Devices utilizing arterial pressure waveform-based assessment of cardiac output (APCO) differ in many technological aspects, including proprietary analysis algorithms and need for calibration. We compared two such devices, LiDCOplus (version 4.0, LiDCO Ltd., UK) and Vigileo (Edwards Lifesciences, V01.10, Irvine, California, USA), to the pulmonary artery catheter thermodilution (PACTD) method of measuring cardiac output (CO) during liver transplantation (OLT) [1,2] in an institutional review board (IRB)-approved study. Our study provided an unanticipated opportunity to observe the performance of these devices during a postreperfusion cardiac arrest and resuscitation.
A 74-year-old woman with primary biliary cirrhosis underwent an OLT with piggy back technique and temporary porto-caval shunt. Haemodynamic monitors included an oximetric pulmonary artery catheter (Opticath Catheter, Hospira, Lake Forest, Illinois, USA) and arterial blood pressure (ABP) through a radial catheter and a FloTrac transducer (Edwards Lifesciences). Haemodynamic recordings and ventilatory data from a Draeger Apollo anaesthesia workstation (Draeger Medical Inc., Telford, Pennsylvania, USA) were displayed on a Philips IntelliVue 70 monitor (Philips Electronics North America Corporation, Andover, Massachusetts, USA). Vigileo was interfaced with the monitor (Philips VueLink). All data from the Philips monitor were recorded on a laptop using TrendFace data acquisition software (Version 1.03, Ixcellence GmbH, Wildau, Germany). LiDCO data were stored in the device's internal drive. LiDCO was calibrated as per manufacturer's instructions prior to induction of anaesthesia.
Internal clocks of all devices were synchronized prior to data collection.
The hepatectomy and anhepatic phase were marked by haemodynamic stability and estimated blood loss of about 1500 ml. Before reperfusion, COs were PACTD 5.70 l min−1, LiDCO 6.15 l min−1 and Vigileo 3.96 l min−1. About 1 min after reperfusion hypotension developed, then bradycardia, progressing to cardiac arrest. After about 23 min of resuscitation, sinus rhythm and effective circulation were restored. Postrecovery COs were PACTD 3.85 l min−1, LiDCO 7.62 l min−1 and Vigileo 3.30 l min−1.
Figure 1 presents, top to bottom, systolic and diastolic ABP, end-tidal CO2 (EtCO2) and corresponding continuous COs displayed by Vigileo and LiDCO during approximately 34 min surrounding the reperfusion. We divided this record into four periods (P). P1 represents stable haemodynamics before reperfusion. ABP increased immediately before the reperfusion due to vasopressor administration. P2, starting immediately after reperfusion, shows rapid decline in ABP, due first to bradycardia and then to asystolic cardiac arrest. The EtCO2 decreased markedly, mirroring the drop in ABP, but remained above 15 mmHg throughout this phase. During the remainder of P2, CPR alternated with spontaneous circulation. During P3, the ABP was generated by continuous CPR. ABP was extremely low, with progressive narrowing of the pulse pressure. Again, the changes in EtCO2 paralleled the changes in ABP. P4 was marked by increasing ABP and EtCO2 secondary to the recovery of spontaneous circulation. Brief interruption of ABP tracing (arrow) was due to blood gas sampling.
Vigileo displayed an initial decrease in CO but the values never decreased below 2 l min−1, even during the asystole. For the remainder of P2, the almost constant Vigileo CO did not seem to reflect the rapidly changing ABP. During most CPR (P3), Vigileo CO ranged between 2.9 and 3.6 min−1 until it plummeted to 0, although the corresponding ABP had not changed much. The CO remained 0 for about 4 min, even as the ABP started to recover (P4). After the blood gas sampling, the rapid increase in ABP was reflected by COs as high as 10 l min−1. Vigileo CO then decreased rapidly towards the value of 4 l min−1, although ABP and EtCO2 remained high. LiDCO showed rapidly changing CO values that overall appeared to reflect changes in ABP and EtCO2. With initial hypotension (P2), LiDCO CO decreased progressively. During the asystole, LiDCO displayed COs as low as 0.5 l min−1, or displayed no values at all. During P3 and P4, LiDCO CO grossly trended with ABP and EtCO2. Of note, LiDCO recorded several relatively high COs that could not be readily correlated to ABP and EtCO2 increases.
