Impact of Obesity on the Respiratory System

Matthew J. Baugh, M.D.Pulmonary and Critical Care Medicine

DuPage Medical Group

Topics

• Effects of obesity on lung volumes and function

• Asthma and obesity• Obstructive sleep apnea• Obesity Hypoventilation Syndrome• Obesity and venous thromboembolism

HOW DOES OBESITY AFFECT THE LUNGS?

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• Reductions of ERV and FRC– Reduced chest wall compliance

• Reductions in TLC, VC, and RV can be seen in morbid obesity

• Airway resistance increases as BMI increases• Overall increased work of breathing due to increased

forces needed to inflate the lungs (can be 60-250% higher)• Weakening of respiratory muscles (impaired diaphragmatic

function)

Oxygenation in obese patients

• In many patients PaO2 is normal or mildly reduced

• Hypoxemia can occur in severe obesity and OHS– Premature airway closure = V/Q mismatch– Hypoventilation further contributes in OHS

Control and pattern of breathing in obesity

• Obese patients often adapt a “rapid and shallow” breathing pattern– Resting respiratory rate can be 40% higher in

obese patients• Ventilatory drive can be reduced in patients

with OHS– Diminished response to rising CO2– Leptin resistance?

Dyspnea

• Very frequent symptom of patients with obesity, especially with exertion

• Patients also have other comorbid diseases such as cardiac disease which can contribute

• Obesity has been shown to increase risk for asthma and VTE

OBESITY AND ASTHMA

• Epidemiologic studies show 1.5 to 3.5x higher risk of asthma in obesity

• Being overweight increases risk by 50-70%

Sin et al 2007

Beuther, et al 2006

Obesity and Asthma

• Leptin resistance leading to airway hyperresponsiveness

• Increased likelihood of atopy in obese• Chronic inflammatory state – Adipokines: leptin (high) and adiponectin (low)

may be involved in pulmonary inflammation.– ? Role of adipose macrophages and alveolar

macrophages

(Proceedings of American Thoracic Society, 2010)

Asthma Control

• Obese patients with asthma have more severe symptoms and increased medication use (even after adjustment for age, sex, race, income, education)

• Obesity increases bronchodilator use by 94%• Less response to inhaled steroids and inhaled

steroid/long-acting bronchodilator combos• Increase risk of asthma-related hospitalizations• Weight loss leads to improvement in asthma

symptoms and control.

Taylor, et al. Thorax 2008

Asthma treatment

• Weight loss (obviously)• Exercise• Treatment of comorbid conditions which are

also associated with asthma and obesity– GERD– OSA

• Prednisone only when necessary

OBESITY AND OBSTRUCTIVE SLEEP APNEA

• Prevalence of OSA– 2-5%, although studies in USA up to 20-30%– >40% in Obese

(Punjabi et al)

(Lopez et al)

BMI % OSA

25-34.9 33.33

35-39.9 71.43

40-49.9 73.48

50-59.9 76.67

60+ 94.83

OSA pathophysiology• Increased tissue thickness of tongue,

pharyngeal soft tissues leading obstruction of the passage to the trachea

• Relaxation of protective muscles of the airway during sleep

Other risk factors

• Age• Gender (Male>Female)• Craniofacial anatomy• Neck circumference (>17in for men, > 16 in for

women)• Nasal congestion• Tobacco use• Family history

Cardiovascular effects of OSA

• Independent risk factor for hypertension– Higher risk depending on severity– OSA is common in drug-resistant hypertension– Treatment with CPAP results in small reduction in

BP (but not as much as BP meds)– BP may not improve with treatment in those with

long-standing hypertension

Cardiovascular effects of OSA

• Myocardial infarction– Severe OSA associated with an increase risk of

fatal and nonfatal myocardial infarction– Treatment with CPAP lowers risk of MI– Incidence of MI no different in treated OSA vs. no

OSA

(Marin et al)

