Module 2 - Upper Airway Obstruction in Sleep Flashcards
(204 cards)
1
Q
What are 4 anatomical abnormalities associated with OSA?
A
- Adenoidotonsillar enlargement
- Micrognathia (small mandible)
- Infiltration of muscles and soft tissues (rare: myxoedema, acromegaly, neoplastic processes, mucopolysaccharidosis)
- Nasal obstruction
2
Q
How is nasal obstruction associated with OSA?
A
It’s a contributing (not major) factor. Needs more negative pressure to breathe so there’s more collapsing force.
3
Q
How does sleep impact the upper airway muscles (x5) in normal subjects?
A
in Non-REM sleep
Palatoglossus, genioglossus & diaphragm all normal-ish to maintain pharyngeal patency.
Levator palatini 50% reduced. Not that important because it elevates to the roof of the mouth.
Tensor palatini 75% reduced. Important for stiffening and maintaining airway by bringing soft palette onto back of the tongue. Important for sleep.
4
Q
Describe the upper airway muscles reflex response to negative airway pressure?
A
Negative airway pressure is sensed by upper airway muscles and reflexively increase activity of upper airway muscles (genioglossus) to improve upper airway patency.
5
Q
How does the upper airway muscles reflex response different from awake to sleep?
A
During sleep, the reflex response is markedly diminished or absent.
6
Q
How do the upper airway muscles control pharyngeal patency?
A
Negative airway pressure is sensed by upper airway muscles and reflexively increase activity of upper airway muscles (genioglossus) to improve upper airway patency.
7
Q
How does the role of the upper airway muscles control of pharyngeal patency different in OSA when awake and asleep?
A
When awake: OSA patients compensate for inadequate airway anatomy by increasing pharyngeal dilator muscle activity (neuromuscular compensation -> reflex).
When asleep: no neuromuscular compensation during sleep leads to airway occlusion in OSA sleep.
8
Q
What are the 5 important upper airway muscles involved in maintaining pharyngeal patency?
A
- Genioglossus muscle
- Geniohyoid muscle
- Tensor veli palatini muscle
- Levator veli palatini muscle
- Palatopharyngeus muscle
9
Q
Where is the genioglossus muscle and what does it control?
A
Base of the tongue, sits on soft palette
Contracts and keeps base of tongue off posterior pharyngeal wall. Important in pharyngeal patency.
10
Q
Where is the geniohyoid muscle and what does it control?
A
From mandible to hyoid bone.
Contraction pulls tongue off pharyngeal wall. Important in pharyngeal patency
11
Q
What does the tensor veli palatini muscle do?
A
Contraction tenses soft palette and pulls of pharyngeal wall. This is important for nasal airflow and pharyngeal patency.
12
Q
What does the levator veli palatini muscle do?
A
Elevates soft palette, closing nasopharynx. Important for swelling and oral breathing.
13
Q
What does the palatoglossus muscle do?
A
Contracts the soft palette putting it on the back of tongue to promote nasal breathing.
14
Q
Do upper airway muscles respond in a uniform way in sleep?
A
No.
15
Q
How do upper airway muscles respond to negative airway pressure?
A
A reflex activation.
16
Q
What are some of the problems of using AHI as a phenotype?
A
- Noisy signal
- Variable definitions (e.g. hypopnea)
- Variable techniques
- Relationship to outcomes isn’t overly strong
- Night to night variability (reporting and physiological changes, body positioning and sleep depth)
- Problems of in-lab recording
- Two patients can have very different clinical characteristics
17
Q
What are the phenotype names in OSA?
(e.g. Risk factors, clinical features)
A
Risk factors: risk factor phenotypes
Clinical features/Complications: clinical phenotypes
Physiological features: Polysomnographic phenotypes
18
Q
What are the new ways that we can use to phenotype for OSA?
A
- Imaging of craniofacial and upper airway structures [narrowing, Box model]
- Ethnicity
- Tongue Fat %
- Mandibular Advancement (SPAM grid)
- Photography for facial phenotyping
- Pathophysiological
- PSG
- Genetic
19
Q
Describe the bone-soft tissues interaction (“Box” model)
A
Soft tissue (small/large) + Bony enclosure (of mandible and maxilla small/large) -> Leads to -> Airway size
Obesity = large soft tissue and normal (or smaller) bony enclosure -> increased tissue pressure and smaller airway
20
Q
What is the main ethnic difference in driving risk factor for OSA?
A
Chinese: craniofacial restriction is bigger driver
Caucasian: obesity is biggest driver
But, BMI has a bigger influence in Chinese population due to craniofacial restriction
21
Q
What is SPAM imaging?
A
magnetic grid of tissue imaging to find tissue deformations
check out grid photos in notes
22
Q
What types of information can be taken from photography for facial phenotyping of OSA?
A
Angles
Areas
Volumes
23
Q
How does photographic facial phenotyping perform in predicting OSA?
A
77% correctly classified based on
Caucasian:
Mandibular width & width angle
Neck width
Lower face width-depth angle
HongKong
Cricomental space area
Mandibular width
Mandibular plane angle
Neck soft tissue area
24
Q
What are the pathophysiological phenotypes in OSA & how much are they present in disease?
A
Anatomical (Pcrit) 81%
Inadequate UA muscle responsiveness 36%
Low respiratory arousal threshold 37%
Oversensitive ventilatory control (high loop gain) 36%
25
What does it mean if someone has an oversensitive ventilatory control (high loop gain)?
They develop an exaggerated response that causes cyclical breathing
26
What is the primary finding regarding clinical clusters in the Icelandic study in OSA?
