Exercise Hemodynamics and Gas Exchange in Patients with Chronic Obstruction Pulmonary Disease, Sleep Desaturation, and a Daytime Pa<sub>O<sub>2</sub></sub>above 60 mm Hg

Fletcher, Eugene C.; Luckett, Rita A.; Miller, Trey; Fletcher, Joyce G.

doi:10.1164/ajrccm/140.5.1237

Cited by 52 publications

(35 citation statements)

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“…Exercising Ppa, measured in 54 patients, was also similar in the two groups, in contrast to the results of FLETCHER et al [29]. Furthermore, Ppa was not significantly correlated with the mean nocturnal Sa,O 2 nor with t Sa,O 2 <90%.…”

Section: Nocturnal Desaturation and Daytime (Permanent) Pulmonary Hypcontrasting

confidence: 54%

Sleep-related O2 desaturation and daytime pulmonary haemodynamics in COPD patients with mild hypoxaemia

Chaouat¹,

Weitzenblum²,

Kessler³

et al. 1997

Eur Respir J

157

102

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It has been hypothesized but not firmly established that sleep-related hypoxaemia could favour the development of pulmonary hypertension in chronic obstructive pulmonary disease (COPD) patients without marked daytime hypoxaemia.We have investigated the relationships between pulmonary function data, sleeprelated desaturation and daytime pulmonary haemodynamics in a group of 94 COPD patients not qualifying for conventional O 2 therapy (daytime arterial oxygen tension (Pa,O 2 ) in the range 7.4-9.2 kPa (56-69 mmHg)). Nocturnal desaturation was defined by spending ≥30% of the recording time with a transcutaneous O 2 saturation <90%. An obstructive sleep apnoea syndrome was excluded by polysomnography.Sixty six patients were desaturators (Group 1) and 28 were nondesaturators (Group 2). There was no significant difference between Groups 1 and 2 with regard to pulmonary volumes and Pa,O 2 (8.4±0.6 vs 8.4±0.4 kPa (63±4 vs 63±3 mmHg)) but arterial carbon dioxide tension (Pa,CO 2 ) was higher in Group 1 (6.0±0.7 vs 5.3±0.5 kPa (45±5 vs 40±4 mmHg); p<0.0001). Mean pulmonary artery pressure (Ppa) was very similar in the two groups (2.6±0.7 vs 2.5±0.6 kPa (19±5 vs 19±4 mmHg)). No individual variable or combination of variables could predict the presence of pulmonary hypertension.It is concluded that in these patients with chronic obstructive pulmonary disease with modest daytime hypoxaemia, functional and gasometric variables (with the noticeable exception of arterial carbon dioxide tension) cannot predict the presence of nocturnal desaturation; and that mean pulmonary artery pressure is not correlated with the degree and duration of nocturnal hypoxaemia. These results do not support the hypothesis that sleep-related hypoxaemia favours the development of pulmonary hypertension. Eur Respir J 1997; 10: 1730-1735 The worsening of hypoxaemia during sleep in patients with chronic obstructive pulmonary disease (COPD) has been documented since the early 1960s [1], and has since been confirmed by polysomnographic studies [2,3], which have included continuous monitoring of oxygen saturation from the late 1970s [4][5][6][7][8][9][10]. It must be emphasized that most of these studies have included patients with severe COPD exhibiting marked daytime hypoxaemia. Is sleep-related hypoxaemia present in patients with less severe COPD with mild or absent daytime hypoxaemia? Several studies of the literature [11][12][13] have shown that a relatively high percentage of these COPD patients exhibit significant nocturnal hypoxaemia, which naturally raises the question: Does this hypoxaemia, limited to sleep, deserve treatment with nocturnal oxygen? Such a treatment could be justified if nocturnal hypoxaemia had deleterious effects on life expectancy, which is rather controversial [14,15], and on pulmonary haemodynamics. It has been hypothesized [16,17] that isolated nocturnal hypoxaemia, occurring in patients without significant daytime hypoxaemia, could lead to permanent (daytime) pulmonary hypertension, but this hypothesis has not, so...

