I used to think that as Pcrit is the same during sedation and natural sleep, this means that the properties of the UA muscles remain intact under sedation, but then I read an old article that explained that because of the methodology to get the Pcrit, where the CPAP is on, the muscles don't have activity, and so you shouldn't expect to have a different Pcrit as, even if the drug would cause muscle relaxation, it would not make a difference in an already relaxed muscle....(Morrison DL, Launois SH, Isono S, Feroah TR, Whitelaw WA, Remmers JE. Pharyngeal narrowing and closing pressures in patients with obstructive sleep apnea.pdf. Am Rev Respir Dis. 1993;148:606–11.)
Now I'm reading an article by Eastwood about increasing dose of propofol and Pcrit and says that it increased Pcrit, so now I don't know what to think (Eastwood PR, Platt PR, Shepherd K, Maddison K, Hillman DR. Collapsibility of the upper airway at different concentrations of propofol anesthesia. Anesthesiology 2005;103(3):470–7.)
Can anyone explain me where's the problem?
Thanks
Pcrit measurements during anesthesia are reportedly higher than during natural sleep or light sedation. It all depends on sedation/anesthesia depth and loss of muscle tone.
Thanks for your answer Pedro
Yes, but in those articles they were using just sedation without muscle relaxants ... What I don't understand is if when you're doing the study of the Pcrit the muscles of the UA have no tone due to the high pressure of the CPAP....
Pcrit is 'the resultant of numerous chemical / biological variables that interact with each other in a different way. Pcrit is 'complex, multi-dimensional and it' difficult to measure in every single patient during DISE. OSA phenotypes have been described according to the different pathogenic mechanisms, the Pcrit varies according to the pathogenetic pattern described
I would say hypotonic. CPAP decreases but does not abolish muscle tone.
Recent studierà suggest that OSA is multifactorial condition and not anatomical problem (wellman 2011, Echert 2013) Alongside anatomical vulnerability,at least three additional physiological traits interact 1) ineffective upper airway dilatator muscle 2) alow threshold for arousal from sleep 3 hight loop Gain . ( see Orr 2014 journal Physiology)
three
Dear Domenico
Thanks for your answer, I know about the different things that interact to create OSAS, that's why there're people with normal anatomy and have OSAS and people with huge tonsils and a really crowded airway are not OSAS.
The question was more about methodology, I understand what is Pcrit, but as in order to calculate it, you have to use CPAP, I had read that this causes a lost in the UA muscle tone, therefore, although sedation may cause a lost in the UA too, this could not be evident because the muscle tone would be lost anyway... but in the article of Eastwood, apparently doing the same, the Pcrit was increased with higher propofol concentrations... I can understand the concepts but it looks like I don't understand something about the methodology to do this studies... and also I might have to integrate all this concepts together
The side of OSA is the collapse of the upper airway during sleep, which raises CO2 and leads to increased ventilatory drive and increasingly negative pharyngeal pressure. These respiratory stimuli can activate the upper airway dilator muscles to restore pharyngeal patency during sleep, which can protect against OSA. However, restoration of sufficient airflow can only occur if ventilatory drive can build up during sleep without an arousal. Instead, invasive procedures, such as an epiglottic or an esophageal pressure catheter, is required. Signals were sampled at 125-150 Hz data acquisition interface and displayed using software This method used to determine in each respiratory arousal threshold (Arth), could be used to measure the Pcrit.( Edwards, Eckert, McSharry, et al.: Predictors of the Arousal Threshold in Am J Respir Crit Care Med Vol 190, 11, pp 1293–1300, Dec 1, 2014)