Near-infrared spectroscopy during stagnant ischemia estimates central venous oxygen saturation and mixed venous oxygen saturation discrepancy in patients with severe left heart failure and additional sepsis/septic shock

Hugo Mozina, Matej Podbregar, Hugo Mozina, Matej Podbregar

Abstract

Introduction: Discrepancies of 5-24% between superior vena cava oxygen saturation (ScvO2) and mixed venous oxygen saturation (SvO2) have been reported in patients with severe heart failure. Thenar muscle tissue oxygenation (StO2) measured with near-infrared spectroscopy (NIRS) during arterial occlusion testing decreases slower in sepsis/septic shock patients (lower StO2 deoxygenation rate). The StO2 deoxygenation rate is influenced by dobutamine. The aim of this study was to determine the relationship between the StO2 deoxygenation rate and the ScvO2-SvO2 discrepancy in patients with severe left heart failure and additional sepsis/septic shock treated with or without dobutamine.

Methods: Fifty-two patients with severe left heart failure due to primary heart disease with additional severe sepsis/septic shock were included. SvO2 and ScvO2 were compared to the thenar muscle StO2 before and during arterial occlusion.

Results: SvO2 correlated significantly with ScvO2 (Pearson correlation 0.659, P = 0.001), however, Bland Altman analysis showed a clinically important difference between both variables (ScvO2-SvO2 mean 72 +/- 8%, ScvO2-SvO2 difference 9.4 +/- 7.5%). The ScvO2-SvO2 difference correlated with plasma lactate (Pearson correlation 0.400, P = 0.003) and the StO2 deoxygenation rate (Pearson correlation 0.651, P = 0.001). In the group of patients treated with dobutamine, the ScvO2-SvO2 difference correlated with plasma lactate (Pearson correlation 0.389, P = 0.011) and the StO2 deoxygenation rate (Pearson correlation 0.777, P = 0.0001).

Conclusions: In patients with severe heart failure with additional severe sepsis/septic shock the ScvO2-SvO2 discrepancy presents a clinical problem. In these patients the skeletal muscle StO2 deoxygenation rate is inversely proportional to the difference between ScvO2 and SvO2; dobutamine does not influence this relationship. When using ScvO2 as a treatment goal, the NIRS measurement may prove to be a useful non-invasive diagnostic test to uncover patients with a normal ScvO2 but potentially an abnormally low SvO2.

Trial registration: NCT00384644 ClinicalTrials.Gov.

Figures

Figure 1
Figure 1
Correlation between mixed venous (SvO2) and central venous saturation (ScvO2) in patients with heart failure and additional sepsis/septic shock. Pearson correlation 0.659, P = 0.001.
Figure 2
Figure 2
Bland Altman analysis of clinically important difference between mixed venous (SvO2) and central venous saturation (ScvO2) in patients with heart failure and additional sepsis/septic shock. ScvO2-SvO2 mean 72 ± 8%, Scv-Svo2 difference 9.4 ± 7.5%.
Figure 3
Figure 3
Correlation of mixed venous (SvO2) and central venous saturation (ScvO2) difference with plasma lactate (mmol/L). Pearson correlation 0.400, P = 0.003.
Figure 4
Figure 4
Correlation of central venous saturation (ScvO2) central venous saturation (SvO2) difference with skeletal muscle tissue oxygenation (StO2) deceleration rate. Pearson correlation 0.651, P = 0.001.

