Septic shock has been defined as a state in which hypotension persists despite adequate fluid resuscitation or the presence of a lactate level more than 4 mmol/L (so-called sepsis-induced tissue hypoperfusion) in patients with confirmed or suspected infection.1 In these conditions, the Surviving Sepsis Campaign Guidelines suggest to restore mean arterial pressure (MAP) more than 65 mm Hg and normalize lactate levels and central or mixed venous hemoglobin saturation (ScvO2/SvO2).1 Basically this reflects restoring perfusion pressure, improving tissue perfusion and restoring the balance between oxygen delivery and oxygen demand.
A recent study showed a 46% mortality rate in septic patients with increased lactate levels and hypotension.2 In addition, a study using ScvO2 as an endpoint of resuscitation3 and a study using both ScvO2 and lactate clearance as endpoints of resuscitation4 showed significant improvements in mortality. However, a study (mostly septic-shock patients) comparing the use of either ScvO2 or lactate clearance in early resuscitation with common goals for central venous pressure and MAP did not show differences in mortality.5 In addition, a recent study in septic-shock patients comparing early goal-directed therapy based on ScvO2 measurements, protocol-based standard therapy based on systolic blood pressure, and heart-rate measurement without mandatory central venous catheter placement and usual-care based on the bedside physician similarly did not show differences in mortality.6
Therefore, controversy exists on how to use ScvO2 or lactate levels in the resuscitation of septic-shock patients. In this chapter, both the background physiology of both parameters and their clinical use in the treatment of septic-shock patients is reviewed.
PHYSIOLOGY OF VENOUS OXYGENATION
Many aspects of venous oximetry have recently been reviewed.7,8 There is an abundance of oxygen available in the circulation. The red blood cells leave the left ventricle with almost 100% saturated hemoglobin to return, after exchanging oxygen in the microcirculation, to the right ventricle with around 75% saturated hemoglobin. When oxygen delivery to the tissues is decreased, stepwise oxygen consumption is maintained by using this surplus of oxygen resulting in a gradual decrease of venous oxygenation.9 When the decrease in oxygen delivery reaches a critical level, lactate levels generally start to increase.10,11 In these models, venous oxygenation is proportional to cardiac output (CO) as arterial oxygen saturation and hemoglobin levels are usually stable. Venous oxygenation in these conditions thus reflects the balance between whole body oxygen demand and CO. It is important to realize that SvO2 does not reflects regional venous oxygenation levels.12 When cardiac function is normal, decreases in oxygen content are met by increases in CO thus minimally affecting venous oxygenation.13 However, when cardiac function is limited or the decrease in oxygen content is excessive, the surplus of oxygen in the system is mainly used to compensate for changes in oxygen ...