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Technology, Computing, and Simulation: Research Reports

The Impact of Phenylephrine, Ephedrine, and Increased Preload on Third-Generation Vigileo-FloTrac and Esophageal Doppler Cardiac Output Measurements

Meng, Lingzhong MD; Phuong Tran, Nam BS; Alexander, Brenton S. BS; Laning, Kathleen BS; Chen, Guo MD; Kain, Zeev N. MD, MBA; Cannesson, Maxime MD, PhD

Author Information
doi: 10.1213/ANE.0b013e31822649fb

Uncalibrated cardiac output (CO) monitoring obtained through pulse contour analysis using the Vigileo-FloTrac system (Edwards Lifesciences, Irvine, CA) has the potential to be used for intraoperative goal-directed hemodynamic management and fluid optimization.14

Although the concept of perioperative hemodynamic optimization has been well validated,5,6 especially using the esophageal Doppler,7 it has only recently been tested with positive results for the second-generation Vigileo-FloTrac system.1,4 However, several studies have suggested that acute changes in arterial blood pressure induced by increased vasomotor tone may alter this device's ability to accurately measure CO.810 This may be of concern in managing high-risk surgical patients in whom the use of a vasopressor is warranted to maintain an “acceptable” arterial blood pressure. A previous study demonstrated that there was a significant discrepancy between changes in CO measured by pulse contour analysis (COPC) on the basis of the second-generation Vigileo-FloTrac system and changes in CO measured by intermittent pulmonary artery thermodilution (COTD) after norepinephrine administration.8 In that study, norepinephrine induced a significant increase in COPC (from ∼4.5 L/min to ∼6.5 L/min) but no changes in COTD. The limitations of this previous study include the following: (1) thermodilution is not a beat-to-beat CO monitor and may not accurately track rapid and transient changes in CO induced by vasopressors; (2) norepinephrine has some inotropic effects that can increase CO, and thus the analysis of how the change in vasomotor tone affects CO is confounded.11

Recently, third-generation Vigileo software (3.02) was released and tested in a multicenter study conducted in septic patients.12 Although the first- and second-generation software were based on a limited human database, the third-generation database relies on a much larger dataset, including a larger proportion of hyperdynamic and vasoplegic patients, who are septic or have end-stage liver disease, to improve the reliability of the software during changes in vasomotor tone.12 Supposedly, this larger dataset allows identifying specific arterial pressure waveform characteristics in these specific settings. These characteristics are then used to calculate and update the κ factor (which is used to estimate arterial compliance) every minute to improve CO determination from the arterial pressure waveform analysis. Moreover, new analytical methods have recently been proposed to evaluate a new device's ability to track trends of change in CO against an established device.13

The major goal of this study was to examine the third-generation Vigileo-FloTrac's ability to track CO changes induced by increased vasomotor tone, increased myocardial contractility, and increased preload. We used the esophageal Doppler as the reference method in the present study because it is a beat-to-beat monitor allowing for detection of transient changes in CO and because it is a device that has been used in several intraoperative goal-directed therapy studies with positive impact on patient outcome.7,14,15



Thirty-three ASA I–III patients (22 males, 11 females, ages 59 ± 13 years old, height 173 ± 9 cm, and weight 77 ± 13 kg [mean ± SD]), scheduled for elective surgery at University of California, Irvine Medical Center, were enrolled after IRB approval. Both verbal and written consent were obtained. The exclusion criteria were (1) symptomatic cardiac diseases (e.g., ischemic myocardial disease, significant valvular disease, or arrhythmia), (2) poorly controlled hypertension (systolic blood pressure ≥160 mm Hg), and (3) history of congestive heart failure.

A radial intra-arterial catheter (Arrow International Inc., Reading, PA) was placed before induction of anesthesia. After being zeroed to atmospheric pressure, the pressure transducer was secured at the midaxillary level. Anesthesia was induced with fentanyl (1.5 to 2 mcg/kg) and propofol (2 to 3 mg/kg). All patients were tracheally intubated and maintained with total IV anesthesia: propofol 100 to 150 mcg/kg/min and remifentanil 0.3 to 0.5 mcg/kg/min. All patients' lungs were mechanically ventilated with a tidal volume of 8 to 10 mL/kg body weight at a frequency of 8 to 12 breaths per minute to keep the end-tidal carbon dioxide between 35 to 40 mm Hg. An esophageal Doppler probe (CardioQ, Deltex Medical, Chichester, UK) and a third-generation Vigileo-FloTrac system (version 3.02, Edwards Lifesciences, Irvine, CA) were placed after endotracheal intubation.