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Section: Nocturnal Desaturation and Daytime (Permanent) Pulmonary Hypcontrasting

confidence: 54%

Sleep-related O2 desaturation and daytime pulmonary haemodynamics in COPD patients with mild hypoxaemia

Chaouat¹,

Weitzenblum²,

Kessler³

et al. 1997

Eur Respir J

157

102

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“…In advanced COPD, patients with resting PH have a marked increase in Ppa during steady-state exercise [42,65,66]: a COPD patient whose baseline P pa is modestly elevated (25-30 mmHg) may exhibit severe PH (50-60 mmHg) during moderate exercise (30-40 W). This is explained by the fact that PVR does not decrease during exercise in advanced COPD patients [65,66], whereas it does in healthy subjects; as cardiac output is doubled for this level of exercise, P pa increases by ,100%.…”

Section: Natural History Of Ph In Copd Exercising Phmentioning

confidence: 99%

“…This is explained by the fact that PVR does not decrease during exercise in advanced COPD patients [65,66], whereas it does in healthy subjects; as cardiac output is doubled for this level of exercise, P pa increases by ,100%. From a practical viewpoint, this means that daily activities, such as climbing stairs, or even walking, can induce marked PH.…”

Section: Natural History Of Ph In Copd Exercising Phmentioning

confidence: 99%

Pulmonary hypertension in COPD

Chaouat¹,

Naeije²,

Weitzenblum³

2008

Eur Respir J

538

418

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Mild-to-moderate pulmonary hypertension is a common complication of chronic obstructive pulmonary disease (COPD); such a complication is associated with increased risks of exacerbation and decreased survival. Pulmonary hypertension usually worsens during exercise, sleep and exacerbation. Pulmonary vascular remodelling in COPD is the main cause of increase in pulmonary artery pressure and is thought to result from the combined effects of hypoxia, inflammation and loss of capillaries in severe emphysema.A small proportion of COPD patients may present with ''out-of-proportion'' pulmonary hypertension, defined by a mean pulmonary artery pressure .35-40 mmHg (normal is no more than 20 mmHg) and a relatively preserved lung function (with low to normal arterial carbon dioxide tension) that cannot explain prominent dyspnoea and fatigue. The prevalence of out-ofproportion pulmonary hypertension in COPD is estimated to be very close to the prevalence of idiopathic pulmonary arterial hypertension.Cor pulmonale, defined as right ventricular hypertrophy and dilatation secondary to pulmonary hypertension caused by respiratory disorders, is common. More studies are needed to define the contribution of cor pulmonale to decreased exercise capacity in COPD. These studies should include improved imaging techniques and biomarkers, such as the B-type natriuretic peptide and exercise testing protocols with gas exchange measurements.The effects of drugs used in pulmonary arterial hypertension should be tested in chronic obstructive pulmonary disease patients with severe pulmonary hypertension. In the meantime, the treatment of cor pulmonale in chronic obstructive pulmonary disease continues to rest on supplemental oxygen and a variety of measures aimed at the relief of airway obstruction.

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“…Pulmonary arterial vasoconstriction secondary to hypoxia may cause pulmonary arterial hypertension but there appears to be significant inter-individual differences in such a response [95][96][97]. In a study by Held et al, a cohort of 18 patients were identified to have with pulmonary hypertension and hypoventilation [68].…”

Section: Long Term Effects Mortality and Prognosis Of Pap Therapymentioning

confidence: 99%

Obesity Hypoventilation Syndrome

2010

IJPM

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Obesity hypoventilation syndrome is a respiratory consequence of morbid obesity that is characterized by alveolar hypoventilation during sleep and wakefulness. The disorder involves a complex interaction between impaired respiratory mechanics, ventilatory drive and sleepdisordered breathing. Early diagnosis and treatment is important, because delay in treatment is associated with significant mortality and morbidity. Available treatment options include noninvasive positive airway pressure (PAP) therapies and weight loss. There is limited long-term data regarding the effectiveness of such therapies. This review outlines the current concepts of clinical presentation, diagnostic and management strategies to help identify and treat patients with obesityhypoventilation syndromes.

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Exercise Hemodynamics and Gas Exchange in Patients with Chronic Obstruction Pulmonary Disease, Sleep Desaturation, and a Daytime Pa_O₂above 60 mm Hg

Cited by 52 publications

References 1 publication

Sleep-related O2 desaturation and daytime pulmonary haemodynamics in COPD patients with mild hypoxaemia

Sleep-related O2 desaturation and daytime pulmonary haemodynamics in COPD patients with mild hypoxaemia

Pulmonary hypertension in COPD

Obesity Hypoventilation Syndrome

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Exercise Hemodynamics and Gas Exchange in Patients with Chronic Obstruction Pulmonary Disease, Sleep Desaturation, and a Daytime PaO2above 60 mm Hg

Cited by 52 publications

References 1 publication

Sleep-related O2 desaturation and daytime pulmonary haemodynamics in COPD patients with mild hypoxaemia

Sleep-related O2 desaturation and daytime pulmonary haemodynamics in COPD patients with mild hypoxaemia

Pulmonary hypertension in COPD

Obesity Hypoventilation Syndrome

Contact Info

Product

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Exercise Hemodynamics and Gas Exchange in Patients with Chronic Obstruction Pulmonary Disease, Sleep Desaturation, and a Daytime Pa_O₂above 60 mm Hg