(# clusters, symptoms and which is more prone to comorbidities)
There are 3 clinical clusters; (1) insomnia-type 33%, (2) minimally symptomatic 25% and (3) textbook OSA with daytime sleepiness 42%
Cluster 2 more prone to hypertension, CVD, diabetes. Not based on severity as no diff in age, gender, AHI.
27
The European clinical phenotypes study on OSA determined there were 4 clinical types of OSA. What were they and what is their distribution?
Excessive Daytime Sleepiness (Y/N)
Insomnia (Y/N)
Roughly even distribution
28
What is the confounding problem when examining phenotypes for OSA?
A lot of comorbidites in OSA that have interrelationships and have bidirectional causalities.
Leads to many moderators and modifiers.
E.g. Obesity (OSA RF) is strongly related to diabetes (OSA comorbidity)
29
What are the conclusions on genetic research in OSA?
Inconsistent, doesn't say much yet.
Likely many genes contributing small amounts.
30
What are the 5 common polysomnographic phenotypes?
- Sleep stage dependency (e.g. REM OSA)
- Position dependency (e.g. supine OSA, common)
- Apnoeas vs hypoponoeas
- Arousal index (e.g. fragmentation)
- SaO2 (fragmentation & time below threshold)
31
What polysomnographic phenotypes could provide information on disease burden?
- Age of onset
- Duration of disease
- Extent of sleep fragmentation and arousal intensity
- Breathing "load"
- Airflow "fingerprints"
- Hypoxic burden
- Haemodynamic effects
- Hypercapnia/acidosis
- Snoring characteristics
- Biomarkers
32
What is residual disease burden?
The amount of remaining AHI when treatment compliance + efficacy is considered
E.g. Residual AHI = (AHI treatment x Hours) + (AHI treatment2 x Hours) / Total sleep time hours
2 treatments could have same effect due to different efficacy and compliance (hrs)
33
What traits predict response to oral appliance therapy in OSA?
Lower loop gain
34
How can the field of OSA improve treatment?
- Shift focus from diagnosis to outcomes (e.g. chronic disease management)
- Fractionating the OSA phenotype (simple, reliable, inexpensive phenotypic tools)
- Create large-scale OSA cohorts
- Collaborate with other disciplines
35
What are the functions of the human upper airway?
Air transmission, swallowing, heat exchange, and vocalization.
36
How does NREM sleep affect upper airway muscles?
What happens in REM sleep that differs?
Reduces tonic and phasic electromyogram (EMG) activity, contributing to airway narrowing.
REM sleep further reduces activity, particularly in phasic dilating muscles like the genioglossus, leading to increased collapsibility.
37
Why is the activation of genioglossus and hypoglossal nerve crucial?
Crucial for airway patency during sleep.
38
Does gender significantly influence negative pressure reflex during wakefulness?
No, limited evidence supports gender differences in baseline muscle activity.
39
How does aging impact reflex responses contributing to airway collapsibility?
Aging may not affect baseline muscle activity but can decrease reflex responses to negative pressure and hypoxia.
40
What histologic changes in upper airway muscles are associated with OSA?
Edema
mucosal gland hypertrophy
neurogenic injury
changes in muscle enzyme activity
leukocytic inflammation.
41
Why is craniofacial structure crucial for upper airway patency?
Various abnormalities are linked to OSA, affecting pharyngeal airway size and function.
42
How can intrinsic properties of the upper airway affect collapsibility?
Intrinsic compliance, influenced by various factors, modifies the collapsing effect of transmural pressure.
43
What challenges does sleep pose to the ventilatory system?
Reduces activity of upper airway dilators, leading to decreased upper airway caliber and increased collapsibility.
44
What happens to upper airway resistance during NREM sleep?
Increases, reaching highest values in slow-wave sleep.
45
How is collapsibility measured during sleep?
Measured by critical closing pressure (P crit), it increases during sleep and is related to the propensity for airway collapse.
46
How does hormonal activity influence upper airway collapsibility?
Leptin, associated with decreased upper airway collapse, can influence collapsibility.
47
How does upper airway resistance change between Non-REM and REM sleep?
No significant increase in resistance during REM sleep compared with NREM sleep in normal humans.
48
What are examples of sensors involved in ventilatory regulation?
Sensors include central and peripheral chemoreceptors, vagal pulmonary sensors, and chest-wall and respiratory muscle afferents.
49
What role does the central controller play in ventilatory regulation?
The central controller receives information from sensors and generates an automated rhythm of respiration, constantly modified in response to receptor input.
50
What are the effectors in ventilatory regulation?
Effectors include respiratory motoneurons and muscles which alter minute ventilation and gas exchange according to the signals from the central controller.
51
Where are the DRG and VRG located?
The Dorsal Respiratory Group (DRG) and Ventral Respiratory Group (VRG) are located within the medullary ventilatory center.
52
What functions do the DRG and VRG serve?
The DRG primarily regulates inspiration, while the VRG controls both inspiratory and expiratory neurons, particularly during forced expiration.
53
What role do pontine influences play in respiratory control?
Pontine influences regulate and coordinate inspiratory and expiratory control, with the pneumotaxic center affecting inspiration duration and the apneustic center terminating inspiratory efforts.
54
What are the types of chemoreceptors involved in ventilatory regulation?
Chemoreceptors include central chemoreceptors in the ventrolateral surface of the medulla and peripheral chemoreceptors in the carotid and aortic bodies.
55
What are the types of pulmonary mechanoreceptors?
Pulmonary mechanoreceptors include PSRs, J-receptors, and bronchial c-fibers, which respond to inflation, dyspnea, and pulmonary inflammation respectively.
56
How does respiration differ during sleep compared to wakefulness?
Respiration during sleep shows changes in ventilation, response to CO2 and O2, and effects on upper-airway muscles and positional changes.
