Non-invasive assessment of fluid responsiveness by changes in partial end-tidal CO2 pressure during a passive leg-raising maneuver

Manuel Ignacio Monge García, Anselmo Gil Cano, Manuel Gracia Romero, Rocío Monterroso Pintado, Virginia Pérez Madueño, Juan Carlos Díaz Monrové, Manuel Ignacio Monge García, Anselmo Gil Cano, Manuel Gracia Romero, Rocío Monterroso Pintado, Virginia Pérez Madueño, Juan Carlos Díaz Monrové

Abstract

Background: The passive leg-raising (PLR) maneuver provides a dynamic assessment of fluid responsiveness inducing a reversible increase in cardiac preload. Since its effects are sudden and transitory, a continuous cardiac output (CO) monitoring is required to appropriately assess the hemodynamic response of PLR. On the other hand, changes in partial end-tidal CO2 pressure (PETCO2) have been demonstrated to be tightly correlated with changes in CO during constant ventilation and stable tissue CO2 production (VCO2). In this study we tested the hypothesis that, assuming a constant VCO2 and under fixed ventilation, PETCO2 can track changes in CO induced by PLR and can be used to predict fluid responsiveness.

Methods: Thirty-seven mechanically ventilated patients with acute circulatory failure were monitored with the CardioQ-ODM esophageal Doppler. A 2-minutes PLR maneuver was performed. Fluid responsiveness was defined according to CO increase (responders ≥ 15%) after volume expansion.

Results: PLR-induced increases in CO and PETCO2 were strongly correlated (R2 = 0.79; P < 0.0001). The areas under the receiver-operating characteristics (ROC) curve for a PLR-induced increase in CO and PETCO2 (0.97 ± 0.03 SE; CI 95%: 0.85 to 0.99 and 0.94 ± 0.04 SE; CI 95%: 0.82 to 0.99; respectively) were not significantly different. An increase ≥ 5% in PETCO2 or ≥ 12% in CO during PLR predicted fluid responsiveness with a sensitivity of 90.5% (95% CI: 69.9 to 98.8%) and 95.2% (95% CI: 76.2 to 99.9%), respectively, and a specificity of 93.7% (95% CI: 69.8 to 99.8%).

Conclusion: Induced changes in PETCO2 during a PLR maneuver could be used to track changes in CO for prediction of fluid responsiveness in mechanically ventilated patients with acute circulatory failure, under fixed minute ventilation and assuming a constant tissue CO2 production.

Figures

Figure 1
Figure 1
Study protocol.
Figure 2
Figure 2
Linear regression analysis of the relationship between PLR-induced changes in cardiac output and PETCO2. PETCO2, partial end-tidal CO2 pressure; PLR, passive leg raising.
Figure 3
Figure 3
Linear regression analysis of the relationship between cardiac output changes induced by volume expansion and PLR-induced changes in cardiac output and PETCO2. CO, cardiac output; PLR, passive leg raising; VE, volume expansion.
Figure 4
Figure 4
Individual values and box-plot of studied fluid-responsiveness parameter in responders (open circles) and non-responders (closed circles). ΔCOPLR, cardiac output changes induced by passive leg raising (PLR); ΔPETCO2-PLR = PETCO2 changes induced by PLR; ΔPP-PLR, arterial pulse pressure changes induced by PLR; FTc: corrected flow time at pre-infusion time.
Figure 5
Figure 5
Comparison of receiver operating characteristics curves regarding the ability of studied fluid responsiveness parameters to discriminate responder patients (cardiac output increase ≥ 15%) and nonresponder patients after volume expansion. ΔCOPLR, cardiac output changes induced by passive leg raising (PLR); ΔPETCO2-PLR, PETCO2 changes induced by PLR; ΔPP-PLR, arterial pulse pressure changes induced by PLR; FTc: corrected flow time at pre-infusion time.

