Obstructive Sleep Apnea

Laura Cadigan, SRNA

University of Miami
Objectives
Overview of Sleep Disordered Breathing
OSA
History highlights of OSA
Incidence and Prevalence
Risk Factors
Signs and Symptoms
Diagnosis
Pathophysiology
Morbidity and Mortality
Effects of sedatives, analgesics, anesthetics on the
respiratory system
Effects of sleep contributing to perioperative risk
Preoperative Evaluation
Preoperative preparation
Intraoperative management recommendations
Postoperative management recommendations
Sleep Disordered Breathing
 Momentary, often cyclical, cessations in breathing rhythm (apneas) or
momentary or sustained reductions in the breath amplitude (hypopneas),
sufficient to cause significant arterial hypoxemia and hypercapnia

 Apneas and hypopneas are specific to the sleeping state and are
accompanied by a:
◦ Obstructive event- compromised or often completely closed extrathoracic
upper airway
◦ Central Event-A marked reduction or cessation of brain stem respiratory
motor output
◦ A combination of central and obstructive events

 Lead to transient arousals from sleep and sleep state fragmentation

throughout the night and cause overcompensatory responses of the ANS

Dempsey et al 2010
 Continuum of sleep disordered
breathing

 Normal: Normal upper airway resistance, no snoring

Primary snoring: not associated with daytime symptoms

UARS: Increased upper airway resistance sufficient to cause symptoms

OH: increased UAR sufficient to cause  PaC02 or  SaO2

OSA: Intermittent upper airway obstruction

Lerman, 2006
 What is Obstructive Sleep Apnea?

 Defined as cessation of airflow for more than

10 seconds despite continuing ventilatory
effort, 5 or more times per/hr during sleep,
and is usually associated with a decrease in
arterial oxygen saturation (SaO2) of more
than 4%

 OSA event results in

◦ Upper airway obstruction
◦ Decreased alveolar ventilation
◦ Decreased alveolar Po2; increased alveolar PC02
◦ Decreased arterial PO2: increased arterial PCO2
◦ Stimiluation of arterial chemoreceptors; central
chemoreceptors
◦ Arousal
◦ Secondary hyperventilation

Benumof 2001
What does OSA look like?
OSA in history
 Earliest description of OSA may
have been as early as 4th century
B.C.
 Tyrant Dionysius who lived during
the time of Alexander the Great
manifested obesity,
hypersomnolence, and snoring

 1836 Charles Dickens published

the Pickwick Papers, in which the
character Joe the Fat Boy
manifested symptoms of what
later was called pickwickian
syndrome
 Salvador Dali suffered from OSA,
which inspired his painting
“Sleep” in 1937
“.... and on the box sat a fat and re-faced
boy, in a state of somnolency....the fat
boy rose, opened his eyes, swallowed a
huge piece of pie he had been in the act
of masticating when he fell asleep....Joe-
dams the boy he's gone to sleep again."
The posthumous paper of the Pickwick
Club, Charles Dickens 1836
Stalford 2003
Salvador Dali’s “Sleep”
Historical highlights-History of OSA
 1956 Burwell coined the “Pickwickian syndrome”
 1950s- The later refuted theory was “Pickwickians “ breathing disorder and
drowsiness was due to carbon dioxide poisoning
 Around 1965 Gestaut, Tassinari, and Duron in France and Jung and Kuhlo in
Germany provide the most accurate descriptions of OSA
 1970: Elio Lugaresi and Colleagues at the University of Bologna perform
tracheostomy. This procedure left little doubt that OSA was due to an
obstructed upper airway and not a dysfunction of the brain’s respiratory
centers.
 1970-1986: tracheostomy and weight loss were the only proven beneficial
remedies for OSA
 1981 Sullivan et al introduced CPAP treatment for OSA, which replaced
tracheostomy as the most useful treatment
 1981: Fugita and colleagues introduced uvulopalatopharyngoplasty
 Other treatments such as oral appliance therapy are now treatment
alternatives
What is the Prevalence of OSA
High prevalence in North American, European, and Asian nations

Estimated 15 to 20 million American adults have OSA

Approximately 20% of adults have at least mild OSA (AHI>5/h)

Approximately 7% of adults have moderate to severe OSA (AHI>/= to 15/hr)

Prevalence twice as high in men than in women

Especially
common in obese individuals
In follow up to Wisconsin Sleep Cohort Study, percentage of obese subjects

(BMI>40) with AHI greater or equal to 15 is:
42-55% of men
16-24% of women

Estimates
vary but some sources state 85% of people with OSA are
undiagnosed It is estimated

Chung et al 2006, Lopez-Jimenez et al 2008

OSA in surgical Population
Noepidemiologic studies have been undertaken to determine
the frequency of OSA in surgical population

Frequency of OSA in the surgical population is markedly higher than in


the general population

7 out of every 10 patients undergoing bariatric surgery were found to


have OSA

More studies needed. One problem- difficult to recruit surgical


patients to undergo Polysomnography studies
In study by fidan et al, less than ½ of the patients identified as being
at risk for OSA agreed to undergo a sleep study.
Out of the patients agreeing to the sleep study, the majority (78%)
were found to have an AHI>/= to 5

