OBESITY

HYPOVENTILATION
SYNDROME

Anthea Grace B. Esver

2nd year Pulmonary Fellow
Objectives:
1. To present a case of OSA with OHS
2. To present the criteria for diagnosis of OHS
3. Discuss the recommendations and management of
OHS
Case:
● C. L
● 41 / M
● Married
● Catholic
 Case
● Chief complaint :Loud
snoring/ apnea

For the past 10 years

● Excessive and loud snoring
● Unrefreshing sleep
● Waking up during the night
● Jerking of legs at night
● Excessively sleepy/ falling
asleep during the day
 Past Medical History
● Non Diabetic

● Hypertensive for 5 years- Irbesartan

● No nose, throat or jaw surgery

● Previously admitted at a local hospital in Bicol  Had alcohol binge

drinking up to the point of intoxication became unconscious and
cyanotic and went into cardiac arrest. He was rushed to a local
hospital intubated and was subsequently admitted
 Personal and Social History

● Works as a production manager

● Non alcoholic drinker
● Non smoker
● Drinks 3 cups of coffee , 1 tea and 2 cola per day

● Sexual history
● Married- 1 lifetime sexual partner
 Family History

● No history of sleep apnea in the family

 Sleep history
● Patient normally sleeps at 9pm Weekdays Weekends
during weekdays and weekends
● It takes him 10 mins to fall asleep Bedtime 9:00 PM 9:00 PM
and does not take any medications
to fall asleep
● He wakes up 6-7am in the morning Waking – 6:00 AM 7:00 AM
up time
● He wakes up 2x times at night to
urinate with no difficulty of falling Nap during 1 hour 3 hours
asleep again the day
● Involved on road accident because
of falling asleep while driving
Physical Examination
● Awake, comfortable and not in distress
● Vital Signs: BP 138/106 HR 73 regular, RR 14
O2sat 90-91%

● Ht 161.5 cm Wt 125 kg BMI 48.2 kg/m2

● Neck Circumference 54 cm STOP BANG of 8 ( high risk for OSA)
● Tonsillar grade 2, Mallampati 4 0-2 low risk
3-4 intermediate
>- 5 high risk
● HEENT: normocephalic, anicteric sclerae (-) Epworth sleepiness scale- 0-10 normal
CLAD 10-12 borderline
● Narrowed pharyngeal opening 12-24 abnormal
Physical examination
Chest/Lungs:
symmetrical chest
Skin: (-) jaundice, expansion, no
good skin turgor (-) adventitious breath
striaes sounds

Cardiovascular:
Abdomen: globular
adynamic precordium,
soft, non tender
with regular rate and
rhythm, no murmurs
Extremities: no gross
deformities, no edema
STOP BANG SCORE
0-2 low risk
3-4 intermediate
>- 5 high risk

Total = 7
Epworth Sleepiness Questionnaire

Epworth sleepiness scale-

0-10- normal
11-14 - mild sleepiness
15-17- moderate sleepiness
18-24 – severe sleepiness

19
ADMITTING
IMPRESSION:

Obstructive Sleep Apnea with probable

Obesity hypoventilation syndrome
Hypertension
 Polysomnography- Diagnostic

EOG

EEG

EMG
● This is a type 1 PSG. I will be orienting to regarding the
different parameters.
● Sleep Parameters
○ EEG
○ EOG
○ EMG
● Cardiopulmonary Parameters
○ ECG
○ Air Flow
○ Effort
○ SaO2
 Polysomnography- Diagnostic

AIRFLOW

EFFORT

O2 SAT
Polysomnography- Diagnostic
Polysomnography- Diagnostic
Result of Diagnostic Part
 Sleep onset: 13.0 minutes
 The patient’s total sleep time: 24.5 minutes
 The sleep efficiency: 14.7%
 Minimum oxygen saturation: 65 percent
 Snoring was present
 The Respiratory Disturbance Index: 134.7 events /hour
 The Periodic Limb Movement Index: 14.7/hr
 Highest ETCO2 during time in bed: 67 mmHg
 Highest wake ETCO2: 65 mmHg
Polysomnography- Therapeutic
 Result of Therapeutic Part
 Sleep onset: 16.6 minutes
 There was REM sleep rebound occurring 46.5 minutes later
 The patient’s total sleep time: 423.5 minutes.
 The sleep efficiency: 85.5%.
Sleep Architecture:
Sleep onset occurred 16.6 minutes after the lights were turned off. There was REM sleep rebound occurring 46.5 minutes later. The patien
total sleep time was 423.5 minutes. The sleep efficiency improved to 85.5%.

