Obesity Hypoventilation Syndrome

This article gives an overview of the obesity hypoventilation syndrome (OHS) and its links with the most common sleep-related breathing disorder, obstructive sleep apnoea (OSA).
OHS is characterised by many symptoms: patient’s body mass index over 30, daytime hypoventilation, hypercarbia (pCO2>45mm Hg), and hypoxemia (pO2 < 70 mm Hg), and night time sleep-related breathing disorder. At the same time, the causes for a daytime and night time breathing disorder are not some other neuromuscular, mechanical, or metabolic disorders.
Several studies have shown a link between obesity and sleep-related breathing disorders: 80% of patients who are very obese suffer from a sleep-related breathing disorder. It is estimated that 10-20% of obese people suffer from OHS; among adults the OHS occurrence is 0.15-0.3%.


Obstructive Sleep Apnoea is the Most Common

Obstructive sleep apnoea is the most common sleep-related breathing disorder. Sleep apnoea is increasingly being diagnosed already in middle age (1-5% of middle-aged people), one of the reasons for which is increasing obesity. In case of OSA, the upper airways are partially or completely closed during sleep, partial pressure of oxygen decreases, and normal sleep rhythm is disturbed.
About 90% of patients with OHS also suffer from OSA. OSA should be suspected also when the patient snores, their bedfellow notices periods when the patient does not breathe at night, and there is sleepiness and/or fatigue during daytime.
The following factors are vital for the formation of OSA: small diameter of upper airways (hypertrophied lateral pharyngeal walls, big tongue, low soft palate, small lower jaw), unstable respiratory control, low lung capacity, and the dysfunction of the upper respiratory tract muscles. A polysomnographic procedure needs to be performed in order to diagnose OSA, during which the existence and severity level (apnoea-hypopnea index – AHI) of a breathing disorder or some other sleep disorder is detected. Important risk factors include obesity and metabolic syndrome, being a male, age, menopause, liquid retention in the body, greater neck and waist measurements, and smoking.


The Clinical Picture of OHS and Pathogenesis

The main symptoms of OHS are daytime fatigue, shortness of breath, low exercise tolerance; depression and headaches could also occur. During the examination, the following are noticeable: excessive obesity; lip, finger, toe, skin cyanosis and/or red skin; failure symptoms on the right side of the heart (swollen feet, calves, shortness of breath, fatigue after a short effort).
The main moments in the pathogenesis of OHS are complicated and worsening breathing due to obesity; leptin resistance which causes central hypoventilation; and the body’s decreasing ability to tolerate acute episodes of hypercapnia.

Heavy Breathing. In case of OHS, there could be severe upper respiratory tract obstruction, restrictive or obstructive lung parenchyma, cypho-scoliosis, severe hypothyreidism, disrupted central breathing, and pulmonary hypertension. In case of OSA, the patient does not have an alveolar ventilation disorder like in the case of OHS. Gradually worsening breathing is caused by mechanical overstrain on the respiratory musculature, thorax wall due to obesity: the breathing muscles get tired quicker and cannot bear the overstrain resulting from obesity. Patients with OHS have a significantly higher BMI than obese patients with no pathogenic changes in their blood gases (eucapnia).

Leptin. Leptin resistance could play an important role in the development of OHS. Leptin is a protein produced in the fat tissue. This protein regulates appetite and the use free energy in the body. This protein penetrates through the blood-brain barrier, having several binding sites within the brain. Patients with OHS have higher leptin levels compared to eucapnic obese patients. It is thought that unbalanced leptin levels are linked to increased breathing in order to compensate for excess carbon dioxide. In case of OHS treatment, the serum’s leptin levels become normal.

The Decompensation of Acute Hypercapnia The compensation of acute hypercapnia is decreased in the case of a sleep-related breathing disorder. Obstructive apnoeas, hypopnea, and long periods of hypoventilation also cause acute episodes of hypercapnia. Short-term hyperventilation occurring in the shallow sleep phase and renal bicarbonate retention are the compensatory mechanisms which help to maintain carbon dioxide balance in the body. Chronic hypercapnia occurs in a situation, in which these compensation mechanisms are damaged.
Patients with eucapnic obstructive apnoea have apnoea episodes separated by periods of hyperventilation and accumulated CO2 is taken out of the body. When apnoea attacks get longer, CO2 starts to cumulate in the body. In case of OHS, the ventilation periods between apnoea are shorter. Presumably, this is an adaptive condition, in which chemoreceptors adapt to the increased bicarbonate level in the serum. Normal breathing also removes excess CO2 from the body via bicarbonate secretion. The transition from acute hypercapnia to chronic happens when a small amount of bicarbonate remains unsecreted via the kidneys, causing decreased sensitivity to bicarbonate.

