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The value of SvO2 measurement
THE VALUE OF Sv02 M E A S U R E M E N T ~. NELSON
The assessment of mixed venous oxygen saturation (SvO~) is an essential element in the care of critically ill patients. The purpose of this review is to examine the role of SvO~ measurements in the assessment of oxygen transport in critically ill patients. As our understanding of the shock state has evolved over the past three decades, the importance of oxygen transport balance has become increasingly clear. In the 1960's when critical care was in its infancy, shock was believed to be a problem of blood pressure control and monitoring of patients in shock focused upon pressure measurements. The treatment of shock was aimed at restoring pressure and the physician's armamentarium was filled with vasopressors. In the 1970's our understanding had evolved and shock was believed to be primarily a problem with tissue blood flow. The thermodilution Swan-Ganz catheter became available and shock resuscitation was oriented to improving cardiac output. The 1970's were the golden age of inotropes. In the 1980's the definition of shock was revised to emphasize that shock was an imbalance between supply and demand of oxygen. Restoring this critical balance became the therapeutic goal of the 1990's.
•
Oxygen transport terminology [1]
Oxygen transport terminology has become increasingly complex in the last several years. There is general agreement that o x y g e n d e l i v e r y defines the volume of gaseous oxygen which is pumped from the left ventricle each minute. Oxygen delivery (DO2) is therefore the product of cardiac output (or its in-
Director, Surgical Critical Care, Department of Surgical Education, Orlando Regional Medical Center, 1414 Kuhl Avenue (MP-35), Orlando, Florida 32806, USA. R~an. Urg., 1996, 5 (2 bis), 200-203
dex, CI) and arterial oxygen content (Ca02). Normal oxygen delivery is about 600 mL/min/m2. The other side of the oxygen transport balance is oxygen c o n s u m p t i o n (V02). Oxygen consumption defines the volume of gaseous oxygen which is actually used by the body each minute. Oxygen consumption is a value which is calculated using the Fick equation. The Fick equation simply says that the volume of oxygen consumed is equal to the difference between the volume of oxygen delivered to the body minus the volume of oxygen returned to the heart. This is calculated by the classic equation of V02 = C(a- v)02 x C1. Normal oxygen consumption is about 140 mL/min/Im2. O y y g e n utilization defines the fraction of delivered oxygen which is actually consumed. Therefore, the oxygen utilization coefficient (OUC) is equal to VOJD02. The OUC (sometimes referred to as the oxygen extraction ratio, OER) is an indicator of the relative oxygen transport balance. The normal OUC ranges from about 0.2 to 0.3. Values greater than 0.35 indicate a severe stress upon oxygen delivery to adequately meet the oxygen consumption requirements of the patient. Oxygen d e m a n d is a relatively new term which is used to define the volume of oxygen which is actually needed by the tissues to function aerobically. At this time we have no technology available to measure actual oxygen demand. Therefore, we must rely on indirect indicators of the relationship between the demand for oxygen (what is needed) and the consumption of oxygen (what is actually used). When the demand for oxygen exceeds the consumption of oxygen, anaerobic metabolism must occur or the tissues will die. Therefore, markers of anaerobic metabolism, such as lactic acid concentration, serve to indicate that the demand for oxygen has exceeded the consumption of oxygen [2, 3]. The last term commonly used today to define oxygen transport is the oxygen uptake. Oxygen uptake defines the volume of gaseous oxygen which is
The value of Sv02 measurement- 201 removed from the patient's gas supply each minute. This value is what is commonly measured through indirect calorimetry on modern metabolic measurement carts. Oxygen uptake can differ from oxygen consumption and oxygen demand depending upon the patient's metabolic and pulmonary status. O x y g e n t r a n s p o r t may be defined as the entire global process of delivering oxygen from the left ventricle, consumption of oxygen by the tissues, and return of partially deoxygenated blood to the lungs for reoxygenation. The overall adequacy of this process is described by the fraction of delivered oxygen which is consumed and, therefore, by the oxygen utilization coefficient. Sv02 measurement is obviously necessary for the assessment of oxygen consumption, utilization, and transport using these definitions. It is also useful in assessing the adequacy of oxygen delivery and the relationship between demand and consumption.
