Advanced investigation showed that ordinary ventilators used at normal atmospheric pressure cannot maintain stable VT during VCV when operated at high atmospheric pressure. Inspiratory flow provided by the ventilator will decrease with increasing ambient pressure [7,8,9,10]. The reason is that during HBO therapy, the ambient pressure is raised by compression air, which results in a high breath gas density and has no influence on breath gas viscosity. High breath gas density results in more turbulent flow in peripheral airways according to an increased Reynold’s value (>1000, Figure 5). To obtain the same inspiratory flow, turbulent flow produces higher airway resistance than laminar flow. Hence, more driving pressure (△P) must be provided by the ventilator to overcome the higher airway resistance; otherwise, it will lead to decreased inspiratory flow. Unless this phenomenon is technically compensated for, hypoventilation may occur due to decreased VT and MV [11,17]. To maintain adequate VT and MV, we need to increase the inspiratory flow as the chamber pressure increases through manual regulation or automatic compensation [7,8,9,10,16].
Evaluating VT during VCV at high ambient pressure
During VCV, the modified Shangrila590 ventilator can provide more △P to overcome the greater resistance and achieve constant VT and MV, even though VT and MV decreased within a narrow range. In the high VTset group (800-1000 ml), the decline in VT as the ambient pressure increased was greater than that in the low VTset group (400-600 ml) (Table 2, Figure 2). However, the degree of decline was smaller than that in previous research at the same ambient pressure scale, which resulted in a 20-56 % decline in VT [7,9]. Nonetheless, compared with the hyperbaric ventilator Siaretron IPER 1000, a 6.5-20 % increase in VT during VCV under 1.0 ATA to 2.2 ATA ambient pressure occurred, which is CE-certified for hyperbaric use in Europe [10]. A modified Penlon Nuffield 200 has been used in a monoplace hyperbaric chamber, fixed outside the chamber, with a 30 % decrease in VT with ambient pressure from 1.0 ATA to 2.0 ATA [16].
When we focused on the accuracy of VT displayed by the ventilator, it was not exactly equal to VT detected by the test lung. For VTset between 400-600 ml, the VT displayed by the ventilator may overestimate the actual VT Otherwise, for VTset between 800-1000 ml, the VT displayed by the ventilator may underestimate the actual VT. The difference in VT displayed by the ventilator and by the test lung was narrow during VTset between 400-600 ml, but it was wide during VTset between 800-1000 ml. However, the accuracy of the test lung in previous studies was controversial at high ambient pressure [7,9]. We used a water tank-simulated lung in pre-experiments, which can roughly reflect the true value of ventilator VT. The data between the ventilator and the water tank-simulated lung seemed good, but the numerical precision of the water tank-simulated lung was low. For statistical analysis, we decided to choose the Michigan test lung (5601i) for the test equipment, according to previous research [7].
During VCV, the goal of maintaining constant VT is to take in enough O2 and ensure expiration of CO2. Factors affecting the expiration of CO2 include not only Vt but also dead space and high PaO2. During HBO therapy, PaO2 is much higher than that under normobaric conditions. Under hyperbaric conditions, respiratory resistance leads to decreased breath gas flow and enlarged dead space. These may reduce exhalation of CO2 [18,19]. In addition to the stable operation of ventilators, it is essential to monitor the expiratory volume, arterial partial pressure of carbon dioxide (PaCO2), transcutaneous carbon dioxide tension (PTCCO2), or end-tide carbon dioxide partial pressure (PETCO2) [11,20].
Changes in Peak during VCV at high ambient pressure
Our data showed that the Ppeak displayed by the ventilator increased obviously during VCV with fixed VTset in the process of ambient pressure rise (Table 4, Figure 4). As Ppeak can reflect inspiratory resistance, the ventilator can provide more △P to overcome increased airway resistance to maintain stable VT. Our data shown in Figure 4 supports this mechanism. However, changes in Ppeak detected by the test lung were gentle because of the different detected positions of the ventilator and the test lung. The breathing gas flow was buffered when detected by the test lung.
Side effect of HBO in pulmonary system and preventive measures
In general, there is no risk of pulmonary barotrauma (PBT) in patients with normal lungs during HBO therapy. Based on Boyle’s Law, there is potential for PBT due to lung overinflation during decompression when disease is present, such as asthma or chronic obstructive pulmonary disease (COPD) with active bronchospasm, mucous plugging, and bullous lung disease. Additionally, pneumothorax (PTX) is a potentially life-threatening phenomenon, especially given the increased risk of tension PTX during decompression. All candidates for HBO therapy must be screened for pulmonary disease to avoid increasing the risk of PBT and PTX [21].
Continuous exposure of the lungs to elevated PaO2, either at normobaric or hyperbaric pressure, leads to toxic effects of O2. Pulmonary O2 toxicity can be avoided if O2 is provided at the proper dose [5,22]. When FiO2 is continuously high in normobaric environments, the lungs are at risk of O2 toxicity: (a) high FiO2 levels promote the formation of absorption atelectasis in the absence of nitrogen; (b) high FiO2 levels also induce ROS-mediated damage; and (c) another side effect of hyperoxemia is the rise in PaCO2 [22]. In the hyperbaric chamber, we can obtain higher PO2 by increasing ambient pressure with lower FiO2 to avoid absorption atelectasis. In rats, HBO exposure caused significant oxidative stress in the first 24 h. However, these effects were resolved at the end of the tenth day of HBO treatment [23]. There are two pathways for the development of CO2 intoxication. PCO2 is increased in inspired breathing gas or expiration of produced CO2 is insufficient [17]. Increased PCO2 in inspired gas may occur when gas exchange occurs in the hyperbaric chamber. To prevent raised PCO2 levels, hyperbaric chambers must be flushed continuously with breathing gas. Increased breathing resistance in the hyperbaric chamber may decrease the expiration of produced CO2. Maintaining stable pulmonary ventilation and monitoring PaCO2 by blood gas, PETCO2, and PTCCO2 must be established during HBO therapy [11,17,21].
Work of breathing in hyperbaric environments is also a concern. Combined with the breathing equipment itself, the work of breathing will be increased compared to breathing the same gas in a normobaric environment [6]. For patients on mechanical ventilation, the endotracheal tube diameter is critical with regard to its effect on airway pressure and work of breathing [18]. During HBO therapy, we must consider that a high breath gas density induces high airway resistance, which cannot be avoided in hyperbaric chambers. In addition to sputum aspiration and exchange for large endotracheal intubation, we can decrease airway resistance by prolonging the inspiratory time appropriately and using a helium oxygen mixture to decrease the gas density. Additionally, we can reduce the high airway resistance and breathing work by downregulating ambient pressure or upregulating the support pressure of the ventilator.