What is the effect of deep procedural sedation with HFNOT on tcPCO2, mitoPO2 and mitoVO2

Deep procedural sedation has seen an increased use indication over the last
couple of years aided by the introduction of high flow nasal oxygen therapy
(HFNOT) during these procedures. However, this level of deep sedation does come
with the increased risk of examining whether a patient is adequately ventilated
during this procedure.
The definition of deep sedation is: *a drug-induced depression of consciousness
during which patients cannot be easily aroused but respond purposefully
following repeated or painful stimulation. The ability to independently
maintain ventilatory function may be impaired. Patients may require assistance
in maintaining a patent airway, and spontaneous ventilation may be inadequate.
Cardiovascular function is usually maintained.* As the definition showed there
may be an insufficient ventilation during deep sedation. Therefore, HFNOT is
used to ensures that the peripheral oxygen saturation is sufficient. However,
there are two potential disadvantages. HFNOT can mask the presence of an
insufficient respiratory minute volume and an insufficient gas exchange, which
can lead to high arterial CO2 (paCO2) levels. Another risk associated with
HFNOT is the fact that high oxygen levels are toxic, and prolonged exposure to
high partial oxygen pressures, can cause oxidative damage to cell membranes,
collapse of the alveoli in the lungs, retinal detachment, and seizures. Most of
this damage can be explained by hyperoxia that increases the 'leak' of
electrons from the mitochondrial electron transport chain and the resulting
increased generation of reactive oxygen species (ROS). Low paCO2 levels and
hyperoxia cannot be examined using standard monitoring techniques therefore,
this study will use the transcutaneous carbon dioxide (tcPCO2) a proven
technique which correlates well to the arterial CO2 (paCO2) to evaluate whether
there is an adequate level of ventilation during deep procedural anesthesia
with HFNOT. Moreover, the cutaneous mitochondrial oxygenation (mitoPO2) will be
monitored to determine the effects that deep procedural sedation with HFNOT has
on the cellular oxygenation.

Primary objectives:
- To examine the effects of deep procedural sedation and use of HFNOT on the
tcPCO2.
- To determine the effects of deep procedural sedation and use of HFNOT on the
mitoPO2

Secondary Objective:
- To determine the effects of deep procedural sedation and use of HFNOT on the
mitoVO2

Single center observational trial in patients undergoing deep procedural
sedation.

The transcutaneous carbon dioxide measurements performed by the SenTec Digital
Monitoring System (SDMS) and the intracellular oxygen measurements performed by
the Cellular Oxygen METabolism (COMET) device are non-invasive and do not
require deviation from standard protocol. Mild possible discomfort may arise
from the use of the aminolevulinic acid plaster or the COMET Sensor Holder
which will be attached to the arm during the study period. Overall the risks
are considered negligible and the burden low.