•
Goals of shock resuscitation
The goals of shock resuscitation have changed with our understanding of the shock state. It is clear that re-establishment of blood pressure is not an adequate indicator of shock resuscitation. Improving cardiac output alone does not necessarily improve tissue oxygenation and normalizing oxygen delivery is often inadequate in highly stressed patients. Twenty years ago Powers [4] suggested that maximizing tissue oxygen consumption may achieve adequate shock resuscitation. The goal is not to increase artificially the demand for oxygen but rather to improve the use of oxygen by the tissue so that the consumption increases to whatever demand is created by the tissue's aerobic needs. Achievement of this goal is often assessed by the clearance or production of markers of anaerobic metabolism. The most widely used clinical marker indicating that demand for oxygen by the tissues has exceeded the actual use (consumption) of oxygen by the tissues, is the excess lactate. Unfortunately, excess lactate (indicated by an increase in the lactate to pyruvate ratio) is frequently not available at the patient's bedside in a timely fashion. Elevations in total serum lactate may indicate ongoing anaerobic metabolism, impaired hepatic elimination of lactate, or washout of lactate from reperfusion of previously underperfused vascular beds. The normal serum half-life of lactate in states of normal hepatic function and perfusion is approximately 2 - 4 hours. The change in venous oxygen saturation occurring after reperfusion of hypoperfused tissues occurs usually in only minutes. The finding of an elevated serum lactate and a low SvO~ should raise the suspicion of continued inadequate perfusion and anaerobic metabolism. The finding of an elevated serum lactate in a patient with a normal or increasing Sv02 raises the suspicion of lactate washout from previously hypoperfused tissue, im-
paired lactate clearance, or aerobic glycolysis (often associated with sepsis). Maximization of oxygen consumption to restore optimal tissue perfusion necessitates the optimization of the oxygen supply-demand balance and SvO~ monitoring may improve the efficiency of this process [5, 6].
•
Monitoring oxygen transport balance
Oxygen transport balance is clearly defined by the variables in the Fick equation. The balance of oxygen supply and demand is dependent upon the relative relationship between those factors which determine supply (cardiac index, hemoglobin concentration, and arterial oxygen saturation) and oxygen consumption (V02). Since these variables are related to one another by physical laws, the relationships are predictable and calculable. For years mixed venous oxygen tension (PvO~) was used to help the clinician assess tissue oxygenation. It is clear that PvO~ does not well define tissue oxygenation but yet is an important predictor of the likelihood of the development of anaerobic metabolism and associated mortality [2]. In the early 1980's, clinicians realized that intermittent measurement of mixed venous oxygen saturation provided equally useful information directly relating to the many factors affecting oxygen supply and demand. When the Fick equation is solved for SvO~, it becomes clear that SvO~ defines the adequacy cardiac output to deliver the volume oxygen needed to meet oxygen consumption requirements [7]. It is, in fact, an indicator of the relative balance between the total body supply and demand of oxygen: V0~ V02 Sv02 = 1 = 1 ---= 1 - 0UC CO x Hgb x Sa02 D0~ Since the Sv02 is determined almost entirely by the mixed venous oxygen content and mixed venous oxygen content is determined by the physical law of conservation of mass, Sv02 is controlled by the balance between the delivery and consumption of oxygen. Mixed venous oxygen tension is secondarily determined by the Sv02 and the position of the oxyhemoglobin dissociation curve. In other words unlike the arterial side of the circulation where oxygen tension determines the saturation, on the venous side, oxygen content determines saturation and saturation determines tension. The mixed venous oxygen saturation is a sensitive but nonspecific indicator that an imbalance between oxygen supply and demand has occurred. It does not define the nature of the imbalance or by itself give insights into the therapy which could be used to improve the oxygen transport balance. Rather, Sv02 is the flow-weighted average of the venous effluents R6an. Urg., 1996, 5 (2 bis), 200-203
- 202 -
The value of Sv02 measurement
from all perfused vascular beds. Therefore, it does not define the oxygen supply/demand adequacy of individual vascular beds but rather the entire body as a whole. Because of this, high flow, low extraction beds (such as the kidney) have greater impact on SvO2 than do high extraction, low flow beds (such as the myocardium).