57
What are examples of drugs that can impair respiration?
Alcohol, anesthetics, narcotics, and sedative-hypnotics are drugs that can impair respiration by reducing hypoxic and hypercapnic ventilatory responses and depressing upper-airway muscle tone.
58
What respiratory disorders are associated with sleep disturbances?
Respiratory disorders such as asthma, COPD, restrictive lung disease, kyphoscoliosis, obesity hypoventilation syndrome, pregnancy, neuromuscular disorders, and obstructive sleep apnea can cause sleep disturbances.
59
How do respiratory patterns differ between NREM and REM sleep?
NREM sleep typically exhibits more regular respiratory patterns with decreased tidal volume, while REM sleep shows increased frequency and reduced regularity in respiration.
60
How do positional changes during sleep affect breathing?
Nonupright positions can significantly alter breathing mechanics, with the supine position potentially increasing airway compromise.
61
How do ventilatory responses differ between wakefulness and sleep in response to increased airway resistance?
Reductions in minute ventilation are more pronounced during NREM sleep compared to wakefulness in response to increased airway resistance.
62
What symptoms characterize nocturnal asthma?
Nocturnal asthma presents with repetitive arousals, breathlessness, coughing, and wheezing during sleep.
63
What contributes to hypoxemia in COPD during sleep?
Hypoxemia in COPD during sleep results from hypoventilation, ventilation/perfusion mismatching, and/or reduction of lung volume, exacerbated in REM sleep.
64
How does pregnancy affect sleep-disordered breathing?
Pregnancy tends to increase snoring prevalence but has less effect on apnea-hypopnea frequency.
65
How do neuromuscular disorders affect respiration during sleep?
Neuromuscular disorders can cause hypoventilation, oxygen desaturation, and apneas/hypopneas during sleep.
66
What characterizes obesity hypoventilation syndrome during sleep?
Obesity hypoventilation syndrome during sleep results from increased work of breathing and metabolic demands, leading to hypoxemia.
67
How does REM sleep exacerbate obstructive sleep apnea?
REM sleep exacerbates obstructive sleep apnea by increasing upper-airway narrowing and breathing work, leading to hypoxemia and hypercapnia.
68
What is alveolar hypoventilation, and how is it defined?
Alveolar hypoventilation is defined as PaCO2 ≥ 45 mm Hg during wakefulness, with nocturnal hypoventilation indicated if sleeping PaCO2 is ≥ 10 mm Hg higher than awake.
69
What PaO2 value on room air indicates severe hypoxemia?
A PaO2 < 55 mm Hg on room air indicates severe hypoxemia, suggesting the need for oxygen therapy.
70
How is PAO2 calculated, and what value is assumed for the respiratory exchange ratio (R)?
The alveolar gas equation computes PAO2 from FiO2 and PaCO2, assuming a respiratory exchange ratio (R) of 0.8.
71
What are some causes of hypoxemia?
Hypoxemia can result from low FiO2 (fraction of inspired oxygen), low barometric pressure (high altitude), hypoventilation (increased PaCO2), ventilation-perfusion mismatch, or shunt.
72
What complications can arise from hypoxemia?
Hypoxemia may occur from hypoventilation without affecting the A-a gradient, whereas lung disease causing increased PaCO2 is associated with an increased A-a gradient.
73
How is oxygen mainly carried in the blood, and what factors affect its saturation?
Oxygen is mainly carried by hemoglobin, with saturation affected by temperature, pH, and other factors. Abnormal hemoglobins, like those in sickle cell disease, can alter this relationship.
74
What happens when the oxygen dissociation curve shifts left or right?
A left shift reduces oxygen release to tissues, while a right shift increases it. Various factors like temperature, pH, and abnormal hemoglobins influence these shifts.
75
What factors influence PaCO2 levels?
PaCO2 is related to metabolic rate and alveolar ventilation, with minute ventilation minus dead space ventilation determining alveolar ventilation.
76
How does ventilation change during sleep, and why?
Ventilation decreases during sleep due to decreased CO2 production, increased upper airway resistance, decreased chemosensitivity, and loss of wakefulness stimulus.
77
What are some tests used to assess ventilatory control?
Chemoreceptors like carotid body and medullary chemoreceptors respond to changes in PaO2, PaCO2, and [H+]. Hypercapnic hypoxemia is a potent stimulus. Sensitivity of chemoreceptors can be measured using rebreathing methods.
78
What does mouth occlusion pressure measure, and how is it assessed?
Mouth occlusion pressure (P0.1) measures respiratory drive and is measured 0.1 second after inspiration start. It is assessed during rebreathing with intermittent airway occlusion.
79
How do ventilatory control parameters change during different sleep stages?
Hypercapnic and hypoxic ventilatory responses are reduced during NREM sleep compared to wakefulness and further decreased during REM sleep compared to NREM sleep.
80
How does CPAP treatment alter ventilatory control in patients with obstructive sleep apnea (OSA)?
CPAP treatment in OSA patients alters the position of the oxygen dissociation curve without changing its slope. This is attributed to reduced nocturnal PaCO2 accumulation and bicarbonate (HCO3) compensation.
81
How are pH, PaCO2, and HCO3 related in acid-base physiology?
pH is related to serum bicarbonate (HCO3) and PaCO2 through the Henderson-Hasselbalch equation. Compensation involves changes in HCO3 in the same direction as PaCO2 changes to minimize alterations in the PaCO2-to-HCO3 ratio, while pH remains outside the normal range.
82
What are the main components and uses of pulmonary function testing (PFT)?
