Effeets of respiration on the circulation have been recognized for many years. Exaggerated falls in blood pressure in association with enhanced variations in intrathoracic pressure (pulsus paradoxus) were first reported by Gauchat and Katz in 1924. Since pulsus paradoxus in patients with bronchial asthma did not appear to indicate an abnormality of the circulation but was thought to reflect transmission of the negative intrathoracic pressure to the vascular tree, it was not considered to be of any particular importance.
Recently, there has been interest in pulsus paradoxus as a clinical indicator of the severity of an attack of bronchial asthma. Rebuck and Read observed in 76 cases of severe asthma that pulsus paradoxus was invariably present when the patient’s forced expiratory volume in one second (FEVi) was less than 20 percent, and was never present when the FEVi exceeded 40 percent of the patient’s best value. In spite of the interest in this clinical sign, very little is known of the influence on pulsus paradoxus of various factors that characterize an acute asthmatic attack. Consequently, we have attempted to examine some of these factors in normal subjects with induced pulsus paradoxus, both from the point of view of better understanding and interpretation of the sign in the clinical setting, and in terms of the possible physiologic mechanisms which give rise to it.
Materials and Methods
We studied five normal male seated subjects selected from laboratory personnel. Measurements of arterial blood pressure, tidal volume, and esophageal and gastric pressures were recorded while the subjects breathed through a variety of inspiratory or expiratory resistances (or both). The effect of increased airway resistance without hyperinflation was investigated by introducing progressively greater inspiratory resistances which increased swings in esophageal pressure (change in intrapleural pressure [Ppl] up to 40 to 50 cm H20). Hyperinflation was induced by expiratory resistances of sufficient magnitude to increase end-expiratory pulmonary volume to 75 to 85 percent of the vital capacity (VC). Increased change in Ppl was achieved by further adding inspiratory resistances until the desired values of change in Ppl were observed. The volume of hyperinflation was checked by asking the subject at intervals to inspire to total lung capacity. In each case, measurements were recorded only after the subject achieved a stable breathing pattern. This was assisted by displaying the change in Ppl in front of the subject on a large display oscilloscope.
To investigate the influence of the mediastinal configuration on pulsus paradoxus, the trained subjects performed periods of “intercostal” and of “abdominal” breathing during inspiratory resistive loading at functional residual capacity (FRC). In the former instance, there was an exaggerated contribution of the intercostal and accessory muscles of inspiration, with the abdominal wall moving inwards during inspiration. During “abdominal” breathing, each inspiration was achieved by descent of the diaphragm with enhanced outward motion of the abdominal wall, resulting in preferential expansion of the lung in the longitudinal direction with stretching of the mediastinum. Gastric and transdiaphragmatic pressures were used as objective indicators that subjects were using the appropriate pattern.
The patients’ examinations with constant respiratory symptoms, breath with wheezing are described in the article: “Research Concerning Expiratory Flow and Bronchodilator Response in Asthma”
To better understand the interaction between the change in Ppl and the arterial pressure, we studied the pattern of change in the latter during sustained Mullers maneuvers. The latter constituted step changes in Ppl. The effect of differences in the configuration of the chest wall during Miiller’s maneuvers was also examined.
Arterial pressures were measured via an indwelling 20-gauge plastic cannula inserted under local anesthesia into a radial (four subjects) or brachial (one subject) artery and connected to a saline-filled pressure transducer (Sanborn 267B). Flow was measured by a pneumotachygraph (Fleisch), and the signal was electrically integrated to give changes in volume. A 10-cm latex balloon was placed in the lower third of the esophagus and another in the stomach for measurement of changes in Ppl and gastric pressure, respectively. These were attached by thin plastic tubing, each to one port of a pressure transducer (Sanborn 267B). A screw-elamp placed on a small piece of rubber tubing was connected to a valve (Hans Rudolph) and served to provide inspiratory and expiratory resistive loads which could be varied as required. All signals were recorded on an eight-channel strip-chart recorder (Hewlett-Packard ).
Pulsus paradoxus was quantitated from the pressure tracings by taking the difference between the greatest systolic pressure in expiration and the lowest systolic pressure during the subsequent inspiration.