br Detection of IFL Assessing

Detection of IFL Assessing for inspiratory flow limitation requires recognition of both flow and intrathoracic pressure changes [21]. A decrease in flow normally is accompanied by a compensatory increase in intrathoracic pressure. This is illustrated in Fig. 1 in the setting of differentiating a central and obstructive event via airflow and esophageal pressure monitoring [18]. Inspiratory flow limitation, which does not meet criteria for an obstructive hypopnea is illustrated in Fig. 2. Esophageal pressure monitoring, by demonstrating intrathoracic pressure changes before EEG arousal, remains key in the clinical diagnosis of UARS [9]. As esophageal pressure monitoring may be uncomfortable and is not practical for routine monitoring, different methods ofidentification are needed. Conventional pneumotachography has demonstrated that plateaus on inspiratory flow waveforms correlate with elevated upper airway resistance [20–22]. Similar to esophageal pressure monitoring, routine application of pneumotachography is limited by discomfort with the monitoring equipment [22]. Respiratory-Inductance-Plethysmography – RIP-has also been shown to be effective for evaluation of upper airway resistance, however there is difficulty in ensuring an accurate tidal volume measurement when using this p2y receptor measure alone [23]. Many studies have been done assessing nasal cannula/pressure transducer system as a non-invasive assessment of IFL, in addition to its role in detection of hypopneas and apneas [2,3,21,22,24]. Ayappa et al. hypothesized that by assessing the contour of flow shape, rather than amplitude of signal, respiratory effort could be detected with similar accuracy to Pes. . Ayappa showed that assessment of RERAs via flattening of the waveform contour was nearly identical to the detection by Pes, with interclass correlation coefficient of 0.96 [24]. In addition, Hosselet showed that upper airway resistance is increased in flow limited breaths by as much as 387% [2].These results suggest that esophageal pressure monitoring may not be required in assessing for inspiratory effort, and that further evaluation of waveform contour via routinely applied nasal cannula/pressure transducer could reveal these very important events. Comparison of different monitoring measures has been done since Ayappa׳s study showing promise of the nasal cannula/pressure transducer. Johnson et al. stimulated upper airway resistance in normal subjects with alcohol consumption and compared nasal cannula/pressure transducer with Pes, respiratory inductive plethysmography and a fourth method including a piezo-electrically treated stretch sensor adhered to the supraclavicular fossa. It was shown that nasal cannula/pressure transducer was superior to all tested modalities in detecting arousals secondary to increased upper airway resistance. Surprisingly, many events culminating in arousals were not associated initially with an increase in negative intraesophageal pressure detected by Pes; and over 90% of arousals were preceded initially by flow limitation seen via nasal pressure transducer [25]. It has been shown that additional metabolic factors exist for increasing respiratory effort during flow limited breathing. Rimpila et al. researched the relationship between transcutaneous carbon dioxide (tcCO2) level, flow limitation, and respiratory effort during sleep. It was found that flow limitation associated with increased respiratory effort correlated with tcCO2 above an individual׳s steady state during sleep. The authors noted that flow changes did exist below this tcCO2 threshold, however not with an increase in respiratory effort. It was concluded that carbon dioxide level can also be utilized to evaluate for flow limitation, and that flattening of flow contour exists without an increase in respiratory effort likely due to stabilization of breathing during sleep [26]. Abnormal flow limitation requires arousal and effort changes; therefore this type of flattening of the waveform without an increase in effort cannot be a scorable event. Carbon dioxide surrogate markers add to the understanding of flow limitation and respiratory effort, and raises questions regarding whether isolated flow limitation without RERAs or increase in arterial carbon dioxide is pathological.