Study Protocol

Patients who demonstrated a 20% or more decrease in mean arterial blood pressure (MAP) in response to anesthesia induction were studied. Three interventions were adopted to challenge hemodynamics: IV phenylephrine bolus (100 to 200 mcg) (to increase vasomotor tone), IV ephedrine bolus (5 to 20 mg) (to increase myocardial contractility and heart rate), and whole-body tilting from the reverse Trendelenburg (head up) position to the Trendelenburg (head down) position (to increase venous return and ventricular preload). The preload change caused by whole-body tilting has been previously described.16,17 The sequence and condition of these interventions are illustrated in Figure 1. Anesthesia-induced hypotension was treated with a vasopressor bolus (either phenylephrine or ephedrine, randomized). When the MAP decreased to the pretreatment level at least 5 minutes after the first vasopressor treatment, whole-body tilting was performed. Finally, if MAP was still 20% lower than the patient's preinduction level at least 10 minutes after the first vasopressor treatment, the alternate vasopressor (the one not chosen as the first vasopressor treatment) was administered. Because there was an interindividual difference in MAP responses to vasopressor treatment as well as severity of anesthesia-related hypotension, varying doses of phenylephrine (100 to 200 mcg) and ephedrine (5 to 10 mg) were used to increase MAP at least 20%. Three successive hemodynamic measurements were recorded immediately before vasopressor interventions and repeated when MAP peaked after treatment. During whole-body tilting, 3 successive measurements were recorded at both reverse Trendelenburg and Trendelenburg positions. The mean value of each trio of consecutive measurements was used for analysis. All measurements were performed before surgical incision. The anesthesia regimen and ventilation settings were kept constant throughout the study.

Figure 1
Figure 1:
Study protocol with intervention sequence and conditions. MAP = mean arterial pressure.

Cardiac Output Determination Using the Vigileo-FloTrac System

The third-generation Vigileo-FloTrac device analyzed the arterial waveform to determine COPC.12 This device does not require prior calibration. Briefly, the Vigileo-FloTrac has a custom-made pressure transducer that connects to both a commercially available arterial catheter and a specific Vigileo monitor. The arterial waveform is assessed at 100 Hz, and the standard deviation (SD) of the pulse pressure is determined over a 20-second period. To calculate CO, the software uses an algorithm based on the relationship between arterial pulse pressure and stroke volume while considering vessel compliance and peripheral resistance. Vessel compliance is estimated from nomograms based on age, gender, height, and weight. Peripheral resistance is determined from arterial waveform characteristics. Apart from monitoring CO, Vigileo-FloTrac allows determination of respiratory variation in stroke volume. This index is displayed continuously on the monitor and was recorded at each step of the protocol.

Cardiac Output Determination Using Esophageal Doppler

The esophageal Doppler (CardioQ, Deltex Medical Ltd., Chichester, Sussex, UK) measures bloodflow in the descending aorta and estimates CO via multiplying the cross-sectional area of the aorta by bloodflow velocity (over time). The aortic diameter is obtained from a built-in nomogram. In addition to monitoring CO, the device provides flow time corrected, an index of ventricular preload, which was recorded at each step of the protocol.

Statistical Analysis

Data are expressed as mean ± SD. The Kolmogorov–Smirnov test was used to test the normality of the distributions. Changes in CO induced by hemodynamic challenges were analyzed using a 2-sided paired Student t test. Bland– Altman analysis18 was used to assess the bias (mean difference) and precision (SD of the bias) between CO by esophageal Doppler (COED) and COPC. The percentage error (2 SD of the difference divided by mean CO of the reference method) between COED and COPC was assessed using the Critchley and Critchley method.19 Finally, because the aim of our study was to compare the trending ability between COED and COPC, we used the 4 quadrant plots recently described by Critchley and Critchley to analyze their concordance (the percentage of the total number of data points that are in 1 of the 2 quadrants of agreement).13 Correlations between MAP and CO were determined by linear regression. For all statistical analyses, P values <0.05 were considered statistically significant.


