Cardiac Output Measured with Both Esophageal Doppler Device and Vigileo-FloTrac Device

To the Editor We disagree with Meng et al.'s1 conclusions in their comparison of cardiac output (CO) measurements using both the third-generation Vigileo-FloTrac device (COFT) (Edwards Lifesciences, Irvine, CA) and the esophageal Doppler device (COED). The authors were wrong to assume that the COED was a valid reference. Furthermore, the significant disconcordance between COED and COFT measurements with phenylephrine boluses was predictable. Knapp et al.2 demonstrated that stroke volume initially increases during the first 4 minutes after initiating a phenylephrine infusion, peaks at 19.3 minutes, after which the stroke volume decreases. Schwinn and Reves3 showed that the time course and hemodynamic effects of bolus phenylephrine administration in anesthetized patients ranges from 40 seconds to 55 seconds depending on the dose administered. The patient's underlying volume status,4,5,6 relative density and activation of α- and β-adrenergic receptors, the underlying catecholamine state and cardiac function, and chronic medication use all influence hemodynamic responses to these study interventions. There is interindividual variability in response to anesthetic and a 20% decrease in mean arterial blood pressure after induction hardly guarantees equivalent volume status (especially considering the variable size of the splanchnic reservoir). The χ (Ķ) factor accounting for arterial compliance in the Vigileo-FloTrac (FT) algorithm is updated every minute in the third-generation FT software. Thus, the FT device was using an “unupdated” correction factor because it was trying to make sense of the acutely increased pulse pressure with a phenylephrine bolus. In other words, Meng et al. were testing the FT in a situation for which it had not been intended to perform. Therefore, we could have anticipated study findings given the lack of synchrony between the time course of phenylephrine bolus effects (well below 60 seconds) and the updating interval for the arterial compliance correction factor on the third-generation FT algorithm (60 seconds). Preload-augmenting effects of phenylephrine are generally predominant5–9 and these effects are largely related to splanchnic and abdominal visceral venous constriction5 (in response to α-agonist effects of phenylephrine) resulting in the displacement of blood from a previously nonstressed compartment into the central circulation.5,9,10 Although stroke volume may increase, CO may decrease secondary to an overall negative effect of phenylephrine on the heart rate. Global CO was not directly measured by Meng et al. The implicit assumption with COED-based monitoring is that the proportion of bloodflow in the ascending and descending aorta remains fixed (at a constant 30:70 ratio), despite fluctuations in various hemodynamic variables. Effects of changes in posture have not been formally examined using the esophageal Doppler device.11 Situations altering the proportion of upper lower body bloodflow will affect Doppler-derived values.11 The physiologic effects of an acute bolus of phenylephrine are not dissimilar to those associated with aortic cross-clamping; acute simultaneous increases in preload and afterload. We contend that the esophageal Doppler device assumed ratio of ascending to descending aortic flow (the relative distribution of global cardiac output) will not hold true after a phenylephrine bolus. With an acute phenylephrine bolus, global bloodflow is redirected away from the lower body (splanchnic viscera) toward the vital organs in the upper body (heart and brain). Therefore, when a phenylephrine bolus is used to treat hypotension occurring after the induction of general anesthesia we would expect the COED to decrease (because it is measuring only descending aortic flow) and the COFT to increase (because it is using an “unupdated” arterial compliance correction factor based off a radial arterial monitoring site). In essence, both the devices (esophageal Doppler device and FT) were not accurately measuring the effects of a phenylephrine bolus on global bloodflow. Karthik Raghunathan, MD, MPH Department of Anesthesiology Baystate Medical Center Tufts University School of Medicine Springfield, Massachusetts email protected Joshua A. Bloomstone, MD Department of Anesthesiology and Perioperative Medicine Banner Thunderbird Medical Center Glendale, Arizona Valley Anesthesiology Consultants, Ltd Phoenix, Arizona William T. McGee, MD, MHA Division of Critical Care Department of Internal Medicine Baystate Medical Center Tufts University School of Medicine Springfield, Massachusetts