Obesity, Respiratory Mechanics and Its Impact on the Work of Breathing, Neural Respiratory Drive, Gas Exchange and the Development of Sleep-Disordered Breathing

Author(s):  
Culadeeban Ratneswaran ◽  
Patrick Murphy ◽  
Nicholas Hart ◽  
Joerg Steier
Author(s):  
Swapna Mandal ◽  
Joerg Steier

Sleep-disordered breathing in the obese is not a small problem. Obesity-related sleep-disordered breathing is common and may include sleep apnoea or obesity hypoventilation syndrome. Patients present with symptoms of excessive daytime sleepiness, breathlessness, and, in severe cases, hypercapnic respiratory failure. In recent decades, the prevalence of obesity has increased exponentially. Although not exclusively responsible, obesity is directly linked to the development of sleep-disordered breathing due to high resistance in the upper airway, increased work of breathing, and high neural respiratory drive. Obese patients with sleep disorders are complicated with multiple metabolic, cardiovascular, and orthopaedic co-morbidities, frequently presenting at an advanced stage. This chapter reviews a common clinical presentation of an obese patient with a respiratory condition and the difficulties in their management. The chapter explains the complex underlying pathophysiology and the long-term management of these patients, and shows how sleep-disordered breathing may develop as a consequence of obesity.


2014 ◽  
Vol 44 (4) ◽  
pp. 1023-1041 ◽  
Author(s):  
Johan Petersson ◽  
Robb W. Glenny

This review provides an overview of the relationship between ventilation/perfusion ratios and gas exchange in the lung, emphasising basic concepts and relating them to clinical scenarios. For each gas exchanging unit, the alveolar and effluent blood partial pressures of oxygen and carbon dioxide (PO2andPCO2) are determined by the ratio of alveolar ventilation to blood flow (V′A/Q′) for each unit. Shunt and lowV′A/Q′ regions are two examples ofV′A/Q′ mismatch and are the most frequent causes of hypoxaemia. Diffusion limitation, hypoventilation and low inspiredPO2cause hypoxaemia, even in the absence ofV′A/Q′ mismatch. In contrast to other causes, hypoxaemia due to shunt responds poorly to supplemental oxygen. Gas exchanging units with little or no blood flow (highV′A/Q′ regions) result in alveolar dead space and increased wasted ventilation,i.e.less efficient carbon dioxide removal. Because of the respiratory drive to maintain a normal arterialPCO2, the most frequent result of wasted ventilation is increased minute ventilation and work of breathing, not hypercapnia. Calculations of alveolar–arterial oxygen tension difference, venous admixture and wasted ventilation provide quantitative estimates of the effect ofV′A/Q′ mismatch on gas exchange. The types ofV′A/Q′ mismatch causing impaired gas exchange vary characteristically with different lung diseases.


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A347-A348
Author(s):  
M Sobremonte-King ◽  
M Chen ◽  
L M DelRosso

Abstract Introduction Refractory spasticity in children is treated with intrathecal baclofen (ITB), which may worsen both central and obstructive breathing events. Sleep disordered breathing (SDB) is seldom investigated prior and/or subsequent to placement of ITB and there are currently no standardized protocols. This study aims to compare occurrence of SDB pre/post ITB placement. Methods Retrospective chart review revealed 104 patients started on ITB therapy from 2009-2019 and those who had pre and/or post ITB polysomnograms (PSG) were included. Medical history and PSG parameters were extracted. Comparison of paired results will occur using the Wilcoxon Signed Rank Sum Tests once collection is complete. Results Thirty-seven patients were identified having pre and/or post ITB PSGs. Results in mean ± SD show: age was 11 ± 4 years and 65% were male. Twenty-five pre ITB PSG had an oAHI of 4 ± 5 with 22/25 (88%) having SDB. There were 15/25 (60%) with mild OSA (oAHI >1 but < 5) and 7/25 (28%) with moderate-severe OSA (oAHI > 5/hr). CAI was 1 ± 2 and oxygen saturation nadir was 88 ± 9 %. Sixteen post ITB PSG had an oAHI of 8 ± 13 with 100% having SDB. There were 11/16 (69%) with mild OSA and 5/16 (31%) with moderate-severe OSA. CAI was 3 ± 7 and oxygen saturation nadir was 84 ± 8 %. Ten patients were initiated on non-invasive ventilation, one on supplemental oxygen and two had adenotonsillectomy. Conclusion Initial data shows high occurrence of SDB in patients pre and post ITB placement leading to medical or surgical intervention in 35%. Post ITB PSGs showed worsened oAHI and CAI and lower oxygen saturation nadir. Possible mechanisms include depression of central respiratory drive and decreased pulmonary reserves. This study may help stratify and address risks of ITB for those with refractory spasticity and SDB. Support None


2012 ◽  
Vol 303 (10) ◽  
pp. L845-L851 ◽  
Author(s):  
John B. West

Extraordinary advances in respiratory physiology occurred between 1941 and 1956 in the Department of Physiology, University of Rochester. These were principally the result of a collaboration between Wallace Fenn, Hermann Rahn, and Arthur Otis. Remarkably, all three scientists had worked in very dissimilar areas of physiology before and, by their own admission, were largely ignorant of respiratory physiology. However, because of the exigencies of war they were brought together to study the physiology of pressure breathing. The result was that they laid much of the foundations of pulmonary gas exchange and pulmonary mechanics and some of their work is still cited today. In pulmonary gas exchange they exploited the new oxygen-carbon dioxide diagram; clarified the effects of changes of altitude, hyperventilation, and pressure breathing; and pioneered the analysis of ventilation-perfusion relationships. In respiratory mechanics, they carried out groundbreaking work on the pressure-volume behavior of the lung and chest wall and went on to analyze aspects of gas flow and work of breathing. This explosion of ideas from what initially appeared to be a poorly prepared group has lessons for us today.


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