Cardiac versus vascular responder types during combined hypoxia and hypoxic orthostatic stress.
- Paper number
IAC-18,A1,IP,32,x43458
- Author
Dr. Michael Nordine, Germany, Center for Space Medicine Berlin (ZWMB)
- Coauthor
Ms. Zeynep Masatli, Germany, Center for Space Medicine Berlin (ZWMB)
- Coauthor
Ms. Katharina Brauns, Germany, Charité Universitätsmedizin Berlin
- Coauthor
Prof.Dr. Hanns-Christian Gunga, Germany
- Coauthor
Dr. Oliver Opatz, Germany, Charité - University Medicine Berlin
- Year
2018
- Abstract
Acute changes in environmental conditions presents a hazard for manned space crews. One such scenario that could occur during take-off, orbital re-entry, or aerobraking maneuvers involves exposure to acute onset hypoxia combined with hypergravity. Hypoxia can result in systemic vasodilation, while resilience to hyper-gravity relies upon effective systemic vasoconstriction. An inability to mount an adequate vasomotor response during hypoxic hyper-gravity could result in an orthostatic event, possibly rendering a pilot of a space vehicle incapacitated, which could lead to critical mission compromise. This study set out to explore cardiovascular reactions occurring during acute onset hypoxia followed by rapid onset hypoxic lower body negative pressure (LBNP). We hypothesized that a vasodilatory response to hypoxia would lead to a greater propensity for orthostatic collapse during hypoxic LBNP. For this study, 29 healthy male subjects took part. Each subject was exposed to rapid onset normobaric hypoxia using a gas mixture of 12% Fi02 until 02 saturation dropped to 85%. Upon reaching 85%, -70 mmHg hypoxic LBNP was activated. The LBNP remained on until >60 seconds, or until an orthostatic event took place. The delta % change in systemic vascular resistance (SVRI mmHg*L/m2), cardiac index (CI L/m2) and absolute Sp02% were recorded throughout the study. During hypoxia, 17/29 subjects (Group D) experienced a -8.1% decrease in systemic vascular resistance index (SVRI), while the other 12 (Group I) exhibited an SVRI increase of 6.0%. This difference in SVRI was significant (p<0.001). In addition to this, Group D had a 15.0% increase in cardiac index during hypoxia, while Group I showed a 2.0% increase in cardiac index (p<0.001). No differences in 02 oxygenation, or time to 85% desaturation were found between the 2 groups. During hypoxic LBNP, there was a significant difference between the 2 groups regarding SVRI (Group D 2.0% vs Group I 45.7% p=0.003) and CI (Group D -12% vs Group I -33% p=0.008). No differences in Hypoxic LBNP time nor 02 Saturation were found between the 2 groups. In conclusion, the original hypothesis proposed was not supported. Despite the vasodilatory effects of hypoxia seen amongst the Group D subjects, resilience to hypoxic LBNP was no different than Group I. This was due to a reliance on cardiac, rather than vascular reactions, to maintain orthostatic stability in the face of an extreme environmental challenge. It appears that 2 types of response patterns are apparent during a combined hypoxic and hypoxic hyperG challenge.
- Abstract document
- Manuscript document
(absent)