Hypovolemia is the condition under investigation. Hypovolemia is induced by the "lower body negative pressure" (LBNP)-model. MedDRA version: 20.0 Level: PT Classification code 10049771 Term: Shock haemorrhagic System Organ Class: 10047065 - Vascular disorders
Conditions
Interventions
Trade Name: Conoxia 100 % medisinsk gass, komprimert
Product Name: Conoxia 100 % medisinsk gass, komprimert
Pharmaceutical Form: Medicinal gas, compressed
Pharmaceutical form of the placebo: Medicinal
Sponsors
Oslo University Hospital
Eligibility
Sex/Gender
All
Inclusion criteria
Inclusion criteria: - Age > 18 years. - Age =65 years) no F.1.3.1 Number of subjects for this age range 0
Exclusion criteria
Exclusion criteria: 1. Any medical condition limiting physical exertional capacity or requiring regular medication (allergy and contraceptives excepted). 2. Pregnancy. 3. Breastfeeding. 4. History of syncope (syncope of presumed vasovagal nature with known precipitating factor excepted). 5. Any known cardiac arrhythmia. Prior/Concomitant Therapy 6. Any drug (contraceptives excepted) used on a regular basis for a chronic condition (allergy excepted).
Design outcomes
Primary
| Measure | Time frame |
|---|---|
| Main Objective: 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. ;Secondary Objective: The secondary objective is to determine the agreement between blood velocity in the medial cerebral and internal or common carotid arteries. ;Timepoint(s) of evaluation of this end point: Continuously during LBNP-exposure. ;Primary end point(s): Determine if there is an effect of supplemental oxygen on cardiac output during LBNP. Cardiac output will be measured continuously by volume-clamp method and suprasternal Doppler if needed (e.g. due to poor signal quality). The primary aim of the study is to test the difference of oxygen compared ro placebo. P-values <0.05 are considered statistically significant. Cardiac output will be entered as a continuous explanatory variable in a linear mixed effects regression model. Analyses will be performed by assigning variables (dummy coding) to each medication. Confidence intervals for the effect of each medication will be calculated using the glht-function of the “multcomp”-package in R with “single step” correction for multiple comparisons. No interim-analyses will be performed. Missing values will not be imputed, but are generally handled well in mixed effects regression models. The exact setup of the statistical model (e.g. random intercept vs. random slope, interaction effects, covariance structures etc.) will depend on details in the data. Analyses will be performed using the statistical software R (https://www.r-project.org/). | — |
Secondary
| Measure | Time frame |
|---|---|
| Timepoint(s) of evaluation of this end point: Continuously during LBNP-exposure. ;Secondary end point(s): • Effect of oxygen and LNBP on changes in middle cerebral artery blood flow velocity (MCAV). • Effect of oxygen and LNBP on changes in cardiac stroke volume. • Effect of oxygen and LNBP on changes time to decompensation. - Change in MCAV with increasing LBNP will be analyzed in a linear mixed effects model corresponding to cardiac output (see above). - Change in stroke volume with increasing LBNP will be analyzed in a linear mixed effects model corresponding to cardiac output (see above). - Time to hemodynamic decompensation will be compared between the three interventions in a mixed proportional hazards model (Cox regression). | — |
Countries
Norway
Contacts
Public ContactDepartment of Anesthesiology
Oslo University Hospital
Outcome results
None listed