Cardiovascular effects of OSA

• Atrial fibrillation– Studies involving 24 hour Holter monitoring have

shown 3x higher risk of AF in patients with OSA compared to general population

– 25% higher risk for recurrent AF after cardioversion or ablation

– Treatment with CPAP reduces risk of recurrence after cardioversion/ablation(Guilleminault et al)

(Ng et al)

Cardiovascular effects of OSA

• Congestive heart failure-men with AHI > 30 were 58% more likely to develop HF than men without OSA

• Sudden cardiac death– More common in patients with moderate to

severe OSA

Cardiovascular effects of OSA

• Pulmonary hypertension– 20-33% of patients with moderate to severe OSA

have pulmonary hypertension– Degree of PH is usually mild unless other

coexisting lung diseases present.– Treatment with CPAP lowers mean PA pressures.

(Sanner et al)

(Bradley, et al.)

OSA and the Central Nervous System

• Stroke– OSA is independently associated with increased

risk of stroke (as well as through its association with other risks such as AF and HTN)

– Stroke survivors with moderately severe OSA have increased risk of early death

– Treatment with CPAP improves acute stroke outcomes at 30 days compared to no treatment

• Seizures and seizure control

• 2x increased risk of motor vehicle accidents in those with OSA

OSA and the Endocrine system

• OSA is an independent risk factor for the development of DM

• This risk is present even after adjusting for body mass index.

• Patients with severe OSA (AHI>30) have 30% higher risk of developing diabetes than in patients without OSA

OSA and Nonalcoholic Fatty Liver Disease (NAFLD)

• OSA associated with 2-3x increased risk for NAFLD, independent of BMI

• NAFLD can progress to cirrhosis over time

Perioperative complications with OSA

• Difficult intubation• Postoperative respiratory depression from

anesthetics and analgesics• Higher risk of postoperative reintubation• Higher risk of cardiac arrhythmias • Increased hospital length of stay, ICU length of

stay

Screening for OSA

• Screening questionnaires– STOP-BANG• Mild OSA (AHI>5): Sens 84%, Spec 56%• Mod-Severe OSA (AHI>15): Sens 93% Spec 43%

– Sleep Apnea Clinical Score (SACS)– Berlin Questionnaire

Snoring (loud enough to be heard through closed doors; bed partner elbows you at night)

Tired (feeling Tired, Fatigue, or Sleepiness during the daytime, falling asleep while driving)

Observed (observed episodes of stopping breathing, gasping or choking during sleep)

Pressure (being treated for high blood pressure)

BMI (BMI >35)

Age (Age > 50)

Neck size large(Shirt collar >17 inches males, > 16 inches females)

Gender=MaleLow Risk = 0-2 Intermediate Risk = 3-4 High Risk = 5-8

Diagnosis of OSA

• Other symptoms– Restless sleep / frequent awakenings– Morning headaches– Poor concentration– Nocturia (occurs in 50% of patients with OSA)• OSA leads to increased secretion of atrial natriuretic

peptide

EPWORTH SCORE> 10 = EXCESSIVE SLEEPINESS

Polysomnography

• First line diagnostic study for OSA• Measured variables– EEG and EMG for monitoring of

sleep stages– Respiratory effort– Airflow– O2 saturation– EKG– Limb movement and body position

OSA Severity

• Apnea hypopnea index (average number of apneas and hypopneas per hour of sleep)

• Mild OSA– AHI 5-15

• Moderate OSA– AHI >15-30

• Severe OSA– AHI>30

Treatment

• Weight loss and exercise• CPAP (continuous positive airway pressure)– Significantly improves sleepiness– Improvements in quality of life– Improvements in cognitive function– Improves systemic blood pressure

• Indications for CPAP– AHI>15 (moderate OSA)– AHI 5-15 with excessive sleepiness, impaired cognitive

function, mood disorders, insomnia, cardiovascular disease or stroke

CPAP (continuous positive airway pressure)

