Our observations and those from Figure 6 in the study of Abel et al demonstrate less variation in SAP during the open chest condition rather than during the closed chest condition. Based on observations in three subjects, Perel et al and Pizov et al hypothesized that the absence of variation in SAP may indicate the presence of an underlying LV dysfunction during the open chest condition. Neither the data of Abel et al nor ours support this conclusion. Although we saw less SAP variation in our study group following cardiopulmonary bypass, when contractility is reduced, there is a considerable overlap in response between subjects before and after bypass. However, the average apneic EDA in our subjects with variation in SA during a positive-pressure breath of < 0.5 cm2 (n = 14) was 12.2 ± 5.5 cm2 compared with a mean apneic EDA of only 7.1 ± 3.7 cm2 in those subjects (n = 11) with > 0.5 cm2 variation. These data are consistent with results from subjects having a relatively fixed stroke volume, as is commonly seen in patients with heart failure. According to these data, it appears that limiting ITP fluctuations (open chest conditions) minimized the SAP changes seen in response to positive-pressure ventilation, whereas impaired LV function minimizes the changes seen in LV area. This impaired LV function could be secondary to postbypass ischemia, stunning myocardium, or hibernating myocardium. contraceptive pills
Massumi et al, Jardin et al, and Perel et al suggested that increases in SAP or reversed pulsus paradoxus during a positive-pressure breath would represent an increase in stroke volume either from an increase in preload or a decrease in afterload. A subset of our subjects appears to behave in a fashion similar to that described by these authors. In 10 of our subjects, SA increased during the positive-pres-sure inspiration, and in all but 1, this increase was in phase with the increase in SAP (Fig 3). In the nine subjects in whom both SAP and SA increased, the increase in SA was associated with an increase in EDA in only three subjects and a decrease in ESA in the remaining six subjects. These data imply that both increasing preload (increase in EDA) and decreasing afterload (decrease in ESA) may be the mechanisms inducing these changes. However, in this subset of our subjects, the reduction in afterload appears to be the more prevalent mechanism responsible for the changes in SAP and LV area.