•
Continuous mixed venous oximetry
Continuous mixed venous oximetry using a fiberoptic pulmonary artery catheter has opened new understanding in the real-time monitoring of oxygen supply/demand balance. Mixed venous oximetry was introduced clinically in the early 1980's. Tremendous controversy has brewed around the ability of mixed venous oxygen saturation measurements to correlate with cardiac output. Early studies suggested that SvO~ should correlate with cardiac output in patients who are otherwise stable. These early studies were supported by the finding of a clinical correlation under general anesthesia. Later studies in the intensive care unit, however, failed to show a high degree of correlation between SvO~ in cardiac output [7-11]. When one examines the determinants of mixed venous oxygen saturation by the Fick equation, it is clear that there are multiple determinants of SvO~. When arterial saturation is maintained at a high level, the previously described relationship holds: SvO~ = 1 -
VO~ Hgb x SaO= x 13.4 x CO
There are four determinants of mixed venous oxygen saturation (SaO~, hemoglobin concentration [Hgb], cardiac output [CO], and VOw). Mixed venous oxygen saturation is determined by the balance between the consumption of oxygen (the numerator) and the delivery of oxygen (the denominator). This relationship has been defined by others as the oxygen utilization or extraction ratio. The tissues normally extract about 25% of the delivered oxygen making a normal mixed venous oxygen saturation in a patient who has a normal arterial oxygen saturation about 0.75. Decreases in consumption or increases in delivery which are uncompensated will lead to an increase in SvO2. On the other hand, increases in consumption or decreases in delivery which are uncompensated will lead to a decrease in Sv02 [7]. The only time in which there would be correlation between mixed venous oxygen saturation and cardiac output would be when SaO~, hemoglobin, and oxygen consumption are unchanged. Mixed venous oxygen saturation is not just an indicator of pulmonary gas exchange but rather an indicator of the relationship between oxygen delivery and oxygen ROan. Urg., 1996, 5 (2 bis), 200-203
consumption. SvO~ does not tell us about tissue oxygenation per se, but rather represents the flowweighted average of the effluents of all perfused vascular beds. A change in mixed venous oxygen saturation alerts the clinician that the oxygen supply/demand balance has changed and further information is needed to assess the cause for this change. Mixed venous oxygen saturation measurements can help to determine the timing of other oxygen transport measurements. It will help minimize unnecessary oxygen transport measurements in the stable patient but yet will alert the clinician as to the need for further measurements in the unstable patient. Continuous SvO~ monitoring therefore may improve the efficiency of the delivery of critical care by improving the timing of our intermittent measurements [7, 8].
•
A s s e s s m e n t of c u r r e n t t e c h n o l o g y
Mixed venous oximetry catheters are both accurate and precise in the measurement of SvO~. In spite of this accuracy, there remains considerable controversy as to whether the catheters are cost effective in the management of critically ill patients. While some studies suggest tremendous cost effectiveness, others suggest that the monitoring catheter may actually increase costs to the patients with no appreciable benefit. The reason for this controversy seems to be quite clear. When the information is used for clinical decision making and is felt to be reliable enough to eliminate the need for other multiple measurements, the technique is not only cost effective but, in fact, is cost saving. When the technique is used only to trigger a response of other multiple measurements and not to direct therapy per se, it is clear that costs are increased above those incurred with traditional pulmonary artery catheters. Therefore, both patient selection and physician utilization of the data will determine whether or not the monitoring technology is cost effective in a given situation. When applied to the most critically ill patients and used in a goal-directed fashion, the technology appears to be safe, reliable, efficient, and cost effective. The future of oxygen transport monitoring seems to be in the area of the computer acquisition of data from multiple sources. The primary inputs in the foreseeable future will be the same (i.e., cardiac output, SaO2 and SvO~) but the data will be combined by dedicated computer systems to allow a more precise and continuous interpretation of the complex data. Dual oximetry combines the input sources of an arterial pulse oximeter and a continuous mixed venous oximeter [12]. Combining these data with a manually entered inspired oxygen fraction, PaC02, and hemoglobin allows calculation of both the oxy-
The value of Sv02 measurementgen utilization coefficient and an index of the intrapulmonary shunt fraction. The recent addition of continuous thermodilution cardiac output measurements gives continuous data regarding both oxygen delivery and consumption.