Pulmonary function testing includes spirometry, lung volume determination, and diffusing capacity for carbon monoxide (DLCO) measurement. It helps evaluate lung function in conditions such as obstructive and restrictive ventilatory dysfunction.
83
What are the main patterns of abnormality seen in pulmonary function testing?
Pulmonary function abnormalities include obstructive ventilatory dysfunction (OVD) and restrictive ventilatory dysfunction (RVD). OVD is characterized by reduced flow rates with increased lung volumes, while RVD involves a reduction in total lung capacity.
84
How does obesity affect ventilatory parameters?
In obesity, functional residual capacity (FRC) may be reduced or reduced relative to residual volume (RV). Simple obesity commonly presents with reduced expiratory reserve volume (ERV), while obesity hypoventilation syndrome may show reductions in total lung capacity (TLC) and vital capacity (VC).
85
How does muscle weakness affect ventilatory parameters?
Muscle weakness can lead to decreased inspiratory and expiratory muscle strength, resulting in low TLC, high RV, and low VC. Maximum inspiratory pressure (MIP) and maximum expiratory pressure (MEP) are sensitive tests of respiratory muscle strength
86
What factors determine arterial oxygen saturation?
Arterial oxygen saturation depends on the position of the oxygen-hemoglobin saturation curve, which is affected by temperature, pH, and abnormal hemoglobins. Pulse oximetry measures arterial oxygen saturation noninvasively during sleep studies.
87
What challenges are associated with measuring oxygen saturation?
Carboxyhemoglobin and methemoglobin are forms of hemoglobin that do not bind oxygen, complicating oxygen-carrying capacity determination. Co-oximeters can accurately measure different hemoglobin forms, while pulse oximetry estimates oxygen saturation using two wavelengths.
88
How do chemoreceptor responses change during sleep compared to wakefulness?
Chemoreceptor responses, including hypercapnic and hypoxic ventilatory responses, are reduced during NREM sleep compared to wakefulness and further decreased during REM sleep compared with NREM sleep.
89
How does CPAP treatment affect ventilatory control in obstructive sleep apnea (OSA) patients?
CPAP treatment in OSA patients alters the position of the oxygen dissociation curve without changing its slope. This is attributed to reduced nocturnal PaCO2 accumulation and compensatory changes in bicarbonate levels
90
How is compensation achieved in respiratory acidosis?
In respiratory acidosis, compensation involves increased bicarbonate (HCO3-) levels to maintain pH within the normal range despite elevated PaCO2 levels.
91
What are some parameters assessed in spirometry?
Spirometry measures parameters such as forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), and the FEV1/FVC ratio.
92
What characterizes obstructive ventilatory dysfunction (OVD) in pulmonary function testing?
OVD is characterized by a reduction in flow rates, often with an increase in absolute lung volumes, such as increased residual volume (RV) compared to total lung capacity (TLC).
93
How does obesity affect functional residual capacity (FRC)?
In obesity, FRC may be reduced or reduced relative to RV, potentially contributing to decreased lung compliance and impaired respiratory function.
94
What parameters are evaluated in measuring muscle strength relevant to respiratory function?
Maximum inspiratory pressure (MIP) and maximum expiratory pressure (MEP) are commonly assessed to evaluate respiratory muscle strength.
95
How does muscle weakness affect lung volumes?
Muscle weakness, especially affecting inspiratory and expiratory muscles, can lead to reductions in total lung capacity (TLC) and vital capacity (VC) due to decreased ability to generate force for lung expansion.
96
How does the presence of carboxyhemoglobin affect pulse oximetry readings?
Presence of carboxyhemoglobin can artificially increase pulse oximetry readings, potentially leading to overestimation of oxygen saturation levels.
97
How was pharyngeal closing pressure (Pcrit) determined in the study?
Pcrit was determined using a technique involving the continuous positive airway pressure (CPAP) method, wherein CPAP pressure was gradually lowered until zero airflow occurred during three breaths.
98
What does loop gain represent in the context of the study on OSA and ventilatory instability?
Loop gain is a measure of the stability of the respiratory control system and represents the sensitivity of the negative feedback loop controlling ventilation. It was measured during sleep using a proportional assist ventilator (PAV).
99
How did the Apnea-Hypopnea Index (AHI) vary among different pharyngeal closing pressure (Pcrit) groups in the study?
AHI varied significantly among different Pcrit groups, with subjects in the negative Pcrit group exhibiting primarily hypopneas.
100
Was there a significant correlation between loop gain and AHI in the study?
While loop gain values did not significantly differ among Pcrit groups, there was a positive correlation between loop gain and AHI for the overall group of subjects.
101
What impact did variations in pharyngeal closing pressure (Pcrit) have on apnea severity in the study?
Significant differences in AHI were observed between negative and positive Pcrit groups, indicating an association between Pcrit levels and OSA severity.
102
What did the study reveal regarding the influence of ventilatory instability on OSA?
The study confirmed a correlation between ventilatory instability and apnea severity, particularly in OSA patients with collapsible upper airways.
103
How can understanding the relationship between ventilatory instability and upper airway collapsibility inform OSA treatment?
Recognizing the heterogeneous nature of OSA and identifying patients where ventilatory instability is a factor could help tailor therapeutic interventions more effectively.
104
How does alcohol influence breathing?
Alcohol reduces hypoxic and hypercapnic ventilatory responses and depresses upper-airway muscle tone, potentially causing or worsening obstructive sleep apnea.
105
What effects do anesthetics have on respiration?
Anesthetics impair the hypoxic ventilatory response, decrease lung volumes, and reduce upper-airway muscle tone, leading to respiratory depression.
106
What is the impact of narcotics on breathing?
Narcotics are potent respiratory depressants that diminish upper-airway muscle tone and decrease ventilatory responses, contributing to respiratory depression.