References

    1. Monnet X, Rienzo M, Osman D, Anguel N, Richard C, Pinsky MR, Teboul JL. Passive leg raising predicts fluid responsiveness in the critically ill. Crit Care Med. 2006;34:1402–1407. doi: 10.1097/01.CCM.0000215453.11735.06.
    1. Maizel J, Airapetian N, Lorne E, Tribouilloy C, Massy Z, Slama M. Diagnosis of central hypovolemia by using passive leg raising. Intensive Care Med. 2007;33:1133–1138. doi: 10.1007/s00134-007-0642-y.
    1. Lamia B, Ochagavia A, Monnet X, Chemla D, Richard C, Teboul JL. Echocardiographic prediction of volume responsiveness in critically ill patients with spontaneously breathing activity. Intensive Care Med. 2007;33:1125–1132. doi: 10.1007/s00134-007-0646-7.
    1. Monnet X, Teboul JL. Passive leg raising: keep it easy! Intensive Care Med. 2010;36:1445. doi: 10.1007/s00134-010-1900-y.
    1. De Backer D. Can passive leg raising be used to guide fluid administration? Crit Care. 2006;10:170. doi: 10.1186/cc5081.
    1. Monnet X, Teboul JL. Passive leg raising. Intensive Care Med. 2008;34:659–663. doi: 10.1007/s00134-008-0994-y.
    1. Preau S, Saulnier F, Dewavrin F, Durocher A, Chagnon JL. Passive leg raising is predictive of fluid responsiveness in spontaneously breathing patients with severe sepsis or acute pancreatitis. Crit Care Med. 2010;38:819–825. doi: 10.1097/CCM.0b013e3181c8fe7a.
    1. Biais M, Vidil L, Sarrabay P, Cottenceau V, Revel P, Sztark F. Changes in stroke volume induced by passive leg raising in spontaneously breathing patients: comparison between echocardiography and Vigileo/FloTrac device. Crit Care. 2009;13:R195. doi: 10.1186/cc8195.
    1. Jabot J, Teboul JL, Richard C, Monnet X. Passive leg raising for predicting fluid responsiveness: importance of the postural change. Intensive Care Med. 2009;35:85–90. doi: 10.1007/s00134-008-1293-3.
    1. Benomar B, Ouattara A, Estagnasie P, Brusset A, Squara P. Fluid responsiveness predicted by noninvasive bioreactance-based passive leg raise test. Intensive Care Med. 2010;36:1875–1881. doi: 10.1007/s00134-010-1990-6.
    1. Lafanechere A, Pene F, Goulenok C, Delahaye A, Mallet V, Choukroun G, Chiche JD, Mira JP, Cariou A. Changes in aortic blood flow induced by passive leg raising predict fluid responsiveness in critically ill patients. Crit Care. 2006;10:R132. doi: 10.1186/cc5044.
    1. Mahjoub Y, Touzeau J, Airapetian N, Lorne E, Hijazi M, Zogheib E, Tinturier F, Slama M, Dupont H. The passive leg-raising maneuver cannot accurately predict fluid responsiveness in patients with intra-abdominal hypertension. Crit Care Med. 2010;38:1824–1829. doi: 10.1097/CCM.0b013e3181eb3c21.
    1. Leigh MD, Jenkins LC, Belton MK, Lewis GB Jr. Continuous alveolar carbon dioxide analysis as a monitor of pulmonary blood flow. Anesthesiology. 1957;18:878–882. doi: 10.1097/00000542-195711000-00009.
    1. Weil MH, Bisera J, Trevino RP, Rackow EC. Cardiac output and end-tidal carbon dioxide. Crit Care Med. 1985;13:907–909. doi: 10.1097/00003246-198511000-00011.
    1. Kolar M, Krizmaric M, Klemen P, Grmec S. Partial pressure of end-tidal carbon dioxide successful predicts cardiopulmonary resuscitation in the field: a prospective observational study. Crit Care. 2008;12:R115. doi: 10.1186/cc7009.
    1. Pernat A, Weil MH, Sun S, Tang W. Stroke volumes and end-tidal carbon dioxide generated by precordial compression during ventricular fibrillation. Crit Care Med. 2003;31:1819–1823. doi: 10.1097/01.CCM.0000069538.12447.82.
    1. West JB. State of the art: ventilation-perfusion relationships. Am Rev Respir Dis. 1977;116:919–943.
    1. Ornato JP, Garnett AR, Glauser FL. Relationship between cardiac output and the end-tidal carbon dioxide tension. Ann Emerg Med. 1990;19:1104–1106. doi: 10.1016/S0196-0644(05)81512-4.
    1. Dubin A, Silva CGC, Valli J, Faruna O, Estenssoro E, Mordujovich P. End-tidal CO2 pressure in the monitoring of cardiac output during canine hemorrhagic shock. J Crit Care. 1990;5:42–46. doi: 10.1016/0883-9441(90)90008-W.
    1. Jin X, Weil MH, Tang W, Povoas H, Pernat A, Xie J, Bisera J. End-tidal carbon dioxide as a noninvasive indicator of cardiac index during circulatory shock. Crit Care Med. 2000;28:2415–2419.
    1. Dubin A, Murias G, Estenssoro E, Canales H, Sottile P, Badie J, Baran M, Rossi S, Laporte M, Palizas F, Giampieri J, Mediavilla D, Vacca E, Botta D. End-tidal CO2 pressure determinants during hemorrhagic shock. Intensive Care Med. 2000;26:1619–1623. doi: 10.1007/s001340000669.