Stress on the Respiratory System. The effect of obesity on breathing function is bad due to the following reasons: lower lung volumes, the flexibility of thorax wall decreases by 2.5 times, respiratory resistance has increased (most likely due to the decrease of functional residual capacity), the patient exerts greater effort when breathing. In case of OHS, the breathing function is even more disturbed. The spirometry indicators for OHS are of the restrictive type: Decreased FEV1 and FVC, but FEV1/FVC is normal. However, the functional residual capacity, total lung volume, and expiratory reserve volume have decreased. The mentioned changes in breathing double the patient’s breathing volume, which increases even more when recumbent, as then the abdominal cave organs press on the thorax organs.

Central Breathing. Due to increased basal oxygen demand, carbon dioxide production, and increased breathing, obese people require higher minute ventilation than people with normal weight to maintain eucapnia. Overweight people experience significant increases in central breathing in order to ensure their increased respiratory need; the sensitivity of chemoreceptors to hypercapnia and hypoxemia have decreased in case of OHS. A patient suffering from OHS does not experience the same hyperventilation as an obese eucapnic patient, if there is carbon dioxide re-use. Decreased sensitivity can be linked with leptin resistance and sleep-related breathing disorder.

Pulmonary Hypertension. In the case of OHS, the pressure in pulmonary circulation has increased. One of the causes in case of OHS is probably chronic alveolar hypoxia and hypercapnia. In some OHS patients, pulmonary hypertension could be related to left ventricle failure because left ventricle hypertrophy is a common find in case of cardiomyopathy that accompanies severe obesity. In case of OHS, the closing pressure of pulmonary artery has also increased.



In order to diagnose OHS, the following needs to be done: analysis of blood gases in arterial blood, CT examination of the chest to eliminate other chest diseases, lung function tests, and polysomnography. As OHS is often also accompanied with OSA, it is reasonable to refer the patient to polysomnography. As a rule, it is clear after the sleep test and CPAP test whether the patient requires further tests concerning OHS. It is recommended that the patient’s OSA risk be assessed before referring him to a sleep test, by using the STOP-Bang survey (see Table 1). This survey is primarily suited for evaluating the OSA risk of an obese male patient.


Treatment of OHS

The treatment components are positive airway pressure treatment PAP, oxygen treatment, losing weight conservatively and surgically, and pharmacological breathing stimulants.


The Short- and Long-Term Effects of PAP Treatment

Currently, two methods are primarily used in PAP treatment: CPAP (continuous positive airway pressure) and bi-level PAP (bi-level positive airway pressure).
The rapid effects of PAP treatment are significant improvement in gas exchange (decrease in PaCO2 and increase in PaO2) and cropping a sleep-related breathing disorder by decreasing the AHI. The long-term effects of PAP treatment are the continuous improvement of gas exchange, increasing of lung volumes, and improving the central breathing response to CO2. The normalisation of PaCO2 and PaO2 values continues; the decrease in breathing restrictive components is a result of a decrease in the premature closing of airways and the opening of micro-atelectasis. Long-term PAP treatment also has a positive effect on FEV1 and FVC indicators.
PAP treatment decreases mortality caused by OHS. Retrospective research has found a 13-19% decrease in the mortality rate during four years of PAP treatment. In case of untreated OHS, the mortality rate within 18 months is 23%.
Short-term PAP treatment improves gas exchange parameters and sleep-related breathing disorder. Long-term treatment increases lung volumes, increases central sensitivity to CO2, and decreases the mortality rate. As this is a non-invasive treatment, it is the primary choice in case of OHS.
For some OHS patients, the CPAP treatment is not efficient because the AHI values remain >5 and the average night SpO2 <95%. In this case, the bi-level PAP is then considered as a treatment method. BiPAP is efficient if the patient cannot tolerate the high pressure of CPAP treatment (>15 mm Hg) or when hypoxemia persists despite diminished apnoea and hypopnea. Patients with OHS who do not respond well to CPAP treatment are observed to have significantly decreased FEV1 and FVC readings.
In case of OHS, two main patient groups can be highlighted: Those who respond to the CPAP treatment, with the main problem being high pre-treatment AHI values (typical to obstruction in upper airways), and those who respond to bi-level PAP treatment and who have restrictive respiratory damage due to being excessively obese, in which case long-term BiPAP treatment is required.


