Mechanism of paradoxic pulse in bronchial asthma.
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 H2O) to a positive level during expiration (7.6 +/- 6.0 cm H2O). 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 less than 0.01) and end-diastole (-32%, p less than 0.01), the leftward septal shift, and the increased right ventricular internal diameter at end-systole (42%, p less than 0.01) and end-diastole (40%, p less than 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.
D000328:Adult; D001249:Asthma / Q000150:complications / Q000503:physiopathology*; D002302:Cardiac Output; D004452:Echocardiography; D005260:Female; D006801:Humans; D008168:Lung / Q000502:physiology; D008297:Male; D008875:Middle Aged; D011312:Pressure; D011669:Pulmonary Wedge Pressure; D011674:Pulse; D012119:Respiration; D013599:Systole; D013610:Tachycardia / Q000209:etiology