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Svo2 Monitoring

Jill Jesurum
Crit Care Nurse. 2004;24: 73-76
© 2004 American Association of Critical-Care Nurses Published online http://ccn.aacnjournals.org Personal use only. For copyright permission information: http://ccn.aacnjournals.org/cgi/external_ref?link_type=PERMISSIONDIRECT

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Critical Care Nurse is the official peer-reviewed clinical journal of the American Association of Critical-Care Nurses, published bi-monthly by The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656. Telephone: 949-362-2000. Fax: 949-362-2049. Copyright 2004 by AACN. All rights reserved.

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ProtocolsforPractice

SVO2 Monitoring
Jill Jesurum, RN, MN, CCRN, CS

Where is SVO2 (percentage of oxygen saturation in the pulmonary arterial blood) measured in the body? SVO2 is measured in the pulmonary artery (PA), where venous blood mixes after circulating through the superior and inferior vena cavae, coronary sinuses, and the chambers in the right side of the heart. Although SVO2 is the percentage of oxygen saturation in the pulmonary arterial blood, SVO2 actually represents an average of all the venous oxygen saturations of the various organs and tissues.1 Q: Describe the technology used to measure SVO2. The components of an SVO2 monitoring system include a flowdirected thermodilution PA catheter that has conventional hemodynamic

Q

monitoring capabilities in addition to fiber optics for transmitting light (Figure 1), an optical module that contains a light-emitting source and a photodetector, and a microprocessor to analyze reflected light. Reflectance spectrophotometry is used to differentiate oxygenated blood from deoxygenated blood in the PA. From the distal end of the PA catheter, light-emitting diodes transmit pulsating light of various wave-

lengths in the red and infrared spectra through an optical fiber to illuminate the blood. The red blood cells absorb various amounts of light depending on the amounts of oxygenated and deoxygenated hemoglobin that are present. The light reflected by the blood cells is transmitted through a second optical fiber to the photodetector, which converts light intensity into electrical signals for transmission to the microprocessor. After the microprocessor receives the electrical signals, the light intensities from oxyhemoglobin and deoxyhemoglobin are analyzed by detecting color changes in the red blood cells, and a ratio is computed.2 The SVO2 value that is displayed on the oscilloscope represents a composite of measurements of multiple samples and is updated every few seconds.

Fiber-optic catheter To oximetry instrument Cardiac output computer connector Receiving fiber optic Transmitting fiber optic

Optical module Proximal (CVP) lumen

Author
Jill Jesurum is a cardiovascular clinical nurse specialist at Swedish Medical Center in Seattle, Wash.
To purchase reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 809-2273 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, reprints@aacn.org.

Distal (PA) lumen

Balloon inflation lumen

Thermistor CVP injection port

Sampling and pressure monitoring lumen

Figure 1 Fiber-optic PA catheter and associated interconnections.
Abbreviations: CVP, central venous pressure; PA, pulmonary artery. Reprinted with permission from Abbott Critical Care Systems, Mountain View, Calif.

