TL;DR: This review summarizes the current knowledge about postoperative pulmonary function, emphasizing recent improvements in the understanding of the etiology of postoperative abnormalities, their prevention, and their treatment.
Abstract: HE POSTOPERATIVE period is frequently asT sociated with clinically important abnormalities of pulmonary function. Following surgery of the abdominal or thoracic cavities, postoperative changes are invariable and severe with recovery of function delayed for days or weeks. This review summarizes the current knowledge about postoperative pulmonary function, emphasizing recent improvements in the understanding of the etiology of postoperative abnormalities, their prevention, and their treatment. Awareness of postoperative pulmonary dysfunction as a major problem is longstanding. Pasteur (I), in 1910, described lobar collapse of the lung after abdominal operations. His speculation about the etiology of the collapse has proved prophetic: “I feel sure that when the true history of postoperative lung complications comes to be written, active collapse of the lung, from deficiency of inspiratory power, will be found to occupy an important position among determining causes.” The role of shallow breathing, without periodic “sighs” in producing hypoxemia (“anoxemia”) was identified by Haldane et al (2) , in 1919. Beecher’s 1932 classic report (3) of reduced lung volumes after laparotomy signaled the start of attempts to quantitate mechanical lung function changes following surgery. Beecher correctly identified the functional residual capacity (FRC) (“subtidal volume”) as “the most significant of all lung volumes (3).” The appvnpriateness of this designation has become more apparent only recently.
TL;DR: Heavy tobacco smoking influenced most lung function tests less than ageing from 20 to 70 years, but for airway resistance, volumic airway conductance, closing volume, phase III, FEV1/VC, volume of isoflow and mean transit time the opposite was found.
Abstract: Prediction formulas for static and dynamic spirometry, gas distribution, static lung mechanics and transfer test were derived from measurements in healthy females. The measurements included total lung capacity, residual volume, airway resistance, static elastic recoil pressure of the lung, static compliance, closing volume, slope of the alveolar plateau (phase III), flow-volume variables (including mean transit time) during breathing of air or a helium/oxygen mixture, and conventional spirometric indices. The results from 86 smokers and 100 never-smokers were evaluated separately and combined. For all lung function tests, a single regression equation including time-related smoking variables, valid for both smokers and never-smokers, was obtained. For many lung function tests, a nonlinear age coefficient resulted in a significant reduction in variance compared with simple linear models. Heavy tobacco smoking influenced most lung function tests less than ageing from 20 to 70 years, but for airway resistance, volumic airway conductance, closing volume, phase III, FEV1/VC, volume of isoflow and mean transit time the opposite was found.
TL;DR: In patients with tidal airway closure (CV > EELV), there is not only impairment of pulmonary gas exchange, but also peripheral airway disease due to injury of the peripheral airways, and assessment of the “open volume”, as opposed to the ‘closing volume’, is proposed because it is easier to perform and it requires less equipment.
Abstract: Measurement of closing volume (CV) allows detection of presence or absence of tidal airway closure, i.e. cyclic opening and closure of peripheral airways with concurrent (1) inhomogeneity of distribution of ventilation and impaired gas exchange; and (2) risk of peripheral airway injury. Tidal airway closure, which can occur when the CV exceeds the end-expiratory lung volume (EELV), is commonly observed in diseases characterised by increased CV (e.g. chronic obstructive pulmonary disease, asthma) and/or decreased EELV (e.g. obesity, chronic heart failure). Risk of tidal airway closure is enhanced by ageing. In patients with tidal airway closure (CV > EELV) there is not only impairment of pulmonary gas exchange, but also peripheral airway disease due to injury of the peripheral airways. In view of this, the causes and consequences of tidal airway closure are reviewed, and further studies are suggested. In addition, assessment of the "open volume", as opposed to the "closing volume", is proposed because it is easier to perform and it requires less equipment.
TL;DR: It is suggested that the premature airway closure observed in this disease may be due to mechanical compression of small airways by dilated blood vessels and/or interstitial pulmonary edema.
Abstract: The lung volume at which the dependent lung zones begin to trap gas as a result of airway closure (i.e., the “closing volume”) was measured with 133Xe in 10 seated patients with hepatic cirrhosis. In all of them the closing volume was increased above normal, and in eight it was greater than the functional residual capacity, indicating the presence of airway closure and gas trapping during resting tidal volume breathing. Direct measurements made with 133Xe in five cirrhotic patients (a) confirmed the presence of increased gas trapping in the lower lung zones both at residual volume and at functional residual capacity, and (b) indicated that in liver cirrhosis the ventilation-perfusion ratio of the dependent lung zones may be very low, primarily as a result of decreased ventilation due to airway closure. It is concluded that in hepatic cirrhosis, gas trapping in the dependent lung zones may be an important cause of impaired gas exchange within the lungs. It is suggested that the premature airway closure observed in this disease may be due to mechanical compression of small airways by dilated blood vessels and/or interstitial pulmonary edema.