Transcript Sleep-Disordered Breathing

Unit I
Integrative Lecture:
Sleep-Disordered Breathing and
Respiratory Failure
Ruwan Amaratunga, MD, FRCPC
Credit: Jackie Sandoz, MD, FRCPC
Objectives
o Sleep-Disordered Breathing (SDB)
o OSAS
o Definition, symptoms, risk factors, pathophysiology, consequences, diagnosis,
severity, treatments, differences between adults & children
o Other types of SDB
o Central apnea, OHS and hypoventilation
o Respiratory Failure
o
o
o
o
Hypoxic vs. Hypercapnic failure
Pathophysiology of hypercapnia
Indications for Home O2
A few words on cor pulmonale
SLEEP-DISORDERED
BREATHING
CASE #1
o 50M
o History
o
o
o
o
o
o
Snoring, witnessed apneas, gasping/choking at night
Non-refreshing sleep, AM headaches, sore throat in AM
Lack of concentration, daytime fatigue, depressed mood
Decreased libido, frequent awakenings, nocturia
Daytime sleepiness
Epworth Sleepiness Score 12 (>10 is abnormal)
o Physical Exam
o BMI 34
o BP 149/92 with HR 80
o Collar size 18 inches
Sleep-Disordered Breathing (SDB)
Obstructive
Simple
snoring
UARS
OSAS
Central
OHS
Drugs (resp. depressants)
Brainstem injury/tumour/bleed
Neuromuscular disorders
Congenital central hypoventilation
Medical conditions (↓T4)
↑PCO2
↓PCO2
Cheyne-Stokes (CHF)
Altitude
Complex sleep apnea
Sleep-onset centrals
Post-arousal / post-sigh centrals
UARS = Upper Airway Resistance Syndrome
OSAS = Obstructive Sleep Apnea
OHS = Obesity Hypoventiation Syndrome
Obstructive Sleep Apnea (OSA)
o Most common form of sleep-disordered breathing
o Prevalence varies by definition
o AHI > 5 events/hr: 20-30% in M and 10-15% in F
o AHI ≥15 events/hr: 15% in M and 5% in F
o Overall prevalence in NA increasing with obesity
Pathophysiology
o Normal UA narrowing during sleep depends upon a balance of
outward and inward forces
o UA dilator muscles must be active to hold airway open against
suction forces created by inspiratory muscles
o However, during sleep, decreased brainstem motor neuron activity
reduces drive to UA dilator muscles (decreased tone)
o Furthermore, soft tissues (tongue, soft palate) are drawn into the
pharyngeal airway by gravity when patient is supine
Pathophysiology
Upper airway collapse
Cessation of air flow +/O2 desaturation, hypercapnia
Increased respiratory effort
Restoration of airway patency
& air flow
Sleep disruption
Key Features of OSA History
o
o
o
o
Classic symptoms
Elicit risk factors
Elicit consequences
Elicit severity/risk
Epworth Sleepiness Scale
Johns, M.W. Sleep 1991
OSAS Diagnosis (ICSD-3)
Diagnosis requires (A+B) or C:
A. The presence of one or more of the following:
–
–
–
–
The patient complains of sleepiness, nonrestorative sleep, fatigue, or insomnia symptoms.
The patient wakes with breath holding, gasping, or choking.
The bed partner or other observer reports habitual snoring, breathing interruptions, or both
during the patient’s sleep.
The patient has been diagnosed with hypertension, a mood disorder, cognitive dysfunction,
coronary artery disease, stroke, congestive heart failure, atrial fibrillation, or type 2 diabetes
mellitus.
B. Polysomnography (PSG) or OCST1 demonstrates:
–
Five or more predominantly obstructive respiratory events2 (obstructive and mixed apneas,
hypopneas, or respiratory effort related arousals [RERAs])3 per hour of sleep during a PSG
or per hour of monitoring (OCST).1
C. PSG or OCST1 demonstrates:
–
Fifteen or more predominantly obstructive respiratory events (apneas, hypopneas, or
RERAs)3 per hour of sleep during a PSG or per hour of monitoring (OCST).1
Risk Factors for OSA
•
•
•
•
•
•
Epidemiologic
Anatomic
Neuromuscular
Medical
Environmental
Family History
Epidemiologic Risk Factors
o Male > Female (2:1)
o Less disparity once post-menopausal
o Increasing Age
o African-American, Asian > Caucasian
o Obesity
o BMI >30 = 63% prevalence of AHI >15
o >10% weight gain within 4 years = 6x increase in AHI >5
Anatomic Risk Factors
o Adenotonsillar hypertrophy
o Nasal obstruction
o Chronic rhinitis
o Polyps
o Septal deviation
o Mid face hypoplasia
o Large or retropulsed tongue
o Retrognathia
o Large neck circumference
o Pharyngeal soft tissue crowding
o Velopharyngeal cleft palate repairs
o Obesity
Tonsils
Uvula
Tongue
Lateral pharyngeal walls
Hyoid bone position
Tissue water/fat
Mandible
Palate
Anatomic Risk Factors
Anatomic Risk Factors
Anatomic Risk Factors
Standardized tonsillar hypertrophy grading scale
Am Fam Physician. 2004 Mar 1;69(5):1147-1155.
