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COMMON MODES OF MECHANICAL

VENTILATION

Continuous Mandatory Ventilation and

Assist Control Ventilation

Continuous mandatory ventilation (CMV) has been supplanted by assist control (AC) ventilation. In CMV, the ventilator is set to deliver a fixed, nontriggered tidal volume at a fixed respiratory rate, ignoring the patient’s ventilatory drive. Assist control was designed to eliminate the synchronization problems inherent in CMV. During a patient-triggered inspiratory effort, there is a pressure drop in the airway sensed by the ventilator followed by delivery of a preset tidal volume.The ventilator is also preset to deliver a minimum number of breaths per minute, analogous to CMV, should the patient fail to trigger the ventilator.The work of breathing is substantial for patients receiving AC but may be reduced by proper sedation or the use of neuromuscular blocking agents in severe cases.

Intermittent Mandatory Ventilation

and Synchronized Intermittent

MandatoryVentilation

Intermittent mandatory ventilation (IMV) is a combination of CMV and spontaneous respiratory efforts. The ventilator is set to deliver nontriggered breaths at a fixed volume and rate. Patient-triggered breaths are also possible similar to the AC mode, but rather than delivering a preset TV, the TV generated is derived entirely from patient effort. Thus total minute ventilation is equal to the sum of tidal volumes generated by spontaneous efforts plus machine-delivered breaths. Synchronized intermittent mandatory ventilation (SIMV) is a variation of IMV in which the ventilator senses spontaneous efforts and times its own mechanical breaths to prevent breath stacking. Like AC, SIMV imposes a significant respiratory and cardiac workload.

Pressure Support Ventilation

Pressure-support ventilation (PSV) differs from AC ventilation and IMV in that the physician sets a level of pressure (rather than volume) to augment spontaneous breathing efforts. Tidal volume is determined by the level of set pressure, patient effort, and pulmonary mechanics (less compliant lungs will generate a smaller tidal volume for a given level of pressure support and vice versa). At any constant level of patient effort, the greater the pressure support, the greater the combined volume. At any constant level of pressure support, the greater the inspiratory effort, the greater the combined

volume.Advantages of PSV include patient comfort due to ventilator synchronization with spontaneous respiratory efforts and decreased work of breathing. Pressure support ventilation, sometimes in conjunction with SIMV, is commonly used as a weaning mode.

Positive End-Expiratory Pressure

Positive end-expiratory pressure (PEEP) is used as an adjunct to the various ventilator modes thus far described. During normal breathing, airway pressure is zero (atmospheric) at end-expiration. If a subject exhales into tubing, the distal end of which is submerged under a column of water, the end-expiratory pressure becomes positive relative to the atmosphere. This applied PEEP is also known as extrinsic PEEP. PEEP can also be measured in the spontaneously breathing subject, especially in someone with chronic obstructive pulmonary disease (COPD), high minute ventilation, and gas trapping.This phenomenon is termed auto-PEEP (or occult PEEP). Similarly, extrinsic PEEP can be applied in the mechanically ventilated patient who exhales against a preset pressure delivered by a one-way valve added to the expiratory circuit. Auto-PEEP, an unwanted complication of positive-pressure ventilation, can result in high airway pressures and an increased risk of barotrauma, and commonly occurs in the setting of bronchospasm, or expiratory airflow obstruction from any cause.

Extrinsic PEEP dialed into the ventilator circuit is useful for patients with alveolar filling processes such as the ARDS. By redistributing lung water from the alveoli to the perivascular interstitial space, intrapulmonary shunting is reduced, leading to an increase in arterial oxygen tension. Addition of PEEP can influence lung mechanics by elevating FRC, shifting tidal breathing to a more compliant portion of the pressure–volume curve, and reducing the work of breathing. In acute lung injury, recent evidence suggests that PEEP may promote the healing process by maintaining the patency of alveoli throughout the respiratory cycle, rather than subjecting alveoli to repeated cycles of opening and closing with each mechanically driven positive pressure breath.