203
-
T he assessment of Sv02 is an essential element in the care of critically ill patients. The continuous in vivo monitoring of this value may be cost effective and result in more timely interventions when the data are used to direct patient care.
Oxygen transport terminology Term
Abbreviation
Definition
Normal Range
Tension
PaO=
partial pressure of oxygen
> 65 mmHg (5 kPa)
Saturation
SaO2
oxyhemoglobin saturation
> 0.92
Content
CaO2
total content of oxygen CaD2 = (Hgb x SaD2 x 1.34) + (PAD2 x 0.0031)
> 20 mL/dL
Transport
---
balance between supply and demand
Delivery
DO2
O5 volume ejected from left ventricle DO2 = CO x CaD= x 10/BSA
500-650 mL/min/m2
Consumption
VO2
O2 volume used by tissue VO= = CO x C(a-v)O2 x 10/BSA
110-150 mL/min/m-b 2
Uptake
- --
O~ volume taken up by lungs
110-150 mL/min/m2
Demand
---
O2 volume needed by tissues
110-150 mL/min/m 2
Utilization
OUC
fraction of delivered 02 consumed OUC = VOJDO2
0.22 - 0.30
- --
CO = cardiac output (L/rain), CaD2 = arterial oxygen content (mL/dL), C(a-v)O2 = arterial-venous oxygen content difference (mL/dL), BSA = body surface area (m 2)
References [1] NELSONL.D., RUTHERFORDE.J. - - Principles of hemodynamic monitoring./n Pinsky MR and Dhainaut J-F: Pathophysiologic foundations of critical care (Eds). Baltimore, Williams and Wilkins, 1993, 3-22. [2] KRASNITZ P., DRUGERG.L., YORRAF., SIMMONSD.H. - - Mixed venous oxygen tension and hyperlactatemia: Survival in severe cardiopulmonary disease. JAMA, 1976, 236, 570-574. [3] KANDELG., ABERMANA. - - Mixed venous oxygen saturation: Its role in the assessment of the critically ill patient. Arch. Int. Med., 1983, 143, 1400-1402. [4] POWERSS.R., DUTTON R.E. - - Correlation of positive endexpiratory pressure with cardiovascular performance. Crit Care Med., 1975, 3, 64-68. [5] SHOEMAKER W.C., APPELP.L., KRAM H.B. et al. - - Prospective trial of supranormal values of survivors as therapeutic goals in high risk surgical patients. Chest, 1988, 94, 1176-1186.
[6] TUCHSCHMIDTJ., FRIEDJ., ASTIZ M., RACKOWE. - - Elevation of cardiac output and oxygen delivery improves outcome in septic shock. Chest, 1992, 102, 216-220. [7] NELSONL.D. - - Continuous venous oximetry in surgical patients. Ann. Surg., 1986, 203, 329-333. [8] ORLANDOR. m Continuous mixed venous oximetry in critically ill surgical patients: 'High-Tech' cost-effectiveness. Arch. Surg., 1986, 121, 470-471. [9] MAGILLIGAN D.J., REASDALL R. et aL - - Mixed venous oxygen saturation as a predictor of cardiac output in the postoperative cardiac surgical patient. Ann. Thorac. Surg., 1987, 44, 260-262. [10] SHENAQS.A., CASAR G., CHELLY J.E. et aL - - Continuous monitoring of mixed venous oxygen saturation during aortic surgery. Chest, 1987, 92, 796-799. [11] DIVERTIEM.D., McMICRAN J.C. - - Continuous monitoring of mixed venous oxygen saturation. Chest, 1984, 85, 423-428. [12] R.~SANENJ., DOWNS J.B., MALECK D.J. et aL - - Estimation of oxygen utilization by dual oximetry. Ann. Surg., 1987, 206, 621-623.
