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Sleep apnea and central sleep apnea

Terms in this set (42)

What is obstructive sleep apnea?
-Repetitive episodes of complete or partial upper airway obstruction during sleep that are associated with oxygen desaturations or arousals
-Hypopharynx is where the tongue meets the back of the mouth
What are signs/symptoms of obstructive sleep apnea?
-Daytime sleepiness
-Difficulty concentrating
-Loud snoring
-Witnessed apneas with resuscitative snorts
-Non-restorative sleep
-Morning headaches/dry mouth
-Insomnia
-Peds: present with over activeness instead of sleepiness
What are risk factors for OSA?
-Age
-Males
-Excess body weight
-Craniofacial abnormalities
-Ethnicity (blacks and Asians)
-Medical comorbiditis
-Nasal congestion (you're a mouth breather)
-Familial/genetic
-Alcohol consumption
-Hypothyroidism
-Polycystic ovarian syndrome (increased androgens)
-Pregnancy (the baby pushes up on the diaphragm and decreases lung volume)
-Menopausal status
-Current smoking (inflammation of the airways)
What is the STOP-BANG Questionnaire?
-Frequently used as a screening tool preoperatively to determine risk factor for OSA, positive if greater than 3
-Sensitive but not specific-->we get a high false positive screening rate
-The Berlin Questionnaire is another example
What is the Epworth sleepiness scale?
-Asks the patient how likely they are to doze/fall asleep in lifestyle situations
What should you look for on PE in someone you suspect OSA?
-BMI
-Neck circumference
-Waist circumference
-Airway features (size of tonsils)
-Craniofacial abnormalities
How do you predict if someone has OSA?
-There is no one thing that is a greater predictor
How do you diagnose someone with OSA?
-Polysomnography (aka sleep study)
-This test measures:
--Airflow (nasal cannula for hypopnea, thermistor for apnea)
--Oxygen saturation
--EEG, extra ocular movements
--Chin EMG (muscle tone)
--Respiratory effort
--ECG
What is obstructive apnea?
-A cessation of airflow with ongoing respiratory effort lasting at least 10 seconds
-So the flow goes away but the patient is still breathing
What is obstructive hypopnea?
-Nasal flow is reduced by 30-50% with an oxygen desaturation of 4% or an arousal
-So the flow goes down a little and there's a consequence
What is apnea-hypopnea index?
-Number of apneas and hypopnea per hour of sleep (the birds eye view of how we score)
What is a home sleep study?
-Includes the airflow (nasal), oximetry (pulse ox), and respiratory effort (belt)
-May underestimate the degrees of sleep apnea bc it goes by recording time and not the total sleep time
-Should be considered primarily for individuals at risk of OSA-->good results for patients with moderate to severe sleep apnea
-Lacks performance with comorbidities and mild OSA
How do you diagnose OSA?
-Apnea-hypopnea index (AHI) greater than 15 events/hour OR
-AHI greater than 5 events/hour with at least one of the following: excessive daytime sleepiness, awaking with choking or gasping, or bed partner reports loud snoring and witnessed apneas
What are the different degrees of severity in OSA?
-Mild: 5-15/hour
-Moderate: 15-30/hour
-Severe: greater than 30/hour
Can we diagnose OSA by our oximetry?
-No!
-If positive for repetitive desaturations it is strongly suggestive, but not definitive
-Also, if it is negative, it doesn't rule out OSA
What are consequences of OSA?
-Cardio: HTN, MI, stroke, sudden death, arrhythmia, pulmonary HTN
-Lost work productivity, MVA
-Metabolic: insulin resistance, DM
What is the connection btw OSA and HTN?
-They are directly correlated to each other
-Individuals with OSA lack the normal nocturnal fall in blood pressure
-Treatment of OSA improves BP
What is the connection btw OSA and nocturnal death?
-In sleep apnea, peak deaths occur btw midnight and 6 am
What is the connection btw OSA and metabolic consequences?