Disturbances of Sleep:
After CPAP was applied, the minimum oxygen saturation during the study was 27 percent.
Snoring was still noted during this recording. The Respiratory Disturbance Index decreased to
37.7 events /hour. The Periodic Limb Movement Index with arousals at 1.1/hr. There were no
cardiac arrhythmias noted during the study.
With BPAP at IPAP 22 cm of water and EPAP 14 cm of water, RDI was at 5.2 events/hour,
minimum oxygen saturation at 87 % and sleep efficiency at 100 %. There was sufficient supine
REM sleep at this pressure to ensure good titration.
Result of Therapeutic Part
After CPAP was applied, the minimum oxygen saturation during the study was
27%.
 Respiratory Disturbance Index: 37.7 events /hour.
 Snoring still recorded
 Periodic Limb Movement Index with arousals: 1.1/hr.
 With BIPAP at IPAP 22 cm of water and EPAP 14 cm of water. RDI was at
5.2 events/hour
 Minimum oxygen saturation: 87 %
 Sleep efficiency: 100 %
DIAGNOSTIC THERAPEUTIC
● This night hypnogram shows the summary of the whole study
which includes the of stages of sleep, position of the patient
( supine), Events ( apneas, hypopneas, central apneas) , Titrating
pressure Ipap, Epap , noted suring diagnostic and therapeutic
part of PSG
● Noted here the during the diagnostic part there are many
hypopneas with desaturation, and apneas noted. Upon
application of pressure there were decreasing trend in events ,
hypopneas until the desired BPAP pressure was achieved which
is Ipap 19, Epap 13
POSITION
HEART RATE
02 SAT
STAGES OF
SLEEP
EVENTS
PRESSURES
DIAGNOSTIC THERAPEUTIC
 DIAGNOSTIC THERAPEUTIC

Sleep onset 13 mins 16.6 mins

Total sleep time 24.5 mins. 423.5 mins

Sleep efficiency 14.7 % 85.5 %

RDI 134.7 events/ hr 5.2 events/hr

● RDI- 134. 7events/hr
● ETCO2- 65 mmHg
 OBESITY
HYPOVENTILATION
SYNDROME
Obesity Hypoventilation Syndrome
Defined by the combination of:

1. OBESITY- BMI ≥ 30 kg/m2; >95th percentile for age and sex for children

2. HYPOVENTILATION during wakefulness- PaCO2 ≥ 45 mm Hg as

measured by arterial PCO2, end tidal PCO2 or transcutaneous PCO2

3. HYPOVENTILATION- not primarily due to lung parenchymal or airway

disease, pulmonary vascular pathology, chest wall disorder, medication use,
neurologic disorder, muscle weakness or a known congenital or idiopathic central
alveolar hypoventilation syndrome

• Source: International Classification of Sleep Disorders 3 rd

Edition; AASM
 Epidemiology
● Among non-Asian populations, the prevalence of OHS is 8% to 11% among
patients with OSA with BMI of 30 to 35 kg/m2 and increases to 18% to 31%
among patients with OSA with BMI of 40 kg/m2 and higher

● East Asian populations are known to have OSA at a lower BMI compared with
other populations, probably because of cephalometric differences

● In these populations, OHS may be more prevalent at a lower BMI range than in
non-Asian populations

• Source: Kryger et al. Principles and Practice of Sleep

Medicine 6th ed
Prevalence of obesity-hypoventilation syndrome in patients with obstructive sleep apnea
(OSA), • Source: Kryger et al. Principles and Practice of Sleep
sorted by body mass index (BMI). As BMI increases prevalence of OHS also Medicine 6th ed
increases
 Onset and Course
● Present initially for evaluation of suspected OSA or are identified following one
or more episodes of severe hypercapnic respiratory failure
● The course is generally slowly progressive

• Source: International Classification of Sleep Disorders 3rd

ed
Essential Features
● characterized by obesity and daytime hypercapnia (arterial PaCO, > 45 mm Hg)
that cannot be fully attributed to an underlying cardiopulmonary or neurologic
disease

● Hypercapnia worsens during sleep and is often associated with severe arterial
oxygen desaturation

● Hypoventilation is often worse during REM than during NREM sleep

● OHS patients without OSA exhibit sustained or intermittent episodes of shallow

breathing during sleep associated with worsening hypoventilation and hypoxemia

• Source: International Classification of Sleep Disorders 3rd

ed
Clinical Features
 Morbidly obese (BMI ≥40 kg/m2)
 Severe OSA (≥30 events/hour of sleep)
 Hypersomnolence
 Morning headaches
 Fatigue & Mood disturbance
 Impairments of memory or concentration