Continuous Positive Airway Pressure

Continuous positive airway pressure (CPAP) was devised to overcome the problem of increased inspiratory work. Here, the positive pressure is not confined to expiration but is sustained throughout the breathing cycle. For some patients with severe airflow obstruction, the addition of CPAP may cause tidal volume to increase as pressure support or the natural force of

breathing effort becomes more effective. For stronger patients, CPAP may be used as a counterspring against which expiratory muscles can store energy for release during subsequent inspiration.

In a child with upper respiratory tract infection, airway congestion, fever, and anxiety may begin a cycle of airway compression, decreased airway radius, and increased work of breathing. In some extreme cases, simple maneuvers such as nasal drops and postural drainage may not be sufficient to overcome the airway

SELF-TEST QUESTIONS

For each question select the correct answer from the lettered alternatives that follow.To check your answers, see Answers to Self-Tests on page 715.

1.Which of the following lung capacities cannot be measured by a spirometer?

A.Total lung capacity

B.Inspiratory capacity

C.Vital capacity

D.Functional residual capacity

2.If arterial oxygen content is 19 mL/100 mL of blood, and mixed venous oxygen content is 16 mL/100 mL

obstruction, and positive airway pressure (CPAP) may be needed to alleviate the extrathoracic obstruction.

SUGGESTED READINGS

Hlastala MP, Berger AJ. Physiology of Respiration. New York: Oxford University Press; 1996

Tobin MJ. Mechanical ventilation. N Engl J Med 1994;330(15): 1056–1061

West JB. Respiratory Physiology—the Essentials. 5th ed. Baltimore: Williams &Wilkins; 1995

of blood, what blood flow is necessary to sustain a volume of oxygen (VO2) of 400 mL/minute?

A.12 L/minute

B.13.33 L/minute

C.10 L/minute

D.Cannot measure with above information

3.Which of the following in arterial blood has the most important control on normal ventilation conditions?

A.PCO2

B.pH

C.PO2

In 1836, Charles Dickens wrote Posthumous Papers of the Pickwick Club, in which he described the classical pickwickian syndrome in the character Joe, the “fat boy.” In Dickens’s novel, the reader is introduced to Joe as follows: “And on the box sat a fat and red-faced boy, in a state of somnolence.”The description is pretty much on target in describing the alveolar hypoventilation syndrome, an extreme form in the spectrum of sleep disordered breathing (SDB) syndromes.

Approximately 50 million Americans snore, and 20 million Americans suffer from a sleep apnea syndrome. Together these syndromes are responsible for increases in spousal complaints and more importantly carry an increased risk of cardiovascular disease and premature death.

Under the label of SDB are classified a spectrum of disease processes, from snoring to the alveolar

hypoventilation syndrome (Fig. 6-1), also known as the pickwickian syndrome. Obstructive sleep apnea syndrome (OSAS) lies somewhere at the center of the spectrum. Of concern is that snoring will progress in a significant number of patients into a more serious entity within the spectrum of SDB syndromes. When the disease entity reaches the levels of severe sleep apnea, it is associated with a 10% increase in mortality, usually related to the cardiovascular system (e.g., stroke, myocardial infarction, and deadly arrythmia). Severe sleep apnea syndrome also is strongly associated with increased body mass index (BMI, in kg/m2), and it is an ongoing debate how much of the morbidity found in patients with OSAS is dependent on the sleep apnea syndrome per se respective to the increased BMI.

The U.S. Department ofTransportation estimates that 200,000 automobile accidents yearly are sleep related, causing 1500 road deaths per year.The loss of productivity in the work place as well as accidents while using heavy machinery at work in patients with sleep disorders has been documented in both the European andAmerican literature.

The complexity of sleep apnea syndromes dictates that multiple specialties are involved in their treatment. Medical specialists such as general internists, endocrinologists, nutritionists, cardiologists, psychiatrists, and neurologists are often involved. On the surgical side, otolaryngologists, prostodontists, maxillofacial surgeons, and general surgeons may be involved.

