In this post I link to and excerpt from The Curbsiders’ “#269 Obesity Hypoventilation Syndrome (OHS) and the Didgeridoo with Dr Aneesa Das“, APRIL 19, 2021 By CYRUS ASKIN.

Please see and review The 2019 American Thoracic Society (ATS) Guidelines on Obesity Hypoventilation Syndrome

See also Sleep Related Questionnaires from the American Thoracic Society. Here is more information on the Functional Outcomes of Sleep Questionnaire (FOSQ) from the ATS. Here is a sample of the Functional Outcomes of Sleep Questionnaire (FOSQ).

All that follows is from the above:

Obesity Hypoventilation Pearls

1. Obesity + daytime hypercapnia (awake ABG with pCO2> 45 mm) + sleep-disordered breathing without an alternative explanation for hypoventilation = OHS
2. OHS and OSA are often comorbid conditions, and therapies targeting OSA often resolve the OHS as well
3. While CPAP is often sufficient to treat OHS (generally, when OSA is also present), some patients do need bilevel PAP to more directly support ventilation and reduce work of breathing
4. Oxygen therapy is not a substitute for PAP therapy!
5. Adherence is critical – having a CPAP or Bilevel PAP on the nightstand is no good if it doesn’t get used!
6. The primary care provider is critical! As a PCP you can reinforce adherence, follow up on results of therapy and most importantly, work with your patient towards a strategy for weight loss – the most important part of OHS treatment!

Obesity Hypoventilation Syndrome (OHS) In-Depth Show Notes 

History, symptoms, and more

• OHS Definition: Obesity (BMI ≥30) + daytime hypercapnia (ABG with pCO2 greater than or equal to 45 mmHg) + sleep-disordered breathing, without another alternative explanation for hypoventilation [Masa 2018]
  • So… BMI ≥30 is a risk factor!
  • Diagnosis of exclusion! If your patient has COPD, Dr. Das explains that they technically cannot meet diagnostic criteria of OHS… but clinical judgement is key to really sort through these challenging cases!
• Symptoms: per Dr. Das, symptoms can be “relatively silent” so need to maintain a high index of suspicion. Ask your patient about:
  • Dyspnea with exertion
  • Headache: specifically morning headaches– may be secondary to retained carbon dioxide
  • Other sleep-disordered breathing questions: Snoring? Poor quality sleep? Mental cloudiness?
  • STOP-BANG or Epworth Sleepiness Scale
    • These are classically for obstructive sleep apnea (OSA), but given concurrence of the two diseases, these can be very helpful for OHS too
  • Dr. Das specifically recommends the FOS-Q that can be useful both during diagnosis and to track improvements (Example – Here)
  • Prior sleep studies, if none done, the patient will almost certainly need one
• Things to look (or test) for:
  • Central obesity (increased waist to hip ratio, increased neck circumference)
  • Airway exam (Mallampati Score of 3 or 4)
  • Signs of cor pulmonale (lower extremity edema, clubbing)
  • A serum bicarbonate less than 27 may help you screen low-to-moderate probability OHS patients (<20%), Dr. Das says this has good negative predictive value and can spare the patient an ABG [2019 ATS OHS Guideline – Mokhlesi 2019]
  • Dr. Das reminds us that PFTs are important: need to rule out obstructive lung disease on PFTs (if present, can be the cause of hypoventilation). In OHS, PFTs can demonstrate extrinsic restriction (reduced TLC, preserved DLCO. Extrinsic restriction from obesity shows low FRC and very low ERV. In contrast neuromuscular disease (which can also cause hypoventilation, and needs to be ruled out to confirm OHS diagnosis) has increased FRC, ERV, and RV. Need a PFT refresher? Check this out!
  • In-Lab Sleep Study: better to evaluate OHS and titrate PAP treatment and/or oxygen if needed. Home sleep tests are great for diagnosing OSA in the general population and these patients can try auto-PAP (insurance coverage for test can be more challenging, depending on payer). See here for more info /  a useful reference
  • Other considerations per Dr. Das include
    • Chest X-Ray
    • Transthoracic echocardiogram to identify comorbid cardiac disease– pulmonary hypertension is a particularly frequent comorbidity
    • Check daytime oxygen saturation – if in the low/mid 90s, that may raise concern

