Shock Syndromes I
CO, Scvo2, and Svo2
Historically, CO was monitored and used as a therapeutic target in most patients with a PAC.
Because treatment of general ICU patients with a PAC has not been shown to improve patient
outcomes, routine use of a PAC has decreased substantially.
ii.
Use of venous oximetry (Scvo2 and Svo2) and echocardiographic findings has largely replaced
use of a PAC.
Scvo2 may be used as a component of an early resuscitation strategy (though it is not a mandatory
component).
A decreased Scvo2 or Svo2 is a sign that tissue oxygen demands are not completely met by Do2.
ii.
Strategies to increase Do2 (and subsequently increase Scvo2 or Svo2) include fluids to optimize
preload, red blood cell transfusion to increase Cao2, and inotropes to increase CO. Because
Pao2 does not contribute significantly to Cao2, it should not be used as a therapeutic target.
If Scvo2 or Svo2 is used as a resuscitation goal, it may be more important to use predefined targets
as well as trends in the early resuscitation period (first 6 hours after presentation) than in the later
resuscitation periods.
| d. | Caution must be used with using Scvo2 or Svo2 in isolation as a resuscitation goal for the following |
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reasons:
The assumption that decreased Scvo2 or Svo2 is synonymous with Do2 and oxygen demand
mismatch is not true because, by definition, tissue oxygen demand exceeds Vo2 in shock.
ii.
During resuscitation, Vo2 depends on Do2, and increasing Do2 will increase the Vo2 without
substantially changing Scvo2 or Svo2 until the critical Do2 threshold is reached.
iii.
Svo2 and CO are not directly proportional and are better described by a hyperbolic relationship.
As such, in hyperdynamic states when the CO is already high, the Svo2 will not increase
substantially with increases in CO.
iv.
Venous hyperoxia may indicate mitochondrial dysfunction and impaired tissue oxygen use or
shunting of blood from peripheral circulation; therefore, achieving a high Scvo2 or Svo2 is not
always best.
CO, Scvo2, and Svo2 are likely best interpreted as either adequate or inadequate (not high or low).
Adequacy is best determined by assessing end-organ perfusion and lactate concentrations.
ii.
If CO, Scvo2, or Svo2 is inadequate, Do2 should be raised.
A strategy of systematically increasing CO to predefined “supranormal” values was not associated
with a mortality benefit; hence, it is not recommended. The decision to augment CO must be
individualized on the basis of organ perfusion.
Lactate clearance (a decrease in lactate concentration from the initial value) suggests improvement
in global tissue perfusion and is associated with a decreased mortality rate.
Significant discordance between lactate clearance and Scvo2 may occur. In one study, 79% of
patients with a lactate clearance of less than 10% had a concomitant Scvo2 of 70% or greater.
A protocol-based approach to resuscitating patients with sepsis or septic shock targeting a lactate
clearance of at least 10% was noninferior to an approach targeting an Scvo2 above 70%.
| d. | Lactate normalization (to a concentration below 2 mmol/L) is a strong independent predictor of |
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survival and may be an even better predictor of outcomes than lactate clearance.
Targeting lactate clearance or normalization is an attractive end point because it does not require
invasive hemodynamic monitoring.
Use of lactate clearance together with Scvo2 as a resuscitation goal may be best because this
improves outcomes compared with use of Scvo2 alone.
Further discussion of lactate clearance as a resuscitation target in patients with sepsis or septic
shock is included later in the chapter.