Key result
A 6 ml/kg fluid bolus significantly decreased carotid peak systolic velocity variation from 14.9% to 6.1% (p=0.0001) in critically ill fluid responders, demonstrating its utility as a surrogate marker for stroke volume variation.
Why the study?
LVOT VTI variability is time-consuming and often difficult to achieve, prompting investigation of carotid peak systolic velocity variation as an alternative surrogate marker of fluid responsiveness.
Does carotid peak systolic velocity variation correlate with LVOT VTI variation and decrease after fluid administration in critically ill fluid responders?
Observational (n=30)
No
Does carotid peak systolic velocity variation correlate with LVOT VTI variation and decrease after fluid administration in critically ill fluid responders?
Carotid peak systolic velocity variation is a feasible and accessible surrogate for LVOT VTI variability to assess fluid responsiveness in critically ill patients.
May support carotid peak systolic velocity variation as a noninvasive surrogate for fluid responsiveness; hypothesis-generating and requires prospective validation.
Background and objectives A fluid responder is a patient who can increase his stroke volume/ cardiac output by more than 10%-15% after a fluid bolus. Left ventricular outflow tract (LVOT) velocity time integral (VTI) variability is widely used as an adynamic parameter of fluid responsiveness, but a transthoracic echo view of LVOT VTI is often time-consuming and, at times, difficult to achieve. So, in the quest for another parameter that might equally be a good surrogate marker of stroke volume variation, carotid peak systolic velocity (CPSV) variation has been studied. The objective was to assess CPSV variation in patients who are already fluid responders. Methods The sample size was calculated considering a minimum correlation coefficient of 0.5. Adult patients in whom the physician wanted to give a fluid bolus and whose average LVOT VTI was more than 15% over 3 respiratory cycles were included in the study. Demographic variables, along with hemodynamic parameters such as heart rate, blood pressure, the need for vasopressors, mode of breathing (spontaneous or mechanical ventilation), and CPSV variation,were noted and averaged over three respiratory cycles. Fluid bolus (Plasmalyte) 6 ml/kg bolus over 10-15 minutes. Post-fluid hemodynamic variables, along with averaged LVOT VTI over three respiratory cycles and averaged CPSV variation over three respiratory cycles, are noted. Results Thirty adult patients were evaluated in the study. In spontaneously breathing patients (n=12), the average CPSV variation expressed as mean + standard deviation before and after fluid administration of 6ml/kg of ideal body weight was 14.1 ± 3.4 and 5.4 ± 2.6, respectively (p < 0.05). In mechanically ventilated patients (n=18), the average CPSV variation expressed as mean + standard deviation before and after fluid administration of 6ml/kg of ideal body weight fluid was 15 ± 5.3 and 6.5 ± 3.1, respectively (p <0.005). Overall, there was a statistically significant positive correlation between LVOT VTI variation and CPSV variation before fluid therapy (correlation coefficient 0.56 and p-value 0.001) and a statistically significant moderate positive correlation post-fluid therapy (correlation coefficient 0.37 and p-value 0.043). Conclusion We found a significant decrease in CPSV variation post-fluid administration in patients who are fluid responders, which mimics a decrease in stroke volume variation after fluid administration in patients who are fluid responsive.
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Roy et al. (2023) conducted an observational in Shock with fluid responsiveness (n=30). Fluid bolus (Plasmalyte) vs. Pre-fluid baseline was evaluated on Carotid peak systolic velocity (CPSV) variation (MD 8.8, 95% CI 7.60-10.00, p=0.0001). A 6 ml/kg fluid bolus significantly decreased carotid peak systolic velocity variation from 14.9% to 6.1% (p=0.0001) in critically ill fluid responders, demonstrating its utility as a surrogate marker for stroke volume variation.
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