107
How do sedative-hypnotics affect respiration?
Sedative-hypnotics are mild respiratory depressants that decrease upper-airway muscle activity, potentially worsening sleep-disordered breathing, especially when coingested with other depressants.
108
Which drugs are known to stimulate respiration?
Almitrine, acetazolamide, certain antidepressants, nicotine, progesterone, and theophylline are drugs that can stimulate respiration through various mechanisms.
109
What is the role of almitrine in respiration?
Almitrine enhances peripheral chemoreceptor sensitivity, mildly improving nighttime oxygenation by stimulating respiration.
110
How does acetazolamide influence breathing?
Acetazolamide induces metabolic acidosis, stimulating respiration, although its efficacy for obstructive sleep apnea treatment is limited.
111
What effects do certain antidepressants have on respiration?
Certain antidepressants decrease apnea-hypopnea frequency and duration by increasing upper-airway muscle tone, thus improving breathing.
112
What role does nicotine play in respiration?
Nicotine acts as a respiratory stimulant, but it is not used for obstructive sleep apnea treatment due to its adverse effects.
113
Describe the balance of forces that determine upper airway patency (a diagram)
Airway suction and dilator muscle tone are the primary influencers (OSA due to these).
Airway suction (impacts inspiratory drive) -> Local reflex -> Dilator muscle tone (impacts upper airway drive)
Central breathing control is sent information from central and peripheral chemoreceptors.
Central breathing control sends information to change inspiratory drive and upper airway drive
114
What happens to nasal and tracheal pressure when you close the nasal airway?
Nasal: don't see much of an increased drive from chemoreceptors
Tracheal: see increased pressure, getting larger until airway opens, due to increasing drive
Direct response of reflexes as carotid body is detecting decrease O2 and increasing CO2
115
How does the hypoxic response change in OSA when someone is normocapnic vs hypercapnia?
Normocapnic: CO2:O2 Interaction increases, Ventilation response increases when PCO2 increases.
Hypercapnic: Decreased or absent peripheral chemoreceptor response so ventilation doesn't increase with PCO2 increases (even when starting higher).
Hypercapnic people have minimal ventilatory response to increasing PCO2 due to absent reflexes from carotid body
116
How do awake ventilatory responses change for hypercapnia, hypoxia and CO2:O2 interactions in people with OSA with/without hypercapnia vs controls?
Hypercapnic Response:
- OSA+Hyper: low response
- OSA+Normo: normal response, maybe slightly lower
- Control: normal (highest)
Hypoxic Response:
- OSA+Hyper: low response
- OSA+Normo: sometimes higher
- Control: middle
CO2:O2 Interaction:
- OSA+Hyper: no/very low response
- OSA+Normo: middle
- Control: normal (highest)
117
How do most people with OSA respond to hypoxia?
Increased hypoxic response -> increased ventilatory drive.
As adaptation to repetitive hypoxia, associated with vascular sensitivity (hypertension)
118
Why do some people with OSA develop hypercapnia?
Likely due to sustained hypoxia leading to depression of carotid body drive
119
Are apneas and hypoventilation the same?
No.
As long as you recover between apneas, most people are okay.
Sustained hypoxia from partial obstruction can be worse for people to develop hypercapnia.
120
How do central chemoreceptors respond to CO2 increases? (what do they release and why?)
When CO2 increases, central chemoreceptors respond by increasing BCO3 to adjust pH so you can tolerate more CO2 -> Progressive adaptation
121
How do progressive partial obstructions lead to hypercapnia?
After apneas, the increased ventilation at arousal help to cope with the apneas deficit. So you maintain ABG's relatively well.
When an airway is partially obstructed, you don't fully arouse, so CO2 progressively increases
122
When depressed hypoxic responses occur in SDB (in the small subset of OSA patients), what is the pathway that leads to central chemoreceptor adaptation?
Depressed hypoxic responses ->
- Depressed arousal -> longer apnea -> higher CO2 -> central adaptation
AND - Depressed ventilatory drive (from carotid bodies) -> Reduced ventilatory recovery and hypopnea (increased partial obstruction likelihood) -> Longer exposure to High CO2 (also influenced by lung disease and high awake upper airway resistance) -> central adaptation
123
What responses underlie obesity hypoventilation syndrome?
Depressed hypoxic responses leading to central chemoreceptor adaptation
124
How do peripheral chemoreceptors respond in severe OSA that leads to increased stroke/heart disease? (not in hypercapnia)
Increased peripheral chemoreceptor response -> Mixed/central apnea pattern -> Alveolar HYPERventilation -> Compromised brain/heart/bloodflow -> increased hypertension risk -> Stroke/Ischemic
125
How do cycles of central apnea change CO2 levels?
Reduces CO2 due to increased respiratory drive
126
What are the limitations of subjective clinical impressions in diagnosing obstructive sleep apnea (OSA)?
Subjective impressions have inadequate sensitivity and specificity.
127
What is the predictive value of nocturnal choking or gasping compared to other symptoms like morning headache, reported apnea, EDS, or snoring?
Nocturnal choking or gasping has higher specificity and positive predictive value for OSA.
128
How do neck circumference and body mass index (BMI) correlate with the presence and severity of OSA?
They correlate well, but their predictive value is not large except in extreme ranges.
129
What are some physical findings associated with OSA in patients who are not obese?
Pharyngeal crowding, obstructed nasal passages, or craniofacial abnormalities.
130
What is the predictive value of the Mallampati score in assessing the risk for OSA?
It was associated with increased odds of OSA and higher apnea-hypopnea index (AHI).
131
What are some examples of physical findings that may increase the likelihood of OSA?