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Q: What clinically useful information can be obtained with SVO2 monitoring? Continuous measurement of SVO2 is a practical method of globally assessing tissue oxygenation and cardiopulmonary function in the clinical setting.3 Clinicians may use continuous SVO2 monitoring to detect cardiopulmonary instability and deterioration, because clinically important changes in SVO2 may be observed before changes in other hemodynamic parameters are detectable.4-7 SVO2 monitoring may be especially useful in patients who have limited cardiac and oxygen reserves and who are at risk for tissue oxygen deprivation including: • Before or during high-risk cardiovascular surgery • Patients in advanced-stage heart failure • Patients with acute myocardial infarction • Patients with acute hypoxemic respiratory failure (eg, pulmonary embolism, pulmonary infarction) • Patients with severe burns • Patients with multisystem organ failure • Neurosurgery patients • High-risk obstetric patients SVO2 monitoring is also used to do the following: • Evaluate the adequacy of tissue oxygenation • Detect adverse changes in oxygen delivery (DO2) and oxygen consumption (VO2) or impaired tissue oxygenation • Evaluate the effectiveness of interventions to improve the balance between DO2 and VO2 including the administration of fluids (blood, crystalloids), pharmacological agents and use of mechanical assistance (eg, intra-aortic balloon pump, positive end-expiratory pressure) • Evaluate the effects of routine medical and nursing procedures on tissue oxygenation • Diagnose intracardiac shunting and cardiac tamponade • Assist in the differential diagnosis of pathological conditions Q: What is the relationship among SVO2, DO2, and VO2? DO2 is the volume of oxygen delivered to the tissues each minute and is determined by the arterial oxygen content (CaO2) and cardiac output. CaO2 comprises arterial oxygen saturation (SaO2), the amount of oxygen dissolved in the plasma (partial pressure of arterial oxygen, PaO2), and hemoglobin level. Normal DO2 is approximately 1000 mL/min. When indexed to body surface area (ie, DO2 index), normal delivery is approximately 600 mL . min-1 . m-2. VO2 is the amount of oxygen consumed each minute by the tissues for aerobic metabolism. Because the amount of oxygen needed for cellular metabolic functions (ie, oxygen demand) is difficult to measure in the clinical setting, VO2 is used as a measurement to estimate oxygen demand.8 In healthy persons, VO2 and oxygen demand are approximately equal. Normal values are approximately 250 mL/min for VO2 and 120 to 140 for VO2 index.9 SVO2 is a nonspecific multifactorial parameter that reflects the dynamic relationship (or balance) between DO2 and VO2 at the tissue level3 (Figure 2). DO2 is normally 3

Figure 2 Cardiopulmonary system including the normal values of tissue oxygenation parameters. Mixed venous oxygen saturation (SvO2) reflects the adequacy of oxygen delivery (DO2) in meeting oxygen demand. As shown, cardiac output (CO), hemoglobin (Hgb), and arterial oxygen saturation (SaO2) make up delivery. Oxygen consumption (VO2) is a reflection of oxygen demand.
Reprinted with permission from Abbott Critical Care Systems, Mountain View, Calif.

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Factors associated with fluctuations in Svo2
Changes that cause a decrease in Svo2 Decrease in cardiac output Factors Hypovolemia or cardiac tamponade Shock Myocardial infarction Arrhythmias Increases in positive end-expiratory pressure Pulmonary edema Adult respiratory distress syndrome Decrease in inspired oxygen Anemia Hemorrhage Dysfunctional hemoglobin Pain Anxiety or fear Agitation or restlessness Hyperthermia or burns Tachycardia Shivering Activity (positioning, suctioning)

Decrease in oxygen saturation

Decrease in hemoglobin level

Increase in oxygen consumption

Changes that cause a decrease in Svo2 Decrease in oxygen consumption

Factors Use of analgesics and anesthetics Neuromuscular blockade or use of paralytics Use of β-antagonists Hypothermia Hypothyroidism Sepsis (dysoxia, shunting) Cyanide poisoning Sleep or rest Increase in fraction of inspired oxygen or hyperoxia Intracardiac shunt or arteriovenous fistula Severe mitral valve regurgitation Distal migration of a pulmonary artery catheter Optimal preload Use of inotropic agents Use of mechanical-assist devices

Increase in oxygen saturation

Increase in cardiac output

or 4 times greater than VO2. Under resting (stable) conditions, approximately 25% of oxygen delivered to the periphery will be consumed, and 75% will be returned to the right side of heart.10 Thus, SVO2 values between 60% and 80% usually indicate a balance between DO2 and VO2.