-Individuals with OSA are 5-9 x more likely to have metabolic syndrome
-It is associated with insulin resistance and glucose intolerance
How do you treat OSA?
-Weight loss (bariatric surgery has shown to improve OSA than non-surgerical)
-Positional therapy
-Nasal CPAP is our best thing
-Bilevel ventilation
-Mandibular advancement devices
-Surgical therapies
-Tracheostomy
Who should you consider for bariatric surgery?
-Acceptable surgery risk
-Previously failed other weight loss strategies
-BMI greater than 35 if comorbidities, including sleep apnea, DM, and joint disease
-BMI greater than 40 if no comorbidities
What is a nasal CPAP?
-Acts as a pneumatic splint to upper airway to prevent collapse
-If titrated properly and used, effectiveness at preventing obstructive events near 100%
-Our best thing!
-Complaints: nasal congestion or dryness, frequent awakenings, inconvenience, noise, claustrophobia, mask leak, lack of benefit
What is bilevel ventilation treatment for OSA?
-Can be considered if patients have difficulty tolerating CPAP pressure
-Provides increased pressure with inspiration compared with expiration and can support ventilation (there's 2 pressures)
What is mandibular advancement for OSA?
-Rarely used
-Holds the tone and jaw in a more anterior position
-Stabilizes the mandible and hyoid bone anteriorly
-Increases palatoglossal and palatophyargneal muscle activity
-Redues pharyngeal tissue folds
-Indicated for mild to moderate OSA if patient preference over CPAP, failure to tolerate or respond to CPAP, inappropriate candidates for CPAP
-Indicated for severe OSA only if the patient fails to tolerate CPAP
-It's better than nothing, but it's not great
-It has to be fitted by a sleep apnea dentist
-They have to do jaw exercises in the morning to get their jaw back in place
What are surgical options for OSA?
-Nasal: septoplasty, rhinoplasty
-Nasopharyngeal: UPPP, palatal advancement, tonsillectomy in children (may be curative, palatal implants
-Hypopharyngeal: tongue reduction, hyoid suspicion, mandibular advancement
-Laryngeal: epiglottoplasty
-If the patient has severe craniofacial abnormalities or obstructing tonsillar hypertrophy then refer to ENT
What is UPPP?
-Uvuloplatatopharyngoplasty that removes excess tissue in the throat to make the airway wider
-Usually combine with adenotonsillectomy and may include tongue resection
-Success rate is 40-50%
-Side effects: dysphagia, velopharygneal insufficiency (food can go up into their nose from their mouth), stenosis
What is central sleep apnea?
-Diminished or absent respiratory effort in an intermittent or cyclic pattern due to CNS or cardiac dysfunction
-On a sleep study, a cessation of decrease of both effort and airflow for a least 10 seconds
-It is considered pathologic if greater than more than 5 per hour
What are the two categories of CSA?
-It is based on daytime PaCO2 levels
1.) Hypercapnic: have impaired ventilatory response to CO2 during wakefulness and increased Co2. Worsens with sleep onset. The brainstem doesn't respond to CO2 and no matter what happens they won't breathe anymore. (Central) or it can be from Myasthenia Gravis in that they're can't breathe (Respiratory)
2.) Hypocapnic:typically marked by a high ventilatory response to CO2. They have Cheyne-Stokes respiration or high altitude periodic breathing, or idiopathic
What can cause central hypercapnic CSA?
-Central meaning the brainstem doesn't respond
-Obesity hypoventilation syndrome
-Opioid medications
-Tumors, stroke or trauma to brainstem structures
-Congenital central hypoventilation syndrome (Ondine's curse)-->require nocturnal ventilation throughout life
What is obesity hypoventilation syndrome?
-Obesity and presence of hypoventilation (PaCO2 > 45mmHg) that cannot be explained by another reason
-Inability to compensate for increased work of breathing from obesity-related impairments in respiratory mechanics (it gets tired!)