Signs of congestive heart failure, polycystic ovary disease, prior stroke, or underlying neuropathy or neuromuscular disease.
132
Name some instruments used to assess the risk for OSA.
Berlin Questionnaire, STOP, STOP-BANG, and Multivariable Apnea Prediction Questionnaire.
133
How are hypopneas scored according to the recommended and acceptable rules in PSG?
Recommended rule requires a 30% airflow drop and arousal or 3% oxygen desaturation; acceptable rule requires a 4% oxygen desaturation.
134
What factors may influence the precision of diagnostic PSG in detecting OSA?
Variability in biologic severity, equipment, or human scoring performance.
135
What are the advantages and limitations of split-night PSG?
It may save time and resources but may not be suitable for all patients. It may not address specific conditions like insomnia or positional OSA adequately.
136
What are home sleep tests (HSATs), and what physiologic signals do they monitor?
They are portable monitoring tools that monitor nasal pressure, chest and abdominal effort, and oximetry.
137
When are HSATs recommended as an alternative to PSG for diagnosing OSA?
In adults with an increased risk of moderate to severe OSA.
138
What are some limitations of HSATs compared to PSG?
They may not identify sleep stage or muscle activity and have limitations in scoring hypopneas.
139
What imaging modalities are used to visualize the upper airway?
Cephalometric radiography, CT, MRI, nasopharyngoscopy, and drug-induced sleep endoscopy (DISE).
140
What are the advantages and limitations of cephalometric radiography, CT, MRI, nasopharyngoscopy, and drug-induced sleep endoscopy (DISE)?
They offer various degrees of detail and accessibility but have limitations in assessing dynamic airway obstruction.
141
How is nasopharyngoscopy used in assessing the response to various OSA treatments?
It can determine the site of obstruction and assess treatment outcomes.
142
What is inspiratory airflow limitation (IFL)?
IFL describes a state of the upper airway during sleep where inspiratory airflow plateaus despite an increase in the pressure gradient, caused by fluttering of the airway, and can be audible (snoring) or silent.
143
What is snoring, and how is it related to IFL?
Snoring is audible inspiratory fluttering of the upper airway during sleep, indicating the presence of IFL. It can occur with or without associated hypopnea and is classified as habitual or isolated.
144
What is the difference between habitual snoring and isolated snoring?
Habitual snoring refers to consistent snoring observed by a bed partner, while isolated snoring occurs in asymptomatic individuals who do not meet diagnostic criteria for obstructive sleep apnea (OSA) on polysomnography.
145
What is respiratory effort-related arousal (RERA)?
RERAs are transient arousals from sleep following a period of inspiratory airflow limitation (IFL), presumed to be caused by increased inspiratory effort to move air across a fluttering airway. They are commonly observed in individuals with sleep-disordered breathing.
146
What is the Starling resistor model of IFL, and how does it differ from the concept of upper airway resistance?
The Starling resistor model describes IFL as a collapsible tube (pharynx) that collapses when the pressure within falls below a critical level (Pcrit), leading to fluttering of the airway and a fixed maximal inspiratory airflow. This model differs from the concept of increased upper airway resistance during sleep, which implies progressive narrowing of the airway.
147
How can inspiratory airflow limitation (IFL) be recognized during polysomnography?
IFL can be recognized by observing a plateau in inspiratory airflow and a prolonged inspiratory time relative to the total respiratory cycle time. Additionally, the presence of snoring may indicate IFL, but it is not as sensitive as airflow criteria.
148
What methods can be used to identify IFL during diagnostic polysomnography?
IFL can be identified by observing a plateau in inspiratory airflow, using a nasal pressure signal, or by analyzing the ratio of inspiratory time to total respiratory cycle time. Additionally, computer algorithms and airflow tracings can aid in recognizing IFL.
149
What defines habitual snoring, and how is it classified according to the ICSD-3?
Habitual snoring is sleep-related sound from soft tissue vibration during inspiration.
ICSD-3 classifies it as "isolated snoring" when occurring without symptoms and with an RDI < 15 per hour.
150
What factors contribute to variability in reported prevalence figures for habitual snoring?
Differences in subject selection, methodology, gender, and obesity rates.
Variations in snoring definition (isolated/habitual) and subjective/objective assessment methods.
151
How does snoring impact pulmonary resistance during sleep?
Increases total pulmonary resistance due to reduced upper airway muscle tone.
Leads to increased inspiratory effort and airflow limitation (IFL).
152
What contributes to the discrepancy between subjective and objective assessments of snoring severity?
Night-to-night variability in snoring intensity, sleeping position, and medication/alcohol use.
Environmental factors like allergens and individual sensitivity to noise.
153
When is polysomnography (PSG) warranted for habitual snorers?
Warranted if symptoms like witnessed apnea, hypersomnolence, or comorbidities are present.
Asymptomatic snorers may be monitored over time for symptom development.
154
What lifestyle modifications and treatments are available for isolated snoring?
Lifestyle changes: weight reduction, avoiding alcohol, maintaining regular sleep schedules.
Treatments: oral appliances, surgery for anatomical abnormalities, CPAP therapy.
155
What are the clinical characteristics and risk factors associated with Upper Airway Resistance Syndrome (UARS)?
Younger, leaner, more frequently female.
Symptoms: hypersomnolence, fatigue, nonrestorative sleep, nonapneic habitual snoring.
Risk factors: craniofacial abnormalities, nasal resistance during childhood.
156
How do signs and symptoms of UARS differ from those of OSA?
UARS: nonrestorative sleep, fatigue, insomnia, nonapneic habitual snoring.
OSA: disrupted sleep, more apneic/hypopneic events.
157
What psychiatric and somatic symptoms are associated with UARS?