Chung et al 2006
Patient Populations having higher prevalence of
OSA Patient Population Prevalence estimates (%)
Smokers 6.7 for heavy smokers
Diabetes 36
Treatment-resistant HTN 63
Overweight men and women Men: OR for BMI> 35 = 95%
with CHF Women: OR for age>60
years= 95%
During the acute phase of 71
first ever stroke
Primary open angle 20
glaucoma
Hypothyroidism 45
Alcoholism (in subjects aged 17
40-59 yrs) Chung et al 2008
 Known and suspected predisposing conditions for OSA (Chung et al 2006)

Known and suspected predisposing

Condition

Obesity, body fat distribution

Examples

Adult Obesity, Prader-Willi syndrome

Contributions

conditions for obstructive sleep apnea

Race/Genetics Complex and ill-defined Anatomical similarity

Age Tissue Laxity; pharyngeal closing

pressure increases with age

Male Gender longer pharyngeal length? Testost.?

Alcohol, Sedatives, Analgesics, Muscle relaxation, depressed arousal

anesthetics

Smoking Chronic nasal congestion, Pharyngeal

edema

Nasal Obstruction Septal deviation, chronic nasal  Pharyngeal negative pres.

congestion

Pharyngeal Obstruction Tonsillar and adenoidal hypertrophy  Pharyngeal negative pres.

Cranio-facial abnormality Down’s, Pierre-Robin, Treacher- mid-face hypoplasia, macroglossia

collins, Aperts, Crouzon’s, or micrognathia , retrognathia
acromegaly, fragile-x,
achondroplasia

Laryngeal obstruction Lryngomalacia, tracheomalacia Laryngeal collapse

Endocrine/Metabolic Hypothyroidism, androgen therapy, Upper airway infiltration or

Cushings Triad myopathy, obesity

Neuromuscular disorders Stroke, cerebral palsy, head injury, Disordered pharyngeal

shy-Drager, Poliomyelitis, myotonic neuromuscular function
dystrophy, dysautonomia, tetraplegia
Symptoms of OSA
 Loud snoring
 Hypersomnolence

(excessive daytime
sleepiness)
 Depressed mentation
 Altered personality
 Impotence
 Headaches upon

waking
 Nocturia

Hillman et al 2004
The 3 Cardinal Symptoms of OSA
 Snoring
 Sleepiness
 Significant other

report of sleep
apnea episodes

 This 3 S pneumonic
is a helpful
pneumonic for
assessing for OSA

Shafazand 2009
Signs of OSA
 Systemic Hypertension

 Pulmonary Hypertension (right axis deviation seen on ECG)

 Polycythemia

 Cor Pulmonale

 Bradycardia during apneic event

 Tachycardia after airflow is restored

 Typically no respiratory abnormality while awake

 Arterial blood gases while awake may show metabolic alkalosis

OSA - Increasing concern for
Anesthetists
 Increasingly common sleep disorder associated with
increased perioperative morbidity and mortality
 OSA is undiagnosed in an estimated 80% of Pts
 Concerns in patients with OSA include:

◦ Potential upper –airway obstruction

◦ Difficult tracheal intubation
◦ Postoperative respiratory depression and airway obstruction
◦ Oxygen desaturation
◦ Hypertension
◦ Dysrhythmias
◦ Postoperative Re-intubation
◦ Prolonged recovery and hospital stay
Minimal diagnostic criteria for
OSAHS
 Pts should have excessive daytime sleepiness
that is not better explained by other factors or
two or more of the following symptoms not
explained by other factors:
◦ Choking or gasping during sleep
◦ Recurrent awakenings from sleep
◦ Unrefreshing sleep
◦ Daytime fatigue
◦ Impaired concentration
 Greater than 5 Apnea-hypopnea events (AHI)
per hour during sleep
Randerath 2006
Polysomnography-Gold Standard for
diagnosis of OSA
 Continuous measurement of breathing effort by plethysmography (chest and
abdominal wall motion)
 Airflow at the nose and mouth using flow sensors (thermistor, pneumotachnograph)
 O2 saturation by pulse oximetry
 Blood pressure
 Esophageal pressure (estimates intrapleural pressure)
 Sleep architecture by EEG
 Chin electromyography (looking for hypotonia)
 Electro-oculograms to assess the occurrence of rapid eye movements
 Polysomnography records help classify stages of sleep and the occurrence and
duration of apneic and hypopneic periods
 Pt is also video recorded
 ECG monitoring is used to determine whether arrhythmias occur in conjunction with
the apneic episodes
 Limb muscle activity is also recorded to assess nonrespiratory casues of sleep
arousal, such as restless leg syndrome and periodic limb movement disorder and
body position (apnea may occur only in supine position)

Eckert and Malhotra 2008

Schematic description of sleep study
(Polysomnography) methodology

Obesity, sleep apnea, the

airway and anesthesia.
Benumof, Jonathan

Current Opinion in
Anaesthesiology. 17(1):21-30,
February 2004.

