Obesity and breathing

Report
OBESITY
and
BREATHING
Dr Christopher Worsnop
Department of Respiratory and Sleep Medicine
Austin Hospital, Melbourne, Australia
After a short visit to America,
David returns to Italy.
OVERVIEW
• Physiology
• Asthma
• COPD
• Obstructive sleep apnoea
LUNG VOLUMES AND OBESITY
• FRC = volume at end of normal expiration
- balance btw. chest wall expanding & lung
contracting
-  in obesity due to  chest expansion
• BMI > 45 to get consistently low FRC.
• FRC is reduced especially when supine.
Pulm Med 2012; 8: 1892. Chest 2006; 130: 827. JAP 2005; 98: 512.
• FRC normal values may be overestimated
as weight is a factor.
• ERV  with BMI > 35.
Chest 2006; 130: 827
Effects of obesity
• RV, TLC, FVC, TLCO are not consistently
below the lower limits of normal.
• In morbid obesity VT is close to RV.
• Volume at which there is airway closure is
less than FRC normally, but may be above
FRC in obesity → V/Q mismatch, atelectasis
and widened A-a gradient.
JAP 2010; 108: 206, 734. AJRCCM 2009; 479: 432. Chest 2001; 119: 1401.
EXERCISE
Obesity
• Low lung volumes with morbid obesity
leads to flow limitation with exercise, or V
exceeds the max flow-volume loop – due to
gas compression.
JAP 2007; 102: 2217
AJRCCM 2009; 180: 964
Effects of obesity on exercise
• VT is at a lower lung volume and EELV may  in
exercise (↓ in normals).
• Respiratory rate and relative dead space ventilation
are higher.
• Work of breathing is higher – partly due to reduced
lung compliance,  airway resistance.
• For the same amount of work there is greater
oxygen uptake (VO2).
• These effects are more marked with truncal than
peripheral obesity.
Chest 2012; 141: 1031. JAP 2007; 102: 2217.
REDUCED TLCO
• Some reference values for women have
weight as a factor.
• Thus in obese women the cut-off for
normal may be artificially high.
• So a TLCO value that is below the normal
cut-off may be normal in an obese woman.
OBESITY and ASTHMA
• 1.5 x  risk of asthma with obesity, but little
association between bronchial hyper-reactivity
and obesity. JAP 2010; 108: 206. Clin Exp Allergy 2013; 43:8.
• Symptoms in obesity such as dyspnoea may
be mistaken for asthma.
• Wheeze may be heard in obese people due to
the low lung volumes and compression of the
airways with deep expiration without there
being an airways disease.
Diagnosis of Asthma in Obesity
• Symptoms in obesity may be due to asthma.
• The diagnosis of asthma requires objective
testing as over and under diagnosis is
common. CMAJ 2008; 179: 1121. Respir Med 2107: 1356.013;
ASTHMA DIAGNOSIS
• There is no ‘gold standard' for the diagnosis
of asthma.
• The diagnosis of asthma is based on:
history
physical examination
supportive diagnostic testing, including
spirometry.
Australian Asthma Handbook 2014
ASTHMA DIAGNOSIS
• Variability over time:
 > 12 - 15 % variation in FEV1
 > 10 - 20 % variation in peak flows
• Variability with bronchodilator:
 > 12 (and 200 ml) increase in FEV1
 > 20 % increase in peak flows
• Variability after challenge:
 methacholine, histamine, mannitol
Management of Asthma in Obesity
• Asthma is more difficult to control in obesity.
Respir Med 2007; 101: 2240. Respir Med 2006; 100: 248. Allergy 2006; 61: 79.
AJRCCM 2008; 178: 682. J Asthma. 2010; 47: 76-82
• This may be due to non-eosinophilic
inflammation in the airways.
• Gastro-oesophageal reflux may be na
exacerbating factor.
• ICS + LABA is the preferred treatment.
• Weight loss has shown to improve asthma
control in obesity.
Cochrane database 2012. Allergy 2013; 68: 425.
COPD: HOW EMPHYSEMA CAUSES AIRFLOW
OBSTRUCTION and DYSPNOEA
– There is loss of the supporting connective
tissue around the airways.
– The airways within the lungs are thus more
collapsible during expiration.
– Over time this can produce hyperinflation.
– This worsens during exercise due to reduced
expiration time leading to dynamic
hyperinflation.
– Loss of elastic recoil means that there is less
pressure generated for expiration, and the
chest tends to spring out.