Symptoms: depression, anxiety, headaches, functional gastrointestinal issues, alpha-delta sleep.
Symptoms may respond to nasal CPAP or rapid palatal expansion.
158
How do polysomnographic findings differ between patients with UARS and those with OSA?
UARS: unstable, nonrestorative sleep, shorter sleep latencies, increased sleep pressure.
Alpha-delta sleep, parasomnias like sleep-related bruxism and chronic sleepwalking may be present.
159
What are the polysomnographic findings associated with sleep architecture in patients with UARS?
Increased alpha frequency intrusion into sleep.
Sleep stage instability characterized by frequent shifts from deeper to lighter sleep stages.
Presence of cyclic alternating pattern (CAP), periodic disruptions of NREM sleep by electroencephalographic events.
160
Describe the phenomenon of alpha-delta sleep observed in patients with UARS.
Alpha-delta sleep refers to the presence of alpha frequency intrusion, typical of quiet wakefulness, within sleep stages.
This intrusion may occur in stage N3 sleep, contributing to nonrestorative sleep, and may resolve with improved sleep quality.
161
How does treatment with nasal CPAP affect sleep stage shifting in patients with UARS?
Nasal CPAP decreases the frequency of sleep stage shifts from deeper to lighter sleep stages.
This reduction in sleep stage shifting is not solely due to eliminating respiratory events but also improves sleep continuity.
162
What is the cyclic alternating pattern (CAP) observed in patients with UARS?
CAP is characterized by periodic disruptions of NREM sleep by electroencephalographic events not meeting arousal criteria.
Increasing levels of CAP correlate with increasing levels of sleepiness and fatigue.
163
How does the chronic stress paradigm explain the varied symptoms associated with UARS?
The chronic stress paradigm posits that individuals sensitized to upper airway resistance perceive it as a chronic stressor.
This leads to symptoms such as insomnia, fatigue, headaches, gastrointestinal irritability, anxiety, and depression, among others.
164
What is the significance of increased alpha frequency intrusion in sleep architecture among patients with UARS?
Increased alpha frequency intrusion reflects altered sleep quality and contributes to nonrestorative sleep.
It may resolve with interventions like rapid palatal expansion, improving sleep quality.
165
Explain the relationship between CAP and sympathetic nervous system tone in patients with UARS.
Increasing levels of CAP correlate with increased sympathetic nervous system tone, indicative of stress.
CAP serves as a marker for increased sympathetic activity commonly observed under stressful conditions.
166
What term was initially used to describe individuals with obesity, hypersomnolence, hypercapnia, cor pulmonale, and erythrocytosis?
The term "pickwickian syndrome" was initially used to describe such individuals.
167
What are the two common diagnostic criteria for diagnosing OSA?
The common diagnostic criteria for OSA include an AHI ≥ 5/hr with symptoms or an AHI ≥ 15/hr with or without symptoms.
168
What is the respiratory disturbance index (RDI), and how is it calculated?
The RDI is the number of apneas, hypopneas, and respiratory effort–related arousals (RERAs) per hour of sleep, calculated as RDI = AHI + RERA index.
169
What are some potential mechanisms linking hypothyroidism and acromegaly to OSA?
Potential mechanisms include upper airway muscle myopathy, increased upper airway mass, and alterations in ventilatory control.
170
What are the recent clinical guidelines recommended for the evaluation of OSA in adults?
Recent clinical guidelines recommend questioning high-risk populations in detail concerning symptoms of OSA, along with basic sleep questions for all patients as part of a general history and physical examination.
171
What is the Epworth Sleepiness Scale (ESS), and how is it used?
The Epworth Sleepiness Scale (ESS) is a subjective estimate of the propensity to doze off in eight situations, with scores greater than 10 indicating excessive daytime sleepiness. It is often used to assess daytime sleepiness in patients with suspected OSA.
172
What physical examinations are recommended for patients suspected of having OSA?
Physical examinations should target abnormalities associated with OSA, including measurement of BMI and systemic blood pressure, examination of the nose, ears, and oropharynx, and observation of signs of right heart failure.
173
What is primary (simple) snoring, and how is it defined?
Primary (simple) snoring is defined as the presence of snoring without associated symptoms of insomnia, daytime sleepiness, or sleep disruption. It is characterized by evidence of snoring on polysomnography (PSG) without a significant number of apneas, hypopneas, or RERAs (Respiratory Effort Related Arousals).
174
What factors contribute to the worsening of snoring?
Snoring worsens with any process that narrows the upper airway, increases nasal resistance, or decreases upper airway muscle tone. Factors such as nasal congestion, supine posture, and the use of ethanol or hypnotics can exacerbate snoring.
175
What are the characteristics of upper airway resistance syndrome (UARS)?
UARS is characterized by subjective and objective daytime sleepiness without an AHI of 5/hr or greater. Patients with UARS exhibit a respiratory arousal index greater than 10/hr using esophageal pressure monitoring, which is not associated with desaturation or changes in thermal device–detected airflow.
176
How is the diagnosis of obesity hypoventilation syndrome (OHS) made?
The definitive diagnosis of OHS requires an arterial blood gas while awake with a PCO2 of 45 mm Hg or greater. However, an elevated serum HCO3 is a useful clue indicating the need for testing for hypoventilation in patients with OSA.
177
What are the treatment options for patients with OHS?
Treatment options for OHS include continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BPAP) with or without supplemental oxygen. Treatment aims to improve daytime and nocturnal gas exchange, prevent apneas and hypopneas, and address underlying ventilatory abnormalities.
178
What is the overlap syndrome, and how is it managed?