Relationship between CO measurements by APCOs, EtCO2 and ABP (systolic, diastolic, mean and pulse pressure) was analysed using linear regression. For the entire recording, the best fit for LiDCO was with pulse pressure (R 2 0.82, P < 0.0001) and for Vigileo with systolic pressure (R 2 0.37, P < 0.0001). Although there was a significant correlation between ABP and EtCO2 (R 2 0.45, P < 0.0001), no correlation was found between either APCO monitor and EtCO2.
This report has several limitations. First, this is a single case report. Second, all ABPs and COs were based on the radial artery pressure waveform. This is important because cardiac arrest and high doses of vasopressors may result in deterioration of this waveform. However, whenever a spontaneous rhythm was restored, the waveform shape and values were plausible.
On the contrary, the abnormal arterial waveform produced by CPR, lacking recognizable peak systolic pressure and dicrotic notch, and the irregular pulse rate may have affected the performance of the two devices. Of note, unlike Vigileo, LiDCO is reportedly minimally influenced by changes in arterial waveform morphology and damping [3,4]. It is possible that femoral artery waveform would have yielded different results . Finally, we were unable to measure PACTD CO during the arrest and resuscitation. However, we can compare APCOs to the continuous EtCO2 which has been recognized as a reliable monitor of cardiac output during CPR .
This is the first comparison of the performance of two APCO monitors during cardiac arrest and resuscitation. Evidently, the two proprietary algorithms process the same haemodynamic data differently and yield quite different results. Vigileo, set at its maximal update rate of 20 s, failed to reflect rapidly changing haemodynamics. First, it displayed relatively unchanged CO for about 19 min of arrest and resuscitation. Then, it abruptly fell to 0 with little change, or even with recovery of ABP. Finally, upon recovery of haemodynamics (P4), Vigileo CO only temporarily increased, then reverted towards the prearrest values, although the increase in ABP and EtCO2 was sustained. In contrast, LiDCO estimated CO beat-to-beat and with a broader dynamic range, giving results that better correlate with ABP. However, LiDCO recorded multiple high COs not corresponding to any significant ABP variations, and omitted multiple data points.
In conclusion, in rapidly changing haemodynamics of arrest and resuscitation, the calibrated beat-to-beat device correlated with ABP and EtCO2 better than the uncalibrated device. More importantly, our concern is that Vigileo did not promptly recognize major changes in haemodynamics, such as cardiac arrest. The displayed monotonous values of COs were implausible during a prolonged period of alternating CPR and spontaneous circulation, and were potentially misleading to the clinician. The manufacturer explicitly warns that Vigileo's performance depends on a normal ABP waveform. But the fact that this monitor accepted an abnormal arterial signal without revising the displayed COs raises questions. How were the CO values during arrest and CPR – only moderately correlated to blood pressure – generated? Why does the CO dramatically decrease during spontaneous circulation when ABP and EtCO2 do not change? Are this device's signal processing function and algorithm at risk of failing in other clinical situations, as previously suggested ? As APCOs are increasingly accepted technologies, a more in-depth understanding of the performance, applicability and limitations of these novel devices, as shown by this report, is of critical importance.
The authors wish to acknowledge Ms Patty Suntrup, a Clinical Research Specialist with the Division of Clinical and Translational Research, Department of Anesthesiology, Washington University School of Medicine, for her valuable help with this study. The study was funded by the Division of Clinical and Translational Research (DOCTR) grant to I.K., ClinicalTrials.gov identifier NCT00682110, Department of Anesthesiology, Washington University School of Medicine, St Louis, MO, USA.
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