© 2004 Lippincott Williams & Wilkins, Inc. Published by Lippincott Williams & Wilkins, Inc. 5
Polysomnography

Eckert and Malhtra 2008

Apnea-hypopnea index (AHI)
 Number of apneas and hypopneas per hour

 Used to define and characterized the severity of the sleep

apnea syndrome

 AHI of >5-10 events per hour is used to characterized

patients with OSA

 Ability to predict OSA related complications is modest at

best

Randerath 2006
 Grading of severity of OSA
AHI, events/hr O2 saturation, %

Normal <5 >95

Mild 5-19 >85

Moderate 20-39 >65

Severe >40 <65

Randerath 2006
Pathophysiology of OSA
 Snoring and obstructive apnea are symptoms of increased
upper airway resistance

 Ability to maintain upper airway patency during the

normal respiratory cycle is the result of a delicate
equilibrium between the forces that promote airway
closure and dilation

 This "balance of forces" concept reflects the current line

of thought regarding the underlying pathophysiological
mechanisms that result in the clinical spectrum of
obstructive apnea

Hillman et al 2007
Pathogenesis of OSA
Narrowing or occlusion of the upper airway is related to
several factors:
◦Abnormal anatomy of the UA

◦Abnormal neural regulation

◦Pathological and insufficient reflex activation of UA dilator muscles

◦Increased collapsibility of the passive UA

◦ The UA collapse occurs during the terminal phase of the expiration preceding the
apnea

Randerath 2006
Multiple factors maintain upper airway patency

Anatomic characteristics
Tonic and phasic upper airway muscle activity
Thoracic volume

 Patency of pharynx is dictated by interaction of a

variety of passive mechanical and active neural
forces that together determine:
◦ Caliber of airway
◦ Compliance of the airway wall
◦ Pressure gradient across the wall

Hillman et al 2007
Reasons why narrow airway is more
vulnerable to collapse
 During inspiration, intraluminal pressure decreases, tending to narrow the
airway- this tendency is increased if airway is already narrow, the airway walls
are compliant, or extraluminal presssure is increased

◦ Poiseulle’s Law: resistance is directly related to the air viscosity () and to
the length (L) of the tube, and inversely related to its radius in the 4th power:
Raw = 8  L/r4. Doubling the length of the airways only doubles the airway
resistance, but halving the radius increases the resistance sixteen-fold

◦ Airway wall compliance is increased at lower calibers

 The velopharynx Is usually the narrowest (most compliant) segment of upper airway
and appears to be most common site of collapse during sleep and anesthesia

 Laplace’s law dictates that recoil pressure generated across a distended

curved elastic surface is inversely proportional to its radius of curvature

Hillman et al 2007
Important Upper Airway Anatomy
 Upper airway begins at the nose and lips
and ends at the larynx

◦ Consists of a potentially collapsible

segment (the pharynx) situated
between two rigid tubes (bony nasal
passages and the cartilaginous larynx
and trachea)

 There are three collapsible pharyngeal

segments-
◦ Retropalatal pharynx (Velo or
nasopharnynx, posterior to the soft palate)
◦ Retroglossal pharynx (oropharynx,
posterior to the tongue from the tip of the
uvula to the tip of the epiglottis
◦ Retroepiglottic pharynx (laryngo or
hypopharynx posterior to the epiglottis)

 These areas are collapsible because the anterior

and lateral walls lack bony support

Benumof 2001
Pharyngeal dilator muscles
 Responsible for maintaining patency
of the collapsible segments in the
pharynx

 Act to stiffen or distend the

collapsible pharyngeal airway during
inspiration

 Greater the negative inspiratory

pressure, the greater the force of
contraction required to keep the
airway open

 This negative pressure reflex

response seem to be driven by
pressure-sensitive airway receptors
because pharyngeal anesthesia
abolishes it

Benumof 2001
Muscles of upper airway patency
Tensor Palatini: retracts the soft palate away from
the posterior pharyngeal wall-maintains patency
during nasal breathing
◦Predominately tonic. Decreased activity during sleep
results in increased airway resistance

Genioglossus: moves tongue anteriorly to open the

retroglossal air space
◦Considered most important muscle for upper airway
patency
◦Phasic with inspiration, decreases during sleep in
normal subjects, almost ceases during REM sleep
and is abolished in OSA pts at onset of an apnea,
and increases at the termination of an obstruction

The hyoid muscles: cause the hyoid bone to move

forward and they enlarge and stabilize the
retroepiglottic hypopharynx
◦Phasic activity with inspiration which correlates
inversely with UAR
◦Factors influencing hyoid position, such as neck
flexion or mandibular abnormalities can negatively
affect the function of these muscles, leading to
narrowing of the laryngopharnyx Benumof 2001
Sites of Obstruction During Sleep
Apnea
Anatomical characteristics
◦Can help determine pharyngeal
collapsibility
◦Not sole cause of OSA
◦Studies have shown various
anatomical correlates are poor
predictors of OSA prevalence or
severity

According to Bachar et al although

the velopharnynx was the most
common site of obstruction (in 89%
of patients), most patients (72%) had •Collapse of nasopharynx at the palatal level
multiple sites of obstruction. •Collapse of oropharynx at the glottic level
AHI increased with the number of
•Collapse of laryngopharynx at the epiglottic
level
obstruction sites

Benumof 2001
Transluminal Pressure Gradient
 Transluminal pressure: difference
between intraluminal pressure and
the surrounding tissue pressure
 Extraluminal pressure increases
with obesity and other increases in
tissue volume (eg. Angioedema) or
narrowing of skeletal structures
(eg. neck flexion or micro or
retrognathia)
 If transmural pressure decreases,
the cross-sectional area of the
pharynx decreases. If this pressure
passes a critical point, pharyngeal
closing pressure is reached
 OSA occurs when the net forces
reach the closing pressure.

