General information on various sleep disorders
Epidemiologic Evidence for a Role of Obstructive Sleep Apnea in Systemic Hypertension
The early observations of hypertension in patients with sleep apnea stimulated several cross-sectional clinics- and community-based studies that attempted to determine whether there was an association between OSA and hypertension:
• Reports from several well-designed epidemiology studies, generally show associations with OSA and hypertension that remain significant even after adjustment for potential confounding factors (i.e., obesity).
• The strongest epidemiologic evidence for a causal association comes from longitudinal analyses of data from the Wisconsin Sleep Cohort Study, (population of middle-aged WI state employees). The incidence of new hypertension, defined as systolic blood pressure of at least 140 mm Hg, diastolic blood pressure of at least 90 mm Hg, or use of antihypertensive medication at follow-up, was dependent on the severity of OSA.
• After considering confounding factors, the odds of developing new hypertension over 4- years was 2X greater for those with an apnea-hypopnea index (AHI) of 5-15 events/hour, and 3X greater for those with an AHI of greater than 15 at baseline, (in comparison to patients without OSA).
• Longitudinal analyses of OSA as a predictor of 5-year incidence of hypertension in the Sleep Heart Health Study (SHHS) and 7.5-year incidence of hypertension in the Vitoria-Gasteiz (Spain) Cohort did not find the same strong association as was found in the Wisconsin cohort; however, the SHHS findings were consistent with about a 50% increased risk for incident hypertension in persons with severe OSA (AHI > 30).
• According to the 2014 update, the actual number of cardiovascular disease deaths per year declined by 16.7%, but cardiovascular diseases still accounted for about 32% or 1 of every 3 deaths in the United States. Based on 2010 death rate data, more than 2,150 Americans die of cardiovascular disease each day, an average of 1 death every 40 seconds. In fact, since 1900, cardiovascular disease has been the number one killer every year except 1918. In 2010, the total direct and indirect cost of cardiovascular disease and stroke in the United States was estimated to be $315.4 billion.
• Hypertension alone, a disorder proved to be caused by OSA, affects 78 million Americans. Many of these patients are erroneously diagnosed as having essential hypertension because of the under diagnosis of OSA.
• Congestive heart failure and stroke, disorders frequently associated with both central sleep apnea and obstructive sleep apnea, are also highly prevalent, each affecting approximately 5.1 to 6.8 million Americans.
Cognitive Behavior Therapies for Insomnia
Stimulus Control Therapy
• Involves five instructions designed to reassociate temporal (bedtime) and environmental (bed and bedroom) stimuli with rapid sleep onset and to establish a regular circadian sleep-wake rhythm:
1. Go to bed only when sleepy—not just fatigued, but sleepy.
2. Get out of bed when unable to sleep (e.g., after 20 minutes), go to another room, and return to bed only when sleep is imminent.
3. Curtail all sleep-incompatible activities: no eating, watching television, using electronic devices, or planning or problem solving in bed.
4. Arise at a regular time every morning regardless of the amount of sleep achieved.
5. Avoid daytime napping.
Cognitive Therapy
• Cognitive therapy for insomnia seeks to alter sleep-disruptive cognitions (e.g., beliefs, expectations) and maladaptive cognitive processes (e.g., excessive self-monitoring, worrying) through Socratic questioning and behavioral experiments.
• For example, worries about the consequences of sleep loss on the next day’s performance can lead to further arousal and more sleep disturbance, thus forming a vicious cycle.
1. Keep realistic expectations about sleep requirements and daytime energy.
2. Do not blame insomnia for all daytime impairments because there may be other explanations (worries about family, conflicts with coworkers) for these deficits.
3. Never try to sleep because it is likely to exacerbate sleep difficulties.
4. Do not give too much importance to sleep. Although sleep should be a priority, it should not become the central point of life.
5. Do not catastrophize after a poor night’s sleep. Insomnia is very unpleasant, but it is not necessarily dangerous to health, at least not in the short term.
6. Develop some tolerance to the effects of insomnia. If you are predisposed to insomnia, it is likely that you will remain vulnerable to sleep disturbances even after treatment, and you can develop strategies to cope with these occasional nights of poor sleep
Relaxation-Based Interventions
• Because stress, tension, and anxiety are often contributing factors to sleep disturbances, relaxation is probably the most used intervention for insomnia.
• The goal of this treatment is to reduce arousal at bedtime or on nighttime awakening.
• Among the different relaxation interventions include:
1. Progressive muscle relaxation, which focuses primarily on reducing somatic arousal.
2. Attention-focusing procedures (e.g., imagery training) focuses on mental arousal in the form of worries, intrusive thoughts, or a racing mind.
• Selection should be based on the patient’s preference or the predominant subtype of arousal (somatic versus mental). There is no formal contraindication to using relaxation, but some patients might have a paradoxical response and become more anxious when trying to relax.
• The most critical issue is to encourage daily practice for at least 2 - 4 weeks. The focus should be on reducing arousal rather than on inducing sleep, and the relaxation method should be done out of bed.
Obstructive Sleep Apnea (OSA)
• Obstructive sleep apnea occurs when there are sleep-related changes that effect your upper airway anatomy.
• Obstruction of the airway during sleep leads to low oxygenation levels and disruptive sleep.
• Chronic obstructive sleep apnea can also lead to a condition called “sleep maintenance insomnia”, which occurs when patients have a difficult time staying asleep, chronically waking up at night many times. This is primarily due to inability one’s inability to effectively breathe adequately while sleeping.
The Upper Airway is Divided Into 5-Regions:
Each of these anatomic regions can become occluded or blocked during sleep due to various anatomic abnormalities.
