Noninvasive and Continuous Fluid Responsiveness Monitoring with Pleth Variability Index (PVI)
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Transcript of Noninvasive and Continuous Fluid Responsiveness Monitoring with Pleth Variability Index (PVI)
Noninvasive and Continuous Fluid Responsiveness Monitoring
with Pleth Variability Index (PVI)
PVI Overview
• Physiology
• Fluid administration challenges
• PVI method
• PVI clinical evidence
Physiology Background• Oxygen delivery components
• Cardiac output x oxygen saturation x hemoglobin
• Cardiac output components• Stroke volume
• Preload • Afterload (Systemic Vascular Resistance)• Contractility
• Heart rate
• Primary methods to increase cardiac output• Increase preload (volume expanders)• Increase contractility (inotropes)
• Decrease afterload (vasodilators)
• Key point• Administering volume may increase intravascular volume and
preload but not stroke volume and cardiac output
Preload
Stroke Volume
00
Frank-Starling RelationshipFrank-Starling Relationship
1 Perel A. Anesth Analg. 2008; 106 (4):1031-33 2 Bundgaard-Nielsen M et al. Acta Anaesthesiol Scand. 2007; 51(3):331-403 Michard F et al. Chest. 2002; 121(6):2000-08 4 Joshi G et al. Anesth Analg. 2005; 101:601-5
Fluid Administration Challenges
• Fluid administration is critical to optimizing oxygen delivery by optimizing cardiac output 1
• Unnecessary fluid administration may be harmful2
• Traditional methods to guide fluid administration often fail to predict fluid responsiveness• Accurate only 50-60% of time 3
• Newer dynamic methods that can predict fluid responsiveness are invasive, complex, and/or costly 4
• Many patients are not candidates for this level of monitoring
Pleth Variability Index (PVI)
• Masimo PVI is clinically proven to help clinicians assess fluid responsiveness and improve fluid management to reduce patient risk.1,2
• Once your Masimo Pulse CO-Oximeter is enabled with PVI-monitoring capability, PVI is automatically displayed for every patient receiving pulse oximetry monitoring
1 Cannesson M et al. Br J Anaesth. 2008;101(2):200-6. 2 Forget P et al. Anesth & Anal. 2010;111(4):910-4.
Pulse Pressure Variation and Changes in PPW During Ventilation
Ventilatory Cycle
Adapted from: Cannesson M et al
PPWmax
PPWmin
Arterial Pulse Pressure Variation
PPmax- PPmin
(PPmax + PPmin) ÷ 2
ΔPP =
Pleth Waveform Variation
PPWmax – PPWmin
(PPWmax + PPWmin) ÷ 2ΔPPW =
• Automated measurement• Changes in plethysmographic waveform amplitude over the
respiratory cycle• PVI is a percentage from 1 to 100%:
• 1 - no pleth variability • 100 - maximum pleth variability
PVI Calculation
2011 Radical-7
Preload
Stroke Volume
00
Higher PVI = More likely to respond to fluid administration24 %
10 % Lower PVI = Less likely to respond
to fluid administration
PVI to Help Clinicians Optimize Preload / Cardiac Output
Maxime Cannesson, MD, PhD
PVI to Help Clinicians Assess Fluid Responsiveness During Surgery: Similar to Arterial Pulse Pressure /
Superior to CI, PCWP, CVP
Adapted from Cannesson M. et. al. Br J Anesth 2008;101(2):200-206
PVI to Help Clinicians Assess Fluid Responsiveness During Surgery:Similar to Stroke Volume Variation / Superior to CVP
Zimmermann M, et al. Eur J Anaesthesiol. 2010;27(66):555-561.
CO
PPV
PVI
PVI to Assess Fluid Responsiveness in the ICUSimilar to Pulse Pressure Variation / Superior to Cardiac
Output
Loupec T et al. Crit Care Med 2011 Vol. 39, No. 2
PVI to Help Clinicians Predict Hypotension During Surgery
Tsuchiya M et al. Acta Anaesthesiol Scand. 2010.
PVI to Help Clinicians Predict Hemodynamic Instability by PEEP
Desebbe O et al. Anesth Analg 2010;110:792–798.
PVI to Help Clinicians Improve Fluid Management and Reduce Patient Risk
Forget P et al. Anesth Analg 2010.
Overall Conclusions: Clinical Utility of PVI
• Fluid administration is critical to optimizing patient status• Traditional methods to guide fluid administration are not
sensitive or specific 1
• Newer methods to improve fluid administration may improve patient outcomes but are impractical, invasive, or costly 2
• PVI is noninvasive and proven to predict fluid responsiveness in mechanically ventilated patients in the OR and ICU 3,4
• PVI improves fluid management and reduces patient risk as evidenced by lower lactate levels 5
1 Michard F, Teboul JL. Chest. 2002 Jun;121(6):2000-8. 2 Joshi G. et al. Anesth Analg. 2005; 101:601. 3 Cannesson M et al. Br J Anaesth. 2008 Aug;101(2):200-6. 4 Feissel M et al. Critical Care. 2009;13(1):P219. 5 Forget P et.al. Critical Care. 2009; 13(1):P204.