References

    1. Rivers E, Nguyen B, Havstad S, Ressler J, Muzzin A, Knoblich B, Peterson E, Tomlanovich M. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001;345:1368–1377. doi: 10.1056/NEJMoa010307.
    1. Reinhart K, Kuhn HJ, Hartog C, Bredle DL. Continuous central venous and pulmonary artery oxygen saturation monitoring in the critically ill. Intensive Care Med. 2004;30:1572–1578. doi: 10.1007/s00134-004-2337-y.
    1. Barratt-Boyes Bg, Wood EH. The oxygen saturation of blood in vena cava, right heart chambers and pulmonary vessels of healthy subjects. J Lab Clin Med. 1957;50:93–106.
    1. Lee J, Wright F, Barber R. Central venous oxygen saturation in shock: a study in men. Anesthesiology. 1972;36:472–478. doi: 10.1097/00000542-197205000-00012.
    1. Scheinman MM, Brown MA, Rapaport E. Critical assesment of use of central venous oxygen saturation as a mirror of mixed venous oxygen saturation in severly ill cardiac patients. Circulation. 1969;40:165–172.
    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. Podbregar M, Mozina H. 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. Crit Care. 2007;11:R6. doi: 10.1186/cc5153.
    1. Reinhart K, Rudolph T, Bredle DL, Hannemann L, Cain SM. Comparison of central-venous to mixed-venous oxygen saturation during changes in oxygen supply/demand. Chest. 1989;95:1216–1221. doi: 10.1378/chest.95.6.1216.
    1. Pareznik R, Knezevic R, Voga G, Podbregar M. Changes in muscle tissue oxygenation during stagnant ischemia in septic patients. Intensive Care Med. 2006;32:87–92. doi: 10.1007/s00134-005-2841-8.
    1. Nanas S, Gerovasili V, Dimopoulos S, Pierrakos C, Kourtidou S, Kaldara E, Sarafoglou S, Venetsanakos J, Roussos C, Nanas J, Anastasiou-Nana M. Inotropic agents improve the peripheral microcirculation of patients with end-stage chronic heart failure. J Card Fail. 2008;14:400–406. doi: 10.1016/j.cardfail.2008.02.001.
    1. Rivers E, Nguyen B, Havstad S, Ressler J, Muzzin A, Knoblich B, Peterson E, Tomlanovich M. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001;345:1368–1377. doi: 10.1056/NEJMoa010307.
    1. Dellinger RP, Carlet JM, Masur H, Gerlach H, Calandra T, Cohen J, Gea-Banacloche J, Keh D, Marshall JC, Parker MM, Ramsay G, Zimmerman JL, Vincent JL, Levy MM. 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. 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. doi: 10.1378/chest.101.6.1644.
    1. Strahovnik I, Podbregar M. Measurment of skeletal muscle tissue oxygenation in critically ill. Signa Vitae. 2008;3:43–50.
    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. doi: 10.1007/BF01709751.
    1. Bland JM, Altman DG. Statistical methods for assessing agreement between two methods of clinical measurements. Lancet. 1986;1:307–310.
    1. Mesquida J, Masip J, Gili G, Artigas A, Baigorri F. Thenar oxygen saturation measured by near infrared spectroscopy as a noninvasive predictor of low central venous oxygen saturation in septic patients. Intensive Care Med. 2009;35:1106–1109. doi: 10.1007/s00134-009-1410-y.
    1. Cargill W, Hickam J. The oxygen consumption of the normal and diseased human kidney. J Clin Invest. 1949;28:526–532. doi: 10.1172/JCI102100.
    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. 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. Patel MB, Kaplan IV, Patni RN, Levy D, Strom JA, Shirani J, LeJemtel TH. Sustained improvement in flow-mediated vasodilation after short-term administration of dobutamine in patients with severe congestive heart failure. Circulation. 1999;99:60–64.
    1. Freimark D, Feinberg MS, Matezky S, Hochberg N, Shechter M. Impact of short-term intermittent intravenous dobutamine therapy on endothelial function in patients with severe chronic heart failure. Am Heart J. 2004;148:878–882. doi: 10.1016/j.ahj.2004.04.013.
    1. Anker SD, Ponikowski P, Varney S, Chua TP, Clark AL, Webb-Peploe KM, Harrington D, Kox WJ, Poole-Wilson PA, Coats AJ. Wasting as independent risk factor for mortality in chronic heart failure. Lancet. 1997;349:1050–1053. doi: 10.1016/S0140-6736(96)07015-8.
    1. Podbregar M, Voga G. Effect of selective and nonselective beta-blockers on resting energy production rate and total body substrate utilization in chronic heart failure. J Card Fail. 2002;8:369–378. doi: 10.1054/jcaf.2002.130238.
    1. Obisesan TO, Toth MJ, Donaldson K, Gottlieb SS, Fisher ML, Vaitekevicius P, Poehlman ET. Energy expenditure and symptom severity in men with heart failure. Am J Cardiol. 1996;77:1250–1252. doi: 10.1016/S0002-9149(96)00176-2.
    1. Mancini DM, Schwartz M, Ferraro N, Seestedt R, Chance B, Wilson JR. Effect of dobutamine on skeletal muscle metabolism in patients with congestive heart failure. Am J Cardiol. 1990;65:1121–1126. doi: 10.1016/0002-9149(90)90325-U.

Source: PubMed

Sponsor e collaboratori

Condizioni mediche

Interventi farmacologici

3
Sottoscrivi