Neuromuscular Risk Factors
o Decreased muscle tone
o Neuromuscular disorder
o Hypothyroidism
o Decreased ventilatory drive
o Arnold Chiari I and II
o Myelomeningocele
o Brain stem injury or mass
Other Risk Factors
•
Medical Conditions
–
–
–
–
–
–
–
•
Heart failure
CNS disease (CVA and TIA)
Chronic lung disease (asthma, COPD, IPF)
End-stage renal disease
Congenital disorders (trisomy 21, myotonic dystrophy)
Acromegaly, amyloidosis, hypothyroidism, GERD
Pregnancy, PCOS
Medications
– Alcohol, opioids, benzodiazepines
•
Environmental
– Smoking
•
Family History
OSA Pathophysiology
Asphyxia
Sleep
Fragmentation
Hypoxemia
Hypercapnia
Inflammatory cascade
Mucosal inflammation
Endothelial dysfunction
Cardiac dysrhythmias
Hypertension
Insulin resistance
Intravascular inflammation
Pulmonary hypertension
Stroke
Sudden death
Excessive daytime sleepiness
Increase risk MVC
Impaired memory/concentration
Depression
Decreased QOL
Screening Tool
 Score of ≥3 identified preoperative patients with OSA (defined as an
AHI >5/hour) with a sensitivity and specificity of 84% and 56%
Chung et al. Anesthesiology 2008
Polysomnogram
National Heart Lung and Blood Institute
Courtesy of Dr. Leech
Obstructive vs. Central Apneas
Definitions
• Apnea
– ≥90% reduction in amplitude of thermistor flow
– Must last for ≥10s
• Hypopnea
– ≥30% reduction in amplitude of nasal pressure transducer
Associated with arousal or ≥3% desaturation
– Must last for ≥10 s
– Obstructive or central
OSA Severity
• Based on AHI:
– Normal: <5 events/hour
– Mild:
5–14.9 events/hour
– Moderate:
15–29.9 events/hour
– Severe:
≥30 events/hour
Treatment Overview
• Conservative Measures
–
–
–
–
–
–
Weight loss
Avoid alcohol and sedatives
Positional therapy (avoid supine sleep)
Elevate head-posts of bed
Avoid sleep deprivation
Treat nasal obstruction (very mild OSA)
• Specific Therapies
–
–
–
–
–
Positive pressure therapy (CPAP, BPAP, ASV)
Mandibular advancement device
Upper airway surgery
Bariatric surgery
Provent
Dental Devices
• Two Main Mechanisms:
– Mandibular advancement
– Tongue suction
– Many brands and types
• Disadvantages:
–
–
–
–
–
–
–
Variable initial efficacy
Loss of efficacy over time
Hypersalivation
Mucosal drying
TMJ/tooth pain and altered bite
Not covered by most insurance
Expensive
Surgical Options
• Most Common
– Adenotonsillectomy (T+A)
• Important consideration in children > adults
– Uvulopalatopharyngoplasty (UPPP)
• Sig ↓ in AHI in 50% of patients
• Less Common
–
–
–
–
–
–
Mandibular advancement
Genioglossal advancement
Hyoid advancement
Palatal implants
Ligualplasty/base of tongue resection
Turbinectomy/septal reconstruction
• Rarely cures OSA, improves CPAP tolerance
Other Treatments
• Tracheostomy
– Curative
– Invasive
– Many adverse effects
• Nasal EPAP
– Provent
– Micro-CPAP
– Works best with lower AHI (<15)
Positive Airway Pressure (PAP)
•
Continuous PAP (CPAP):
– Continuous pressure during inhalation + exhalation
– “Stents” open airway
– Most effective therapy
•
Bilevel PAP (BPAP):
–
–
–
–
–
•
Different pressures on inhalation (IPAP) + exhalation (EPAP)
IPAP > EPAP and the difference is ventilation (removal of CO2)
Thus, helps to reduce work of breathing and treat hypoventilation
Often more comfortable than high pressure CPAP
However, more costly and one most qualify for coverage/tx
Disadvantages:
– Adherence 60%, nasal septal ulceration, nasal congestion
– Skin abrasion or allergy, eye discomfort, claustrophobia,
– Nuisance factor
Positive Airway Pressure (PAP)
• Clinical Benefits:
– Superior to dental devices and surgery
– Observational data of ↓ fatal & non-fatal CV events
–
–
–
–
–
↓ AHI and oxygen desaturations
↓ Blood pressure
↓ Daytime sleepiness
↓ MVC
↓ Atherosclerosis
–
–
–
–
↑ Ejection fraction
↑ Cardiac-transplant free survial time in HF
↑ Quality of life
↑ Cognitive function
When to Treat?