mmn
R#an. Urg., 1996, 5 (2 bis), 200-203
The assessment of mixed venous oxygen saturation (SvO~) is an essential element in the care of critically ill patients. The purpose of this review is to examine the role of SvO~ measurements in the assessment of oxygen transport in critically ill patients. As our understanding of the shock state has evolved over the past three decades, the importance of oxygen transport balance has become increasingly clear. In the 1960's when critical care was in its infancy, shock was believed to be a problem of blood pressure control and monitoring of patients in shock focused upon pressure measurements. The treatment of shock was aimed at restoring pressure and the physician's armamentarium was filled with vasopressors. In the 1970's our understanding had evolved and shock was believed to be primarily a problem with tissue blood flow. The thermodilution Swan-Ganz catheter became available and shock resuscitation was oriented to improving cardiac output. The 1970's were the golden age of inotropes. In the 1980's the definition of shock was revised to emphasize that shock was an imbalance between supply and demand of oxygen. Restoring this critical balance became the therapeutic goal of the 1990's.
•
Oxygen transport terminology [1]
Oxygen transport terminology has become increasingly complex in the last several years. There is general agreement that o x y g e n d e l i v e r y defines the volume of gaseous oxygen which is pumped from the left ventricle each minute. Oxygen delivery (DO2) is therefore the product of cardiac output (or its in-
Director, Surgical Critical Care, Department of Surgical Education, Orlando Regional Medical Center, 1414 Kuhl Avenue (MP-35), Orlando, Florida 32806, USA. R~an. Urg., 1996, 5 (2 bis), 200-203
dex, CI) and arterial oxygen content (Ca02). Normal oxygen delivery is about 600 mL/min/m2. The other side of the oxygen transport balance is oxygen c o n s u m p t i o n (V02). Oxygen consumption defines the volume of gaseous oxygen which is actually used by the body each minute. Oxygen consumption is a value which is calculated using the Fick equation. The Fick equation simply says that the volume of oxygen consumed is equal to the difference between the volume of oxygen delivered to the body minus the volume of oxygen returned to the heart. This is calculated by the classic equation of V02 = C(a- v)02 x C1. Normal oxygen consumption is about 140 mL/min/Im2. O y y g e n utilization defines the fraction of delivered oxygen which is actually consumed. Therefore, the oxygen utilization coefficient (OUC) is equal to VOJD02. The OUC (sometimes referred to as the oxygen extraction ratio, OER) is an indicator of the relative oxygen transport balance. The normal OUC ranges from about 0.2 to 0.3. Values greater than 0.35 indicate a severe stress upon oxygen delivery to adequately meet the oxygen consumption requirements of the patient. Oxygen d e m a n d is a relatively new term which is used to define the volume of oxygen which is actually needed by the tissues to function aerobically. At this time we have no technology available to measure actual oxygen demand. Therefore, we must rely on indirect indicators of the relationship between the demand for oxygen (what is needed) and the consumption of oxygen (what is actually used). When the demand for oxygen exceeds the consumption of oxygen, anaerobic metabolism must occur or the tissues will die. Therefore, markers of anaerobic metabolism, such as lactic acid concentration, serve to indicate that the demand for oxygen has exceeded the consumption of oxygen [2, 3]. The last term commonly used today to define oxygen transport is the oxygen uptake. Oxygen uptake defines the volume of gaseous oxygen which is
The value of Sv02 measurement- 201 removed from the patient's gas supply each minute. This value is what is commonly measured through indirect calorimetry on modern metabolic measurement carts. Oxygen uptake can differ from oxygen consumption and oxygen demand depending upon the patient's metabolic and pulmonary status. O x y g e n t r a n s p o r t may be defined as the entire global process of delivering oxygen from the left ventricle, consumption of oxygen by the tissues, and return of partially deoxygenated blood to the lungs for reoxygenation. The overall adequacy of this process is described by the fraction of delivered oxygen which is consumed and, therefore, by the oxygen utilization coefficient. Sv02 measurement is obviously necessary for the assessment of oxygen consumption, utilization, and transport using these definitions. It is also useful in assessing the adequacy of oxygen delivery and the relationship between demand and consumption.