• Utilizes pressure to provide a pneumatic splint to maintain airway patency

• More than 100 different mask options to customize treatment to an individual patient

Effects of weight loss on OSA

• Reduction of weight (BMI) can lead to a reduction in AHI, associated with improvements in sleepiness & QOL (Norman, et al 2000)

• Weight loss in morbidly obese patients has been shown to convert non-positional OSA to positional OSA; obviating need for CPAP

Bariatric surgery and OSA

• Many patients will have improvement or even resolution of OSA after bariatric surgery

• AHI can be reduced by 71% (Greenberg et al, 2009)

• 86% resolution of OSA after gastric bypass (Buchwald et al 2004)

• Sleep study / CPAP titration should be repeated after significant weight loss has occurred

THE OBESITY HYPOVENTILATION SYNDROME

Definition of OHS

• Awake hypercapnia (PaCO2>45mmHg)• Obese patient (BMI>30) • Exclusion of other causes for hypoventilation

(lung disease, neuromuscular disease)• 90% of these patients have co-existing OSA• OHS is associated with higher mortality,

reduced quality of life, and higher rates of comorbidity (Pulmonary hypertension, heart failure, angina, HTN)

Which patients have OHS?

• 0.3-0.4% of the population• 10-20% of outpatients presenting to sleep

clinics• 50% of patients with BMI > 50• OHS patients more likely to have central

obesity compared to obese patients without OHS

Pathogenesis of OHS

• Upper airway obstruction during sleep (OSA) leads to increased CO2– Eucapnic OSA patients are able to normalize their CO2 levels between

these events, patients with OHS are not– Rise in bicarbonate levels further blunts ventilatory response to rise in

CO2• Increased work of breathing due to restrictive effects of obesity• Ventilation / perfusion mismatch • Respiratory muscle impairment• Patients with OHS lack the usual increased ventilatory drive seen

in patients with obesity• Leptin resistance (leptin normally stimulates ventilation)

Symptoms of OHS

• Many indistinguishable from OSA– Snoring– excessive daytime sleepiness– choking

• Pulmonary hypertension / RV dysfunction– JVD– pedal edema– hepatomegaly

Diagnosis of OHS

• Awake hypoxemia on pulse oximetry• High serum bicarbonate can be a clue• Arterial blood gas– PaCO2 > 45– Often hypoxemia with PaO2<70– Normal A-a gradient (widened in lung disease)

• Pulmonary function tests and CXR to exclude other diseases

• Sleep study to evaluate for OSA

Treatment of OHS

• Nocturnal positive airway pressure– BIPAP or CPAP +/- O2 (if necessary)– Goal of eliminating obstructive events at night (if

present) and improving alveolar ventilation– Follow up daytime blood gases should be done to

see that hypoventilation has improved• Daytime supplemental oxygen• Interventions directed at weight loss– Dietary, pharmacologic, bariatric surgery

Prognosis of OHS

• Patients who are not treated with NIV have a higher mortality– 18 months 23%– 7 years 46%

• Untreated patients have increased levels of daytime sleepiness and reduced quality of life

OBESITY AND VENOUS THROMBOEMBOLISM

Obesity and Venous Thromboembolism

• Relative risk of DVT in obese: 2.5• Relative risk of Pulmonary embolism in obese:

2.21 (Stein et al 2005)• Association is stronger as BMI increases

Potential mechanisms for VTE in obese patients

• Increased abdominal fat and intra-abdominal pressure leading to decreased blood velocity in femoral vein

• Inactivity/Poor gait• Endothelial dysfunction• Leptin: leads to higher levels of PAI-1 leading to

prothrombotic state• Chronic inflammatory state leading to increased

thrombosis

Conclusion

• Obesity can have a significant impact on lung function and lead to higher risk of lung diseases

• Obesity often leads to chronic dyspnea which can significant impact quality of life

• Obstructive sleep apnea and OHS pose a significant health risk; health care providers should try to appropriately screen patients who may benefit from treatment.

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