 Patients with OHS are more likely to report dyspnea and to manifest cor
pulmonale

• Source: Kryger et al. Principles and Practice of Sleep

Medicine 6th ed
● Physical examination: features suggestive of COR PULMONALE
Eg: circulatory congestion: plethora, scleral injection, peripheral edema

● Diagnostics:
Polycythemia and elevated serum CO2 on electrolyte testing
PFT-reduced forced vital capacity
ECG- right heart strain, RV hypertrophy and right atrial enlargement
2D echo- ventricular dysfunction

• Source: International Classification of Sleep Disorders 3rd

ed
Predisposing and Precipitating Factors
● Obesity is believe to be the primary pathophysiologic factor responsible for
hypoventilation and hypoxemia.

● Greater degrees of Obesity are often associated with worse sleep related
hypoventilation

● The use of CNS depressants such as alcohol, anxiolytics and hypnotics may
further worsen respiratory impairment.

• Source: International Classification of Sleep Disorders 3rd

ed
 Pathophysiology- Abnormal Ventilatory Drive
● Abnormal ventilatory control (blunted hypercapnic ventilatory response) 
allows hypercapnia to persist into wakefulness after the cause of acute hypercapnia
is no longer present
● Chronic Hypercapnia  Elevation of HCO3  compensatory CO2 ventilatory
response
● Impaired renal bicarbonate excretion rate  seen in hypoxia, heart failure, or
diuretic-related chloride deficiency, may contribute to the persistence of
hypercapnia

• Source: International Classification of Sleep Disorders 3rd

ed
 Pathophysiology- Mechanical Overload
● Obesity  predispose to CO2 retention due to increase CO2 production

● Increased work of breathing  mass loading from the additional weight on the
respiratory pump

● Resistive loading due to intermittent upper airway obstruction during sleep

● Ventilation-Perfusion abnormalities  due to atelectasis or pulmonary

congestion, reduced chemosensitivity and load responsiveness

• Source: International Classification of Sleep Disorders 3rd

ed
 Pathophysiology- Humoral Factor

● Leptin (respiratory stimulant)  suppression of respiratory drive due to obesity-

related humoral factors

● Patients with OHS have resistance to the elevated leptin levels

• Source: International Classification of Sleep Disorders 3rd

ed
Objective Findings
● Arterial Blood Gas  during wakefulness shows hypercapnia and often hypoxemia in
untreated patients

● Polysomnographic finding  sleep related hypoventilation and arterial oxygen

desaturation during sleep with or without obstructive apnea and hypopneas.

● Chronic hypoxia can be associated with polycythemia. ECG, chest xray, and 2ded may
demonstrate evidence of pulmonary hypertension

● Serum bicarbonate level is usually elevated due to renal compensation for chronic
respiratory acidosis (hypercapnia).

• Source: International Classification of Sleep Disorders 3rd

ed
Management
 CPAP is effective in the majority of patients with stable OHS, particularly in the
subgroup with severe OSA.
 Bilevel PAP should be strongly considered in patients who fail CPAP, patients
with OHS who experience acute-on-chronic respiratory and patients who have
OHS without OSA
 Improvement in symptoms and blood gases is directly related to adherence with
therapy and maximal improvement in blood gases can be achieved as early as 2
to 4 weeks

• Source: Kryger et al. Principles and Practice of Sleep

Medicine 6th ed
• Source: Kryger et al. Principles and Practice of
Sleep Medicine 6th ed
Complications:
The course can be variable but is generally slowly progressive.
Many affected individuals with severe hypercapnia and hypoxemia develop:
1. Pulmonary Hypertension
2. Heart Failure
3. Cardiac Arrhythmias
4. Neurocognitive dysfunction
5. Polycythemia

• Source: International Classification of Sleep Disorders 3rd

ed
 Take Home Points:
 Upper airway obstruction is an important factor in the pathogenesis of OHS
and there is evidence that strategies for reversing upper airway
obstruction, such as tracheostomy and nasal continuous positive airway
pressure (CPAP) are effective
 Failure of normal mechanisms that prevent hypoventilation during sleep
are implicated in OHS and therefore noninvasive or even invasive
ventilation to support breathing and reverse hypoventilation has been
advocated.
 Finally, by definition, OHS does not occur in the absence of obesity.

• Source: Kryger et al. Principles and Practice of Sleep

Medicine 6th ed
THANK
YOU!