and the sympathetic nervous system counteracts the pressure increase.

Under most circumstances (in our study hyperoxia and stress from hyperbaric treatment), the body attempts to maintain a steady mean arterial pressure.

But the response is not the same for all subjets. Future studies are important to have a comprehensive classification between responders and non‐responders or normotensive, prehypertensive and hypertensive subjets. That suggest complex patterns of regulation.

The results may have clinical implications for healthing subjets using oxygen‐enriched gas mixtures as well as for patients using oxygeno‐therapy as medical treatment.