Although determination of pulsus paradoxus (change in systolic pressure greater than 10 mm Hg) in the clinical setting is most commonly done by means of a sphygmomanometer cuff and stethoscope, in our experience, as well as that of other investigators, this is an inaccurate and difficult measurement; yet in very few studies of pulsus paradoxus in man has the arterial blood pressure been measured directly. In this study, direct measurement of systolic and diastolic pressures provided the necessary degree of accuracy to enable us to observe relationships between the variables studied.
In man, systolic and diastolic blood pressures vary with respiration, reaching a minimum when pleural pressure is at its lowest during inspiration and reaching a maximum during expiration when pleural pressure is greatest. In normal subjects the addition of external resistive loads to breathing produces increased negative swings in pleural pressure and in doing so leads to exaggerated falls in systolic arterial blood pressure2 (Fig 1). It is possible that in spontaneously occurring bronchial asthma, other factors may contribute to the development of pulsus paradoxus; however, its rapid diminution on reversal of the obstruction of airflow and its ready production in normal subjects breathing through resistances point to mechanical factors associated with large swings in pleural pressure as being the most important.
The mechanism of pulsus paradoxus in asthma has been the subject of conjecture. The negative swing in pleural pressure (change in Ppl) alone could be transmitted to the intrathoracic vasculature and recorded peripherally. This is almost certainly partly responsible, and the correlation between the change in systolic pressure and the change in Ppl (Fig 2) supports this hypothesis; however, it is not the sole mechanism, for two reasons. First, the change in systolic pressure was greater than the change in Ppl in four of the five subjects (Fig 2). Secondly, direct transmission should have dropped diastolic pressure as well as systolic pressure so that pulse pressure should have been little affected. In fact, the latter decreased in every case (Fig 4), reflecting a greater decrease in systolic than diastolic pressure.
The most likely additional mechanism is the decrease in left ventricular stroke volume during inspiration. This was thought to be analogous to that in cardiac tamponade, with cardiac compression being produced by pulmonary overdistention and high intrathoracic pressure; however, high intrathoracic pressure is not usually a feature of bronchial asthma at rest, as the persistent activity of the inspiratory muscles keeps pleural pressures negative throughout most of expiration. The same is true during induced hyperinflation with expiratory resistances (Fig 1).
During acute asthma, there is almost invariably an elevation of the FRC, and this was proposed as an important prerequisite for the development of pulsus paradoxus; however, we found that pulsus paradoxus was readily induced by external inspiratory resistive loading without concomitant hyperinflation. Indeed, in four of five subjects, the magnitude of pulsus paradoxus was less at high pulmonary volumes, for a given swing in pleural pressure (change in Ppl), than at FRC. More accurate determination of pulsus paradoxus from the directly measured arterial pressure tracings in our study could be responsible for the different conclusion; however, Amyot and Tremblay recently observed a similar effect of pulmonary volume without direct arterial pressure recordings.
Hyperinflation must contribute to pulsus paradoxus in so far as the decreased pulmonary compliance at high pulmonary volumes requires greater change in Ppl for tidal breathing. Thus, for a given airway resistance, Ppl at high pulmonary volumes is greater due to the elastic component In spontaneously occurring or induced bronchial asthma, the linear correlation between pulmonary resistance and pulmonary hyperinflation results in both resistive and elastic pressure components increasing with severity of obstruction of airflow (following the link to learn more).
We observed virtually identical values of pulsus paradoxus during “intercostal” and “abdominal” breathing. Although the configuration of the chest wall was not objectively monitored in this study, all of the subjects were trained in these breathing patterns from experiments where both gastric and transdiaphragmatic pressures, as well as anteroposterior diameters of the rib cage and abdomen, were measured. The fact that gastric and transdiaphragmatic pressures changed appropriately, as well as our visual observations of excursions of the abdominal wall, convinced us that the desired breathing patterns were indeed achieved in the present study. The enhanced descent of the diaphragm during an “abdominal” inspiration should be associated with greater tension of the mediastinal structures than an “intercostal” inspiration, yet the effect on the magnitude of pulsus paradoxus was negligible. These findings militate against some form of external cardiac compression as a mechanism of pulsus paradoxus in bronchial asthma; however, they are consistent with the concept that reduction in left ventricular stroke volume during enhanced negative pleural pressure swings is partly due to increased right ventricular volume and partlv to an increase in the transmural (relative to Ppl) aortic diastolic pressure, reflecting an increase in the effective left ventricular afterload.
The results obtained from “intercostal” and “abdominal” Mullers maneuvers are at variance with those of “intercostal” and “abdominal” breathing. The greater fall in systolic pressure consistently observed after an “intercostal” Mullers maneuver (Table 2) was due to the greater fall in diastolic pressure. These differences may be due to the greater gastric pressures employed during “abdominal” Muller s maneuvers than during “abdominal” breathing or may reflect differences due to pulmonary inflation during breathing, while a negligible change in pulmonary volume occurs with Mullers maneuvers. The marked rise in gastric pressure during the “abdominal” Mullers maneuvers are unlikely to be encountered in asthma.
