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Though we could not make a clear differentiation between primary (when patients want to be sedated approaching the moment of death) and secondary sedation (when sedation results as a "side-effect" in otherwise refractory symptom control [ 46], it must be clear to all, that the intention of sedation in the terminal and final phase is not a concealed form of euthanasia [ 47].
However, increased sedation results in disrupted sleep architecture that may impede the normal restorative functions of sleep.
A significant feature of murine physiology is that even mild sedation results in a loss of lung volume and subsequent hypoxemia [12].
Progressively increasing sedation results eventually in anesthesia which has been defined as "drug-induced loss of consciousness during which patients are not rousable, even by painful stimulation".
Also, the sensitivity analyses comparing dexmedetomidine separately with propofol or midazolam indicated that dexmedetomidine sedation results in lower ICU costs (Additional file 9: Tables S7 and S8).
Because anxiety is directly related to amount of sedation, results were modeled using a mixed-effects analysis to predict anxiety, sedation frequency, and intensity while adjusting for covariates of interest.
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For the ACC, no connectivity with the PCC was observed at baseline, but sedation resulted in increases in positive correlation in activity in the two regions.
Restarting sedation resulted in an ICP decrease to normal values without the need for additional osmotherapy.
Deep sedation resulted in greater physician satisfaction with procedural conditions as well as lower BIS scores but no significant difference in patient satisfaction compared with conscious sedation.
In a pre-post study, protocolized analgesia and sedation resulted in reduced sedative and opioid doses and reduced ventilation and ICU times [ 31].
One patient in the HFNC group deteriorated after the application of intravenous sedation resulting in apnea while on HFNC requiring transitioning to NIV.
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