The pathophysiologic trifecta [Masa 2018]

• Leptin resistance (leptin being a powerful ventilatory stimulus)
• Extrathoracic chest wall restriction (central obesity) –> PFT changes as discussed above
• Airway obstruction (OSA) – 70-90% overlap between OHS and OSA [Lacedonia 2017]

Getting into the weeds: Central & Peripheral Sleep Apnea

• “Peripheral” Sleep Apneas:
  • Obstructive Sleep Apnea: Must have at least 5 apneas or hypopneas to meet criteria for OSA
  • Obesity Hypoventilation Syndrome: some patients may have NO apneas or hypopneas
    • Up to 90% of OHS patients will meet OSA criteria… but that means 10% won’t
• Central Sleep Apnea: often overly brisk ventilatory response to small changes in CO2 – example, Cheyne-Stokes Breathing in heart failure, or periodic breathing in opioid use or high altitude  [Eckert 2007]

Treatment Considerations

• The 2019 ATS guidelines cite that “more than 70% of patients with OHS also have severe OSA” and thus, those patients with findings consistent with both OHS and OSA, who are stable/ambulatory patients – especially with AHI >30 should be trialed on CPAP first, as opposed to starting with Bilevel
• Oxygen monotherapy is not appropriate and may result in worsening hypercapnia
• Goals of treatment:
  • Improvement/normalization of the pCO2
  • Improvement/normalization of the pH
  • Improvement/normalization of the serum bicarbonate, often elevated in these patients before initiation of therapy.

CPAP, Bi-Level, APAP… What does it all mean?!

• PAP: Positive airway pressure – comes in three basic flavors, APAP (automatic or auto-titrating PAP), CPAP and Bi-Level (often referred to as BiPAP)
• CPAP: continuous positive airway pressure – Dr. Das: “think of it as an airway stent”
  • Increases pressure at mouth and nose to keep the airway open
• Bi-Level=BIPAP: two different pressures, a type of non-invasive ventilation (NIV)
  • Expiratory (E-PAP): Like CPAP
  • Inspiratory (I-PAP): Initiates when the patient attempts to breathe in– critical for ventilation
  • Delta pressure: the difference between IPAP and EPAP
  • Example – Bi-Level at 12/8 would be a constant pressure of 8 cm H₂O (E-PAP), with an additional 4 H₂O (the “delta”)  to “assist” the patient every time they try to take a breath (resulting in the I-PAP of 12 cm H₂O)
  • Benefit? The E-PAP keeps the airways stented open while the I-PAP kicks in when the patient inhales to assist with work of breathing/increase tidal volume
  • For OHS: the delta pressure can be quite high, e.g, greater than 8 cm H₂O
  • Don’t get confused…Bilevel settings are not perfectly analogous to pressure support on a ventilator! Pressure Support, a term reserved for ventilators, in the example above would refer to the “4”  or the “delta” between the expiratory pressure (which on a ventilator is PEEP) and the inspiratory pressure
• Oxygen? Dr. Das explains that sometimes patients may need oxygen initially. However, after treatment with PAP they may no longer need oxygen as their lungs start to work better.
  • OHS is not a set-it-and-forget-it diagnosis – treatment needs to be revisited periodically, and changes may be needed during the course of one’s clinical journey

Take Home Points

•  Obesity is a disease!he higher the BMI the greater the risk of OHS (and other obesity-related comorbidities)
• The greater the AHI (in OSA) the greater the risk of OHS
• Oxygen is not a substitute for PAP– VENTILATION is key
• Adherence, adherence adherence! The best thing any PCP can do is to ask about adherence frequently, and help address issues (e.g. follow up with sleep, patient calls DME company)