Of the 33 patients recruited, 32 phenylephrine treatments, 30 ephedrine treatments, and 26 whole-body tilting hemodynamic challenges were performed. We were unable to administer vasopressors on 4 occasions because the decrease in MAP did not meet the treatment criteria. Because of unstable MAP and significant esophageal Doppler signal interference caused by body position change, we were not able to obtain the data of whole-body tilting on 7 occasions.

For the 176 pairs of CO measurements (pulse contour versus esophageal Doppler), the mean COED was 5.4 ± 1.9 L/min and mean COPC was 5.3 ± 1.9 L/min (P = 0.37). The difference between paired measurements of COED and COPC was 0.14 ± 2.13 L/min (mean ± SD) (Fig. 2), and the percentage error was 66%. When analysis was limited to the 88 pairs of CO measurements obtained before hemodynamic challenges, the mean COED was 5.7 ± 1.6 L/min and mean COPC was 4.5 ± 1.3 L/min (P < 0.01). The difference between paired measurements of COED and COPC was 1.1 ± 1.6 L/min (Fig. 2), and the percentage error was 41%. When analysis was limited to the 88 pairs of CO measurements obtained after hemodynamic challenges, the mean COED was 5.3 ± 2.0 L/min and mean COPC was 6.2 ± 1.8 L/min (P < 0.01). The difference between paired measurements of COED and COPC was −0.94 ± 2.14 L/min (Fig. 2), and the percentage error was 79% (mean percentage error was 101% after phenylephrine, 74% after ephedrine, and 49% after preload increase).

Figure 2
Figure 2:
Agreement between cardiac outputs measured by esophageal Doppler and Vigileo-FloTrac based on Bland–Altman analysis. A, Pooled data (pre- and posthemodynamic challenges). B, Prehemodynamic challenge (prephenylephrine, pre-ephedrine, and reverse Trendelenburg values). C, Posthemodynamic challenge (postphenylephrine, postephedrine, and Trendelenburg values). COED = cardiac output by esophageal Doppler; COFT = cardiac output by Vigileo-FloTrac.

Hemodynamic variables are reported in Table 1. All 3 challenges significantly increased MAP. Overall, we found no statistically significant relationship between percentage change in MAP and percentage changes in COED induced by phenylephrine, ephedrine, and preload increase (r2 = 0.06; P = 0.46), whereas we found a statistically significant relationship between percentage change in MAP and percentage changes in COPC induced by phenylephrine, ephedrine, and preload increase (r2 = 0.11; P = 0.02).

Table 1
Table 1:
Summarized Physiological Data During Each Intervention

When we studied trending abilities of COPC against COED, we found that changes in CO induced by phenylephrine were 23% concordant, changes in CO induced by ephedrine were 69% concordant, and changes in CO induced by preload increase were 96% concordant (Fig. 3).

Figure 3
Figure 3:
Trending ability of Vigileo-FloTrac against esophageal Doppler based on 4-quadrant concordance analysis. ΔCO = change in cardiac output (postintervention minus preintervention).


This study is the first to evaluate the third-generation Vigileo-FloTrac system and to compare COPC with COED in anesthetized patients subjected to common hemodynamic challenges (phenylephrine, ephedrine, and increased preload). COPC and COED demonstrate opposite trends after phenylephrine administration. This may suggest that the third-generation Vigileo software is still impacted by acute changes in vasomotor tone. In comparison, concordance between the esophageal Doppler and Vigileo-FloTrac was acceptable (>60%) after ephedrine treatment and good (>90%) after preload increase. This study emphasizes the limit of the pulse contour analysis on the basis of the third-generation Vigileo-FloTrac system in measuring CO during acute changes in vasomotor tone. Consequently, clinicians should be aware that when conducting goal-directed therapy using this device, acute changes in vasomotor tone affect its accuracy.