PATHOGENESIS AND RISK FACTORS

Snoring is caused by the turbulence of air currents secondary to the partial collapse of the airway. Excessive relaxation of the pharyngeal musculature during sleep may be a single factor that causes the soft tissues of the soft palate, lateral pharyngeal walls, posterior pharyngeal wall, and tongue base to vibrate against each other. However, there are usually other anatomical factors; that is, tonsillar hypertrophy, lingual tonsil hypertrophy, nasal obstruction, and hypoplastic mandibles, which further contribute to the narrowing of the air space. Patients who are mouth breathers secondary to nasal obstruction may have excessive relaxation of the genioglossus muscle that retrodisplaces the tongue, reducing the size of the posterior airway space, which when combined with pharyngeal muscle relaxation, can cause snoring.

An increase in BMI of greater than 120% of ideal body weight and an increase in neck size (larger than 17 inches in males and 15 inches in females) correlate positively with the diagnosis of sleep apnea in greater than 60% of the patients diagnosed with this syndrome. Furthermore, according to several authors, maintaining or reducing weight regardless of the other modalities of therapy is the best predictor of overall success in the management of patients with OSAS. Patients with

endocrine disorders like hypothyroidism and acromegaly are also at increased risk of developing the syndrome.

The degree of collapse, partial or total, of the pharyngeal musculature will determine whether the patient will suffer from snoring or obstructive apnea. Extreme fatigue, alcohol, sedative pills, and deeper stages of sleep diminish the pharyngeal muscle tone and can further aggravate the symptoms of snoring and sleep apnea. One pathophysiological mechanism underlying the progression from snoring to OSAS is believed to be local neurogenic lesions in the oropharynx caused by the low-frequency vibration of habitual snoring.This suggestion is based on results from biopsies of the palatopharyngeal muscle in which morphological abnormalities, including neurogenic signs, were found in snorers with and without OSAS. Together these data suggest that a disturbance in the efferent and/or afferent nerve pathways involved in the reflexogenic mechanism of the upper airway contribute to the pharyngeal collapsibility seen in patients with OSAS.

In patients with sleep apnea, the redundant tissues in the palate and retropharynx can be further elongated by the negative pressure effects of the lungs against a closed pharynx, creating a vicious cycle that can allow the progression of pathological events in the chain of sleep disordered breathing.

There are three key pathophysiological features of OSAS that can adversely affect the cardiovascular system: generation of exaggerated negative intrathoracic pressure, development of asphyxia during apnea, and arousal from sleep at the termination of apnea. These effects are schematically represented in Fig. 6-2. Muscle sympathetic nerve activity increases during apnea. It is also constantly elevated during the daytime in sleep apnea subjects. The heart rate decreases during apnea and increases afterward.The blood pressure has a typical pattern of variation during OSAS. It increases during the latter part of apnea with a peak immediately after apnea termination, whereafter the pressure declines. Simultaneously with arterial pressure, pulmonary artery pressure, central venous pressure, and intracranial pressure increase during apnea and

Figure 6-2 Pathophysiological effects of obstructive sleep apnea syndrome on the cardiovascular system. BP, blood pressure; HR, heart rate; PaCO2, arterial carbon dioxide partial pressure exerted by carbon dioxide (CO2) dissolved in arterial plasma and red blood cell

decrease after apnea. Cardiac output declines during apnea and increases after the resumption of ventilation. Intrathoracic pressure as low as 80 cm of water occurs during obstructive apnea as a result of the inspiratory efforts.This increases the central venous blood volume during apnea, with resulting increases in both central venous pressure and intracranial pressure.The augmented venous return to the right heart induces a leftward shift of the ventricular septum that in turn reduces left ventricular filling.The low intrathoracic pressure can also cause esophageal reflux.

