Many therapeutic treatments are administered to a patient while they are sleeping or are attempting to fall asleep. While these treatments may achieve their intended result, they also often severely affect the quality of sleep that the patient gets while undergoing these treatments. These treatments often interrupt the patient's normal progression of sleep, causing transient arousals. While these arousals do not result in the awakening of the patient, they often pull patients from deeper stages or higher quality states of sleep. Patients often do not reenter these deeper stages of sleep for a relatively long period of time.
In some instances, a therapeutic treatment may cause numerous arousals. This fragments the patient's sleep and prevents the patient from reaching the deeper stages of sleep. Studies have shown that fragmented sleep results in excessive daytime sleepiness. This, in turn, is a direct contributor to many accidents, to a general feeling of lethargy, deterioration of cognitive performance, and/or daytime sleepiness, in the patient.
One example of therapeutic treatments causing sleep fragmentation is in the treatment of sleep disorders. Continuous Positive Air Pressure (CPAP) treatments are a primary remedy for a number of sleep disorders such as sleep apnea, hypopnea, and snoring. CPAP treatments consist of delivering a constant positive airway stream of air pressure into a patient's airway during sleep in order to keep the patient's airway from collapsing upon itself. State-of-the-art CPAP machines, often called auto-titration PAP (APAP) machines, automatically adjust the pressure of the delivered air in order to accommodate a patient's respiratory pattern. to the rapid changes of pressure in the patient's airway caused by the APAP machines. Another drawback of current state-of-the-art APAP machines is that they are subject to either false positives (such as when UAR and/or natural irregular breathing events are not pre-empted or do not occur, despite false detection of such and associated treatment control change) or false negatives (such as when genuine upper airway resistance (UAR) and/or related events are pre-empted or do occur but are not detected or responded to with treatment control change). This is due in part to the reliance of these machines on the correct interpretation of an inspiratory waveform and the inaccuracies related to the interpretation of the underlying waveform by the APAP machine. This can also be due to current state of the art gas delivery (or other treatment control such as pacemaker devices) devices inability to enable suitable algorithms to detect and adapt their computation detection sufficiently to pre-empt or predict the probability or onset likelihood of shallow breathing, UAR, arousals, and or associated sleep fragmentation or sleep quality deterioration.
The inspiratory waveform varies periodically for reasons not always associated with upper airway resistance. The use of inspiratory waveform as the primary or only means of detection of UAR-related events can cause remedial auto titration measures to be taken when none should be. This is particularly evident where the inspiratory waveform analysis technique does not employ an underlying time-course computational method. The time-course computational method refers to comparing a previous sequence of breaths (prestored from previous treatment session or stored from current session breathing data) or the current breath and comparing the variations or changes as an inferred measure of arousal or sleep fragmentation onset. Excessively rapid or excessively insensitive pressure changes often occur when an auto-CPAP machine tries to correct a normal non-UAR related event, or misses detecting the presence of subtle shallow breathing, hypopnea or UAR, respectively. It is believed that the primary cause of sleep fragmentation is the rapid pressure changes in the patient airway produced by the current APAP machines.
In addition to the above, studies have also suggested that some APAP machines are limited in their ability to accurately detect the onset or incidence of shallow breathing, mild hypopnea, or UAR events. This limitation is also possibly attributed to limitations of the machines in interpreting the wave form. Misdiagnosis of such mild hypopnea events results in increased UAR which in turn results in arousal and subsequent sleep fragmentation.
Current state-of-the-art therapeutic devices do not optimally adapt to minimize arousals during therapy. Each patient's arousal threshold is affected by varying parameters, yet current state of the art devices do not have adaptive control algorithms that can adapt their treatment levels to accommodate a number of these varying parameters. These varying parameters include (but are not limited to) sleep history such as sleep deprivation or sleep propensity, physiological factors, psychological factors including (but not limited to) stress or anxiety, environmental factors including temperature; noise; lighting; vibration, factors such as varying threshold to arousals with changing age, drugs and alcohol effects to arousal thresholds and others.
Consequently, in light of the inherent drawbacks in current therapeutic methods for administering treatments to patients who are sleeping or are attempting to sleep, there exists a need for an apparatus and method of monitoring for patient arousal and for adapting a therapeutic treatment to minimize arousal.