Toshinori Kasai1, Eiji Hashiba2, Junichi Saito2, Kazuyoshi Hirota2. 1. Department of Anesthesiology, Hirosaki University Postgraduate School of Medicine, 5 Zaifu-cho, Hirosaki, 036-8563, Japan. tosi_1984@yahoo.co.jp. 2. Department of Anesthesiology, Hirosaki University Postgraduate School of Medicine, 5 Zaifu-cho, Hirosaki, 036-8563, Japan.
Abstract
The initial distribution volume of glucose (IDVG) has been reported to be a surrogate marker of cardiac preload. However, the relationship between cardiac output and IDVG is not fully understood. We investigated the effects of cardiac output on IDVG in the absence of fluid gain or loss in pigs. MATERIALS AND METHODS: Thirteen pigs were anesthetized and allocated to either the modified cardiac output group (m-CO group, n = 10) or the control group (control group, n = 3). In the m-CO group, CO was sequentially modulated from high CO (high CO) to two grades of low CO (low CO-1 and low CO-2) with dobutamine and propranolol with lidocaine, respectively, in the absence of any apparent change in basal fluid volume status. Thermodilutional CO and IDVG were measured at each CO condition. The IDVG was measured according to a one-compartment model with 2 g glucose. The same parameters were measured in the control group using the same time schedule as for the m-CO group but without inotropes and at a stable CO state. Thereafter, 250 ml of 10% dextran were infused over 15 min to compare the effects of a preload-dependent increase in CO on IDVG measurements to the effects of the pharmacological modification of CO. Data were expressed as the mean ± SD. Statistical analysis was performed with repeated measures ANOVA followed by Dunnett's test. Pearson's correlation test was also used. A P value of <0.05 was considered to indicate statistical significance. RESULTS: In the m-CO group, where CO increased to 147.2 ± 26.7% of the baseline CO value in the high CO state and decreased to 65.9 ± 11.0 and 37.3 ± 14.4% of the baseline CO value in the low CO-1 state and the low CO-2 state, respectively, the IDVG did not change as CO was modified. IDVG significantly increased in response to volume loading of dextran in the control group. There was no correlation between the IDVG and CO in the m-CO group when there was no fluid gain or loss (r = 0.097, n = 40, P = 0.554), but the IDVG was well correlated with CO in the control group with volume loading (r = 0.764, n = 18, P = 0.0002). CONCLUSION: This study suggests that the IDVG is dependent on the central extracellular fluid volume and not on cardiac output.
The initial distribution volume of glucose (IDVG) has been reported to be a surrogate marker of cardiac preload. However, the relationship between cardiac output and IDVG is not fully understood. We investigated the effects of cardiac output on IDVG in the absence of fluid gain or loss in pigs. MATERIALS AND METHODS: Thirteen pigs were anesthetized and allocated to either the modified cardiac output group (m-CO group, n = 10) or the control group (control group, n = 3). In the m-CO group, CO was sequentially modulated from high CO (high CO) to two grades of low CO (low CO-1 and low CO-2) with dobutamine and propranolol with lidocaine, respectively, in the absence of any apparent change in basal fluid volume status. Thermodilutional CO and IDVG were measured at each CO condition. The IDVG was measured according to a one-compartment model with 2 g glucose. The same parameters were measured in the control group using the same time schedule as for the m-CO group but without inotropes and at a stable CO state. Thereafter, 250 ml of 10% dextran were infused over 15 min to compare the effects of a preload-dependent increase in CO on IDVG measurements to the effects of the pharmacological modification of CO. Data were expressed as the mean ± SD. Statistical analysis was performed with repeated measures ANOVA followed by Dunnett's test. Pearson's correlation test was also used. A P value of <0.05 was considered to indicate statistical significance. RESULTS: In the m-CO group, where CO increased to 147.2 ± 26.7% of the baseline CO value in the high CO state and decreased to 65.9 ± 11.0 and 37.3 ± 14.4% of the baseline CO value in the low CO-1 state and the low CO-2 state, respectively, the IDVG did not change as CO was modified. IDVG significantly increased in response to volume loading of dextran in the control group. There was no correlation between the IDVG and CO in the m-CO group when there was no fluid gain or loss (r = 0.097, n = 40, P = 0.554), but the IDVG was well correlated with CO in the control group with volume loading (r = 0.764, n = 18, P = 0.0002). CONCLUSION: This study suggests that the IDVG is dependent on the central extracellular fluid volume and not on cardiac output.
Entities:
Keywords:
Cardiac preload; Fluid volume monitoring; Fluid volumetry; Initial distribution volume of glucose