Frank Bloos
Konrad Reinhart
Introduction
The primary physiological task of the cardiovascular system is to deliver enough oxygen (O2) to meet the metabolic demands of the body. Shock and tissue hypoxia occur when the cardiorespiratory system is unable to cover metabolic demand adequately. Sustained tissue hypoxia is one of the most important cofactors in the pathophysiology of organ dysfunction [1]. Therefore determining the adequacy of tissue oxygenation in critically ill patients is central to ascertain the health of the patient. Unfortunately, normal values in blood pressure, central venous pressure, heart rate, and blood gases do not rule out tissue hypoxia or imbalances between whole-body oxygen supply and demand [2]. This discrepancy has led to increased interest in more direct indicators of adequacy
of tissue oxygenation such as mixed and central venous oxygen saturations.
Pulmonary artery catheterization allows obtaining true mixed venous oxygen saturation (SvO2) while measuring central venous oxygen saturation (ScvO2) via central venous catheter reflects principally the degree of oxygen extraction from the brain and the upper part of the body. This brief review discusses the role and limitations of SvO2 and ScvO2 as indicators of the adequacy of tissue oxygenation.
Physiology of mixed venous and central venous oxygen saturation O2 delivery (DO2) describes whole-body oxygen supply according to the following formula:
DO2 ¼ CO CaO2 ð1Þ where CO is cardiac output and CaO2 is arterial oxygen
content, which itself is the sum of oxygen bound to hemoglobin [product of hemoglobin concentration (Hb) and arterial O2 saturation (SaO2)] and physically dissolved
oxygen [arterial PO2 (PaO2)]: CaO2 ¼ ðHb 1:36 SaO2Þ þ ðPaO2 0:0031Þ ð2Þ
Oxygen demand can be summarized in the whole-body oxygen consumption (VO2), which is expressed mathematically by the Fick principle as the product of CO and
arteriovenous O2 content difference (CaO2 CvO2): VO2 ¼ CO ðCaO2 CvO2Þ ð3Þ where mixed venous O2 content (CvO2) is:
CvO2 ¼ ðHb 1:36 SvO2Þ þ ðPvO2 0:0031Þ ð4Þ Equation 3 may be transposed to: CvO2 ¼ CaO2 VO2 CO ð5Þ As physically dissolved oxygen can be neglected, Eq. 5 may be written as: Hb 1:36 SvO2 ðHb 1:36 SaO2Þ VO2 CO , SvO2 VO2 CO ð6Þ Equation 6 also demonstrates that SvO2 is directly proportional
to the ratio of VO2 to CO. Thus SvO2 reflects the relationship between whole-body O2 consumption and cardiac output. Indeed, it has been shown that the SvO2 is well correlated with the ratio of O2 supply to demand [3].Pathophysiology of central or mixed venous O2 saturation during shock Usually VO2 is independent of DO2 since tissues can maintain O2 needs by increasing O2 extraction when DO2 decreases. However, this mechanism has its limits. Below a so-called critical DO2 compensatory increase in O2 extraction is exhausted, and VO2 becomes dependent on DO2. In this case tissue hypoxia occurs, and a rise in
serum lactate levels may be observed [4]. A decrease in SvO2 and ScvO2 represents an increased metabolic stress, because the O2 demands of the body are not completely met by DO2. The causes of a decreasing SvO2 are multiple and reflect the forces operative in Eqs. 5 and 6. That is, either DO2 does not increase in such a way to cover an increased VO2, or DO2 drops because of decrease in either arterial O2 content, cardiac output, or both. Importantly, the normal cardiovascular response of increasing VO2 is to increase O2 extraction and cardiac output. Thus SvO2 normally decreases during exercise despite increasing
DO2. Therefore a drop in SvO2 or ScvO2 does not necessarily mean that tissue hypoxia occurs. The magnitude of the decrease indicates the extent to which the physiological reserves are stressed (Table 1). Whereas in otherwise healthy individuals anaerobic metabolism may occur when SvO2 drops below its normal value of 75% to 30–40% for a substantial period of time, patients with chronic heart failure may live with an SvO2 in this low range without apparent tissue hypoxia, presumably because they have adapted to higher oxygen extraction. These patients can increase their VO2 to a limited degree, however, because O2 extraction is close to its limits as is cardiac output. The cardiocirculatory system may be challenged by two different conditions. Firstly, a drop in DO2 can be induced by anemia, hypoxia, hypovolemia, or heart failure. Secondly, fever, pain, stress etc. may also decrease SvO2 or ScvO2 by increasing whole-body VO2 (Table 2) Since central venous catheterization is commonly performed for a variety of reasons in critically ill patients, it would be useful if ScvO2 could function as a surrogate for SvO2. The central venous catheter sampling site usually resides in the superior vena cava. Thus central venous blood sampling reflects the venous blood of the
