Clinical Trial Details
— Status: Completed
Administrative data
NCT number |
NCT05150418 |
Other study ID # |
1_08-06-2021 |
Secondary ID |
|
Status |
Completed |
Phase |
Phase 1
|
First received |
|
Last updated |
|
Start date |
November 26, 2021 |
Est. completion date |
June 14, 2022 |
Study information
Verified date |
July 2022 |
Source |
Oslo University Hospital |
Contact |
n/a |
Is FDA regulated |
No |
Health authority |
|
Study type |
Interventional
|
Clinical Trial Summary
Supplemental oxygen is frequently administered in acutely and critically ill patients,
specifically, it is often administered in trauma patients to avoid arterial hypoxemia and
tissue hypoxia. There is also an increasing focus on potentially deleterious effects of
hyperoxia. Further, the hemodynamic response to hyperoxia in hypovolemia is poorly
understood.
The present study aims to investigate the effects of supplemental oxygen on systemic and
cerebral hemodynamics in simulated hypovolemia in healthy volunteers.
Description:
The overriding goal for the resuscitation of any critically ill patient is to ensure adequate
oxygen delivery. In critically ill patients, SaO2 and PaO2 may be reduced due to lung
dysfunction (e.g. atelectasis and shunt flow). Under normal circumstances, SaO2 is near to
100%, and supplemental oxygen can not increase this further. Thus, in this circumstance,
providing supplemental oxygen will only increase a small, dissolved proportion. Although this
proportion may be a significant fraction in some circumstances, the intention of giving
supplemental oxygen is in most circumstances to ensure a high SaO2. Supplemental oxygen has
been extensively used in acutely critically ill patients to avoid hypoxemia, and is
recommended in severely injured trauma patients, as given by the statement: "Supplemental
oxygen must be administered to all severely injured trauma patients." in the ATLS (Advanced
Trauma Life Support) guidelines.
Accordingly, supplemental oxygen is often given to trauma patients, often resulting in
hyperoxia. The clinical evidence for providing supplemental oxygen in all trauma patients is
however scarce. The liberal use of supplemental oxygen has also largely been founded on a
perception that supplemental oxygen is harmless, and that it is safer to err on the side of
hyperoxia. There is however an increasing focus on possible deleterious effects of hyperoxia,
especially in specific clinical circumstances. This has led to recommendations of more
restrictive use of supplemental oxygen, often titrated to no more than what is necessary to
achieve an adequate arterial oxygen saturation (e.g. in the range 94-98%).
In the initial treatment of trauma patients, detection and treatment of hypovolemia is of
paramount importance. Hypovolemia leads to reduced cardiac filling and stroke volume. Under
normal circumstances in unanesthetized humans, this is compensated by an increase in systemic
vascular resistance and heart rate to maintain a normal or near-normal mean arterial pressure
(MAP). At some point, these compensatory mechanisms are exhausted, and MAP typically falls
abruptly.
Lower body negative pressure (LBNP) is a model of central hypovolemia where negative pressure
is applied to the body from the waist-down. Thereby, blood is displaced from the central
compartment of the upper body to the lower extremities and pelvis. The model has been used
for more than half a century and is considered useful model for studying hypovolemia in
conscious volunteers.
Normobaric hyperoxia induces vasoconstriction and reduced blood flow to several organs,
including the brain, heart and skeletal muscle. One could therefore hypothesize hyperoxia
leading to both an increased tolerance to hypovolemia mediated by vasoconstriction as well as
a reduced tolerance mediated by reduced cerebral blood flow. One study using the LBNP-model
did not find that supplemental oxygen significantly affected the hemodynamic response to
simulated hypovolemia. This study did however only apply one level of LBNP and did not
specifically study cerebral circulation.
Based on the above, there is a need for studies on the effects of normobaric hyperoxia on the
hemodynamic response to hypovolemia. In the present study, we will study the effect of
supplemental oxygen in the LBNP-model of hypovolemia in a crossover study on healthy
volunteers.
In the present study, 15 healthy volunteers will be exposed to LBNP with oxygen or room air
in randomized order in a crossover fashion. We will measure cardiac outout, stroke volume and
middle cerebral artery blood velocity to explore effects of oxygen on these variables during
hypovolemia.