SLEEP ARCHITECTURE

There are two kinds of sleep: non–rapid eye movement (N-REM) and rapid eye movement (REM).Within N-REM sleep, three stages are recognized, stage I, stage II, and delta sleep, corresponding to the different depths of sleep. REM sleep, of which there are also subcategories, is considered an important part of the overall sleep architecture where there is active dreaming during sleep. REM sleep alternates with N-REM sleep throughout the sleeping period.

A normal person will usually start the resting period with N-REM sleep stage I, which is a transitional phase

water; PaO2, arterial oxygen partial pressure exerted by oxygen (O2) dissolved in arterial plasma and red blood cell water; SNA, sympathetic nervous (system) activity.

between full wakefulness and sleep, that usually lasts between 1 and 7 minutes and that is characterized by a decrease in reactivity to outside stimuli. Stage II follows and is marked by the appearance of electroencephalogram (EEG) sleep spindles and by K complexes. In this stage, mental activity consists of short, mundane, and fragmented thoughts; it usually lasts between 35 and 45 minutes, at which time the person will enter delta sleep, which is a deeper level of sleep. Here the characteristic EEG delta waves appear (2 Hz and higher amplitude). The amount of time spent in this stage varies with the age of the person and ranges from a few minutes to 1 hour; it then yields to stage II sleep.

About 70 to 90 minutes after sleep onset the first REM period of the night occurs. It usually lasts about 5 minutes and is by far the least intense REM period of the night. The second sleep cycle begins while stage II sleep redevelops after the first REM period. On some occasions, delta sleep reappears, but there is generally less delta sleep in the second cycle than the first. Following this, the second REM period of the night occurs about 3 hours after falling asleep and lasts for about 10 minutes.

Following the second REM period and until awakening in the morning, stage II sleep and REM sleep alternate in

90-minute cycles. In these latter sleep cycles, delta sleep is rarely seen, whereas REM periods become more intense and are longer toward the morning.The mean length of a REM period is 15 minutes, but some may last for 1 hour.

Although the separation of sleep into mutually exclusive stages is convenient for understanding, sleep stages actually merge. Delta waves, for example, gradually become more abundant and gain amplitude following the onset of sleep. There is no clear threshold of delta sleep, except by arbitrary definition. Similarly, indices of REM sleep are strongest in the middle of the REM period, whereas the transition point between stage II sleep and REM is often difficult to define.

Of the N-REM stages, delta sleep is the deepest and stage I lightest (if it is sleep at all). However, REM sleep is not easily classified on a sleep-depth scale. By measuring the noise necessary to awaken a person from REM sleep, it appears that REM in humans is about as deep as stage II N-REM sleep.

Several physiological systems are profoundly influenced by the patient’s awake, N-REM, or REM state. In some persons, these systems may work normally during wakefulness but abnormally during sleep. In patients with OSAS, respiration may be normal during wakefulness, but relaxation of the musculature in the upper airway during sleep may have the potential for lethal complications.

CLINICAL SIGNS AND

SYMPTOMS OF OSAS

There are two cardinal manifestations of OSAS in adults: one indicates a disturbance during sleep, the other the resulting disturbance during wakefulness. The first is loud snoring that typically has caused the bed partner to move out of the bedroom and occasionally out of the house.This is unlike the quiet, steady snoring that usually does not interfere with family life.The snoring of obstructive sleep apnea is frequently a crescendo variety, indicating increasingly severe narrowing of the airway. It can also be just a series of snorts interspersed with ominous silence. The daytime symptom is severe sleepiness. The patient shows evidence of falling asleep in all permissive situations. Occasionally,sufferers deny that they are sleepy and say that they fall asleep only when they sit down or are “bored.”The truth is that boredom does not cause sleepiness. Unfortunately, one of the permissive situations is driving, and so patients with OSAS are at high risk for accidents.These two symptoms of loud, intermittent snoring and daytime sleepiness are so important that any person having them should be considered to have obstructive sleep apnea syndrome until proven otherwise. Conversely, it is

TABLE 6-1 SIGNS AND SYMPTOMS OF OBSTRUCTIVE SLEEP

APNEA SYNDROME

extremely unlikely that clinically important OSAS exists in a patient who has no problem with daytime alertness and whose sleep at night is completely quiet.