upper body but neglects venous blood from the lower body (i.e., intra-abdominal organs). As presented in Fig. 1, venous O2 saturations differ among several organ systems since they extract different amounts of O2. ScvO2 is usually less than SvO2 by about 2–3% because the lower body extracts less O2 than the upper body making inferior vena caval O2 saturation higher. The primary cause of the lower O2 extraction is that many of the vascular circuits that drain into the inferior vena cava use blood flow for nonoxidative phosphorylation needs (e.g., renal blood flow, portal flow, hepatic blood flow). However, SvO2 and ScvO2 change in parallel when the wholebody ratio of O2 supply to demand is altered [5]. The difference between the absolute value of ScvO2 and SvO2 changes under conditions of shock [6]. In septic shock ScvO2 often exceeds SvO2 by about 8% [7]. During cardiogenic or hypovolemic shock mesenteric and renal blood flow decreases followed by an increase in O2 extraction n these organs. In septic shock regional O2 consumption of the gastrointestinal tract and hence regional O2 extraction increases despite elevated regional blood flows [8]. On the other hand, cerebral blood flow is maintained over some period in shock. This would cause a delayed drop of ScvO2 in comparison to SvO2, and the correlation between these two parameters would worsen. Some authors therefore argued that ScvO2 cannot be used as surrogate for SvO2 under conditions of circulatory shock [9]. However, changes in SvO2 are closely mirrored by changes in ScvO2 under experimental [10] and clinical conditions [7] despite a variabledifference between these two variables. This may explain why Rivers et al.
were able to use ScvO2 higher than 70% in addition to conventional hemodynamic parameters as therapeutic endpoint for hemodynamic resuscitation to improve outcome in patients with severe sepsis and septic shock. From a physiological point of view, SvO2 monitoring for “early goal directed therapy” should provide similar re-sults. Given the fact that ScvO2 exceeds SvO2 on average by 8% in patients with septic shock, an SvO2 of about 62– 65% should suffice as endpoint for hemodynamic resuscitation in these conditions, although this has not been tested prospectively. However, the placement of pulmonary artery catheters and the potentially higher risk of this should not result in a delay in the start of the resuscitation of critically ill patients.
Venous oximetry can reflect the adequacy of tissue oxygenation only if the tissue is still capable of extracting O2. In the case of arteriovenous shunting on the microcirculatorylevel or cell death, SvO2 and ScvO2 may not decrease or even showelevated values despite severe tissue hypoxia. As demonstrated in patients afterprolonged cardiac arrest, venous hyperoxia with an ScvO2 higher than 80% is indicative of impaired oxygen use [12].
Conclusion
Low values of SvO2 or ScvO2 indicate a mismatch between O2 delivery and tissue O2 need. While measurement of SvO2 requires the insertion of a pulmonary artery catheter, measurement of ScvO2 requires only central venous catheterization. ScvO2 directed early goal-directed therapy improves survival in patients with septic shock who are treated in an emergency department. However, ScvO2 values may differ from SvO2 values, and this difference varies in direction and magnitude with cardiovascular insufficiency. ScvO2 should not be used alone in the assessment of the cardiocirculatory system but combined with other cardiocirculatory parameters and indicators of organ perfusion such as serum lactate concentration and urine output.