In a study published in 2009, Chatti et al. compared the first 2 versions of the Vigileo-FloTrac to esophageal Doppler.20 The authors concluded that the precision of stroke volume estimation using Vigileo-FloTrac was improved with the second version of the software (1.07), but remained insufficient to allow replacement of the reference technique (esophageal Doppler) in the populations studied (critical care patients and surgical patients).20 However, given the fact that there is still a lack of consensus in terms of the “gold standard” for absolute CO measurement in humans, a conclusion regarding the accuracy of any device to measure CO in comparison with esophageal Doppler cannot be definitive. Esophageal Doppler measures the flow velocity in the descending aorta, and its accuracy can also be affected by several variables such as changes in aortic diameter.21 However, its ability to track changes in CO reliably13 and to guide fluid management has been demonstrated in multiple studies.5 Moreover, esophageal Doppler is a beat-to-beat monitor allowing detection of rapid and transient changes in CO. For this reason, we chose esophageal Doppler for this comparison study because thermodilution, which requires a significant averaging time, may not be able to detect rapid changes in CO.

Statistical tools used to assess agreement between CO monitors have been extensively discussed during the past 10 years. Recent studies suggest that a method that can evaluate a CO monitor's ability in trending the change in CO is needed because an accurate absolute value is difficult to determine (and methodology varies considerably). This is especially true if these monitors are meant to be used for CO optimization and goal-directed fluid management.13,2226 A recent meta-analysis by Peyton and Chong assessed the accuracy of minimally invasive methods for CO measurements in comparison with thermodilution and found that the percentage error for these 4 methods was between 41.3% and 44.5%.26 They concluded that none of the 4 methods they evaluated has achieved acceptable agreement with bolus thermodilution (30% percentage error).19 Subsequently, it was suggested that the appropriateness of this arbitrary limit (30% percentage error) in clinical practice should be reassessed.26 In this study, we found similar agreements and percentage errors (prehemodynamic intervention data) to those published by Peyton and Chong. In addition, we studied the ability of Vigileo-FloTrac and esophageal Doppler to track changes in CO induced by phenylephrine, ephedrine, and increased preload (via whole-body tilting), all of which are commonly encountered in clinical practice.

In this study, phenylephrine induced opposite changes in CO as measured by esophageal Doppler and Vigileo-FloTrac. Phenylephrine consistently decreased COED while it consistently increased COPC. A similar observation has been described with norepinephrine (from 2.6 mcg/min to 6.6 mcg/min8) in studies comparing COPC with thermodilution or transpulmonary thermodilution.810 The methodological limits of those studies have been discussed in the introduction paragraphs. Our results clearly demonstrate that phenylephrine, a pure α1-agonist vasoconstrictor, induces opposite changes in COPC and COED. By inducing a rapid and transient vasoconstriction, phenylephrine is responsible for an increase in left ventricular afterload on one side (potentially inducing a decrease in CO), and on the other side it induces a venous constraint that may induce an increase in venous return (potentially inducing an increase in CO). Even though the effects of phenylephrine on cardiac afterload and preload are not totally clear, most studies thus far have found a decrease in CO after phenylephrine administration, suggesting that esophageal Doppler is more accurate than is pulse contour analysis in this setting.27,28 This discrepancy deserves further exploration. In contrast, we found that increased preload (via whole-body tilting) induced very similar changes in COED and COPC (96% concordance), suggesting that COPC is behaving properly when vascular compliance is constant. This high concordance may explain why clinical studies found a positive impact of goal-directed fluid management using both Vigileo-FloTrac and esophageal Doppler devices, even though their agreement on absolute CO values is poor.1,4 Our study also cautions that the use of the Vigileo system for fluid optimization in clinical settings should consider the fact that vasoconstrictors impair its trending abilities.

Study Limitations

Esophageal Doppler does not allow aortic diameter measurement, which may be a possible limitation in our study. The inability to measure aortic diameter could theoretically impair the esophageal Doppler's ability to accurately track CO changes induced by intravascular volume expansion21 or vasopressor administration. Vasoconstriction could potentially affect the esophageal Doppler's accuracy because of its impact on aortic diameter. However, it is more likely that phenylephrine could impact the radial artery compliance, which is critical to the CO-measuring methods based on pulse contour analysis. This fact, combined with phenylephrine's obvious ability to increase arterial blood pressure, make us speculate that this is responsible for the erroneous values reported by the FloTrac after phenylephrine administration. The new-generation software is not able to detect short-term changes in systemic vascular resistances and to discriminate between changes in arterial pressure waveform induced by a change in stroke volume or by a change in arterial compliance. Future studies are warranted to address this concern. For this purpose, studies conducted in the cardiac surgery setting using an aortic flowprobe would be of major interest. Last, we used whole-body tilting instead of intravascular volume expansion (used in other studies) to induce changes in preload (as demonstrated by the increase in flow time corrected and the decrease in stroke volume variation; Table 1), but preload cannot be quantified in either method or compared with other studies.