Hillman et al 2007
 Starling Resistor Model of Upper Airway
 Flow through a collapsible segment depends on how the pressures upstream and downstream of
it relate to the pressure surrounding it (tissue pressure)

 Where Pupstream >Pdownstream> Tissue Pressure (Pcrit)

◦ the segment remains distended and flow varies with pressure gradient from upstream to downstream

 Where Pupstream> Tissue pressure (Pcrit) >Pdownstream of the collapsible segment

◦ flow limitation will occur with flow rate now independent of a downstream pressure, being determined by the gradient b/w upstream and
tissue pressures. A fall in pressure occurs across the collapsible segment which results in a near constant pressure at the site of flow
limitation that approximates tissue pressure

 Where Tissue pressure (Pcrit) > Pupstream

◦ Segment is occluded and no flow occurs

 The upstream pressure at which flow ceases is the critical closing pressure (Pcrit) of the collapsible segment
and provides a measure of its collapsibility

Hillman et al 2007
 Airway Wall Compliance
Is an expression of its degree of flaccidity and, in the absence of muscle activity,
is a function of its passive elastic properties and the radial and longitudinal
tension to which it is subjected

A highly compliant (flaccid) airway is more likely to collapse and upper airway
compliance is increased in OSA

Increased compliance occurs with low lung volumes-predisposing to airway

collapse
Contraction of the diaphragm against the high resistance offered by the nose
during inspiration creates a subatmospheric intra-airway pressure which may
narrow the collapsible segments in the pharynx

Longitudinal tension on the upper airway increases with increasing lung volume
(“tracheal tug”), acting to decrease compliance. This along with reflex muscle
activation stabilizes the airway during inspiration when the associated negative
intraluminal airway pressure favors airway narrrowing

Hillman et al 2007
Bernoulli Effect
 Plays an important dynamic role
in OSA pathology
 Airflow velocity increases at the
site of stricture in the airway
 As airway velocity increases,
pressure on the lateral wall
decreases
 If transmural closing pressure is
reached, airway collapses
 Bernoulli effect is exaggerated in
areas where the airway is most
compliant
 Loads on the pharyngeal walls
increase adherence and , thus.
increase the likelihood for
collapse
Downey 2009
Normal Sleep
 Relation between anatomy and muscle
function in upper airway becomes critical
during sleep

 Typical night sleep: 4-6 cycles of NREM sleep followed

by REM sleep
◦ 4 stages of NREM and one stage of REM sleep
which represent increasing deeper sleep with
progressive slowing of Electroencephalogram
waves

◦ Deep NREM (stages 3&4) and all REM stages are:

 Slow wave or deep sleep
 Restorative periods of sleep
 Characterized by generalized loss of muscle tone
 Loss of muscle tone results in pharyngeal collapse
 Most important site of collapse is lateral pharyngeal
walls, which is major pharyngeal site of adipose tissue
deposition in obese patient

Benumof 2004
NREM SLEEP REM SLEEP

 Rhythmic activity of upper  Activity of upper airway

airway muscles decreases muscles can completely
disappear
 Upper Airway resistance
increases significantly (up to
 Upper airway resistance is
twice that of awake state) higher than NREM sleep

 As upper airway resistance

increases, the pharyngeal
pressure generated by a given
diaphragmatic contraction
increases- Pharyngeal pressure
becomes more negative and
pharyngeal collapse increases

Benumof 2004
Changes in upper airway anatomy and
airway function seen in persons with
OSA
 Smaller pharyngeal airway

 Larger anatomic structures of upper airway have been described in the apnea
patient, including the tongue, parapharyngeal fat pads, and the lateral walls
surrounding the pharyngeal airway

 Men have significantly longer pharyngeal airway than women even when
corrected for body height. Airway length is associated with increased
pharyngeal collapsibility

 Genioglossus is more active in awake OSA patients(increased EMG) and that at

sleep onset this activity falls to a greater extent than in healthy subjects

 Insufficient reflex activation of dilator muscles during sleep

 Increased compliance of the velopharynx in apnea patients

De Backer 2006
Arousal
 Respiratory events leading to increased neural traffic in the RAS stimulating
arousal
◦ Decreased PaO2 –due to initial PaO2, decreased FRC, duration of apnea
◦ Increased PaCo2- as a function of duration of apnea
◦ Increased ventilatory effort progressively increases function of both
decreasing PaO2 and increasing PaC02
◦ Increasingly more negative intra-airway pressures

 Arousal expressed as Increased electroencephalogram (EEG)

activity,vocalization, extremity twitching, turning, gasping or snorting on
airway opening

