|CPAP TRAINING MANUAL
POSITIVE AIRWAY PRESSURE OVERVIEW
APNEA – Defined as a cessation of airflow for at least 10 seconds, occurring during sleep.
HYPOPNEA-In adults, is defined as an abnormal respiratory event lasting at least 10 seconds, during sleep, with at least a 30% reduction in the airflow as compared to baseline, and with at least a 4 % oxygen desaturation.
CPAP- Continuous Positive airway Pressure
CPAP machines work by using air pressure to prop the upper airway open during sleep, thus preventing the upper airway from collapsing. CPAP machine pump room air through a compressor that is connected by smooth bore tubing to a mask or nasal pillows.
CPAP therapy was developed in 1981, and was available in the home in 1985. CPAP therapy is the most effective treatment for OSAS, and has become the standard of care for this condition. When the airflow from the CPAP machine is directed through the upper airway, the caliber of the airway in the retropalatal and retroglossal regions. It increases the lateral dimensions of the upper airway and thins the lateral pharyngeal walls, which are thicker in patients with OSAS than in people without OSAS. Effectively, CPAP acts as a pneumatic split to maintain upper airway patency during sleep, preventing the soft tissues from collapsing. By this mechanism, it effectively eliminates the apneas and/or hypopneas, decreases the arousals, and normalizes the oxygen saturation.
There are many varieties of CPAP masks and interfaces. The patient should be fitted with a mask that is comfortable and fits well. The smallest possible mask (that fits) which should only have a minimal leak is the best mask for the patient.
The patient should be told to breathe through their nose at all times. Even when fitting the patient with a full face mask. Sometimes, it is difficult to exhale initially when using CPAP. The patient should be instructed to resist the temptation to breathe through his mouth. If the patient insists that he is a “mouth breather” he can be given a full face, with instructions to make every attempt at breathing through his nose.
The patient who has untreated apnea has frequent cessations in breathing due to obstruction. When the patient’s airway is compromised, the oxygen level decreases. This is evidenced by a low reading in the pulse oximeter during the sleep study. When the patient arouses from the apnea, the oxygen saturation climbs, only to return to a low level with the next apneic event.
Exceptions: Some patients will not improve their oxygen levels on CPAP alone. This may be due to poor tolerance, or because of a pulmonary condition such as COPD (chronic obstructive pulmonary disease).
CPAP maintains the airway
Oxygen levels are both higher and more stable in the patient on a CPAP, because the airway is splinted open with air. The uncollapsed airway maintains normal breathing and thus normal saturation levels.
Treatment other than CPAP
For patients whose oxygenation does not improve with CPAP, there are other options to consider, such as Bilevel or the addition of oxygen via concentrator.
During the PAP Titration, passover or heated humidification is the standard of care and should always be used.
Effectiveness of CPAP
Application of adequate levels of nasal CPAP during sleep almost always resolves OSAS and/or hypopnea, desaturations, RERAs, and snoring from sleep. It also results in adequate sleep continuity. CPAP has been shown to improve daytime sleepiness, mood, and cognitive function in people with both mild and moderate apnea. CPAP has been shown to decrease blood pressure, primarily in patients with severe OSAS. Evidence also indicates that it may improve the left ventricular ejection fraction in patients with CHF and OSAS. CPAP plus an antihypertensive medication may synergistically improve systemic hypertension. In addition, it improves right-sided heart function and pulmonary hypertension. CPAP has also been shown to increase quality of life and decrease health care costs. CPAP has also been shown to reduce mortality in OSAS. The benefits parallel those observed after tracheostomy.
Pressure Relief CPAP
A system that lowers the pressure at the onset of expiration is hypothesized to improve adherence by reducing the uncomfortable sensation of breathing against high pressure while maintaining a patent upper airway. Often, pressure relief settings will be applied to all patients who require a setting of greater than 10 cmH20.
CFlex- CFlex is a feature that provides selectable pressure (1-3) relief during exhalation. The higher the number selected, the higher the pressure relief. The sensation of being unable to fully exhale against CPAP or pressure intolerance is a frequent complaint of intolerant patients. C-Flex was developed to provide a base pressure to abolish pharyngeal collapse, as well as decrease the cumulative pressure during exhalation. C–Flex therapy allows for pressure reduction at the start of exhalation followed by a sinusoidal rise in pressure as exhalation ends.