Reference Slides
Cannesson M et al. Br J Anaesth. 2008 Aug;101(2):200-6
PVI to Assess Fluid Responsiveness During Surgery: Summary
• Methods• 25 surgical patients under general anesthesia• Recorded CVP, PCWP, cardiac index, delta PP, PVI
• Before and after volume expansion (500 ml of hetastarch 6%)• Fluid responsiveness was defined >15% increase in cardiac index
• Results• Response to volume expansion
• Cardiac index increase from 2.0 to 2.5 l/min/m2
• PVI decrease of 14 to 9• PVI >14% before volume expansion
• Discriminated between responders and non-responders with 81% sensitivity and 100% specificity
• Significant relationship between PVI before volume expansion and change in cardiac index after volume expansion (R=0.67; P<0.01)
• Conclusion• PVI can predict fluid responsiveness non-invasively in mechanically
ventilated patients during general anesthesia
• Method• 20 patients scheduled for elective major abdominal surgery• After induction of anesthesia, all hemodynamic variables were recorded
immediately before (T1) and subsequent to volume replacement (T2) by infusion
• Results• The volume-induced increase in SVI was at least 15% in 15 patients
(responders) and less than 15% in five patients (non-responders).• Baseline SVV correlated significantly with changes in SVI as did baseline
PVI whereas baseline values of central venous pressure showed no correlation to DSVI
• No significant difference between the area under the receiver operating characteristic curve for SVV (0.993) and PVI (0.973)
• The best threshold values to predict fluid responsiveness were more than 11% for SVV and more than 9.5% for PVI
• Conclusion• SVV and PVI can serve as valid indicators of fluid responsiveness in
mechanically ventilated patients undergoing major surgery
Zimmermann M, et al. Eur J Anaesthesiol. 2010;27(66):555-561.
PVI to Help Clinicians Assess Fluid Responsiveness During Surgery: Summary
• Method• Forty mechanically ventilated patients with circulatory insufficiency • Fluid challenge with 500 mL of 130/0.4 hydroxyethyl-starch if
respiratory variations in arterial pulse pressure were >13% or with passive leg raising if variations in arterial pulse pressure were <13%
• Results• 21 were responders and 19 were non-responders.• Differences in responders vs. non-responders
• PVI 28 + 13% vs. 11 + 4% (p<0.05)
• Arterial pulse pressure variation 22 + 11% vs. 5 + 2% (p<0.05)• PVI correlation with change in cardiac output after fluid challenge
(0.72, p<0.0001)• Values at baseline were significantly higher in responders than in
non-responders• Conclusion
• PVI can predict fluid responsiveness noninvasively in intensive care unit patients under mechanical ventilation
PVI to Assess Fluid Responsiveness in the ICU: Summary
Loupec T et al. Crit Care Med 2011 Vol. 39, No. 2
PVI to Help Clinicians Predict Hypotension During Surgery: Summary
• Method• Measured PVI, HR, SBP, DBP, and MAP in 76 adult healthy patients under
light sedation with fentanyl to obtain pre-anesthesia control values• Anesthesia induced w/bolus administrations of 1.8 mg/kg propofol and 0.6
mg/kg rocuronium • During the 3-min period from the start of propofol administration, HR, SBP,
DBP, and MAP were measured at 30-s intervals
• Results• HR, SBP, DBP, and MAP were significantly decreased after propofol
administration by 8.5%, 33%, 23%, and 26%, respectively, as compared with the pre-anesthesia control values
• Linear regression analysis that compared pre-anesthesia PVI with the decrease in MAP yielded an r value of -0.73
• Conclusion• PVI can predict a decrease in MAP during anesthesia induction with
propofol. Its measurement may be useful to identify high-risk patients for developing severe hypotension during anesthesia induction
Tsuchiya Acta Anaesthesiol Scand. 2010.
PVI to Help Clinicians Predict Hemodynamic Instability by PEEP: Summary
• Method• 21 mechanically ventilated and sedated patients in the
postoperativeperiod after coronary artery bypass grafting
• Patients were monitored with a pulmonary artery catheter and a pulse oximeter sensor attached to the index finger
• Cardiac index [CI], PVI, pulse pressure variation, central venous pressure) were recorded at 3 successive tidal volumes
• Results• PEEP induced changes in CI and PVI for VT of 8 and 10 mL/kg.• For VT of 8 mL/kg, a PVI threshold value of 12% during ZEEP
predicted hemodynamic instability with a sensitivity of 83% and a specificity of 80% (area under the receiver operating characteristic curve 0.806; P 0.03)
• Conclusion• PVI may be useful in automatically and noninvasively detecting the
hemodynamic effects of PEEP
Desebbe O et al. Anesth Analg 2010;110:792–798.
Optimization of Fluid Management by PVI: Summary
• Methods• Randomized Clinical Trial
• Intra-operative PVI-directed fluid management vs. standard care
• Abdominal surgery patients
• PVI Group – 41 patients• 500 ml crystalloids followed by 2ml/kg/hr• Colloids added at 250ml for PVI values between 10-13
• Control Group – 41 patients• 500 ml crystalloids followed by standard fluid management care
(challenges and CVP)
• Outcomes• Primary: Perioperative lactate levels• Secondary: Hemodynamic data and post-op complications
Forget P et al. Anesth Analg 2010.
Optimization of Fluid Management by PVI: Summary Cont.
• Results• PVI group had lower lactate levels
• Max intraoperative (1.2 vs. 1.6, p<0.05)• 24 hours (1.4 vs. 1.8, p<0.05)• 48 hours (1.2 vs. 1.4, p<0.05)
• PVI group received lower amounts of intra-operative crystalloids• 1363 vs. 1818 mL (p<0.01)
• No significant differences in morbidity or mortality
• Conclusion• PVI-based goal-directed fluid management reduced the volume
of intraoperative fluid infused and reduced intraoperative and postoperative lactate levels
Forget P et al. Anesth Analg 2010.