 Once arousal occurs upper airway muscles reactivate, and pharyngeal airway
opens; Ventilation resumes; hypercapnia and hypoxia are corrected, the
individual returns to sleep; cycle begins

 Physiological events that surround the arousal response, when repeated

often, will ultimately lead to serious systemic pahtophysiologic consequences

Benumof 2004
Schematic representation of the typical
pathophysiological sequence that occurs in
OSA

Protective/restorative (outside the circle)

Perpetuating (Inside the circle)
 Inside the main circle represents possible sites where various pathophysiological traits
would either predispose or worsen OSA

 ____ OVALS represent some of the factors that may alleviate OSA at various points
throughout the typical Physiological cycle (located outside the main circle) .* some are
only theoretical and largely untested compared to other proven therapies (CPAP)
Morbidity and Mortality
OSA
SYSTEMIC PATHOPHYSIOLOGY OF OSA

© 2004 Lippincott Williams & Wilkins, Inc. Published by Lippincott Williams & Wilkins, Inc. 4
EXCESSIVE DAYTIME SLEEPINESS
 One of most common and most difficult symptoms to treat

 Reduces quality of life

 Impairs daytime performance

 Causes neurocognitive deficits (memory deficits

 CPAP effective in reversing EDS, however poor compliance and low

treatment due to large undiagnosed pt population

 Increased risk for motor vehicle accidents

 Modanafinil has been effectively used to treat refractory daytime

somnolence despite effective CPAP use

Castronovo et al 2009
Performance and neurocognitive deficits
Due to sleep fragmentation and hypoxemia
patients with OSA experience impaired:
 Daytime functioning
 Intellectual capacity
 Memory
 Pschomotor vigilance (decreased attention
and concentration)
 Motor coordination

In a study by Castronova et al OSA pts showed

an over-recruitment of brain regions compared
with controls, in the presence of the same level
of performance on a working-memory task

Decreases of activation in prefrontal and

hippocampal structures were observed after
CPAP treatment in comparison to baseline. These
findings may reflect a neural compensation
mechanism in never-treated patients, which is
reduced by effective treatment

Castronovo et al 2009
OSA and Cardiovascular Disease
 AHA and the ACC published an expert review in 2008
◦ Somers et al stated “OSA patients often have hypoxemia,
reoxygenation, sleep arousals, less sleep time than healthy individuals,
elevated negative intrathoracic pressure, and some cases hypercapnia”

◦ “The commonly accepted contributions of these OSA related factors may

affect sympathetic activation, metabolic dysregulation, left atrial
enlargement, endothelial dysfunction, systemic inflammation, and
hypercoagulability. These mechanisms can lead to HTN (systemic and
pulmonary), heart failure, cardiac arrhythmias, renal disease, stroke, and
myocardial infarction, and sudden death in sleep”

◦ The do not recommend evaluation and for OSA in all patients with
cardiovascular disease, but threshold for a referral for a PSG study should
be low because OSA affects younger individuals with cardiovascular
disease to greater extent than older individuals with cardiac disease

Somers 2008
Stimulus for cardiovascular and
respiratory responses occuring during
apnea
 Primarily stimuli are Hypoxemia and Hypercapnia

 As Pao2 levels decrease and PaC02 levels increase during apnea, chemoreceptors in the carotid
bodies, aortic arch, and brainstem (medulla) are activated, leading to an increased inspiratory
drive

 The chemoreceptor sensitivity to carbon dioxide is the primary drive for increased ventilation
◦ Initially during apnea Stimulation of arterial chemoreceptors without stretching the lungs causes bradycardia
◦ After arousal leads to restoration of airflow, large tidal volumes stretch lungs and cause tachycardia
 an increase in pulmonary stretch receptor activity leads to inhibition of the cardiac vagal motor neurons and an
elevation of heart rate (tachycardia)
◦May hyperventilate immediately after arousal, then hypoventilate until Co2 is restored

 Changes in intrathoracic pressure (from ineffective respiratory efforts) during apnea also play a
role in the acute cardiovascular responses. These changes in intrathorcic pressure can influence:
◦venous return
◦ventricular filling
◦arterial and cardiopulmonary baroreflexes
◦Release of atrial natriuretic peptide

◦It is the interplay of all these physiologic stimuli that result in the autonomic and cardiovascular
changes associated with OSA.

Somers 2008
Putative Mechanisms by which OSA activates
the SNS initiating cascade of events that
results in cardiovascular disease

Dempsey et al 2010
Mechanisms of cardiovascular disease and arrhythmias
in OSA

 The acute pathophysiological events of OSA  may elicit multiple intermediate

cardiovascular disease mechanisms  which may promote the development of several
cardiovascular conditions

Libby et al 2007
 Pathophysiological effects of OSA on the cardiovascular system

Bradley, T. D. et al. Circulation 2003;107:1671-1678

Copyright ©2003 American Heart Association

Hypertension
Repeated increases in sympathetic tone and systemic systemic blood pressure during
arousals may cause vascular remodeling and changes in endothelial function

Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High

Blood Pressure now lists sleep apnea as a significant cause of Secondary HTN

Several studies have shown that sleep apnea increases the relative risk for hypertension,
independent of other confounding factors
 In a cross-sectional analysis of more than 6000 patients, the Sleep Heart Health Study
showed a linear relationship between mean systolic and diastolic blood pressures and
OSA severity
 Prevalence of hypertension linearly increased with the presence and severity of
OSA
 A large Canadian population-based study found that each apneic event per hour
increased the odds of hypertension by 1%, and each 10% reduction in nocturnal oxygen
saturation increased the likelihood of hypertension developing by 13%.
 Approximately 50% of patients with OSA have hypertension, compared with only 30% of
the general public

CPAP treatment for 1 year was associated with decreases in both systolic and diastolic
pressure
 Only evident if patient uses CPAP device for >5.6 hrs per night

Clonidine, a rapid eye movement sleep (REM) suppressant, may improve OSA by reducing
the patient’s percentåge of REM sleep because the REM sleep is when OSA is most severe
Lettieri 2010
Arrhythmias
Cardiac arrhythmias, especially tachy-brady syndrome, ventricular ectopy, and
atrial fibrillation are commonly identified in patients with OSA

Bradyarrhythmia occurs in 10% OSA patients, especially in the REM sleep state
when a greater than 4% drop in oxygen saturation occurs

The Sleep Heart Health Study noted that patients with sleep-disordered
breathing have a higher likelihood of having complex arrhythmias compared with
control patients OSA patients have a fourfold increase in atrial fibrillation, a
threefold increase in non-sustained ventricular tachycardia, and a twofold
increase in complex ventricular ectopy

Rhythm disturbances likely correlate with nocturnal hypoxia, sleep

fragmentation, and elevated sympathetic tone

Treatment of OSA in patients with known congestive heart failure has been
shown to reduce the frequency of premature beats, which in turn may decrease
the morbidity of ventricular arrhythmias

CPAP therapy has been shown to reduce the rate of arrhythmias even after
controlling for heart failure and other independent variables

Lettieri 2010
Pulmonary Hypertension and OSA
 OSA results in hemodynamic derangements and dysfunction of the
pulmonary vasculature and may contribute to the progression of underlying
pulmonary hypertension
 The 2004 American College of Chest Physicians (ACCP) consensus panel
found that pulmonary hypertension occurred in 17% to 53% of individuals
with OSA
 A review from Johns Hopkins found that 82% of patients with pulmonary
hypertension had underlying sleep-disordered breathing
 The nocturnal desaturation, hypoxic-vasoconstriction, reperfusion injuries,
ventilatory instability, impaired nitric oxide synthesis, endothelial
dysfunction, and vascular remodeling that result from repetitive obstructive
respiratory events can lead to the development of pulmonary vascular disease
 To date, whether OSA independently causes clinically significant pulmonary
hypertension remains controversial. Thus, the current ACCP guidelines do not
recommend evaluating patients with OSA for pulmonary hypertension unless
it is clinically suspected.

Lettieri 2010
Stroke
 Association between OSA and stroke has been
observed in multiple cross sectional studies

 So far, studies unable to determine if OSA precedes

onset of stroke and thus involved in pathogenesis

 Arzt et al found that moderate to severe SDB (AHI>

20 ) was associated with increased risk of stroke,
and no increased risk was observed in subjects
with mild SDB

Dempsey et al 2010
Perioperative concerns -OSA
 Increased risk of difficult intubation
 Post-operative hypoxemia
 Post-operative airway obstruction requiring

the need for reintubation

 Myocardial ischemia
 Arrhythmia
 Death

Lovich-Sapola 2010
OSA and postoperative complications
 Increase in postopertive complication rates
 Increase need for intensive care intervention
 Prolonged hospital stays

 Mayo clinic study compared post operative complications in

OSA patients in a retrospective study of 4yrs of data for 101
patients with OSA who had hip or knee replacement surgery
 Outcomes were compared with those of 101 matched controls
without OSA who underwent the same operations
◦ Complications occurred in 39% in OSA patients vs 18% in control
patients
◦ Serious complications requiring ICU transfer for cardiac ischemia or
respiratory failure occurred in 24% of OSA patients vs 9% in controls

Shafazand 2009
Pathophysiology of OSA during the
Peri-operative Period
 All central nervous system (CNS) depressant drugs (inhaled agents,
hypnotics, narcotics) and neuromusclular blocking agents cause (to
varying degrees) relaxation of pharyngeal muscles

 Relaxation of pharyngeal muscles predisposes the OSA patient to

airway collapse and obstruction

 CNS depressants also impair the arousal state, which terminates the
apneic episodes, which predisposes the patient to hypoxemia and
hypercarbia

 Among 23 patients with previously unrecognized sleep apnea

undergoing outpatient diagnostic procedures under conscious
sedation, Sharma et al. noted that OSA developed in 17 Pts (74%)

Lovich-Sapola 2010, Sanjay and Rajiv 2004

Influence of anesthetic drugs on the upper
airway
 Central control of pharyngeal dilator muscles is diminished by
virtually all drugs used in anesthetic care including propofol, opioids,
benzdiazepenes, nitrous oxide and halogenated inhalation agents