Fig. 1 Arterial and venous oxygen saturations in various vascular
regions [2]
Table 1 Limits of mixed venous oxygen saturation SvO2 >75% Normal extraction
O2 supply >O2 demand 75% >SvO2 >50% Compensatory extraction Increasing O2 demand or decreasing O2 supply 50% >SvO2 >30% Exhaustion of extraction
Beginning of lactic acidosis O2 supplySvO2 >25% Severe lactic acidosis SvO2 <25%>
Physiology of mixed venous and central venous oxygen saturation O2 delivery (DO2) describes whole-body oxygen supply according to the following formula:
DO2 ¼ CO CaO2 ð1Þ where CO is cardiac output and CaO2 is arterial oxygen
content, which itself is the sum of oxygen bound to hemoglobin [product of hemoglobin concentration (Hb) and arterial O2 saturation (SaO2)] and physically dissolved
oxygen [arterial PO2 (PaO2)]: CaO2 ¼ ðHb 1:36 SaO2Þ þ ðPaO2 0:0031Þ ð2Þ
Oxygen demand can be summarized in the whole-body oxygen consumption (VO2), which is expressed mathematically by the Fick principle as the product of CO and
arteriovenous O2 content difference (CaO2 CvO2): VO2 ¼ CO ðCaO2 CvO2Þ ð3Þ where mixed venous O2 content (CvO2) is:
CvO2 ¼ ðHb 1:36 SvO2Þ þ ðPvO2 0:0031Þ ð4Þ Equation 3 may be transposed to: CvO2 ¼ CaO2 VO2 CO ð5Þ As physically dissolved oxygen can be neglected, Eq. 5 may be written as: Hb 1:36 SvO2 ðHb 1:36 SaO2Þ VO2 CO , SvO2 VO2 CO ð6Þ Equation 6 also demonstrates that SvO2 is directly proportional
to the ratio of VO2 to CO. Thus SvO2 reflects the relationship between whole-body O2 consumption and cardiac output. Indeed, it has been shown that the SvO2 is well correlated with the ratio of O2 supply to demand [3].Pathophysiology of central or mixed venous O2 saturation during shock Usually VO2 is independent of DO2 since tissues can maintain O2 needs by increasing O2 extraction when DO2 decreases. However, this mechanism has its limits. Below a so-called critical DO2 compensatory increase in O2 extraction is exhausted, and VO2 becomes dependent on DO2. In this case tissue hypoxia occurs, and a rise in
serum lactate levels may be observed [4]. A decrease in SvO2 and ScvO2 represents an increased metabolic stress, because the O2 demands of the body are not completely met by DO2. The causes of a decreasing SvO2 are multiple and reflect the forces operative in Eqs. 5 and 6. That is, either DO2 does not increase in such a way to cover an increased VO2, or DO2 drops because of decrease in either arterial O2 content, cardiac output, or both. Importantly, the normal cardiovascular response of increasing VO2 is to increase O2 extraction and cardiac output. Thus SvO2 normally decreases during exercise despite increasing
DO2. Therefore a drop in SvO2 or ScvO2 does not necessarily mean that tissue hypoxia occurs. The magnitude of the decrease indicates the extent to which the physiological reserves are stressed (Table 1). Whereas in otherwise healthy individuals anaerobic metabolism may occur when SvO2 drops below its normal value of 75% to 30–40% for a substantial period of time, patients with chronic heart failure may live with an SvO2 in this low range without apparent tissue hypoxia, presumably because they have adapted to higher oxygen extraction. These patients can increase their VO2 to a limited degree, however, because O2 extraction is close to its limits as is cardiac output. The cardiocirculatory system may be challenged by two different conditions. Firstly, a drop in DO2 can be induced by anemia, hypoxia, hypovolemia, or heart failure. Secondly, fever, pain, stress etc. may also decrease SvO2 or ScvO2 by increasing whole-body VO2 (Table 2) Since central venous catheterization is commonly performed for a variety of reasons in critically ill patients, it would be useful if ScvO2 could function as a surrogate for SvO2. The central venous catheter sampling site usually resides in the superior vena cava. Thus central venous blood sampling reflects the venous blood of the