C-Flex Plus- This feature provides selectable pressure (1-3) relief during the latter stages of inspiration and during active exhalation (the beginning part of exhalation). C-Flex plus provides pressure relief at the end of inspiration and at the beginning of expiration, as opposed to C-Flex which provides pressure relief at the start of exhalation.
C-FLEX AND C-FLEX PLUS-are patient comfort features and are used at the discretion of the technician. When a patient experiences difficulty with exhalation, try Cflex and increase the numbers to increase the relief. And you can also try C-Flex Plus if regular C-Flex is not helping. Make notes of what you tried and when and what the patient’s response was.
Pressure and airflow related complications
Patients will sometimes relate a sensation of suffocation or claustrophobia, difficulty exhaling, inability to sleep, musculoskeletal chest discomfort, aerophagia, and sinus discomfort. Patients with claustrophobia may try using nasal pillows or behavioral management or may benefit from a PAP NAP prior to titration. Decreasing the CPAP pressure after an awakening and resuming the pressure increases once asleep is often helpful. Often the confidence displayed by the technician will allow the patient to be comfortable enough with the procedure and the study will proceed much easier.
UPPER AIRWAY RESISTANCE SYNDROME-A sleep disorder characterized by airway resistance to breathing during sleep. The primary symptoms include daytime sleepiness and excessive fatigue. The gold standard diagnostic test for UARS is the use of an esophageal pressure probe during the Polysomnography. UARS can also be diagnosed using a nasal cannula/pressure transducer to measure the inspiratory airflow Vs time signal. During sleep, the muscles of the airway become relaxed. The relaxation of these muscles in turn reduces the diameter of the airway. Typically, the airway of a UARS patient is already restricted or reduced in size, and this natural relaxation reduces the airway further. Therefore, breathing becomes labored. It can be likened to breathing through a coffee straw. The pathophysiology of UARS is similar to OSAS/Hypopnea syndrome in that abnormal airway resistance in the upper airway during sleep leads to unwanted physiologic consequences. Increased upper airway resistance in this disorder does not lead to apnea or hypopnea, but instead leads to an arousal secondary to increased work of breathing to overcome the resistance. Repeated and multiple arousals (which the patient is usually unaware of) result in an abnormal sleep architecture and daytime somnolence. Arsousals result in sympathetic activation, and UARS is therefore likely to cause hypertension similar to OSAS (studies are being conducted to determine relationships). Treatment of UARS is essentially the same as for OSAS. UARS should not be overdiagnosed. Three essential clinical features consistently have been used to diagnose UARS: EDS, an elevated EEG arousal index, with the arousal related to increased respiratory efforts: and a normal respiratory disturbance index of less than five events per hour of sleep. UARS is present only if there are documented elevations in upper airway resistance, sleep fragmentation, and a daytime dysfunction or EDS. The clinical complaint of fatigue or EDS can be documented by an abnormal increase in the Epworth Sleepiness Scale score to a value greater than 10. A low respiratory disturbance index is also needed to distinguish UARS from OSAS. The elevated EEG arousal index related to increased respiratory efforts is the specific measurement that distinguishes UARS from idiopathic hypersomnolence. The clinical complaint of snoring (including crescendo snoring), an increase in snoring intensity before EEG arousals, and clinical improvement with a shorit-term trial of nasal CPAP can be regarded as supporting a diagnosis of UARS.
RESPIRATORY EFFORT RELATED AROUSALS (RERA) – Sometimes the throat narrows enough to cause loud snoring and hard breathing, but not enough to produce apneas or hypopneas. Breathing in this situation can be difficult enough to wake the patient, an occurrence referred to as respiratory effort related arousal (RERA). Often, genetic skeletal abnormalities will cause the mandible and/or maxilla to be misshapen to the point that the airway cannot support normal respiration during sleep.