In taking a history from the patient, one must rely heavily on the bed partner’s observation, in terms of both nighttime and daytime behavior. Patients clearly are not aware of snoring because it occurs during sleep. They may also be unaware of how sleepy they are. Sleepiness frequently comes on very gradually, and these patients forget what it is like to be fully alert. Patients should be asked more than just “are you sleepy?” They should be specifically asked about falling asleep under permissive situations such as reading, watching television, and driving. The other clinical features of OSAS are not seen in every patient and are listed in Table 6-1.

PHYSICAL EXAMINATION

In the examination of the adult patient, one looks specifically for any abnormalities involving the upper airway such as nasal obstruction, hypertrophied tonsils and adenoids, retrognathia or micrognathia, and tumors.The majority of patients with OSAS are obese. One must look for frequently associated diseases such as hypothyroidism, acromegaly, and amyloidosis. Hypertension is more frequent in patients with OSAS than in control populations. Most patients with OSAS have normal pulmonary function, but any abnormalities in the respiratory system increase the risk of severe hypoxemia during sleep. A small subset of patients with OSAS develop daytime hypoventilation, so one should be alert for any evidence of hypercapnia or right heart failure. A summary of things to look for is enumerated on the physical examination sheet (Fig. 6-3). In our

experience, it is important to keep in mind the classification of obstructions as described by Fujita et al (1981), in which they note obstructions in the oropharynx, hypopharynx, or both.

We have also noted a higher increase in hypopharyngeal obstruction, more specifically lingual tonsillar hypertrophy in OSAS patients who have had a previous tonsillectomy. Lastly, the degree and site of collapse of the airway can be determined using the Müller maneuver, in which the patient is asked to breathe against closed nose and mouth while observed with a fiberscope.

LABORATORY EVALUATION AND DIFFERENTIAL DIAGNOSIS

POLYSOMNOGRAM

The cornerstone in confirming our diagnostic impression of sleep disordered breathing, which has snoring as one of its components, is a polysomnograph.This can be performed in a hospital laboratory as a polysomnogram (PSG), with multiple leads analyzing a great amount of parameters, usually 12 or more, including EEG, electrocardiogram (ECG), and electromyogram (EMG), or in an ambulatory setting, in which portable units measuring a limited number of parameters are secured to the patient in the comfort of his or her home. Either way, the importance is to be able to define various components of sleep, in particular periods of apnea, hypoxemia, and cardiac arrhythmias, that when placed in a formula are able to confirm or exclude the diagnosis of habitual snoring, upper airway resistance syndrome (UARS),

OSAS, and central sleep apnea. Polysomnogram definitions are listed in Table 6-2.The differential diagnoses of other sleep disorders are listed in Table 6-3 and at times may require other specific tests for definitive diagnosis. The scope of this chapter will remain on obstructive sleep disorder breathing syndromes.

SNAP TEST

This inexpensive and simple test has been available since 1998 and is still in the process of acquiring clinical acceptance.The test is basically an acoustic analysis of snoring that can be performed singularly or in combination with an oxygen saturation monitor. The proponents of this

TABLE 6-3 DISORDERS OF EXCESSIVE SOMNOLENCE

Psychophysiological

Psychiatric disorders

Use of drugs and alcohol

Sleep-induced respiratory impairment

Sleep apnea syndrome

Alveolar hypoventilation syndrome

Nocturnal myoclonus and restless legs

Narcolepsy

Medical, toxic, and environmental conditions

Other

Kleine-Levin syndrome

Menstrual associated syndrome

Insufficient sleep

Sleep drunkenness

diagnostic test claim that they can with a significant degree of accurateness differentiate those patients with habitual snoring from those with sleep apnea syndrome. Furthermore, this simple recording of snoring with a nasal cannula can quantify the loudness of snoring (in decibels) and localize the anatomical site or sites of snoring (by analyzing the pitch), determining if the sound originates from the nose, soft palate, tongue base, hypopharynx, or chest. We have found this test to be accurate when combined with clinical findings.

