Uncertainties in the current understanding of gas exchange in spontaneous pneumothorax: effective lung ventilation may persist in a smaller-sized pneumothorax.
Clinical aspects of spontaneous pneumothorax (SP) are far more clear than some patophysiological issues. The exact mechanism that maintains adequate oxygenation in spontaneous pneumothorax of lesser size is still unclear. Experimental and rare studies in humans could not explicitely confirm whether it is hyperventilation of the nonaffected lung, still effective gas exchange within the affected lung, or hypoxic vasoconstriction. Similarly, it is unclear why the severity of dyspnoea sometimes differs between patients with the same size of SP. The idea that a certain degree of effective lung ventilation might exist in SP of lesser size was based on clinical observation of these patients on admission, on our measurements of pleural pressures and oxygenation in a group of patients with SP of different size and on rare experimental studies. Clinical observation that oxygenation was not significantly impaired in patients with SP of lesser size, without documented hyperventilation, served as a base for critical analysis of possible factors influencing oxygenation in SP of lesser size. Our hypothesis that pleural pressure swings in a partially collapsed lung, but still slightly expanding in inspiration, enable a certain degree of gas exchange, was confirmed both by several experimental studies and by our measurements. On the other hand, our clinical observation that patients with SP of greater size frequently differ in the severity of dyspnoea suggested the need of a more detailed analysis of the causes of hypoxaemia in these patients. The fact that hypoxaemia in these patients usually cannot be abolished by the existing hyperventilation, means that in SP of greater size, despite minimal lung volume, circulation in the pulmonary artery system still exists, causing right to left blood shunting. The fact that the severity of dyspnoea is not equal in all patients with complete SP means that hypoxic vasoconstriction exists only in some of them, following a still unknown pattern. Literature data and our measurements suggest that without further studies of hypoxic vasoconstriction in the acute phase of SP, the exact answer is not possible.
Subotic
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Clinic for the Thoracic Surgery, Clinical Center of Serbia, Institute for Lung Diseases, University Clinical Center, Visegradska 26/20, 11000 Belgrade, Serbia and Montenegro. grudhir@yubc.net
Mandaric
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Gajic
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Vukcevic
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D002245:Carbon Dioxide / Q000097:blood; D004417:Dyspnea / Q000209:etiology; D006801:Humans; D000860:Hypoxia / Q000209:etiology; D001239:Inhalation; D008168:Lung / Q000098:blood supply / Q000503:physiopathology*; D008954:Models, Biological; D010100:Oxygen / Q000097:blood; D010313:Partial Pressure; D035422:Pleural Cavity / Q000503:physiopathology; D011030:Pneumothorax / Q000097:blood / Q000150:complications / Q000473:pathology / Q000503:physiopathology*; D011312:Pressure; D001261:Pulmonary Atelectasis / Q000503:physiopathology; D011659:Pulmonary Gas Exchange / Q000502:physiology*; D012422:Rupture, Spontaneous; D014661:Vasoconstriction
D002245:Carbon Dioxide; D010100:Oxygen