• Indications for Treatment:
– All patients with symptoms (i.e. somnolence)
– All patients with AHI ≥15
– All patients with safety critical occupation (AHI ≥5)
• i.e. Pilot, transport truck driver, taxi driver
– Patients with comorbid disease
• Hypertension, dyslipidemia, DM-2
• Ischemic heart disease
• Heart failure
• Pulmonary hypertension
• Cerebrovascular disease
How to Treat?
•
General Measures
– Weight loss
– Avoidance of alcohol and sedatives before bedtime
– Refrain from driving if tired or sleepy
•
Mild–Moderate OSA (AHI 5-29.9):
– Positive pressure ventilation
– Mandibular device – for those who fail/don’t tolerate CPAP or prefer
dental device to CPAP
– Avoid supine sleep if positional OSA
– Surgery if appropriate anatomy
•
Severe OSA (AHI ≥30)
– Positive pressure ventilation
– UA or bariatric surgery if cannot tolerate PAP
– Tracheostomy if all else fails
Courtesy of Dr. Leech
OSA in Children
• Prevalence
– Snoring 3.2 – 12.1%
– OSAS 0.7 – 10.3%
• Peak Incidence
– Age 2-8 years
• Height of lymphoid hyperplasia &
adenotonsillar hypertrophy
– Older obese children
Clinical Differences in Children
•
Additional nocturnal signs
– Restless, thrashing sleep
– Sweating, increased work of breathing, more obvious rib cage retraction
and rib flaring
– Mouth breathing
– Head extended
•
Additional daytime signs
– Mimics ADHD, learning difficulties, irritability, mood changes
• OR for neurobehavioural abnormalities is 2.93
– Increased somatic complaints, decreased appetite
Treatment in Children
•
Mild cases
– Weight loss, nasal steroids, leukotriene antagonists may suffice
•
Otherwise, primary treatment is adenotonsillectomy:
–
–
–
–
•
If enlarged
If between ages 2 – 8
If other indications for removal
Often have surgery without a sleep study
If residual snoring and/or OSA symptoms post-op:
– Perform a follow-up PSG
•
If significant residual disease on follow-up PSG:
– Dental device
– Upper airway surgery
– Positive airway pressure
RESPIRATORY FAILURE
Case #2
o History
o 40 M with severe COPD (FEV1 20%)
o Increased productive cough x 3 days
o Increasing shortness of breath x 2 days
o Physical Examination
o
o
o
o
o
BP 110/90, HR 115 bpm, T 37.0 celcius
Oxygen saturation 86%, RR 40 (rapid/shallow)
+ Accessory muscle use, diffuse expiratory wheeze
+ Thoracoabdominal paradox
+ Confusion
Case #2
Arterial Blood Gas - Interpretation 1/2
pH 7.05 / pCO2 99/ pO2 52 / HCO3 27
1. Acid/Base Status
– pH < 7.4  ACIDOSIS
– PCO2 >40 and HCO3 >24  RESPIRATORY BASIS
– Compensation  49 pCO2: 3 HCO3 = 10:0.6  ACUTE
2. Oxygen Status
– PO2 < 80  hypoxic
– A-a gradient?
ABG - Interpretation 2/2
Step One:
Calculate PAO2 using the alveolar gas equation:
PAO2 = FiO2 (PB – PH2O) – PACO2/R
PAO2 = 0.21 (760 – 47) – 99/0.8 = 161.45
Step Two:
Calculate |A-a| gradient and compare to expected
|A-a| gradient = PAO2 - PaO2
|A-a| gradient = 161.45 – 52 = 109.5
Normal A-a gradient ≈ 10-20 or [(Age/4) + 4]
Thus, the |A-a| gradient is increased!
