Flow Limitation
Posted: Fri May 25, 2018 6:19 am
What cause flow limitation? The last to night I've had limitation of ,85 and .93 this is much higher than I've been in a long time.
Thanks
Thanks
My personal interpretation based on extending the application of those principles? For some of us, using PAP at a pressure higher than our APAPs give us, in order to smooth out more of the flattening of our waveforms, might actually improve our sleep. For others, not.Stanford dudes, including Guilleminault, wrote:While there is ample evidence that excessive flow limitation is abnormal and leads to pathologic changes in sleep and wakefulness, it is currently unclear whether including this in the diagnostic criteria for OSA would have any value. . . . Meurice et al. conducted an experiment in which two groups of patients diagnosed with OSA were treated with different CPAP pressures. The first group was treated with CPAP pressures targeted to eliminate flow limitation and the second group treated with CPAP pressures targeted to treat apneas, hypopneas and snores. The pressure requirements for the first group were higher than for the second group; however the first group had an increase in sleep time and more consistent improvement in maintenance of wakefulness testing. These results are suggestive that titration to eliminate flow limitation would lead to improved clinical outcomes. . . . Analysis of multiple indices for quantifying recorded SDB [sleep-disordered breathing] has shown that scoring flow limitation events in addition to apneas and hypopneas has a better sensitivity and specificity of correlating symptoms with their respiratory causes than currently used strategies. In particular, it is necessary to detect more subtle forms of SDB such as IFL [inspiratory flow limitation] in certain patient populations that do not present with frank apneas. Standardized IFL scoring should lead to better detection and characterization of IFL. A reasonable threshold to define abnormal IFL would be greater than 30% of sleep, however other quantifiable techniques should be considered. While there is data that IFL may be linked to clinical consequences in certain circumstances, more research is needed to establish guidelines in reproducible scoring of IFL. In addition, further evidence of its negative health associations are warranted before routinely incorporating into PSG interpretation. -- "The role of flow limitation as an important diagnostic tool and clinical finding in mild sleep-disordered breathing," Nevin Arora, Gerard Meskill, Christian Guilleminault; Stanford University Sleep Medicine Division, Redwood City, California, USA, September 2015. -- https://pdfs.semanticscholar.org/262b/4 ... 6d1dbc.pdf
That's not really correct.
a narrowing of the airway, it's like breathing through a straw...
From a historical overview from 2009:Guilleminault initially proposed a liberal definition of a hypopnea as “a reduction—but not complete cessation—of air exchange.” More recent liberal definitions of a hypopnea have ranged all the way up to any visually discernible change in the appearance in the airflow signal or effort signals. This change may be a decrease in the amplitude or change in the shape of either the airflow signal (airflow flattening) or one of the two effort signals (abdominal or thoracic movement signals). Authorities agree that in order for a hypopnea to be clinically significant, it must be followed by either an arousal of some sort and/or an oxygen desaturation. [One] slide show presentation produced by the American Academy of Sleep Medicine . . . defines a hypopnea as any visually discernible reduction in the amplitude of either the airflow or the effort signals. This decrease in airflow must last for 10 seconds or longer. Also, in order to be counted as clinically significant, either an arousal of some sort and/or an oxygen desaturation of three points or more must follow the hypopnea. . . . I used to abide by the strict definition of an apnea argument (an apnea had to be an 80% to 100% reduction in airflow for the entire duration of the event). I have changed my mind to a more liberal interpretation of an apnea as being an event that contains the requisite 80% to 100% reduction in airflow but sometimes only during a portion of the event. The reason why I changed my mind is that nowhere in any of the definitions of an apnea does it specifically say that the entire apnea has to be an 80% to 100% reduction in airflow. They just say that there has to be an 80% to 100% reduction in nasal/oral airflow for 10 seconds or longer. Those 10 seconds could be anywhere within an event that would otherwise be counted as a hypopnea. Second, the shape and duration of the oxygen saturation level change parallel the duration of the entire apnea/hypopnea complex, not just the apnea portion of the event. . . . -- http://www.sleepreviewmag.com/2001/04/t ... hypopneas/
The operational definition for hypopnea remains controversial. One problem stems from recording technique; that is, most sleep laboratories measure flow qualitatively, and such measures do not proportionally estimate tidal volume. Therefore, couching airflow changes in terms of percentage decrease from baseline is problematic. Guilleminault et al.'s original definition of hypopnea as a reduction in airflow without complete cessation of breathing adhered closely to the general principle but left open the question of how much decrease in airflow was minimally required to score a hypopnea. A wide assortment of definitions were developed using different cutting scores for percentage of airflow decrease. Then in 2001, the AASM Clinical Practice Review Committee defined hypopnea largely based on the definition used in the Sleep Heart Health epidemiologic studies. -- https://www.sciencedirect.com/topics/me ... y/hypopnea