PAP-Positive Airway Pressure- This acronym is often used when scheduling patients for a return laboratory visit for CPAP, Bilevel (BPAP), ASV or Bilevel with a back up rate.
Positive airway pressures treat:
Obstructive Sleep Apnea-generally caused by relaxed muscles in the throat while the patient is sleeping, enlarged uvula, palate, tonsils, tongue or an anatomical defect such as a small jaw (micrognathia), a recessed jaw (retrognathia), a smaller than normal or narrower than normal airway or an airway prone to resistance, etc. The patient generally has unrestful sleep and excessive daytime sleepiness (somnolence) or EDS. The patient generally suffers from oxyhemoglobin desaturations (O2 desats) and frequent arousals and fragmented sleep.
Airway obstruction can occur in many areas of the nasopharynx, oropharynx, and hypopharynx.
See the below illustrations:
The above picture is a normal airway. The soft palate and uvula are normal in length and total size. The tongue is normal in size and is angled forward. The upper airway at the level of the nasopharynx, oropharynx and hypopharynx is normal in size and contour.
picture shows an abnormal airway during sleep. An elongated and enlarged soft palate impinges on the posterior airway at the level of the nasopharynx and oropharynx. In addition, a retruding jaw pushes an enlarged tongue posteriorly to impinge on the hypopharyngeal space.
Most airway obstructions occur in the oropharynx, but as you can see from the above picture, there can be several sites of abnormality.
Central Sleep Apnea-Generally there is a defect of some sort in the nervous system that prevents the brain from being able to properly control breathing during sleep. The brain will stop sending signals to the muscles that control breathing. CSA can develop in persons who have life threatening problems with the brainstem (which controls breathing). Some conditions that can cause or lead to central sleep apnea include:
Arthritis and degenerative changes in the cervical spine or base of the skull
Complications of cervical spine surgery
Neurodegenerative illnesses such as Parkinson’s
Radiation of the cervical spine
Primary Hypoventilation syndrome
The use of certain medications such as narcotic-containing painkillers
A form of CSA is common in patients with CHF (Congestive Heart Failure)
If the CSA is not associated with another disease, it is called idiopathic CSA
CSA is not the same as Obstructive Sleep Apnea
Cheyne-Stokes respiration can mimic central sleep apnea. This condition involves breathing to a variable depth, usually while sleeping.
Complex Sleep apnea-A condition which has a combination of obstructive and central sleep apnea.
Sleep Related Breathing Disorder-The concept of the SRBD suggests that optimal OSAS treatment must correct OSAS, Upper airway Resistance Syndrome (UARS), and snoring. If it does not eliminate all 3 problems, the symptoms and the pathophysiological process that was evident at the start of the disease recur. Therefore, in the treatment of SRBD, the PAP corrects OSAS first, UARS next, and snoring last.
An unlikely occurrence is snoring being corrected before OSAS and/or UARS; if this is thought to have occurred, and then consideration should be given to the integrity of the snoring microphone or other vibrations that transduce a “snoring” signal such as: mask leak, oral leak, and excessive moisture in the tubing. When a mask leak occurs, the noise may be transferred by the microphone to the snore channel and may sound like snoring. One can determine the difference between snoring and a leak because snoring occurs at the point of peak inspiration and the beginning of expiration; mask leak occurs during expiration. Consider also: if the patient has had upper airway corrective surgery. If the pharyngeal tissue has been eliminated, snoring may not occur, but OSAS can still develop (so-called silent apnea).
BILEVEL THERAPY (BPAP) – Bilevel therapy permits independent adjustment of the pressures delivered during inspiration and expiration. The levels are set so that the expiratory positive airway pressure eliminates apneas and the inspiratory positive airway pressure eliminates the hypopneas. The ability to adjust inspiratory and expiratory pressures independently results in lower mean airway pressures compared with those of CPAP. In a given patient, the expiratory positive airway pressure level that must be applied is lower than the corresponding CPAP level required to maintain airway patency.
Bilevel is generally used in patients who cannot tolerate high pressures, or who have barotrauma complications (multiple ear infections, bloating in the abdomen). Most patients who need more than 15 cmh20 of CPAP could be titrated more easily with Bilevel.