Q: What constitutes a clinically significant change in SVO2? As previously stated, SVO2 reflects the adequacy of DO2 to satisfy the oxygen requirements of the tissues. The basic premise of continuous SVO2 monitoring is that hemoglobin can release

oxygen and that cells can extract oxygen from the blood, depending on the cellular oxygen needs and partial pressures of oxygen.11 When oxygen demand increases, extra oxygen is made available to the tissues by increases in cardiac output or oxygen extraction. • If the oxygen extraction ratio (O2ER) increases while cardiac output remains constant, less oxygen will remain in the venous blood, and SVO2 will decrease. • If cardiac output increases in response to an increase in oxygen demand and consumption, SVO2 may remain stable. SVO2 values less than 60% may indicate either inadequate DO2 or excessive VO2.3 A clinically significant change in SVO2 (>10% from baseline) may be an early indicator of physiological instability and cardiopulmonary deterioration.12,13 Conditions that may cause SVO2 to decrease include decreases in cardiac output, hemoglobin level, and SaO2 and an increase in VO2. When DO2 decreases to a critically low level, VO2 may be limited to an amount of oxygen that is less than the amount required to meet the metabolic demand of the tissues (ie, VO2 depends on DO2). In comparison, high SVO2 values (>80%-95%) may be related to an increase in cardiac output, a decrease in oxygen demand, or a reduction in O2ER.1 Various conditions, clinical events,10,14 and factors that may affect tissue oxygenation can cause significant changes in SVO2 as described in the Table. Q: How accurate is SVO2 monitoring and what conditions may affect its accuracy?

