A typical record of induced pulsus paradoxus during hyperinflation is shown in Figure 1. On inspiration, there is a fall in systolic blood pressure which reaches a minimum usually on the second heartbeat following the fall in Ppl. Diastolic blood pressure also falls but to a lesser extent, resulting in a fall in pulse pressure. There follows a gradual recovery of systolic and diastolic pressures to a maximum in middle to late expiration.
Figure 2 shows the curvilinear relationship of the induced pulsus paradoxus (change in systolic pressure) to the change in Ppl at FRC in five subjects. The largest falls in systolic pressure per unit pressure change in Ppl occur for small swings in Ppl. In four of the five subjects, the change in systolic pressure is greater than the change in Ppl for l6w values of change in Ppl. In three of the five subjects, this was the case at all values of change in Ppl. During hyperinflation (Fig 2, open circles) in four of the five subjects, the change in systolic pressure for any given value of change in Ppl was less than the value at FRC. In one subject (subject 2), the change in systolic pressure was greater at high pulmonary volumes.
The breathing frequency and duration of inspiration under conditions of inspiratory loading (at FRC) and expiratory loading (75 to 80 percent of VC) are shown in Table 1. In three subjects the breathing frequency during hyperinflation was significantly greater than during inspiratory resistive loading at FRC. In each subject the duration of inspiration shortened substantially when breathing with high expiratory resistances.
Figure 3 illustrates the course of systolic pressure over time during a sustained Mullers maneuver. The minimum systolic pressure is observed on the second heart beat after the fall in Ppl and thereafter shows a partial recovery despite the constant Ppl. Although not seen in this example, systolic pressure in expiration often showed an initial overshoot before falling to control levels.
Changes in pulse pressure (systolic minus diastolic pressure), expressed as a percentage of the control value, were also curvilinearly related to the change in Ppl (Fig 4). In all subjects, most of the change in pulse pressure was achieved at a change in Ppl of 15 to 20 cm H2O. Falls in Ppl of greater magnitude produced little further fall in pulse pressure. In three of the five subjects, changes in pulse pressure induced at FRC and at high pulmonary volumes were comparable. In subject 2, the reduction in pulse pressure was greater during hyperinflation, whereas in subject 4, the opposite was the case.
During “intercostal” breathing, gastric pressure decreased by 7.7 ± 2.8 cm H2O (mean ±: 1 SE; n = 5) during inspiration. During “abdominal” breathing, gastric pressure rose by 17.8 ±: 5.4 cm H2O with every breath. Changes in Ppl were — 31.9 ± 1.4 cm H2O and —30.3 ± 2.7 cm H2O for “intercostal” and “abdominal” breathing, respectively. Thus, similar inspiratory efforts (change in Ppl) were achieved with different configurations of the chest wall. The magnitude of the pulsus paradoxus during “intercostal” breathing exceeded that during “abdominal” breathing by 5.7 cm H2O in three of the subjects, while it was less by 2.5 cm H2O in the other two; however, these differences did not reach the level of statistical significance by paired f-test, due to substantial breath-to-breath variability.
To further explore the possibility that differences in the configuration of the chest wall during inspiratory efforts may lead to differences in the magnitude of the pulsus paradoxus, we examined a series of sustained ‘intercostal” and “abdominal” Muller’s maneuvers. Data for four of the subjects are shown in Table 2. The pulsus paradoxus induced by “intercostal” maneuvers, in which gastric pressure either fell or stayed constant during inspiratory efforts, was consistently greater than that measured during “abdominal” maneuvers. In three of the subjects, this was due to a greater fall in diastolic pressure, while in the remaining subject a greater fall in pulse pressure was responsible.
There were no systematic differences in the patterns of the swing in gastric pressure with inspiration between loading with and without hyperinflation, either within or between individuals.
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Table 1—Data under Conditions of Resistive Loading
|Subject||Breathing Frequency, breaths per min||Duration of Inspiration, sec|
|ResistiveInspiratoryLoading||ResistiveExpiratoryLoading||Resistive Resistive Inspiratory Expiratory Loading Loading|
|1||11.1 ±0.4||15.4 ±0.3||2.9±0.1||1.2±0.2|
|2||14.9 ±0.6||11.3 ±2.3||2.0 ±0.2||1.3 ±0.5|
|3||10.7 ±0.4||20.6 ±1.5||2.9 ±0.3||0.8±0.1|
|4||11.4 ± 1.1||15.2 ±0.9||2.5 ±0.3||0 8±0.1|
|5||20.5 ±0.3||21.7 ±2.0||1.6 ±0.1||0.6 ±0.1|
Table 2—Data during Sustained “Intercostal” and “Abdominal Muller’s Maneuvers
|Subject and Type of Maneuver||Change in Pressure, cm H20|
Figure 1. Pulsus paradoxus induced by expiratory resistance in normal subject. A five second time interval is indicated.
Figure 2. Pulsus paradoxus (change in systolic blood pressure [APsys]) at different magnitudes of swings in pleural pressure (APpl) at FRC(solid circles) and during hyperinflation (ojien circles) in five subjects. Each point of data represents mean for eight consecutive breaths. Bars indicate ±1 SD. Curves were visually fitted through points obtained at FRC.
Figure 3. Changes in pleural pressure (Ppl) and systolic blood pressure (Psys) in sustained Muller’s maneuver, illustrating delayed fall and gradual recovery of systolic pressure during constant value of Ppl.
Figure 4. Decrease in pulse pressure (systolic minus diastolic pressure [Psys-Pdias]) as percentage of control value at different magnitude of swing in pleural pressure (APpl) in five subjects. Solid circles indicate values at FRC, and open circles indicate values during hyperinflation.