upper body but neglects venous blood from the lower body (i.e., intra-abdominal organs). As presented in Fig. 1, venous O2 saturations differ among several organ systems since they extract different amounts of O2. ScvO2 is usually less than SvO2 by about 2–3% because the lower body extracts less O2 than the upper body making inferior vena caval O2 saturation higher. The primary cause of the lower O2 extraction is that many of the vascular circuits that drain into the inferior vena cava use blood flow for nonoxidative phosphorylation needs (e.g., renal blood flow, portal flow, hepatic blood flow). However, SvO2 and ScvO2 change in parallel when the wholebody ratio of O2 supply to demand is altered [5]. The difference between the absolute value of ScvO2 and SvO2 changes under conditions of shock [6]. In septic shock ScvO2 often exceeds SvO2 by about 8% [7]. During cardiogenic or hypovolemic shock mesenteric and renal blood flow decreases followed by an increase in O2 extraction n these organs. In septic shock regional O2 consumption of the gastrointestinal tract and hence regional O2 extraction increases despite elevated regional blood flows [8]. On the other hand, cerebral blood flow is maintained over some period in shock. This would cause a delayed drop of ScvO2 in comparison to SvO2, and the correlation between these two parameters would worsen. Some authors therefore argued that ScvO2 cannot be used as surrogate for SvO2 under conditions of circulatory shock [9]. However, changes in SvO2 are closely mirrored by changes in ScvO2 under experimental [10] and clinical conditions [7] despite a variabledifference between these two variables. This may explain why Rivers et al.
were able to use ScvO2 higher than 70% in addition to conventional hemodynamic parameters as therapeutic endpoint for hemodynamic resuscitation to improve outcome in patients with severe sepsis and septic shock. From a physiological point of view, SvO2 monitoring for “early goal directed therapy” should provide similar re-sults. Given the fact that ScvO2 exceeds SvO2 on average by 8% in patients with septic shock, an SvO2 of about 62– 65% should suffice as endpoint for hemodynamic resuscitation in these conditions, although this has not been tested prospectively. However, the placement of pulmonary artery catheters and the potentially higher risk of this should not result in a delay in the start of the resuscitation of critically ill patients.
Venous oximetry can reflect the adequacy of tissue oxygenation only if the tissue is still capable of extracting O2. In the case of arteriovenous shunting on the microcirculatorylevel or cell death, SvO2 and ScvO2 may not decrease or even showelevated values despite severe tissue hypoxia. As demonstrated in patients afterprolonged cardiac arrest, venous hyperoxia with an ScvO2 higher than 80% is indicative of impaired oxygen use [12].
Conclusion
Low values of SvO2 or ScvO2 indicate a mismatch between O2 delivery and tissue O2 need. While measurement of SvO2 requires the insertion of a pulmonary artery catheter, measurement of ScvO2 requires only central venous catheterization. ScvO2 directed early goal-directed therapy improves survival in patients with septic shock who are treated in an emergency department. However, ScvO2 values may differ from SvO2 values, and this difference varies in direction and magnitude with cardiovascular insufficiency. ScvO2 should not be used alone in the assessment of the cardiocirculatory system but combined with other cardiocirculatory parameters and indicators of organ perfusion such as serum lactate concentration and urine output.
Fig. 1 Arterial and venous oxygen saturations in various vascular
regions [2]
Table 1 Limits of mixed venous oxygen saturation SvO2 >75% Normal extraction
O2 supply >O2 demand 75% >SvO2 >50% Compensatory extraction Increasing O2 demand or decreasing O2 supply 50% >SvO2 >30% Exhaustion of extraction
Beginning of lactic acidosis O2 supply
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