Abstract
Abstract In a series of 76 patients with asthma of varying severity, pulsus paradoxus developed in 34. Those had more severe airways obstruction than patients without pulsus paradoxus (p less than 0.001). In five normal subjects, we simulated various mechanical changes seen in patients with pulsus paradoxus, to determine the extent to which these factors interacted in the production of the abnormal blood pressure. A combination of increased functional residual capacity (54 to 78 per cent rise above resting level) and high intra-alveolar pressure (14 to 22 cm of water) was necessary for the development of pulsus paradox-us. Neither of these factors acting alone was associated with its occurrence. These findings suggest that in severe airways obstruction, right ventricular filling is limited by pericardial stretching in the hyperinflated chest. Volume discrepancy between pulmonary vascular bed and right ventricular stroke output is exaggerated by the wide inspiratory pressure swings.
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