The aortic pulse pressure has been shown to be a good index of the left ventricular stroke volume. This is true to a lesser extent of the peripheral arterial pulse pressure (http://hyper.ahajournals.org/content/44/2/121.full). In our experiments the maximum decreases in pulse pressure, and presumably also stroke volume, occurred for small falls in pleural pressure, reaching a plateau after a change of about 20 cm HfeO in pleural pressure (Fig 4). Further increases in the change in Ppl result in similar falls in systolic and diastolic pressures, which are probably for the most part due to physical transmission of pleural pressure to the aorta and vascular tree; however, these conclusions have to be regarded with some caution, as the magnitude of the pulse pressure change consequent upon a change in left ventricular stroke volume depends on the elastic properties of the arterial tree. Furthermore, the influence of the increase in aortic transmural pressure during inspiration on the characteristics of the pulse wave in its transmission to the periphery is unknown.
Changes in frequency of respiration and the duration of inspiration, singly or in combination, may influence the magnitude of pulsus paradoxus. During Mullers maneuvers, systolic pressure reached a minimum on the second heart beat after the fall in Ppl (Fig 1). One might expect that a fall in pleural pressure which was not sustained for the duration of at least two cardiac cycles would not produce the maximum possible fall in systolic pressure for that change in pleural pressure. Thus, if the onset of expiration occurs before the systolic pressure has fallen to its minimum possible value on inspiration, the magnitude of pulsus paradoxus may be smaller than if the duration of inspiration were longer. Our results are consistent with this hypothesis. When breathing through high expiratory resistances, all subjects hvperinflated and altered their breathing pattern (Table 1). In the four subjects who showed a smaller change in systolic pressure at hgh pul-monarv volumes (Fig 2), the duration of inspiration fell by 1.0 to 2.1 seconds, and breathing frequency increased by 1.2 to 9.9 breaths per minute, relative to the values observed at FRC during inspiratory loading. In contrast, in the one subject who increased the change in systolic pressure at high pulmonary volumes, the duration of inspiration fell by only 0.7 second, and breathing frequency decreased. Thus, it is possible that the effect of hyperinflation on pulsus paradoxus in our subjects was due to the altered temporal pattern of breathing.
During loading without hyperinflation, identical changes in pericardial and pleural pressures have been demonstrated to occur in dogs. During positive-pressure breathing with hyperinflation, changes in pericardial pressure do not equal changes in pleural pressure, presumably due to a cardiac compressive effect by the hyperinflated lungs. It is possible that changes in pleural pressure as measured by the esophageal balloon do not equal the swings in pleural pressure adjacent to the pericardium, in particular during hyperinflation, accounting for the differences in pulse pressure changes between loading with and without hyperinflation.
It is perhaps surprising that greater falls in pulse pressure did not occur during “abdominal” breathing and “abdominal” Mullers maneuvers than during the corresponding “intercostal” maneuvers. The fall in pressure in the thoracic aorta (Pao) induced by a fall in pleural pressure should be less when a concomitant rise in gastric pressure occurs. The left ventricular afterload (Pao minus Ppl) should be increased under these circumstances, resulting in greater falls in pulse pressure than during “intercostar maneuvers. On the other hand, for a given fall in pleural pressure, the increase in transdia-phragmatic pressure is greater when gastric pressure rises. This may result in a smaller venous return from the inferior vena cava and hence smaller right ventricular volume than when gastric pressure falls on inspiration, as during an “intercostar maneuver. Since increases in right ventricular volume have been demonstrated to alter the left ventricular pressure-volume curve, and in this way to reduce left ventricular stroke volume, it is possible that these factors counterbalanced to account for the failure to observe a difference in pulse pressure changes between “intercostal” and “abdominal” maneuvers.
In patients with bronchial asthma, a different pattern of breathing may alter the degree of paradox at a given degree of obstruction of airflow. While a rapid inspiration may tend to decrease the change in systolic pressure, for the reasons given previously, it will tend to increase the change in Ppl, and hence the change in systolic pressure, because of a higher inspiratory flow through a given resistance. In addition, changes in tidal volume will alter the elastic component of the change in ppi, thus affecting the change in systolic pressure. This may explain in part the poor correlation between severity of obstruction of the airways and the magnitude of pulsus paradoxus observed both between and within patients with bronchial asthma. Differences in the configuration of the chest wall during breathing seem unlikely to play an important role in determining the magnitude of pulsus paradoxus.
Earlier issued articles are available on our website:
Factors Influencing Pulsus Paradoxus in Asthma
Outcomes of Pulsus Paradoxus in Asthma