•
Goals of shock resuscitation
The goals of shock resuscitation have changed with our understanding of the shock state. It is clear that re-establishment of blood pressure is not an adequate indicator of shock resuscitation. Improving cardiac output alone does not necessarily improve tissue oxygenation and normalizing oxygen delivery is often inadequate in highly stressed patients. Twenty years ago Powers [4] suggested that maximizing tissue oxygen consumption may achieve adequate shock resuscitation. The goal is not to increase artificially the demand for oxygen but rather to improve the use of oxygen by the tissue so that the consumption increases to whatever demand is created by the tissue's aerobic needs. Achievement of this goal is often assessed by the clearance or production of markers of anaerobic metabolism. The most widely used clinical marker indicating that demand for oxygen by the tissues has exceeded the actual use (consumption) of oxygen by the tissues, is the excess lactate. Unfortunately, excess lactate (indicated by an increase in the lactate to pyruvate ratio) is frequently not available at the patient's bedside in a timely fashion. Elevations in total serum lactate may indicate ongoing anaerobic metabolism, impaired hepatic elimination of lactate, or washout of lactate from reperfusion of previously underperfused vascular beds. The normal serum half-life of lactate in states of normal hepatic function and perfusion is approximately 2 - 4 hours. The change in venous oxygen saturation occurring after reperfusion of hypoperfused tissues occurs usually in only minutes. The finding of an elevated serum lactate and a low SvO~ should raise the suspicion of continued inadequate perfusion and anaerobic metabolism. The finding of an elevated serum lactate in a patient with a normal or increasing Sv02 raises the suspicion of lactate washout from previously hypoperfused tissue, im-
paired lactate clearance, or aerobic glycolysis (often associated with sepsis). Maximization of oxygen consumption to restore optimal tissue perfusion necessitates the optimization of the oxygen supply-demand balance and SvO~ monitoring may improve the efficiency of this process [5, 6].
•
Monitoring oxygen transport balance
Oxygen transport balance is clearly defined by the variables in the Fick equation. The balance of oxygen supply and demand is dependent upon the relative relationship between those factors which determine supply (cardiac index, hemoglobin concentration, and arterial oxygen saturation) and oxygen consumption (V02). Since these variables are related to one another by physical laws, the relationships are predictable and calculable. For years mixed venous oxygen tension (PvO~) was used to help the clinician assess tissue oxygenation. It is clear that PvO~ does not well define tissue oxygenation but yet is an important predictor of the likelihood of the development of anaerobic metabolism and associated mortality [2]. In the early 1980's, clinicians realized that intermittent measurement of mixed venous oxygen saturation provided equally useful information directly relating to the many factors affecting oxygen supply and demand. When the Fick equation is solved for SvO~, it becomes clear that SvO~ defines the adequacy cardiac output to deliver the volume oxygen needed to meet oxygen consumption requirements [7]. It is, in fact, an indicator of the relative balance between the total body supply and demand of oxygen: V0~ V02 Sv02 = 1 = 1 ---= 1 - 0UC CO x Hgb x Sa02 D0~ Since the Sv02 is determined almost entirely by the mixed venous oxygen content and mixed venous oxygen content is determined by the physical law of conservation of mass, Sv02 is controlled by the balance between the delivery and consumption of oxygen. Mixed venous oxygen tension is secondarily determined by the Sv02 and the position of the oxyhemoglobin dissociation curve. In other words unlike the arterial side of the circulation where oxygen tension determines the saturation, on the venous side, oxygen content determines saturation and saturation determines tension. The mixed venous oxygen saturation is a sensitive but nonspecific indicator that an imbalance between oxygen supply and demand has occurred. It does not define the nature of the imbalance or by itself give insights into the therapy which could be used to improve the oxygen transport balance. Rather, Sv02 is the flow-weighted average of the venous effluents R6an. Urg., 1996, 5 (2 bis), 200-203
- 202 -
The value of Sv02 measurement
from all perfused vascular beds. Therefore, it does not define the oxygen supply/demand adequacy of individual vascular beds but rather the entire body as a whole. Because of this, high flow, low extraction beds (such as the kidney) have greater impact on SvO2 than do high extraction, low flow beds (such as the myocardium).
