Regional Distribution of Pulmonary Ventilation and Perfusion in Obesity *

Abstract

Summary. Five women and three men, all obese and weighing 95 to 140 kg, were studied by routine pulmonary function tests and by a radioactive xenon technique, while seated upright at rest, to measure the regional ventilation and perfusion distribution in the lung.In four subjects in whom the expiratory reserve volume averaged 49% of predicted normal, the ventilation distribution as measured with 133xenon was normal. In the remaining four subjects, in whom the expiratory reserve volume was reduced to less than 0.4 L and averaged only 21% of predicted values, the distribution of a normal tidal breath was predominantly to the upper zones.In all subjects the perfusion distribution was predominantly to the lower lung zones but was slightly more uniform than in normal nonobese subjects. During tidal-volume breathing, therefore, in four subjects the ventilation and perfusion distribution was substantially normal, whereas in the remaining four perfusion was maximal in the lower zones, to which ventilation was significantly reduced.These findings show that there may be significant ventilation/perfusion abnormality on a regional basis in obese subjects, this abnormality bearing a close relationship to the reduction in expiratory reserve volume, a finding predictable from recently published data on normal nonobese subjects (1). The abnormalities of ventilation/perfusion relationships that were demonstrated in four of the eight obese subjects could cause a reduction in arterial oxygen tension during resting tidal ventilation. IntroductionThe term "Pickwickian syndrome" was introduced by Burwell, Robin, Whaley, and Bickelmann (2) to describe a patient with alveolar hypoventilation, polycythemia, and right heart failure. As the patient lost weight, his pulmonary and

Diurnal PaCO2 tension in obese women: relationship with sleep disordered breathing

“…A reduced lung function of variable degree was found in subjects with severe obesity and OHS. 3,17 In aggreement with our data, Sahebjiami and Gartside 7 demonstrated that obese subjects with hypercapnia, in the absence of any other disease process and with normal FEV 1 /FVC, were characterized by higher BMI and worse respiratory function. However, not only body weight, but also the fat distribution has been found to play a pivotal role in determining the reduction of FVC in obese subjects.…”

“…Therefore, ventilation can be reduced at lung bases, mainly in patients with reduced ERV, leading to arterial hypoxaemia. 3 Several studies on diurnal hypoventilation in patients affected by obesity hypoventilation syndrome (OHS) have been performed, [4][5][6] whereas few data exist on diurnal PaCO 2 tension in apparently healthy nonsmoking obese patients. 7 It is noteworthy that several studies demonstrated a wide array of respiratory disturbances during sleep (hypoventilation, obstructive apnoea-hypopnoea events, and 'flow limitation') in obese individuals, 8,9 but no information is available about the possible relationship between diurnal PaCO 2 tension and sleep-respiratory disturbances.…”

Avaliação da função pulmonar na obesidade graus I e II

“…As a consequence of obesity, especially in those cases presenting abdominal fat deposition, ventilation of the base of the lungs is reduced, especially in those individuals presenting lower ERV values (32) . Various studies have shown altered pulmonary function in individuals with class III obesity.…”

Increased airway closure is a determinant of airway hyperresponsiveness

“…Closure in nonasthmatics was predominantly in the lung bases, whereas in asthmatic subjects the distribution of closure was patchy, with peripheral wedge-shaped defects in both apical and basal lung regions [5]. Basal ventilation appears to be impaired in obese subjects [29], suggesting that closure may be confined to the basal lung zones i.e. topographically similar to that in nonasthmatics [5].…”