Skeletal muscle oxygen saturation does not estimate mixed venous oxygen saturation in patients with severe left heart failure and additional severe sepsis or septic shock

Matej Podbregar, Hugon Mozina, Matej Podbregar, Hugon Mozina

Abstract

Introduction: Low cardiac output states such as left heart failure are characterized by preserved oxygen extraction ratio, which is in contrast to severe sepsis. Near infrared spectroscopy (NIRS) allows noninvasive estimation of skeletal muscle tissue oxygenation (StO2). The aim of the study was to determine the relationship between StO2 and mixed venous oxygen saturation (SvO2) in patients with severe left heart failure with or without additional severe sepsis or septic shock.

Methods: Sixty-five patients with severe left heart failure due to primary heart disease were divided into two groups: groups A (n = 24) and B (n = 41) included patients without and with additional severe sepsis/septic shock, respectively. Thenar muscle StO2 was measured using NIRS in the patients and in 15 healthy volunteers.

Results: StO2 was lower in group A than in group B and in healthy volunteers (58 +/- 13%, 90 +/- 7% and 84 +/- 4%, respectively; P < 0.001). StO2 was higher in group B than in healthy volunteers (P = 0.02). In group A StO2 correlated with SvO2 (r = 0.689, P = 0.002), although StO2 overestimated SvO2 (bias -2.3%, precision 4.6%). In group A changes in StO2 correlated with changes in SvO2 (r = 0.836, P < 0.001; DeltaSvO2 = 0.84 x DeltaStO2 - 0.67). In group B important differences between these variables were observed. Plasma lactate concentrations correlated negatively with StO2 values only in group A (r = -0.522, P = 0.009; lactate = -0.104 x StO2 + 10.25).

Conclusion: Skeletal muscle StO2 does not estimate SvO2 in patients with severe left heart failure and additional severe sepsis or septic shock. However, in patients with severe left heart failure without additional severe sepsis or septic shock, StO2 values could be used to provide rapid, noninvasive estimation of SvO2; furthermore, the trend in StO2 may be considered a surrogate for the trend in SvO2.

Trial registration: ClinicalTrials.gov NCT00384644.

Figures

Figure 1
Figure 1
Correlation between skeletal muscle StO2 and SvO2. Group A includes patients with severe left heart failure without severe sepsis/septic shock, and group B includes patients with primary heart disease and additional severe sepsis/septic shock. A statistically significant correlation was found in group A (r = 0.689, P = 0.002) but not in group B (r = -0.091, P = 0.60). StO2, tissue oxygenation; SvO2, mixed venous oxygen saturation.
Figure 2
Figure 2
Agreement between SvO2 and thenar muscle StO2 in the absence of severe sepsis/septic shock. Shown are Bland and Altman plots of agreement between SvO2 and thenar muscle StO2 in patients with left heart failure without severe sepsis/septic shock (n = 24), The unbroken line indicates the mean difference (bias), and broken lines indicate 95% limits of agreement (mean ± standard deviation). StO2, tissue oxygenation; SvO2, mixed venous oxygen saturation.
Figure 3
Figure 3
Concordance between changes in SvO2 and changes in thenar muscle StO2 in the absence of severe sepsis/septic shock. Shown are changes in SvO2 and thenar muscle StO2 in 10 patients with severe left heart failure without additional severe sepsis/septic shock (group A; n = 40, r = 0.836, R2 = 0.776, P < 0.001; equation of the regression line: ΔSvO2 [%] = 0.84 × ΔStO2 [%] - 0.67). StO2, tissue oxygenation; SvO2, mixed venous oxygen saturation.