-They're typically hypoxemic
-Almost all people with obesity hypoventilation syndrome also have OSA
-If we put them on CPAP it makes it worst bc we are preventing them from waking up and ventilating more
-Weight loss led to increased ventilatory response to CO2
-It is linked to higher inflammation and mortality then severe obesity or OSA
What is the connection btw opioids and CSA?
-Patients on methadone treatment have decreased ventilatory response to hypercapnia and increased hypoxic ventilatory response
-They have an irregularly irregular pattern of breathing
What is respiratory hypercapnic CSA?
-"Can't breathe"
-Abnormalities occur anywhere along the axis from UPN to respiratory muscles
-Ex: ALS (motor neuron), Myasthenia gravis (NM junction), Myopathies (muscles), chest wall disease (kyphoscoliosis)
-They have a lot of headaches in the morning bc their CO2 is rising
What is the transition to sleep?
-The most vulnerable period
-Loss of behavioral control of breathing
-Decreased upper airway tone
-Decreased respiratory pump muscle tone (increased upper airway resistance and decreased ventilation for a given level of respiratory drive)
-Decreased chemosensitivity
What has the greatest effects in ventilation?
-REM sleep
-Ventilation decreases
-It leads to a rise in CO2 during sleep by 3-8mmHg
What is apnea threshold?
-The PaCO2 at which the brain sends no respiratory signal to breathe
-It is typically 2-6 mmHg below sleeping PCO2 level
-Cheyne Stokes!
-The brain recognizes the decreased breathing so they hyperventilate and then we over compromise and then you stop and you have increased CO2 again and it's a cycle pretty much
-Heart failure
What is Cheyne-stokes respiration?
-Crescendo-decresendo pattern of breathing with apneas or hypopnea alternating with hyperpneas
-Seen in non-REM sleep and largely goes away in REM
-Can be seen in wakefulness as well
-Seen in Heart failure cases
-At least 10 apneas or hypopnea per hour
-Associated with a serious medical illness (CHF, atrial fibrillation, renal failure, acute stroke)
-Worse in acute decompensation of CHF
-Symptoms are not required but patients frequently complain of fragmented sleep and daytime somnolence
What is the patho behind Cheyne-stokes respiration?
-Pulmonary congestion in stimulates a stretch receptor in the lungs resulting in hyperventilation during wakefulness
-More fluid=increased stretch, so the feedback loop doesn't work as well
-At sleep onset eucapnic PaCO2 is below apneic threshold resulting in CSA
-Arousals perpetuate hyperventilation and lead to overshoot in PaCO2 leading to repetitive cycles
What is high altitude periodic breathing?
-Looks like Cheyne-Stokes respiration, but short cycle time (15-34 seconds) and circulation time is short
-Occurs after rapid ascent to altitude
-More common in individuals with high hypoxic ventilatory drive
-Not associated with the development of mountain sickness of high altitude pulmonary or cerebral edema
-Individuals will adapt over the course of the first few nights although may persist at extremes of altitude
What is the patho behind high altitude periodic breathing?
-Related to the hyperventilation that occurs due to hypoxia seen at altitude
-Waking PaCo2 is lower than apneic threshold
What is idiopathic CSA?
-Rare
-Unknown etiology
-Waking PaCo2 is usually low normal
-Cycle length is 20-40 seconds
-Less severe desaturations
-No crescendo-decrescendo pattern
What is the treatment of CSA?
-Medical management of heart failure-->we need help from cardio
-Oxygen-->Non-hypercapnic CSA and considered the "standard" for treating CSA in the most recent AASM guidelines. It improved AHI by around 15 events/hour on oxygen
-Positive airway pressure (CPAP, bilevel)-->used in Cheyne stokes which leads to improved hemodynamics but does not lead to improvements in mortality
-Positional therapy (head of the bed is up)
-CPAP and/or oxygen for Cheyne stokes respiration
-CPAP or bilevel for hypercapnic CSA
As a PCP, when should I suspect CSA?
-Morbidly obese with right heart failure and somnolence
-Those on chronic opioids or with neuromuscular disease
-Chronic heart failure and low EF
-Refer to sleep specialist for management as it is more difficult as well
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