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: 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, T L CO are not consistently below the lower limits of normal. In morbid obesity V T 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.
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 V T 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 (VO 2 ). These effects are more marked with truncal than peripheral obesity. Chest 2012; 141: JAP 2007; 102: 2217.
REDUCED T L CO 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 T L CO 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: Respir Med 2107: ;
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: > % variation in FEV1 > % 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: Respir Med 2006; 100: 248. Allergy 2006; 61: 79. AJRCCM 2008; 178: 682. J Asthma. 2010; 47: 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 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 V T with exercise and there is no change in IC. In COPD there is limited ability to V T so there is ↓ IC. Chest 2012; 141: 753 The maximum V T /IC is about % in exercise at which point dyspnoea becomes intolerable. (~IRV is 5-10 % of TLC) Chest 2012; 141: 753 In COPD RR relatively more than V T 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.
Flow Volume Tidal breathing at rest Tidal breathing during exercise IC rest IC exercise Start exercise Dynamic hyperinflation (quantitative) Dynamic Hyperinflation in COPD 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.