Effects of optimizing cardiac output by fluid loading on the indocyanine green plasma disappearance rate and splanchnic microcirculation

Introduction

Hypovolemia may be associated with splanchnic hypoperfusion and reduced in liver blood flow and function. In general, optimizing the cardiac preload to increase the cardiac output – a major determinant of systemic oxygen delivery – is a primary clinical goal. In this study, we tested the hypothesis that increasing the cardiac output by optimizing the intravascular fluid status leads to an improved regional (i.e. hepato-splanchnic) blood flow and function as assessed by the indocyanine green plasma disappearance rate (ICG-PDR), which has been shown to be of major prognostic relevance [1].

Methods

With approval by our ethics committee and written patient consent we prospectively studied 12 postoperative cardiac surgical patients (mean age 66 ± 13 years) who underwent elective coronary artery bypass grafting. All patients underwent extended hemodynamic monitoring by a pulmonary artery and left atrial catheter for clinical indication. Microcirculation within the splanchnic area was assessed by gastric tonometry, and liver blood flow and function were determined non-invasively by transcutaneous measurement of ICG-PDR. All these patients who were considered hypovolemic underwent hemodynamic optimization by infusion of hydroxyethylstarch (130 kDa). Global and regional parameters were measured at baseline and 1 hour after fluid challenge. All patients received pressure-controlled mechanical ventilation and respirator settings remained unchanged throughout the study. Data are expressed as mean ± standard deviation. For statistical analysis, a paired t test was used and P < 0.05 was considered significant.

Results

Overall, 630 ± 130 ml hydroxyethylstarch were administered. In all patients, the cardiac index significantly increased following fluid administration, on average from 2.8 ± 0.7 to 3.6 ± 0.6 l/min/m² and the stroke volume index from 30 ± 7 to 38 ± 8 ml/m², respectively. With respect to cardiac preload, the central venous pressure significantly increased from 6 ± 2 to 12 ± 2 mmHg and the left atrial pressure from 5 ± 3 to 11 ± 3 mmHg, respectively. However, the ICG-PDR and PCO₂ gap (difference between gastric mucosal and end-tidal CO₂ tension) did not change significantly (i.e. from 21.2 ± 6.5 to 21.6 ± 6.5%/min and from 0.9 ± 0.5 to 1.0 ± 0.7 kPa).

Conclusion

Optimizing cardiac output by fluid loading per se is not associated with a significant change in ICG-PDR or gastric mucosal PCO₂. However, since ICG-PDR in all patients with a value <18%min increased, we hypothesize that particularly patients with an a priori low ICG-PDR may benefit from optimizing cardiac index by fluid loading. Further studies are needed to test this hypothesis.