    1. Isserles SA, Breen PH. Can changes in end-tidal PCO2 measure changes in cardiac output? Anesth Analg. 1991;73:808–814.
    1. Guzman JA, Lacoma FJ, Najar A, Kruse JA. End-tidal partial pressure of carbon dioxide as a noninvasive indicator of systemic oxygen supply dependency during hemorrhagic shock and resuscitation. Shock. 1997;8:427–431. doi: 10.1097/00024382-199712000-00006.
    1. Idris AH, Staples ED, O'Brien DJ, Melker RJ, Rush WJ, Del Duca KD, Falk JL. End-tidal carbon dioxide during extremely low cardiac output. Ann Emerg Med. 1994;23:568–572. doi: 10.1016/S0196-0644(94)70080-X.
    1. Shibutani K, Muraoka M, Shirasaki S, Kubal K, Sanchala VT, Gupte P. Do changes in end-tidal PCO2 quantitatively reflect changes in cardiac output? Anesth Analg. 1994;79:829–833.
    1. Wahba RW, Tessler MJ, Beique F, Kleiman SJ. Changes in PCO2 with acute changes in cardiac index. Can J Anaesth. 1996;43:243–245. doi: 10.1007/BF03011742.
    1. McLellan S, Walsh T, Burdess A, Lee A. Comparison between the Datex-Ohmeda M-COVX metabolic monitor and the Deltatrac II in mechanically ventilated patients. Intensive Care Med. 2002;28:870–876. doi: 10.1007/s00134-002-1323-5.
    1. Cecconi M, Rhodes A, Poloniecki J, Della Rocca G, Grounds RM. Bench-to-bedside review: the importance of the precision of the reference technique in method comparison studies--with specific reference to the measurement of cardiac output. Crit Care. 2009;13:201. doi: 10.1186/cc7129.
    1. Husted JA, Cook RJ, Farewell VT, Gladman DD. Methods for assessing responsiveness: a critical review and recommendations. J Clin Epidemiol. 2000;53:459–468. doi: 10.1016/S0895-4356(99)00206-1.
    1. Guyatt G, Walter S, Norman G. Measuring change over time: assessing the usefulness of evaluative instruments. J Chron Dis. 1987;40:171–178. doi: 10.1016/0021-9681(87)90069-5.
    1. King SL, Lim MS. The use of the oesophageal Doppler monitor in the intensive care unit. Crit Care Resusc. 2004;6:113–122.
    1. Madan AK, UyBarreta VV, Aliabadi-Wahle S, Jesperson R, Hartz RS, Flint LM, Steinberg SM. Esophageal Doppler ultrasound monitor versus pulmonary artery catheter in the hemodynamic management of critically ill surgical patients. J Trauma. 1999;46:607–611. doi: 10.1097/00005373-199904000-00008. discussion 611-602.
    1. Singer M, Allen MJ, Webb AR, Bennett ED. Effects of alterations in left ventricular filling, contractility, and systemic vascular resistance on the ascending aortic blood velocity waveform of normal subjects. Crit Care Med. 1991;19:1138–1145. doi: 10.1097/00003246-199109000-00008.
    1. Cavallaro F, Sandroni C, Marano C, La Torre G, Mannocci A, De Waure C, Bello G, Maviglia R, Antonelli M. Diagnostic accuracy of passive leg raising for prediction of fluid responsiveness in adults: systematic review and meta-analysis of clinical studies. Intensive Care Med. 2010;36:1475–1483. doi: 10.1007/s00134-010-1929-y.
    1. Michard F, Teboul JL. Predicting fluid responsiveness in ICU patients: a critical analysis of the evidence. Chest. 2002;121:2000–2008. doi: 10.1378/chest.121.6.2000.
    1. Critchley LA, Lee A, Ho AM. A critical review of the ability of continuous cardiac output monitors to measure trends in cardiac output. Anesth Analg. 2010;111:1180–1192. doi: 10.1213/ANE.0b013e3181f08a5b.
    1. Marik PE, Monnet X, Teboul JL. Hemodynamic parameters to guide fluid therapy. Ann Intensive Care. 2011;1:1. doi: 10.1186/2110-5820-1-1.
    1. Callaham M, Barton C. Prediction of outcome of cardiopulmonary resuscitation from end-tidal carbon dioxide concentration. Crit Care Med. 1990;18:358–362. doi: 10.1097/00003246-199004000-00002.
    1. Tyburski JG, Collinge JD, Wilson RF, Carlin AM, Albaran RG, Steffes CP. End-tidal CO2-derived values during emergency trauma surgery correlated with outcome: a prospective study. J Trauma. 2002;53:738–743. doi: 10.1097/00005373-200210000-00020.
    1. Lucangelo U, Blanch L. Dead space. Intensive Care Med. 2004;30:576–579. doi: 10.1007/s00134-004-2194-8.
    1. Fougeres E, Teboul JL, Richard C, Osman D, Chemla D, Monnet X. Hemodynamic impact of a positive end-expiratory pressure setting in acute respiratory distress syndrome: Importance of the volume status. Crit Care Med. 2010;38:802–807. doi: 10.1097/CCM.0b013e3181c587fd.

Source: PubMed

스폰서 및 공동 작업자

건강 상태

약물 개입

3
구독하다