The overlap syndrome occurs in patients with both obstructive sleep apnea (OSA) and chronic obstructive pulmonary disease (COPD). Management involves treating upper airway obstruction during sleep with CPAP or BPAP, addressing underlying COPD with bronchodilators and smoking cessation, and possibly using supplemental oxygen as needed.
179
What is an alternative to PSG for diagnosing obstructive sleep apnea (OSA) in high-risk patients?
Attended cardiorespiratory pulmonary studies are an alternative to PSG for diagnosing OSA in high-risk patients.
180
What is the recommended approach for evaluating patients with suspected narcolepsy and OSA?
PSG on PAP treatment followed by MSLT is recommended to confirm treatment efficacy for suspected narcolepsy and OSA.
181
What are the indications for portable monitoring (PM)?
PM may be indicated for diagnosing OSA in high-risk patients or documenting efficacy of non-PAP treatments for OSA.
182
What is recommended before interpreting a polysomnography (PSG)?
A review of clinical history, including medications and underlying conditions, is recommended before interpreting PSG.
183
What are some co-morbidities that may degrade PM accuracy, and why?
Patients with severe pulmonary disease, neuromuscular disease, or congestive heart failure (CHF) may exhibit hypoventilation without discrete respiratory events or Cheyne-Stokes breathing, which could affect PM results.
184
What are some potential drawbacks of PM devices in patients with certain conditions?
PM devices may miss arrhythmias because they rely on pulse rate from an oximeter rather than an ECG tracing. Additionally, patients with certain co-morbidities may ultimately require a PSG PAP titration, making PM less cost-effective in those cases.
185
What are the minimum parameters recommended for monitoring in PM?
The minimum parameters recommended for PM monitoring include airflow, respiratory effort, and oxygen saturation (SaO2).
186
How does CMS measure respiratory disturbance in PM, and why is it different from AHI?
CMS uses the Respiratory Disturbance Index (RDI), which includes apneas, hypopneas, and respiratory effort-related arousals (RERAs), divided by monitoring time, whereas AHI typically excludes RERAs. This difference should be considered when interpreting PM results for clinical decision-making.
187
What factors should be considered when choosing a PM device?
Factors to consider include the number of sensors, complexity of sensor application, level of information provided, durability, and cost of expendables like nasal cannulas.
188
What are some features of PM devices that enhance reliability and backup?
Some PM devices offer features like XFlow, which estimates total airflow derived from respiratory effort bands, providing a backup if airflow sensors fail. Additionally, disposable band materials for RIP bands enhance convenience and reliability.
189
What are some common challenges in PM studies, and how can they be addressed?
Common challenges include dislodgment of sensors or leads, which can be addressed through strategic placement of tape or patient education on proper device application.
190
What is the next step if a PM test is positive for OSA?
If a PM test is positive for OSA, various treatment pathways can be considered, including PSG PAP titration, auto-PAP treatment, or prediction equations for CPAP pressure adjustment.
191
What is the normal relationship between airflow and pressure and what happens in airflow limitation?
It is normal when you increase pressure, you increase flow linearly.
but at some point, flow stops or fails to increase despite the pressure increasing.
192
Describe how flow limitation is related to snoring
Snoring is airflow limitation. The airway is initially sucked closed by suction pressure and then opens/closes at a frequency around 30Hz. Air is still flowing but it's not determined by the pressure drive (which would usually lineraly increase with increasing flow), but influenced by airway opening and closing at a finite rate.
193
What influences the level of sound of a snore?
Increased pressure, increased loudness
194
What is the fluttering sound of a snore?
The soft palate that divides the oral and nasal airway is fluttering and blocking the oral then nasal then oral airway
195
What frequency is snoring at?
30Hz
196
What happens to CO2 when snoring is occurring?
When you start snoring, CO2 increases, which increases the reflexes to CO2 which makes you suck harder, this increases the vibration intensity of snoring
197
Why do partial obstructions cause hypercapnia and not complete repetitive apneas?
OSA: At each arousal, there is often pretty good recovery of ABG
Partial obstruction: constant airflow but not enough to decrease CO2 levels so it rises slowly. Generally happens when redlexes aren't good so they don't respond properly
198
Why are the spectrums of sleep disordered breathing often incorrectly labelled?
They say they are demonstrating severity but they are really showing level of obstruction and how often it happens, which isn't related to severity
199
Why is snoring often measured incorrectly?
The recommended settings are 500Hz (or 200hz is okay) but the filter is (<10Hz and >100Hz), so you wouldn't even pick up the signals from the 500Hz trace.
PSG would filter out a large portion of snoring sounds
200
How do tracheal microphones, cannula and calibrated microphones perform in picking up snoring signal?
Tracheal: Best (some over and under shoot due to filter settings) but it's the best way on PSG
Cannula: mostly underestimates as it can't get high frequency
Calibrated mic: Mostly overestimates as it shows blip on recording which could be breathing but is marked as snoring
Stethoscopes are often used as gold standard
201
What is different between adults and kids in picking up snoring on PSG?
In children, significantly underestimates snoring due to smaller airway so their snoring is a higher frequency which is filtered out
202
What is stertor?
Non-vibrating very high frequency obstructive breathing.
A tight sound, like gasping
203
What do bubble plots tell us about snoring and stertor in OSA?
People with OSA of all severities have :
- long durations of snoring and stertor AND
- frequent runs of snoring and stertor
But, in kids with daytime problems with OSA, all have snoring and stertor runs just as often as those without OSA.
204
What is the relationship between snoring, ESS and OSA in kids?
In kids who snore, it doesn't matter if they also have OSA, they can have daytime functioning problems.
Some of these kids could have termination of snoring runs (some form of arousal) 100s more times than terminations of arousals, so they may not have high AHI but they have problems