 Fogel et al demonstrated the sensitivity and vulnerability of airway

reflex components
◦ LA was applied to the nasopharynx and oropharynx of awake pts with
OSA which resulted in partial airway obstruction due to:
 obtundation of airway pressure-sensing reflexes
 Decreased genioglossus muscle activity
 Increased pharyngeal resistance

 Eastwood et al demonstrated collapsibility of the airway with

isoflurane
◦ With decreasing depth of anestheia, the pharynx was less collapsible
◦ Found that the primary site of obstruction was the soft palate, challenging
widespread view of tongue as primary site of UA obstruction
Stalford 2003
Effects of sedatives, anesthetics, and
analgesic agents on the respiratory
system
 Reduce FRC
 Predispose to atelectasis
 Increase upper airway collapsibility
 Reduce ventilatory response to hypoxemia and

hypercapnia
 Can induce sleep apnea in patients who otherwise do

not have clinically significant OSA

 Decrease arousal and ventilatory response to

respiratory events and worsen hypoxemia

◦ These responses can worsen the severity of underlying OSA

Lan and Rose 2006

Effects of sedative, anesthetic, and
anaglesics on respiratory system
GENERAL EFFECT LOCAL EFFECTS
CNS Depression Depressed consciousness

Reduced arousal responses

Decreased skeletal muscle tone

Decreased upper airway tone

Reduced neural input to upper

airway muscle

Respiratory depression Decreased FRC

Ventilatory depression
Diminished ventilatory response to
Lan and Rose 2006
Effects of sleep contributing to
perioperative risk
 Sleep deprivation
◦ anticipation of surgery,anxiety, pain, medications, conditions r/t surgery
◦ Exacerbates OSA and increases the complications associated with OSA

 REM REBOUND (once patient finally does sleep , the amount of REM sleep
increases to compromise for the deprivation)
◦ REM stage is when most apneas occur
◦ Sleep apneic events tend to be more frequent and severe during this period of
recovery and can cause significant hypoxemia
◦ This post op hypoxemia has been associated with :
 Increased cardiovascular events ie. arrhythmias
 Poor wound healing
 Mental confusion
 Surgical delirium

 Positioning- most patients are nursed in the supine position, and this
may worsen airway obstruction in some pts with position dependent
apnea
Lan and Rose 2006
Type and extent of surgery can contribute to the
variation in responses among patients with OSA
 Surgery for heavy snoring (uvulopalatopharyngosplasty) or for
relieving upper airway obstruction (adenoidectomy, tonsillectomy,
tracheostomy)

 Surgery of the thorax and upper abdomen

◦ Ventilatory function may be depressed, and ability to overcome
upper airway obstruction could be compromised

 Upper airway surgery

 Perioperative swelling may further compromise the narrowed

upper airway lumen

 Surgery of the lower abdomen, pelvis, and extremities

Jain & Dhand 2004

PREOPERATIVE Screening for OSA
 Assessment of OSA risk need not be lengthy
 Pt’s generally don’t volunteer information
about sleep so it is important to ask
 Screening tools can assist in identifying
relevant questions about sleep
 Each screening tool improves the likelihood of
identifying OSA preoperatively
 Berlin Questionaire
 ASA checklist
 STOP Questionaire

Shafazand 2009
STOP-BANG QUESTIONAIRE

STOP-BANG
S (SNORE) Do you snore loudly Yes/No
(louder than talking or
loud enough to be heard
through closed doors)?

T (TIRED) Do you often feel tired, Yes/No

fatigued or sleep during
daytime?

O (Observed) Has anyone observed you Yes/No

stop breathing during
sleep?

P (blood Pressure) Do you have or are you Yes/No

being treated for high BP?

B (body mass index) BMI > 35? Yes/No

A (Age) Age>50 years? Yes/No

N (neck) Neck circumfrence >40 Yes/No

cm? Yes to >3= high risk of OSA
Yes to <3= low risk of OSA
G (Gender) Gender Male? Yes/No
Chung and Elsaid 2009
ASA recommendations
 ASA task force for Perioperative Management of
OSA recommends that any patient who possesses
two of the following characteristics should be
assumed to have moderate OSA

◦ Clinical Signs and Symptoms suggestive of OSA

◦ History of apparent airway obstruction
◦ Somnolence

◦ ASA also notes that any severe manifestations of any of

these symptoms should be treated as though severe OSA
is present

Chung and Elsaid 2009

Preoperative Evaluation
 Early preoperative evaluation in perianesthesia clinic (if avail)
or by direct consultation from surgeon to anesthesia provider
 Preoperative evaluation should include
◦ Review of previous medical records
 hx. of difficult airway, HTN, cardiovascular problems ,
congenital or acquired medical conditions. Sleep studies)
◦ Interview with patient an/or family
 Focused questions r/t snoring, apneic episodes, frequent
arousals during sleep, morning headaches, daytime
somnolence
◦ Physical examination
 Airway evaluation, nasopharyngealcharacteristics, , neck
circumfrence, tonsil, tongue volume

ASA practice guidelines for management of OSA 2006

Preoperative Recommendations
Screening for OSA by questionaire, physical examination

Evaluate for possible difficult intubation

Defer elective surgery and consider overnight sleep study in patients with high
degree of suspicion for severe OSA

