As a final note of validation, Leithner et al demonstrated in normal subjects that lung distention to levels similar to those used in our study reduced LV end-diastolic volume and induced an anterior rotational movement on the heart. They used MRI techniques and thus were limited to end-expiratory analysis as lung volume was progressively increased by the application of 15 cm H2O positive end-expiratory pressure. Because the movement they saw did not alter the midventricular short-axis orientation, if TEE had been used in their subjects, TEE would have not seen this movement as a volume artifact. Thus, it seems highly unlikely that our data in this selected population reflect rotational artifacts.
The variations that we measured in SAP were small, especially if they were expressed as a percent-age.2 However, we did not limit our analysis to patients in which pulsus paradoxus, defined by a change in SAP > 10 mm Hg, was present. Indeed, Rooke et al have shown in a human hemorrhage model that a SAP variation < 5 mm Hg or A down < 2 mm Hg indicates minimal intravascular depletion. Their observed changes in SAP following a 500-mL blood removal was 15.2 ± 7.5 mm Hg (their Table 1). We cannot exclude the possibility that, for larger variations in SAP, changes in ventricular volumes may play a more important role. Our data on closed chest conditions are similar to those obtained by Coriat et al, especially with regard to their Figure 4, which relates the percentage change in EDA with the A down. in detail
It illustrates how variable the response can be. Two patients had < 10% changes in EDA with a A down of > 5 mm Hg, and two others had EDA changes > 40% with a A down < 5 mm Hg. We both observed an average fall in EDA and an increase in A down, but there are large individual variations. However, Coriat et al did not record the area measurement simultaneously with the arterial and airway pressure and did not demonstrate that changes in SAP reflect simultaneous changes in LV volume. It has been previously shown that for the same decrease in SAP or pulsus paradoxus occurring during normal inspiration, the aortic flow will decrease when associated with tamponade, but it will remain constant when associated with airway obstruction. Consequently, we observed that SAP variation with respiration in the range cannot be explained entirely by changes in LV volume.