There was no difference in prebolus PCWP, CO, SV, EDA, and fractional area of contraction values between both groups of patients (Tables 1 and 2). Four patients of 20 responded to fluid administration in the ICU group and 12 patients of 20 in the cardiac surgical group. There were 17 ICU patients receiving inotropic support and only 2 in the cardiac surgical group.
In all patients, the PCWP rose significantly in both responders (12.3 ± 2.2 to 15.4 ± 3.1 mm Hg, P = 0.023) and nonresponders (15.9 ± 3.1 to 21.1 ± 4.2 mm Hg, P < 0.001) (Figure 1, A and B). The prebolus PCWP was significantly smaller in responders when compared with nonresponders (P = 0.003). There was a significant increase in responder EDA after volume administration (15.3 ± 5.4 to 20.1 ± 5.0 cm2, P = 0.026), which was not observed in nonresponders (20.2 ± 4.8 to 21.5 ± 5.3 cm2, P = not significant) (Figure 1, C and D). The prebolus EDA was significantly smaller in responders when compared with nonresponders (P = 0.012).
There was a modest relationship between the SV and EDA in all patients (r = 0.60) (Figure 2A), whereas none was found for SV and PCWP (r = 0.15, Figure 2B).
There was no relationship between EDA and PCWP for cardiac surgical patients (r = 0.35, Figure 3A) and for ICU patients (r = 0.21, Figure 3B). In the cardiac surgical responders (Figure 3A), the prebolus EDA range was 7 to 23 cm2 (n = 12). In the ICU responders (Figure 3B), the prebolus EDA range was 7 to 12 cm2 (n = 4).
PCWP remains the most commonly used variable to assess preload. The EDA is a rapid and direct measurement of LV dimension. We found no correlation between the EDA and the PCWP, which has previously been demonstrated (7,16). In cardiac surgical patients, the EDA has been shown to be sensitive in detecting changes in blood volume (7–10), even in the presence of wall motion abnormalities (7). In surgical patients undergoing hypervolemic hemodilution (8), volume administration resulted in significant increases in SV and EDA, which increased up to a threshold beyond which no further increases were observed. The PCWP, however, continued to rise. In a study in dogs (17), both the LV EDA and the PCWP increased in response to volume administration. These changes correlated well with changes in CO. Further volume administration did not result in any further increases in EDA or CO; however, the PCWP continued to rise. These studies suggest that a threshold or endpoint for fluid administration can be determined for EDA.
We defined responders as those who increased SV by 20% or more. After volume administration, the PCWP increased significantly in responders and nonresponders alike (Figure 1, A and B). There was no significant increase, however, in nonresponder EDA after volume administration. The nonresponders may have already reached their optimal EDA where none or only modest increases in size would be observed. Indeed, nonresponders had a lower LV compliance, as the EDA changed little while the PCWP increased. Some nonresponders, however, did demonstrate an increase in EDA after volume administration. This may have been the result of technical errors in measurement. Alternatively, some patients with poor LV function may have dilated without appreciable increases in SV. Finally, our definition of 20% for increases in SV may have been too high. The nonresponders who increased EDA may have had SV increases slightly less than 20%.
The optimal EDA was difficult to determine as loading conditions, ventricular function, and previous heart disease were not controlled and may have played a large role in determining optimal size. Although responders had significantly smaller prebolus EDA (15.3 ± 5.4 cm2) when compared with nonresponders (20.2 ± 4.8 cm2), the range in both was wide and overlapped significantly (Figure 1, C and D). Furthermore, in patients with wall motion abnormalities or dilated cardiomyopathies, the LV EDA may not have accurately reflected end diastolic volume.
Curiously, a few patients demonstrated a decrease in EDA after volume administration. This may have been the result of technical errors such as probe movement during the study or poor border definition. Alternatively, improvements in loading conditions in response to volume may have resulted in a decreased EDA with little change in SV. The ventilatory cycle may have also influenced the EDA, especially in relatively hypovolemic patients.
We found no correlation between SV and PCWP (Figure 2B). We found only a very modest correlation between the SV and EDA (r = 0.60, Figure 2A) in all our patients. However, in a study examining 16 hemodynamically unstable (mean arterial pressure < 60 mm Hg or cardiac index < 3.0 L · min−1 · /m−2) postoperative patients admitted to an ICU, a good correlation (r = 0.89) was found between the SV and the LV EDA (18). Our poorer relationship may have been the result of a larger proportion of patients with chronic heart disease, who demonstrated large variations in optimal LV sizes and in whom EDA did not reflect true preload. Furthermore, studying a hemodynamically unstable population likely improved the relationship between preload and performance as a larger proportion of patients might have been on the steeper portion of the Starling curve.
It is interesting to note that few ICU patients responded to volume administration when compared with the postoperative cardiac surgical patients (Figure 3). Indeed, it has previously been reported that critically ill patients respond poorly to fluid and show no appreciable increases in LV EDA after volume administration (13). The ICU responders seemed to cluster at an EDA ≤ 12 cm2 (Figure 3B). The small number of responders in the ICU patients could be the result of a septic syndrome, for example, in some patients a high CO would preclude any significant SV increases. Alternatively, overall poor LV performance may have prevented any appreciable recruitment of SV for various LV sizes. Indeed, most of the ICU patients were receiving inotropes when compared with the cardiac surgical group. In the cardiac surgical group, responders were distributed over a wider range of EDA (Figure 3). It was not possible to establish a threshold below which a large proportion of patients respond to volume administration.
In summary, this study provides evidence that the TEE gives information additive to the pulmonary artery catheter in the assessment of preload in an ICU population. Although there may not be a specific threshold EDA value that reliably predicts a response to fluid administration in all patients, the LV EDA may be useful in identifying some critically ill patients who could benefit from volume administration. The decision to administer fluid still relies on clinical judgment.
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