Causes of Hypoxemia
1. Hypoventilation
2. Low inspired FiO2
3. V/Q mismatch
4. Shunt
5. Impaired Diffusion
Causes of Hypoxemia
1. Hypoventilation
- Normal A-a gradient
2. Low inspired FiO2
- Normal A-a gradient
3. V/Q mismatch
- Increased A-a gradient
4. Shunt
- Increased A-a gradient
5. Impaired Diffusion - Increased A-a gradient
Approach to Hypercapnea
Won’t Breathe
Decreased CNS drive to breath
•Medications (ie. opioids, BDZ)
•Brainstem insult (tumour, infarct,
bleed, infection, infiltration)
•Medical condition (ie. ↓T4)
•Congenital central hypoventilation
(CCHS)
•Obesity hypoventilation syndrome
(OHS)
•Patients with hypoxic drive to breathe
administered high flow oxygen
Can’t Breathe
Normal drive to breathe, but
unable to keep up with demand
•Spinal cord disease
•Peripheral nerve disease
•NMJ disease
•Respiratory muscle
weakness/disadvantage
•Pleural disease
•Chest wall disease
•Increased dead space with limited
ability to compensate
•Asphyxia (ie. OSA)
Types of Respiratory Failure
•
Hypoxic – failure to oxygenate (↓ PaO2)
– PCO2 often normal or low initially
– PCO2 may ↑ with respiratory muscle fatigue
•
Hypercapnic – failure to ventilate (↑PaCO2)
– Low PAO2 and PaO2 due to high PCO2
– Normal A-a ∆
•
Mixed - ↓ PaO2
AND ↑PaCO2 AND ↑
A-a ∆
Acute vs. Chronic Respiratory Failure
•
Acute
– Rapid onset (minutes to hours)
– Insufficient time for kidneys to retain HCO3
– This results in low blood pH (<7.35)
•
Chronic
–
–
–
–
•
Develops slowly (days to years)
Kidney has time to retain HCO3
Compensation is never perfect
Therefore, pH will always be slightly acidemic (7.35-7.39)
Acute on Chronic
– Acute worsening of chronic condition
– pH will be low (<7.35) with an elevated HCO3
Why is the patient hypercapnic?
•
PaCO2 = ⩒CO2/ ⩒A
– Increased CO2 production
• Rarely the cause, and requires significant respiratory limitation
– Decreased alveolar ventilation
•
Minute ventilation = ⩒E = RR x VT
•
Alveolar ventilation = ⩒A = RR x (VT – VD)
– Tidal volume (VT), dead space (VD)
Back to the Case
•
Can’t Breathe
– Respiratory muscle problem
•
•
•
•
Fatigue from increased WOB in during COPD exacerbation
Air trapping  flat diaphragms  disadvantageous position
Air trapping  chest wall on stiff portion of PV curve
Together, there is a high cost to deep inhalation  so, the patient opts for
shallow breathing (lower VT = higher dead space ratio) at a higher respiratory
rate (to maintain ⩒E)
• This pattern perpetuates air trapping = positive feedback loop
– High dead space
• Due to emphysema with limited ability to increase ventilation to better parts of
the lung because of above issues
•
Won’t Breathe
– Some patients with chronic hypercapnea rely on a hypoxic drive to
breathe, which in turn is lessened with administration of high flow
supplemental O2
How does O2 worsen hypercapnia?
•
Worsening V-Q Mismatch
– Areas of lung with pulmonary arterial vasoconstriction due to hypoxia will
vasodilate as oxygen diffuses into those alveoli even though the
ventilation to that lung unit may be poor
•
Haldane Effect
– Oxygen binds more strongly to Hb than CO2 and therefore displaces CO2
from Hb into blood
•
Loss of Hypoxic Drive to Breathe
– Some patients with chronic respiratory acidosis may rely on hypoxia as
their primary drive to breathe (CO2 drive is blunted due to chronic PaCO2
>45)
– Contentious theory
Cor Pulmonale
•
Right-sided heart failure due to the development of high blood
pressure in the lungs (pulmonary hypertension) due to chronic lung
disease
•
Also referred to as WHO Class III pulmonary hypertension
•
Classic examples include:
–
–
–
–
–
Pulmonary fibrosis
COPD
Cystic Fibrosis
OSA + OHS
Chronic hypoventilation (ie. opioids, brain stem injury, CCHS)
Indications for Home Oxygen
QUESTIONS?
THANK YOU!