Mechanism of paradoxic pulse in bronchial asthma.

Abstract

SUMMARY To elucidate the mechanism of paradoxic pulse in severe bronchial asthma, we performed hemodynamic studies and measured esophageal pressure in nine patients who had status asthmaticus and clinical paradoxic pulse. Two-dimensional echocardiography allowed simultaneous assessment of cyclic changes in right-and left-heart size throughout the respiratory cycle. Esophageal pressure varied from a markedly negative level during inspiration (-24.4 ± 6.5 cm H20) to a positive level during expiration (7.6 + 6.0 cm H20). Competition between right-and left-heart chambers for pericardial space during inspiration was suggested by the reduced left ventricular cross-sectional area at end-systole (-24%, p < 0.01) and end-diastole (-32%, p < 0.01), the leftward septal shift, and the increased right ventricular internal diameter at end-systole (42%, p < 0.01) and end-diastole (40%, p < 0.001). Competition for filling, however, could not entirely account for the paradoxic pulse, for systemic and pulmonary pulse pressures were almost (within one cardiac cycle) in phase: both were minimal at inspiration and maximal at expiration. The increase in impedance to right ventricular ejection is another major factor reducing left ventricular preload at inspiration. This reduction in preload was shown to be the predominant mechanism for the decrease in left ventricular stroke output at inspiration.INSPIRATORY DECLINE of the arterial pulse was first described during attacks of bronchial asthma.' This inspiratory decrease in systolic arterial pressure was later referred as "paradoxic pulse" and emphasized as a cardinal manifestation of pericarditis.2 Pulsus paradoxus has been recognized in many patients with status asthmaticus,3 and is now considered an index of the severity of airways obstruction.4 Paradoxic pulse has been noted in other clinical settings, including acute pulmonary embolism,5 chronic obstructive pulmonary disease6 and tricuspid atresia.]Hemodynamict and echocardiographic9 studies in patients with cardiac tamponade due to a tense pericardial effusion have improved our understanding of the mechanisms of pulsus paradoxus,'0 emphasizing the severe competition for filling between the right and left ventricle. In other clinical settings, however, the mechanism of paradoxic pulse may differ. In bronchial asthma, pleural pressure is very negative at inspiration," and several mechanisms, all related to these large swings in pleural pressure, have been suggested to explain paradoxic pulse. Most of our knowledge of the pathophysiological mechanisms derives from observations of the hemodynamic alterations induced by a markedly negative pleural pressure during the Muller maneuver in experimental animals'2 " and in man. echocardiography to assess right and left ventricular dimensions and configurations. Materials and Methods PatientsNine adults with a clinically detectable (cuff-measured decrease of 10 mm Hg in systolic blood pressure) pulsus paradoxus during a severe attack of asthma were included in the study. There were four men ...

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“…26 A decrease in systolic blood pressure by more than 10 mm Hg during inspiration is termed pulsus paradoxus. 27 The negative intrapleural pressure generated favors transcapillary fluid edema to the alveolar space. 28 There appear to be 2 subsets of children who die from severe acute asthma, perhaps representing some differences in their pathophysiology.…”

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