•
Continuous mixed venous oximetry
Continuous mixed venous oximetry using a fiberoptic pulmonary artery catheter has opened new understanding in the real-time monitoring of oxygen supply/demand balance. Mixed venous oximetry was introduced clinically in the early 1980's. Tremendous controversy has brewed around the ability of mixed venous oxygen saturation measurements to correlate with cardiac output. Early studies suggested that SvO~ should correlate with cardiac output in patients who are otherwise stable. These early studies were supported by the finding of a clinical correlation under general anesthesia. Later studies in the intensive care unit, however, failed to show a high degree of correlation between SvO~ in cardiac output [7-11]. When one examines the determinants of mixed venous oxygen saturation by the Fick equation, it is clear that there are multiple determinants of SvO~. When arterial saturation is maintained at a high level, the previously described relationship holds: SvO~ = 1 -
VO~ Hgb x SaO= x 13.4 x CO
There are four determinants of mixed venous oxygen saturation (SaO~, hemoglobin concentration [Hgb], cardiac output [CO], and VOw). Mixed venous oxygen saturation is determined by the balance between the consumption of oxygen (the numerator) and the delivery of oxygen (the denominator). This relationship has been defined by others as the oxygen utilization or extraction ratio. The tissues normally extract about 25% of the delivered oxygen making a normal mixed venous oxygen saturation in a patient who has a normal arterial oxygen saturation about 0.75. Decreases in consumption or increases in delivery which are uncompensated will lead to an increase in SvO2. On the other hand, increases in consumption or decreases in delivery which are uncompensated will lead to a decrease in Sv02 [7]. The only time in which there would be correlation between mixed venous oxygen saturation and cardiac output would be when SaO~, hemoglobin, and oxygen consumption are unchanged. Mixed venous oxygen saturation is not just an indicator of pulmonary gas exchange but rather an indicator of the relationship between oxygen delivery and oxygen ROan. Urg., 1996, 5 (2 bis), 200-203
consumption. SvO~ does not tell us about tissue oxygenation per se, but rather represents the flowweighted average of the effluents of all perfused vascular beds. A change in mixed venous oxygen saturation alerts the clinician that the oxygen supply/demand balance has changed and further information is needed to assess the cause for this change. Mixed venous oxygen saturation measurements can help to determine the timing of other oxygen transport measurements. It will help minimize unnecessary oxygen transport measurements in the stable patient but yet will alert the clinician as to the need for further measurements in the unstable patient. Continuous SvO~ monitoring therefore may improve the efficiency of the delivery of critical care by improving the timing of our intermittent measurements [7, 8].
•
A s s e s s m e n t of c u r r e n t t e c h n o l o g y
Mixed venous oximetry catheters are both accurate and precise in the measurement of SvO~. In spite of this accuracy, there remains considerable controversy as to whether the catheters are cost effective in the management of critically ill patients. While some studies suggest tremendous cost effectiveness, others suggest that the monitoring catheter may actually increase costs to the patients with no appreciable benefit. The reason for this controversy seems to be quite clear. When the information is used for clinical decision making and is felt to be reliable enough to eliminate the need for other multiple measurements, the technique is not only cost effective but, in fact, is cost saving. When the technique is used only to trigger a response of other multiple measurements and not to direct therapy per se, it is clear that costs are increased above those incurred with traditional pulmonary artery catheters. Therefore, both patient selection and physician utilization of the data will determine whether or not the monitoring technology is cost effective in a given situation. When applied to the most critically ill patients and used in a goal-directed fashion, the technology appears to be safe, reliable, efficient, and cost effective. The future of oxygen transport monitoring seems to be in the area of the computer acquisition of data from multiple sources. The primary inputs in the foreseeable future will be the same (i.e., cardiac output, SaO2 and SvO~) but the data will be combined by dedicated computer systems to allow a more precise and continuous interpretation of the complex data. Dual oximetry combines the input sources of an arterial pulse oximeter and a continuous mixed venous oximeter [12]. Combining these data with a manually entered inspired oxygen fraction, PaC02, and hemoglobin allows calculation of both the oxy-
The value of Sv02 measurementgen utilization coefficient and an index of the intrapulmonary shunt fraction. The recent addition of continuous thermodilution cardiac output measurements gives continuous data regarding both oxygen delivery and consumption.