Third-generation Vigileo-FloTrac's ability in tracking changes in CO is profoundly affected by phenylephrine-induced change in vasomotor tone, and the software enhancement does not seem to improve the ability of this device to measure CO adequately when arterial compliance is modified. However, even though the concordance of the COs measured with esophageal Doppler and Vigileo-FloTrac was poor after phenylephrine administration, it was acceptable after ephedrine administration and good after preload increase. When using the third-generation Vigileo-FloTrac for perioperative fluid optimization, one must be aware that vasopressors impact the ability of this device to accurately track changes in CO. This suggests that the method adopted by the third-generation Vigileo-FloTrac still does not effectively compensate for acute changes in arterial vasomotor tone.


Name: Lingzhong Meng, MD.

Attestation: Lingzhong Meng participated in the study design, data acquisition and analysis, manuscript drafting, and final approval of the manuscript.

Conflict of Interest: Lingzhong Meng has no conflict of interest to report.

Name: Nam Phuong Tran, BS.

Attestation: Nam Phuong Tran participated in data acquisition and analysis, manuscript drafting, and final approval of the manuscript.

Conflict of Interest: Nam Phuong Tran has no conflict of interest to report.

Name: Brenton S. Alexander, BS.

Attestation: Alexander Brenton participated in data acquisition and analysis, manuscript drafting, and final approval of the manuscript.

Conflict of Interest: Alexander Brenton has no conflict of interest to report.

Name: Kathleen Laning, BS.

Attestation: Kathleen Laning participated in data acquisition and analysis, manuscript drafting, and final approval of the manuscript.

Conflict of Interest: Kathleen Laning has no conflict of interest to report.

Name: Guo Chen, MD.

Attestation: Guo Chen participated in data acquisition and analysis, manuscript drafting, and final approval of the manuscript.

Conflict of Interest: Guo Chen has no conflict of interest to report.

Name: Zeev N. Kain, MD, MBA.

Attestation: Zeev Kain participated in manuscript drafting and final approval of the manuscript.

Conflict of Interest: Zeev Kain has no conflict of interest to report.

Name: Maxime Cannesson, MD, PhD.

Attestation: Maxime Cannesson participated in the study design, data acquisition and analysis, manuscript drafting, and final approval of the manuscript.

Conflict of Interest: Maxime Cannesson is a consultant for Edwards Lifesciences, Masimo Corp., Covidien, ConMed.


Special thanks go to Debra E. Morrison, MD (Professor, Department of Anesthesiology and Perioperative Care, University of California, Irvine, Irvine, CA) for her insightful discussions.


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It would not be an understatement to say that the Foundation for Anesthesia Education and Research (FAER) Medical Student Fellowship has been career changing. In many ways, FAER has been a crystal ball that has offered me glimpses of my ideal medical career: taking care of patients on an individual basis as well as through active academic research. The FAER Fellowship provided me with a research stipend, the opportunity to present at the 2010 ASA Annual Meeting, and more important, the opportunity to explore the field of anesthesiology. During my fellowship, I was able to help with various projects that used the most up-to-date statistical analyses in the evaluation of new technologies, improved upon the computation of stroke volume variation as an indicator of fluid responsiveness, explored the relationship between ventilation and stroke volume variation, monitored cerebral bloodflow using near-infrared spectroscopy, and assessed a new cardiac output monitor for the setting of the operating room. I have participated in other research projects, but this was the first time I was able to directly interact with patients in the perioperative setting as well as observe the benefits of research on patient care decision-making in front of me in real time. FAER's support enabled me to work on many clinical research projects in one summer; this support also equipped my medical student 1.5 self (during the summer between my first and second years of medical school) with the confidence to explore the operating room and intensive care unit with purpose. Interacting with a team of incredibly knowledgeable researchers lead by Dr. Cannesson in the Department of Anesthesiology and Perioperative Care at the University of California, Irvine, enabled me to ask questions of “how” and look at the field in new perspective. For this invaluable experience, I wish to wholeheartedly thank the Foundation for Anesthesia Education and Research.

© 2011 International Anesthesia Research Society