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ProtocolsforPractice
The correlation between SVO2 measurements (range, 24%-85%) obtained with a bedside SVO2 monitor (in vivo) and simultaneous measurements obtained with a laboratory oximeter (in vitro) are between r=.90 and r=.97.1,7,15-19 The average amount of difference (bias) between in vitro and in vivo SVO2 measurements is ±4% (±2 SD) for 95% of all measurements.15,20-22 Numerous studies support the accuracy of SVO2 monitoring systems. Reliability is enhanced by a feature that monitors the optical intensity of the reflected light to guard against abnormal signal conditions (eg, a kink in the catheter, an occlusion or clot on the end of the catheter). An indicator of signal quality is continuously displayed on the monitor and is updated every few seconds. The signal quality indicator should be used by clinicians to evaluate the accuracy of SVO2 measurements. Manufacturers of continuous SVO2 monitoring systems recommend that the system be calibrated in vitro before the catheter is inserted to ensure the accuracy of the measurements.2 Generally, an in vivo calibration is recommended every 24 hours for the duration of use of the system, if the system was not calibrated in vitro before insertion of the catheter, if the fiber optics may have been damaged, if the SVO2 value may be incorrect, and if the optical module becomes disconnected from the fiber-optic PA catheter.10 Conditions that may alter the accuracy of the SVO2 measurement include hematocrit level, blood-flow characteristics, motion artifacts due to catheter “whip” against the vessel wall, blood temperature, and pH.23-24
References
1. Nelson LD. Continuous venous oximetry in surgical patients. Ann Surg. 1986; 203: 329333. 2. Sperinde JM, Senelly KM. The Oximetrix Opticath oximetry system: theory and development. In: Fahey PJ, ed. Continuous Measurement of Blood Oxygen Saturation in the High-Risk Patient. Mountain View, Calif: Abbott Critical Care Systems; 1987:81-89. 3. Lehot JJ, Durand PG. Mixed venous oxygen saturation monitoring in surgery. In: Edwards JD, Shoemaker WC, Vincent JL, eds. Oxygen Transport: Principles and Practice. Philadelphia: Pa: WB Saunders; 1993:125-138. 4. Divertie MB, McMichan JC. Continuous monitoring of mixed venous oxygen saturation. Chest. 1984;85:423-428. 5. Hardy GR. SvO2 continuous monitoring techniques. Dimens Crit Care Nurs. 1988;7:8-17. 6. Stevens PM. Clinical usefulness of continuous monitoring of mixed venous oxygen saturation. In: Fahey P J, ed. Continuous Measurement of Blood Oxygen Saturation in the High-Risk Patient. Mountain View, Calif: Abbott Critical Care Systems; 1987:2:33-44. 7. Waller JL, Kaplan JA, Bauman DI, Craver JM. Clinical evaluation of a new fiberoptic catheter oximeter during cardiac surgery. Anesth Analg. 1982;61:676-679. 8. McGee WT, Veremakis C, Wilson GL. Clinical importance of tissue oxygenation and use to the mixed venous blood gas. Resmedica. 1988;4(2):15-24. 9. Epstein CD, Henning RJ. Oxygen transport variables in the identification and treatment of tissue hypoxia. Heart Lung. 1993; 22:328-348. 10. White KM. Using continuous SvO2 to assess oxygen supply/demand balance in the critically ill patient. AACN Clin Issues Crit Care Nurs. 1993;4:134-147. 11. Ahrens T, Rutherford K, eds. Essentials of Oxygenation: Implication for Clinical Practice. Boston, Mass: Jones and Bartlett Publishers; 1993. 12. White KM. Completing the hemodynamic picture: SvO2. Heart Lung. 1985; 14:272-280. 13. Winslow EH, Clark AP, White KM, Tyler DO. Effects of a lateral turn on mixed venous oxygen saturation and heart rate in critically ill adults. Heart Lung. 1990;19:557561. 14. Fahey P J. Clinical experience with monitoring of mixed venous oxygen saturation in respiratory failure. In: Fahey PJ, ed. Continuous Measurement of Blood Oxygen Saturation in the High-Risk Patient. Mountain View, Calif: Abbott Critical Care Systems; 1987;2:17-26. 15. Baele PL, McMichan JC, Marsh HM, Sill JC, Southorn PA. Continuous monitoring of mixed venous oxygen saturation in critically ill patients. Anesth Analg. 1982;61:513-517. 16. Fahey PJ, Harris K, Vanderwarf C. Clinical experience with monitoring of mixed venous oxygen saturation in respiratory failure. Chest. 1984;86:749-752. 17. Karis JH, Lumb PD. Clinical evaluation of the Edwards Laboratories and Oximetrix mixed venous oxygen saturation catheters. J Cardiothorac Anesth. 1988;2:440-444. 18. Leighton T, Liu SY, Lee TS, Klein S, Bongard F. Simultaneous in-vivo comparison of 2- versus 19. 3-wavelength mixed venous oximetry catheters. Anesthesiology. 1991;75(3A): A408. Abstract. Pond CG, Blessios G, Lappas DG, McCawley C. Perioperative evaluation of a new mixed venous saturation catheter in cardiac surgical patients. Anesthesiology. 1991;75(3A): A411. Abstract. Gettinger A, De Traglia MC, Glass DD. In vivo comparison of two mixed venous saturation catheters. Anesthesiology. 1987;66:373-375. Haney MF, Tait AR, Tremper KK. Carboxyhemoglobin effects on mixed venous oximetry in dogs. Anesth Analg. 1992;74: S130. Abstract. Scuderi PE, MacGregor DA, Bowton DL, James RL. A laboratory comparison of three pulmonary artery oximetry catheters. Anesthesiology. 1994;81:245-253. Hecker BR, Brown DL, Wilson D. A comparison of two pulmonary artery mixed venous oxygen saturation catheters during the changing conditions of cardiac surgery. J Cardiothorac Anesth. 1989;3:269-275. Rouby JJ, Poete P, Bodin L, et al. Three mixed venous saturation catheters in patients with circulatory chock and respiratory failure. Chest. 1999;98:954-958.

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Note: This article was first published
in Critical Care Nurse February 2001.

This article is based on the protocol SVO2 Monitoring by Jill Jesurum. It was taken from the Hemodynamic Monitoring series of AACN’s Protocols for Practice. Protocols can be obtained from AACN, 101 Columbia, Aliso Viejo, CA 92656-1491, (800) 899AACN, (949) 362-2000. ($11, AACN members; $14, nonmembers).

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