The Snap test (from the SPAP® laboratories) is one of several commercially available systems designed to be used in the patient’s home to analyze the degree and character of sleep apnea. These systems have greatly improved in recent years, and a test with one of them can often replace a conventional PSG.

RADIOLOGICAL EXAMINATION

Cefalometry is the most widely available and inexpensive method for evaluating the skeletal and soft tissues of the head and neck. This two-dimensional modality provides useful information in patients with skeletal deformities, such as retrognathia, and is of aid in evaluating the usefulness of dental and lingual appliances. Computed tomographic (CT) scan examination, particularly spiral CT, provides direct three-dimensional volumetric reconstruction images of the airway and bony structures. It is useful in evaluating the efficacy of dental appliances and maxillomandibular advancement in patients with sleep apnea. At the present time the gold standard of imaging studies is dynamic magnetic resonance imaging (MRI). Although expensive, it has distinct advantages over other imaging modalities. Dynamic MRI provides the clinician with excellent airway and soft tissue resolution and an accurate determination of the upper airway cross-sectional area and volume. Because it is void of the risks of radiation, the studies could be repeated during wakefulness and sleep. Three-dimensional reconstruction of soft tissue structures (tongue, soft palate, fat pads, lateral pharyngeal walls) and the airway is possible.

CLASSIFICATION OF OSAS

The importance of the diagnostic tests is their ability to classify and quantify the severity of sleep disorders (Fig. 6-1). The classification of the degree of apnea is important because it correlates with the overall success of treatment. Patients with snoring, UARS, and mild OSAS have an overall better prognosis than those

patients with moderate to severe OSAS. The various modalities of therapy have a predictable reduction in the apnea/hypopnea index (AHI) and will be discussed in the appropriate section.

The diagnosis of a specific sleep disordered breathing disorder is derived by a careful history and office questionnaire plus the physical findings and diagnostic testing. A brief discussion of each entity will follow.

HABITUAL SNORING

Identified as a partial obstruction of the upper aerodigestive tract without having a total collapse of the airway, characteristic habitual snoring is like a rhythmic seesaw whose loudness varies with individuals. Contributing factors to the frequency and loudness of snoring include excessive tiredness, heavy meals prior to retiring for sleep, and the use of sedative pills or alcohol.The patient may or may not have an increase in BMI.The patient does not report symptoms of daytime somnolence, and bed partners do not report patients gasping for breath. Polysomnography will determine the patient to have an AHI index of less than 10.

UPPER AIRWAY RESISTANCE SYNDROME

Patients with UARS present with symptoms of snoring that are accentuated by contributing factors including weight increase and alcohol and sedative drug use. The snoring is characterized by a crescendo pattern with associated arousals. After arousals there is a decrease in the upper airway resistance and temporary abolition of snoring. The multiple arousals lead to fragmentation of sleep with some tiredness throughout the day.

Polysomnography will demonstrate an RDI between 5 and 15, with no or occasional mild oxygen desaturations. Discussion exists whether this is a real entity or an intermediate stage in the spectrum of patients with sleep apnea. The only way to really identify an increase in the airway pressure is with an extensive 12-lead PSG, which will include esophageal pressure monitoring as one of its recording parameters.