Assess and encourage adherence to nasal CPAP

4 to 6 weeks of nasal CPAP before surgery has been shown to increase pharyngeal
size and decease tongue volume on MRI

In another investigation, patients with OSA who received nasal CPAP before surgery
and on a near continuous basis for 24-48 hrs after extubation and thereafter for all
sleep periods did not experience major complications

 CPAP started before and resumed immediately after extubation allowed these
investigators to safely perform a variety of surgical procedures in patients with
OSA, and to freely use sedative, analgeisc and anesthetic drugs without
complications

Jain & Dhand 2004

Preoperative Preparation
 Preoperative initiation of CPAP should be considered, especially for severe OSA

 Non invasive Positive Pressure Ventilation (NIPPV) should be considered for

patients who don’t tolerate adequately to CPAP

 Preoperative use of mandibular advancement, oral devices and pre operative

weight loss should be considered when feasible

 Pt who has had corrective surgery for OSA should still be treated as being at
increased risk for OSA complications unless a normal sleep study has been
obtained

 Pts with known or suspected OSA should be managed as possible difficult airway
with utilization of the difficult airway algorithm

 Determination must be made in patients at risk for OSA complications if a

procedure should be performed in an outpatient or inpatient setting

ASA practice guidelines for management of OSA 2006

CPAP (continous Positive airway pressure)

 Acts as a pneumatic stent

 Controlled pressure is induced
through the nasal passage, holding
the soft tissue of the uvula, soft palate
and the soft pharyngeal tissue in the
upper airway in position

 Applying positive end expiratory

pressure when assisting ventilation with
bag and mask can be a useful strategy in
helping relieve upper airway obstruction

 For pts being treated with CPAP device

should be immediately available post
extubation after removal of
nasopharyngeal or oral airway

Yim, Jordan, Malhotra 2006

 CPAP Treatment
 Benefits
 Improved breathing during sleep
 concentration
 Alertness
 neurocognitive function
 Mood
 Even some cardiovascular outcomes
 Efficacy of long term CPAP treatment in lowering
Arterial BP has been demonstrated
 Reduces number of cardiac arrhythmias and beneficial effects of CPAP on sinus
arrest and episodes of heart block during sleep have been reported

 Efficacy has not been established in the perioperative setting due to insufficient evidence in
the literature

Adherence and acceptance has been limited

 According to Yim et al 1/3 of eligible patients refuse to wear it

Factors affecting adherence to CPAP

 Symptomatic relief
 Initial experience with CPAP
 Side effects-nasal congestion, airleaks
 Recent life events
 Social Support system

Yim, Jordan, Malhotra 2006, Chung et al 2008

Intraoperative Management
 In selecting intraoperative medications (sedatives, opioids, and PIAs) the
potential for postoperative respiratory compromise should be considered
 Peripheral nerve blocks and local anesthesia, with or without sedation should
be considered for superficial procedures
 If moderate sedation is used, ventilation should be continuously monitored
by capnography
 Consider administering CPAP or using an oral appliance during sedation in
patients previously treated with these modalities
 General anesthesia with a secure airway is preferable to deep sedation
without a secure airway, particularly for procedures that may mechanically
compromise the airway
 Regional (spinal or epidural) should be considered for peripheral procedures
unless there is a contraindication.
 Patients should be extubated fully awake. Full reversal of neuromuscular
block should be verified before extubation.
 When possible extubation should be carried out in the lateral, semiupright, or
other non supine position

ASA practice guidelines for management of OSA 2006

Postoperative Management-OSA
Regional analgesic techniques should be considered to reduce or eliminate the requirement
for systemic opioids

If Neuraxial analgesia is planned benefits vs risks of using an opioid or opioid-local

anesthetic mixture compared to a local anesthetic alone should be considered

If controlled PCAs are used continuous background infusions should be used with extreme
caution or avoided entirely

Nonsteroidal antiinflammatory agents should be considered if appropriate to reduce opioid

requirements

Supplemental oxygen should be administered to all pts at increased risk from OSA until they
are able to maintain their baseline on room air
 Task force cautions that supplemental oxygen can increase the duration of apneic
episodes (removes the hypoxic drive) and can hinder detection of atelectasis, transient
apnea, and hypoventilation by pulse oximetry

Continuous use of CPAP or NIPPV (Pts receiving treatment preoperatively) with or without
supplemental oxygen when patient is not ambulating

If possible patients should be placed in non supine positions throughout the recovery
process

Patients at increased risk of respiratory compromise should have continuous pulse oximetry
monitoring after discharge from the recovery room

ASA practice guidelines for management of OSA 2006

In Conclusion
 OSA surgical patients are at increased risk for perioperative complications

 OSA can be induced, unmasked, and exacerbated by the effect of sedative,

analgesic, and anesthetic agents

 Once OSA develops these patients are at higher risk of several life
threatening complications

 Increased awareness of the risk posed by an obstructed upper airway and

appropriate management are important to optimize the perioperative care
with OSA

 Preoperative recognition of OSA, constant control of the airway, titration

of analgesic and sedative drugs and vigilant monitoring could avoid many
unexpected complications after surgery

Janin and Dhand 2004