INSPIRATORY CAPACITY
• IC is from end of tidal expiration to
maximum inspiration.
• IC normally increases with exercise
(decreases in COPD – gas trapping, dynamic
hyperinflation).
• IRV = end of tidal inspiration to maximum
inspiration. When it reaches 0.5 l it is
associated with intolerable dyspnoea.
• Hyperinflation
is measured with IC and is
reproducible during CPET. ERJ 2009; 34: 860
• Obesity reduces lung volumes and IC and so
hyperinfaltion can be underestimated. Chest
2011; 140:461
• Normally VT  with exercise and there is no
change in IC. In COPD there is limited ability to
 VT so there is ↓ IC. Chest 2012; 141: 753
• The maximum VT/IC is about 70-80 % in
exercise at which point dyspnoea becomes
intolerable. (~IRV is 5-10 % of TLC) Chest 2012; 141:
753
• In COPD RR  relatively more than VT Proc ATS
2006 O’Donnell
• In hyperinflated lungs the work of breathing
is greater as breathing is higher on the
pressure-volume curve where compliance is
reduced.
• There is also intrinsic PEEP, and  elastic
force against inspiration and ↓ muscle force as
the muscle fibres are stretched.
• Dyspnoea
in mild COPD has been shown to
be related to the reduction in IC during
exercise.
• Those without dyspnoea do not have the fall
in IC.
• Effects seen in GOLD 1 AJRCCM 2008 O’Donnell,
Thorax 2009 O’Donnell
• It is also associated with reduced thigh
muscle strength.
Respiratory Medicine 2013; 107: 570.
Dynamic Hyperinflation in COPD
Tidal breathing
during exercise
Flow
Tidal breathing
at rest
Volume
Start
exercise
IC rest
IC exercise
Dynamic hyperinflation (quantitative)
With acknowledgements to RL Jones
OBESITY and COPD
• Obese people with COPD have lower lung
volumes at rest so there is more room for
dynamic hyperinflation.
Thorax 2008; 63: 1110 JAP 2010: 108; 206
AJRCCM 2009; 180:964. JAP 2011; 111: 10
Annals ATS 2014; 11: 635.
Pulmonary Rehabilitation in Obesity
• Obesity has no negative impact on
pulmonary rehabilitation, so it is recommended
in obese COPD patients. Respirology 2012; 17: 899
OBSTRUCTIVE SLEEP APNOEA
Current prevalence
• The prevalence is increasing and directly
related to the rising prevalence of obesity.
• So the old prevalence figures from the
early 1990’s probably no longer apply.
• Not only are adults becoming more
obese, more are entering adulthood
already obese.
• 13 % in men and 6 % in women
Peppard Am J Epidemiol 2013; 177: 1006
PATHOPHYSIOLOGY OF OSA
• Due to an interaction between airway
anatomy and compliance, and changes in the
upper airway muscles during sleep.
• The pharynx is a floppy tube and so acts like
a Starling resistor.
Respirology 2012; 17: 213
Anatomy - obesity
Obstructive Sleep Apnoea
30 s
5 min
The Effects of Weight Loss on OSA
• Weight loss of 10 % associated with a 26 %
reduction in AHI. JAMA 2000; 284: 3015
• or 50 % reduction in AHI BMJ 2009: 339
Thorax 2011;66: 797
AIM 2011; 155: 434
OBESITY HYPOVENTILATION SYNDROME
• BMI > 30; awake PCO2 > 45 mmHg; no other
reason for hypoventilation.
• 70 – 90 % also have OSA.
• Increased work of breathing and reduced V
responses due to lower VC, TLC, FRC and
lower chest wall and lung compliance.
• Management is weight loss, NIV and/or
CPAP.
• 60 % who do not respond to CPAP initally
may respond after 3 months on NIV.
Respirology 2012; 17:601. Respirology 2012; 17:402.
OBESITY HYPOVENTILATION SYNDROME
• Raised pulmonary artery pressures and RV
overload in about half of OHS patients.
• These are reduced with NIV.
Respirology 2012; 17:601. Respirology 2012; 17:1289. ERJ 2013; 41:39.
OBESITY AND BREATHING SUMMARY
• Obesity can reduce lung volumes.
• Obesity increases the work of breathing and
oxygen needs.
• Asthma may be both under and over
diagnosed in obesity.
• Obesity may reduce hyperinflation in COPD.
• Obesity is a major risk factor for OSA.

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