References

    1. Vincent JL, De Backer D. Oxygen transport: the oxygen delivery controversy. Intensive Care Med. 2004;30:1990–1996. doi: 10.1007/s00134-004-2384-4.
    1. Lim N, Dubois MJ, De Backer D, Vincent JL. Do all nonsurvivors of cardiogenic shock die with low cardiac index? Chest. 2003;124:1885–1891. doi: 10.1378/chest.124.5.1885.
    1. Goldman RH, Klughaupt M, Metcalf T, Spivak AP, Harrison DC. Measurement of central venous oxygen saturation in patients with myocardial infarction. Circulation. 1968;38:941–946.
    1. Kasnitz P, Druger GL, Zorra F, Simmons DH. Mixed venous oxygen tension and hyperlactemia. Survival in severe cardiopulmonary disease. JAMA. 1976;236:570–574. doi: 10.1001/jama.236.6.570.
    1. Krafft P, Steltzer H, Hiesmayr M, Klimscha W, Hammerle AF. Mixed venous oxygen saturation in critically ill septic shock patients. The role of defined events. Chest. 1993;103:900–906.
    1. Edwards JD. Oxygen transport in cardiogenic and septic shock. Crit Care Med. 1991;19:658–663.
    1. Dalen JE, Bone RC. Is it time to pull the pulmonary artery catheter? JAMA. 1996;276:916–918. doi: 10.1001/jama.276.11.916.
    1. Reinhart K, Radermacher P, Sprung CL, Phelan D, Bakker J, Steltzer H. PA catheterisation – quo vadis? Do we have to change the current practice with this monitoring device. Intensive Care Med. 1997;23:605–609. doi: 10.1007/s001340050379.
    1. Boushel R, Piantadosi CA. Near-infrared spectroscopy for monitoring muscle oxygenation. Acta Physiol Scand. 2000;168:615–622. doi: 10.1046/j.1365-201x.2000.00713.x.
    1. Wahr JA, Tremper KK, Samra S, Delpy DT. Near-infrared spectroscopy: theory and applications. J Cardiothorac Vasc Anesth. 1996;10:406–418. doi: 10.1016/S1053-0770(96)80107-8.
    1. Pareznik R, Voga G, Knezevic R, Podbregar M. Changes of muscle tissue oxygenation during stagnant ishemia in septic patients. Intensive Care Med. 2006;32:87–92. doi: 10.1007/s00134-005-2841-8.
    1. Bone RC, Balk RA, Cerra FB, Dellinger RP, Fein AM, Knaus WA, Schein RM, Sibbald WJ. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. The ACCP/SCCM Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine. Chest. 1992;101:1644–1655.
    1. Dellinger RP, Carlet JM, Masur H, Gerlach H, Calandra T, Cohen J, Gea-Banacloche J, Keh D, Marshall JC, Parker MM, et al. Surviving Sepsis Campaign guidelines for management of severe sepsis and septic shock. Intensive Care Med. 2004;30:536–555. doi: 10.1007/s00134-004-2398-y.
    1. Vincent JL, Moreno R, Takala J, Willatts S, De Medonca A, Bruining H, Reinhart CK, Suter PM, Thijs LG. The SOFA (Sepsis-related Organ Failure Assessment) score to describe organ dysfunction/failure. Intensive Care Med. 1996;22:707–710.
    1. Bland JM, Altman DG. Statistical methods for assessing agreement between two methods of clinical measurements. Lancet. 1986;21:307–310.
    1. De Blasi RA, Palmisani S, Alampi D, Mercieri M, Romao R, Collini S, Pinto G. Microvascular dysfunction and skeletal muscle oxygenation assessed by phase-modulation near-infrared spectroscopy in patients with septic shock. Intensive Care Med. 2005;31:1661–1668. doi: 10.1007/s00134-005-2822-y.
    1. Sair M, Etherington PJ, Winlove P, Ewans TW. Tissue oxygenation and perfusion in patients with systemic sepsis. Crit Care Med. 2001;29:1343–1349. doi: 10.1097/00003246-200107000-00008.
    1. Kreymann G, Grosser S, Buggisch P, Gottschall C, Matthaei S, Greten H. Oxygen consumption and resting metabolic rate in sepsis, sepsis syndrome, and septic shock. Crit Care Med. 1993;21:1012–1019. doi: 10.1097/00003246-199307000-00015.
    1. Rosser DM, Stidwill RP, Jacobson D, Singer M. Oxygen tension in the bladder epithelium increased in both high and low output endotoxemic sepsis. J Appl Physiol. 1995;79:1878–1882.
    1. Ince C, Sinaasappel M. Microcirculatory oxygenation and shunting in sepsis and shock. Crit Care Med. 1999;27:1369–1377. doi: 10.1097/00003246-199907000-00031.