SLEEP APNEA SYNDROMES

Patients with sleep apnea syndromes usually have an increase in BMI of more than 20%. Hypertension or a family history of hypertension is present in more than half of the patients with this diagnosis. Easy fatigability and daytime hypersomnolence are characteristic symptoms, particularly in the patients with moderate to severe apnea. In the case of obstructive and mixed sleep apnea,

the patient or a family member has witnessed a pattern of sleep with severe snoring, with cessation of breath for long periods of time and gasping for air upon arousal from sleep. Conversely, central sleep apnea is characterized by the absence of respiratory efforts during the periods of apnea.The differentiation between central, obstructive, and mixed sleep apnea is done by polysomnographic studies.

TREATMENT OF OSAS

The treatment of obstructive sleep apnea syndrome and sleep-related disorders is multifaceted and requires a careful analysis of the individual factors contributing to this entity. In some patients hypertrophied tonsils may be the single contributing factor causing the syndrome, whereas in the majority there are several factors that have been discussed previously.The point is that all contributing factors must be addressed for the best possible outcome. The severity of sleep apnea may itself be a predictor of outcome. Statistically, patients with mild to moderate sleep apnea will respond better to treatment than those with severe sleep apnea, regardless of the number of therapeutic modalities employed.

MEDICAL TREATMENT

Weight control, continuous positive airway pressure (CPAP), and oral appliances are the major vectors in medical management of OSAS. Other medical conditions such as acromegaly and hypothyroidism, which can contribute to OSAS, have to be ruled out. Medications or substances such as alcohol, sedative hypnotics, narcotics, anesthetics, and sedating antihistamines, all of which have a depressive effect on the central nervous system, should be avoided. Control of hypertension is important in reducing the risk of cardiovascular complications in patients suffering from OSAS.

Weight Control

Obesity, most specifically the presence of a fat neck, is a major risk factor for the development of obstructive sleep apnea. Weight loss, therefore, is the cornerstone of treatment in every overweight patient, even those only mildly overweight. This treatment can be curative by itself, even with a minimal amount of weight loss. Studies have shown that as little as 10 to 15% reductions in weight can be associated with a 50% reduction in the number of apneas and a clinically significant improvement.

Continuous Positive Airway Pressure

In the majority of cases initial treatment of OSAS should be performed by CPAP.The equipment used consists of a mask or cannula that attaches to the nose, mouth, or both, and a generator that provides the delivery of air under pressure, which in turn acts as a “pneumatic stent” to prevent upper airway collapse.The amount of pressure required to maintain an open-air passageway varies depending on the severity of the disease and the collapsibility of the airway. Each patient’s pressure level must be determined individually. The standard procedure is to observe the patient while sleeping and titrate the pressure to a level that eliminates apnea and snoring in all body positions and sleep stages.

There are conflicting reports regarding the long-term patient compliance with this form of treatment. The best long-term reports have a compliance rate of 70%; however, only one third of the patients adhere to the prescribed regimen when scrutinized. The reasons for abandonment of CPAP are varied, such as interference with the patient’s lifestyle (i.e., intimacy, travel) and as a result of complications developing from the treatment itself (i.e., nasal congestion with rhinorrhea, facial irritation from the mask, eustachian tube dysfunction, and aerophagia with gastric distention).

Mandibular Advancement Devices

A mandibular advancement device (MAD) is a promising new approach in the treatment of snoring and obstructive sleep apnea syndrome. Satisfactory results are found more frequently in patients with mild OSAS than in those with a severe syndrome.The dental appliance pulls the lower jaw and thereby also the base of the tongue forward, which increases the size of the upper airway in the hypopharynx. The appliance also causes an increased tension in the oropharyngeal muscles.

Because the device applies strong force to the teeth and the temporomandibular joint, it is important that this type of treatment be performed by a dentist, preferably a specialist in orthodontics. Each device has to be made individually, and possible side effects must be carefully followed. Devices that are occluded, and hence prevent the possibility of oral breathing when the patient opens the mouth, are not recommended. Before intervention with a MAD, a clinical examination of the stomatognathic system including the mandibular joint has to be performed. To use an oral appliance, the patient has to have sufficient teeth and cannot have severe periodontal disease or cariogenic problems.