• For example, the nose/nasopharynx may become occluded due to nasal congestion or structural polyps. The oropharynx may become occluded due to hypertrophy of tonsils, large tongue/macroglossia.
• The nasopharynx and oropharynx are the 2 most common areas we see occlusion/obstruction leading to OSA.
• The retro-palatal region / (area behind the tongue), from awake to sleep-this area decreases by 70% on average. This predisposes to airway resistance and difficulty breathing while asleep in many people who present with sleep apnea.
• The upper airway contains 24 different pairs of muscle groups extending from the nasopharynx down to the hypopharynx.
• These muscle groups are active in controlling important function such as swallowing and speaking.
• 2 very important muscles of the upper airway are the genioglossus and the tensor palatini muscle groups. These 2 muscle groups control the patency or opening of the upper airway to help facilitate breathing.
• While asleep, these 2 muscle groups dramatically decreased their activity. This results in upper airway narrowing and increased resistance to air movement.
The Effects of Sleep on Respiration:
1. Decrease metabolic rate
2. Loss of wakefulness effort/drive to breathe
3. Decrease activity of upper airway muscles and decreased activity of other respiratory and ventilatory motor activity.
• Some patients have susceptible anatomy predisposing them to upper airway narrowing while asleep. (Genetic craniofacial anatomic structure)
• Narrowing of the upper airway can occur even in healthy people. This occasionally results in snoring. Snoring is due to increase airflow turbulence through the upper airway which can result in fluttering of the soft palate and tissue within the oropharynx.
• In patients with OSA, increase upper airway resistance can lead to rising carbon dioxide levels in the blood stream.
• Men have an increase in retro-palatal tissue compliance compared to women. This may be one reason why men are more predisposed to sleep apnea than women.
• Age is associated with an increase in upper airway resistance during sleep resulting in further narrowing of the pharyngeal airway space.
• During REM sleep, minute ventilation decreases, and respiratory rate becomes more irregular.
• Patients with pulmonary disease or obesity are more prone to low oxygen levels or hypoxia while asleep.
• There are 3 categories which determine structural propensity for obstructive sleep apnea:
1. Cranial facial/bone anatomy. The surrounding upper airway soft tissue, including adipose/fat tissue.
2. Vascular structures
3. Neuromuscular factors, ventilatory motor output and upper airway muscle activity.
Cranial facial structural features
A recessed jaw line (mandible/lower jaw), described as a conditioned called retrognathia. This can create decreased in space behind the tongue and cause compression of the retro-pharyngeal space leading to upper airway resistance or complete airway obstruction. Retrognathia is typically a result of inherited cranial facial features.
Vascular factors
• Increased vascular volume in the neck (i.e. rostral fluid shifts) can promote upper airway obstruction by increasing the soft tissue volume and pressure
• For example, during recumbent sleep patients with congestive heart failure or end-stage kidney disease may experience increase in soft tissue volume or edema. Diuretics and compression stockings can help reduce AHI, neck circumference and leg fluid volume.
Neuromuscular factors
1. Loss of wakefulness/drive to breathe reduces muscle activity and decreases the respiratory pump muscles of the upper airway musculature.
2. During wakefulness, application of negative pressure on the upper airway results in a robust reflexive increase in upper airway muscle activity.
3. During sleep, this negative pressure reflex normally present during wakefulness is suddenly absent when you fall asleep.
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3-types of sleep-related breathing disorders:
1. OSA, due to anatomical obstruction in the upper airway, decrease in upper airflow with an increased effort to breathe while asleep.
2. Central sleep apnea (CSA), abnormal signaling from the brain to the respiratory muscles, resulting in a lack of effort to breathe while asleep.
3. Sleep-related hypoventilation disorder, characterized as abnormal ventilation during sleep resulting in increased carbon dioxide levels.**
Note: These 3 groups are not mutually exclusive, a patient can meet criteria for more than 1 of these conditions.
Clinical significance of untreated moderate /severe obstructive sleep apnea may include:
1. Hypertension
2. Cardiac arrhythmias
3. Cardiovascular disease
4. Increased mortality risk
5. Metabolic abnormality
Obesity & OSA:
Longitudinal data of the Wisconsin cohort indicated that a 10% gain in body weight increased the chance of developing moderate to severe OSA by a factor of 6x fold. Every 1% increase in body weight was associated with a 3% increase in AHI. Conversely, weight loss reduced OSA severity but to a less substantial degree than that seen with exacerbation with weight gain.
Type II diabetes & OSA:
Recently, an RCT of CPAP in 39 subjects with prediabetes and OSA found that 8 hours of CPAP use every night for 2 weeks, documented by nightly in-laboratory sleep monitoring, could reduce glucose response to oral glucose tolerance testing and improve insulin sensitivity. As with a previous 1-week RCT in nondiabetic men, these findings can be regarded as proof-of-concept for an adverse effect of untreated OSA on glucose metabolism, which is reversible with control of OSA, but the relevant clinical impact remains elusive.
Obstructive sleep apnea in patients with seizure disorder:
OSA is common in epileptic patients.
General prevalence of OSA in previous investigations have found a general incidence of 10% in adult epileptic patients. In children the incidence of OSA has reported to be approximately 20%.
(CPAP), continuous positive airway pressure treatment in patients with epilepsy and OSA was found to reduce EEG interictal epileptiform activity and improved seizures particularly in drug resistant epilepsy. (Reduction by 50% or more in 28% of patients with OSA & seizure disorder versus 15% reduction in OSA & epileptic patients not on CPAP).
Obstructive sleep apnea can worsen nocturnal seizures by increasing sleep instability during NREM sleep and by inducing daytime sleepiness with an activating effect on epileptic phenomena.