Oxygen Treatment

About 40% of OHS sufferers have ongoing SpO2 desaturations of <90 mm Hg despite adequate CPAP treatment, due to which supplemental oxygen is required. Oxygen treatment requires great care because oxygen treatment at too high a concentration and without positive pressure treatment may lead to the worsening of hypercarbia, reducing minute ventilation. OHS patients require the lowest O2 concentration that has an effect, in order to maintain normal oxygenation.


Surgical Weight Loss Treatment

Bariatric surgical treatment is currently a generally accepted treatment method for lowering pathological obesity if conservative treatment methods have been exhausted and the patient also has concurrent diseases (high blood pressure, type II diabetes, hyperlipidemia). Surgical bariatric treatment improves lung function in case of OHS. One year after the operation, PaO2, PaCO2, FEV1, and FVC figures have improved significantly.
Bariatric operation contributes to weight loss, but many patients fail to achieve normal weight and continue to remain obese. The symptoms of sleep apnoea decrease too, but less than half of OSA sufferers who have undertaken surgical bariatric treatment achieve the AHI value <5. It is important to refer an OHS sufferer to a sleep test before and after operation in order to specify the need for CPAP or BiPAP treatment before and after the surgery. About 15% of OHS sufferers who undergo bariatric surgery still need PAP treatment.
The pre-op preparation of an OHS sufferer for bariatric surgery is very important because untreated OSA involves an increased risk for perioperative venous thromboembolism, repeated surgical interruption, lengthened hospitalisation, and also death (0.5-1.5%).


Pharmacological Treatment

Medroxyprogesterone-1-acetate and acetazolamide are used as respiratory stimulants. Medroxyprogesterone-1-acetate stimulates breathing at the hypothalamic level; the drug’s role in OHS treatment is, however, unclear. Research has shown an increase in PaO2 percentage and decrease in PaCO2. As medroxyprogesterone increases the risk for venous thromboembolism, the use of this drug is limited in cases of OHS.
Acetazolamide is a carbonic anhydrase inhibitor which increases minute ventilation by inducing metabolic acidosis (increased renal excretion of bicarbonate). Acetazolamide decreases AHI by increasing the PaO2 and decreasing the partial pressure of PaCO2. Pharmacological treatment is currently not the main treatment method for OHS.



The main treatment objectives of OHS are controlling OSA, obesity, and hypoventilation; identifying concurrent metabolic and cardiovascular diseases. Cardiac failure, angina, and cor pulmonale are more frequent in case of OHS. In case of untreated OHS, the mortality rate is higher than for eucapnic obese apnoea sufferers.
Previous venous thromboembolism, obesity, being a male, high blood pressure, bad treatment response to PAP treatment increase the death risk. Untreated OSA is a risk factor for the development of coronary artery disease, cardiac failure, and type II diabetes. The frequency and severity of concurrent diseases rise with an increase in obesity. Hypertension and type II diabetes respond less favourably to the treatment if the patient suffers from badly controlled sleep apnoea. The consequences of untreated sleep apnoea are sleepiness, road accidents; most likely, a patient with sleep apnoea is more at risk when it comes to a heart attack.


Used Literature

1.Jordan AS, McSharry DG, Malhotra A. Adult obstructive sleep apnoea. 2014 Feb 22; 383 (9918): 736-47.
2. Alea C, Banzon A. The Association of Obstructive Sleep Apnoea and Metabolic Syndrome 2014; 145 (3).
3. Alzaabi A, Fizal S, Mahboub B, Nagelkerke. Obesity hypoventilation syndrome in obstructive sleep apnoea patients in the United Arab Emirates: a retrospective cross-sectional study. JRSM Short Rep. 2013 Nov 21; 4 (12).
4. Chau E, Lam D, Wong J, Mokhlesi B, Chung F. Obesity Hypoventilation Syndrome. A Review of Epidemiology, Pathophysiology, and Perioperative Considerations. Anaesthesiology 2012; 117: 188–205.


Table 1. STOP-Bang Survey

Do you snore loudly (louder than you speak, snoring can be heard through closed doors)? Yes No
Are you often tired or sleepy during the daytime? Yes No
Has someone noticed that your breathing is disrupted during sleep? Yes No
Do you use or have you used drugs to treat increased blood pressure? Yes No
Is your body mass index over 35 kg/m2? Yes No
Are you over 50 years old? Yes No
Is your neck size over 40 cm? Yes No
Are you male? Yes No

High risk for OSA: yes-answer three or more times
Low risk for OSA: yes-answer less than three times

The author of this article is Dr. Heisl Vaher


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