Central Venous Oxygen Saturation monitoring (SCVO2) and DO2 (oxygen delivery)
In the normal oxygen cycle:
Blood enters the R side of the heart; as it flows through the lungs alveoli, O2 molecules attach to hemoglobin (4:1 ratio)
The oxygenated blood passes through the L side of the heart and out into the tissue
Upon reaching capillary beds, an average patient extracts one molecule of oxygen from each hemoglobin, leaving RBC 75% saturated with oxygen as they return back to the R side of the heart
The amount of O2 saturation in oxygenated blood filling the arterial system as it passes into the capillary bed is DO2 (potential oxygen delivery).
Delivery of oxygen is dependent on hemoglobin molecules to carry the oxygen, cardiac output, and the saturation of the hemoglobin molecules (SpO2). There are four ways to increase potential oxygen delivery.
Increase FiO2: as long as disease process does not inhibit the transfer of O2 in alveolar beds
Mechanical Ventilation: increase pressure (PEEP) for O2 to transfer across alveolar membranes. BiPAP does this as well but to a lesser extent
Give blood: increasing Hgb levels through transfusion may result in extra O2 carrying capacity, although increased blood transfusions can increase mortality
Deliver more blood volume: increase cardiac output (SV x HR)
When blood returns to the R side of the heart after passing through the arterial system, venous oxygenation can be measured through the saturation of hemoglobin molecules. This central venous oxygen satuation is meant to reflect the balance of DO2 to consumption (VO2); although it only gives you a snapshot in time
Patients conditions can vary from minute to minute and you must take this into account
Continuous SCVO2 monitoring exists; often through a PA catheter (SVO2) or CVL (SCVO2).
Advocated by surviving sepsis guidelines as part of EGDT; goal >70%. Controversial
This is because it showed a significant mortality reduction in sepsis (17%)
Normal SCVO2 - drawn from a central line; 70-80% (because normal oxygen cycle delivers one molecule of oxygen to capillary bed, leaving ~75% of O2 still bound to hemoglobin)
SCVO2 measure O2 sat returning from upper body; this runs 5-10% higher than SVO2. SVO2 measures blood returning from lower and upper body mixed with coronary return - which is why it is a mixed venous oxygen saturation.
>80% SCVO2: cytoxic dystoxia (e.g. severe sepsis, mitochondrial dz, cyanide poisoning); microcirculatory shunting (e.g. sepsis, liver failure, hypothyroidism); L—>R shunts
how should i approach a low scvo2?
Like many things in medicine, by determining the cause. The ideal time to intervene is when SCVO2 is at 50-70% range.
Ways to treat:
Decrease patients metabolic demand (need for extraction) - hypothermia, relaxation/sedation, sepsis, positive support ventilation
Increase O2 delivery/saturation of hemoglobin - increase FiO2
Increase hemoglobin circulating - give blood
Increase cardiac output - positive inotropes such as dobutamine, afterload reduction, fluid administration, IABP
Dobutamine: Low dose (<5) primarilly is positive inotrope, higher dose (5-20) reduces some afterload by decreasing SVR as well as produces positive inotropy