203
-
T he assessment of Sv02 is an essential element in the care of critically ill patients. The continuous in vivo monitoring of this value may be cost effective and result in more timely interventions when the data are used to direct patient care.
Oxygen transport terminology Term
Abbreviation
Definition
Normal Range
Tension
PaO=
partial pressure of oxygen
> 65 mmHg (5 kPa)
Saturation
SaO2
oxyhemoglobin saturation
> 0.92
Content
CaO2
total content of oxygen CaD2 = (Hgb x SaD2 x 1.34) + (PAD2 x 0.0031)
> 20 mL/dL
Transport
---
balance between supply and demand
Delivery
DO2
O5 volume ejected from left ventricle DO2 = CO x CaD= x 10/BSA
500-650 mL/min/m2
Consumption
VO2
O2 volume used by tissue VO= = CO x C(a-v)O2 x 10/BSA
110-150 mL/min/m-b 2
Uptake
- --
O~ volume taken up by lungs
110-150 mL/min/m2
Demand
---
O2 volume needed by tissues
110-150 mL/min/m 2
Utilization
OUC
fraction of delivered 02 consumed OUC = VOJDO2
0.22 - 0.30
- --
CO = cardiac output (L/rain), CaD2 = arterial oxygen content (mL/dL), C(a-v)O2 = arterial-venous oxygen content difference (mL/dL), BSA = body surface area (m 2)
References [1] NELSONL.D., RUTHERFORDE.J. - - Principles of hemodynamic monitoring./n Pinsky MR and Dhainaut J-F: Pathophysiologic foundations of critical care (Eds). Baltimore, Williams and Wilkins, 1993, 3-22. [2] KRASNITZ P., DRUGERG.L., YORRAF., SIMMONSD.H. - - Mixed venous oxygen tension and hyperlactatemia: Survival in severe cardiopulmonary disease. JAMA, 1976, 236, 570-574. [3] KANDELG., ABERMANA. - - Mixed venous oxygen saturation: Its role in the assessment of the critically ill patient. Arch. Int. Med., 1983, 143, 1400-1402. [4] POWERSS.R., DUTTON R.E. - - Correlation of positive endexpiratory pressure with cardiovascular performance. Crit Care Med., 1975, 3, 64-68. [5] SHOEMAKER W.C., APPELP.L., KRAM H.B. et al. - - Prospective trial of supranormal values of survivors as therapeutic goals in high risk surgical patients. Chest, 1988, 94, 1176-1186.
[6] TUCHSCHMIDTJ., FRIEDJ., ASTIZ M., RACKOWE. - - Elevation of cardiac output and oxygen delivery improves outcome in septic shock. Chest, 1992, 102, 216-220. [7] NELSONL.D. - - Continuous venous oximetry in surgical patients. Ann. Surg., 1986, 203, 329-333. [8] ORLANDOR. m Continuous mixed venous oximetry in critically ill surgical patients: 'High-Tech' cost-effectiveness. Arch. Surg., 1986, 121, 470-471. [9] MAGILLIGAN D.J., REASDALL R. et aL - - Mixed venous oxygen saturation as a predictor of cardiac output in the postoperative cardiac surgical patient. Ann. Thorac. Surg., 1987, 44, 260-262. [10] SHENAQS.A., CASAR G., CHELLY J.E. et aL - - Continuous monitoring of mixed venous oxygen saturation during aortic surgery. Chest, 1987, 92, 796-799. [11] DIVERTIEM.D., McMICRAN J.C. - - Continuous monitoring of mixed venous oxygen saturation. Chest, 1984, 85, 423-428. [12] R.~SANENJ., DOWNS J.B., MALECK D.J. et aL - - Estimation of oxygen utilization by dual oximetry. Ann. Surg., 1987, 206, 621-623.
mmn
R#an. Urg., 1996, 5 (2 bis), 200-203