    1. Brealey D, Brand M, Hargreaves I, Heales S, Land J, Smolenski R, Davies NA, Cooper CE, Singer M. Association between mitochondrial dysfunction and severity and outcome of septic shock. Lancet. 2002;360:219–223. doi: 10.1016/S0140-6736(02)09459-X.
    1. Barratt-Boyes BG, Wood EH. The oxygen saturation of blood in the venae cavae, right-heart chambers, and pulmonary vessels of healthy subjects. J Lab Clin Med. 1957;50:93–106.
    1. Cargill W, Hickam J. The oxygen consumption of the normal and diseased human kidney. J Clin Invest. 1949;28:526.
    1. Scheinman MM, Brown MA, Rapaport E. Critical assessment of use of central venous oxygen saturation as a mirror of mixed venous oxygen in severely ill cardiac patients. Circulation. 1969;40:165–172.
    1. Lee J, Wright F, Barber R, Stanley L. Central venous oxygen saturation in shock: a study in man. Anesthesiology. 1972;36:472–478. doi: 10.1097/00000542-197205000-00012.
    1. Edwards JD, Mayall RM. Importance of the sampling site for measurement of mixed venous oxygen saturation in shock. Crit Care Med. 1998;26:1356–1360. doi: 10.1097/00003246-199808000-00020.
    1. Martin C, Auffray JP, Badetti C, Perrin G, Papazian L, Gouin F. Monitoring of central venous oxygen saturation versus mixed venous oxygen saturation in critically ill patients. Intensive Care Med. 1992;18:101–104. doi: 10.1007/BF01705041.
    1. Forsyth R, Hoffbrand B, Melmon K. Re-distribution of cardiac output during hemorrhage in the unanesthetized monkey. Circ Res. 1970;27:311.
    1. Boekstegers P, Weidenhoefer St, Pilz G, Werdan K. Peripheral oxygen availability within skeletal muscle in sepsis and septic shock: comparison to limited infection and cardiogenic shock. Infection. 1991;19:317–323. doi: 10.1007/BF01645355.
    1. Parker MM, Parrillo JE. Septic shock: hemodynamics and pathogenesis. JAMA. 1983;250:3324–3327. doi: 10.1001/jama.250.24.3324.
    1. Boekstegers P, Weidenhoefer , Kapsner T, Werdan K. Skeletal muscle partial pressure of oxygen in patients with sepsis. Crit Care Med. 1994;22:640–650. doi: 10.1097/00003246-199404000-00021.
    1. Mancini DM, Bolinger L, Li H, Kendrick K, Chance B, Wilson JR. Validation of near-infrared spectroscopy in humans. J Appl Physiol. 1994;77:2740–2747.
    1. Taylor JH, Beilman GJ, Conroy MJ, Mulier KE, Dean Myers Gruessner A, Hammer BE. Tissue energetics as measured by nuclear magnetic resonance spectroscopy during hemorrhagic shock. Shock. 2004;21:58–64. doi: 10.1097/01.shk.0000101674.49265.93.
    1. Clavijo-Alvarez JA, Sims CA, Pinsky MR, Puyana JC. Monitoring skeletal muscle and subcutaneous tissue acid-base status and oxygenation during hemorrhagic shock and resuscitation. Shock. 2005;24:270–275. doi: 10.1097/01.shk.0000172364.89128.28.
    1. Crookes BA, Cohn SM, Bloch S, Amortegui J, Manning R, Li P, Proctor MS, Hallal AH, Blackbourne LH, Benjamin R, et al. Can near-infrared spectroscopy identify the severity of shock in trauma patients? J Trauma. 2005;58:806–816.
    1. McKinley BA, Marvin RG, Cocanour CS, Moore FA. Tissue hemoglobin O2 saturation during resuscitation of traumatic shock monitored using near infrared spectroscopy. J Trauma. 2000;48:637–642.
    1. Franceschini MA, Boas DA, Zourabian A, Diamond SG, Nadgir S, Lin DW, Moore JB, Fantini S. Near-infrared spiroxymetry: noninvasive measurements of venous saturation in piglets and human subjects. J Appl Physiol. 2002;92:372–384.
    1. Sakr Y, Vincent JL, Reinhart K, Payen D, Wiedermann CJ, Zandstra DF, Sprung CL. Use of the pulmonary artery catheter is not associated with worse outcome in the ICU. Chest. 2005;128:2722–2731. doi: 10.1378/chest.128.4.2722.
    1. Verdant C, De Backer D. How monitoring of the microcirculation may help us at the bedside? Curr Opin Crit Care. 2005;11:240–244. doi: 10.1097/01.ccx.0000158849.94225.11.
    1. Rivers EP, McIntyre L, Morro DC, Rivers KK. Early and innovative interventions for severe sepsis and septic shock: taking advantage of a window of opportunity. CMAJ. 2005;173:1054–1065.

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