My small presentation on practical aspect of Mixed venous oxygen and tissue utility of oxygen

1. SvO2 and ScvO2
Monitoring
Dr. Ahsan Ahmed

2. • Measurement of
oxygenation
saturation from mixed
venous blood (SvO2)
in the pulmonary
artery
• Requires Pulmonary
Artery Catheter
insertion
SvO2

3. • The pulmonary artery receives a mixture of
blood from the superior vena cava, inferior
vena cava, and coronary sinus. It serves as a
sample of whole body oxygen utilization.
• Mixed venous oxygen saturation is measured
from blood in the pulmonary artery to sample
deoxygenated blood entering the pulmonary
artery before passing through the lungs

4. Why measure it?
• If SvO2 decreases, it indicates that the tissues are
extracting a higher percentage of oxygen from
the blood than normal.
• A rise in SvO2 demonstrates a decrease in oxygen
extraction, and usually indicates that the cardiac
output is meeting the tissue oxygen need.
• A rise in SvO2 in the presence of a rising lactate is
inappropriate - the patient who has resorted to
anaerobic metabolism

5. • Unfortunately, the cardiac output
measurement only gives us a value, it does
not indicate whether the measured cardiac
output is meeting the patient's needs
• An SvO2 in the normal range, along with a
normal lactate, suggests that the cardiac
output is adequate.

6. • Measuring SvO2 before and after a change can
assist in determining whether the therapy
made the patient better or worse
• By measuring the SvO2 before and after a
change in PEEP, the optimal level of PEEP can
be determined. The "best" PEEP is the level
that improves the SaO2 without causing the
SvO2 to fall.

7. Physiology
• Tissue oxygen need is met when the amount of
oxygen being delivered to the tissues is sufficient
to meet the amount of oxygen being consumed
(VO2). When the oxygen delivery falls below
oxygen consumption needs, lactic acidosis
develops.
• VO2 (Oxygen Consumption) = Cardiac Output X
Hb X (SaO2 - SvO2)
• Oxygen Delivery (DO2) = Cardiac Output X
Oxygen Content (Hb X SaO2)

8. Physiology
• There are 4 fundamental causes for a drop in
SvO2:
• The cardiac output is not high enough to meet
tissue oxygen needs
• The Hb is too low
• The SaO2 is too low
• Oxygen consumption has increased without
an increase in oxgyen delivery

9. Physiology
• ATP (energy) is needed for all cell function and survival.
Tissues require oxygen in order to make ATP
(energy). If the amount of oxygen being received by
the tissues falls below the amount of oxygen required
(because of an increased need, or decreased supply),
the body attempts to compensate as follows:
• First Compensation: Cardiac Output increases
• Second Compensation: Tissue oxygen extraction
increases.
• Third Compensation: Anaerobic Metabolism
increases

10. Techniques
1. Intermittent sampling
Spectrophotometry
Co-oxymetry
2. Indwelling catheter
Incorporating optical fibre in PA and CVC catheter
Continuous spectrophotometry

11. Utility
Correct clinical interpretation of SvO2, or its properly
measured ScvO2 surrogate, can be used to-
• Estimate cardiac output using the Fick equation
• Better understand whether a patient's oxygen delivery
is adequate to meet their oxygen demands
• Help guide clinical practice, particularly when
resuscitating patients using validated early goal
directed therapy treatment protocols
• Understand and treat arterial hypoxemia, and
• Rapidly estimate shunt fraction (venous admixture).

12. Utility
• ScvO2 and SvO2 measurements should never be
interpreted in isolation. Rather, clinical context
must always be considered.
• For example, SvO2 over 70% is generally a good
indicator.
• Yet in the setting of extreme vasodilatory shock
or following mitochondrial poisoning where
organ function is poor and lactate is rising,
an SvO2 of 90% provides is not good at all

13. Disadvantage
• Must be measured from a PAC thus patient exposed to risks
associated with pulmonary artery catheterization (arrhythmia,
pulmonary infarction, embolism, bleeding, pneumothorax, line
sepsis)
• Can be high in a number of situations (sepsis, liver failure,
wedged PAC, administration of high FiO2)
• Can be low in a number of situation (multiple organ failure,
cardiac arrest)
• Requires calibration for changing haematocrit
• Gattinoni RCT showed no benefit from SvO2 monitoring

14. INTERPRETATION
High SvO2
• increased O2 delivery (increased FiO2,
hyperoxia, hyperbaric oxygen)
• decreased O2 demand (hypothermia,
anaesthesia, neuromuscular blockade)
• high flow states: sepsis, hyperthyroidism,
severe liver disease

15. INTERPRETATION
• Low SvO2
• decreased O2 delivery:
• 1. decreased Hb (anaemia, haemorrhage,
dilution) 2. decreased SaO2 (hypoxaemia) 3.
decreased Q (any form of shock, arrhythmia)
• increased O2 demand (hyperthermia,
shivering, pain, seizures)

16. INTERPRETATION
• Causes of High SvO2 despite evidence of End-
organ Hypoxia
• microvascular shunting (e.g. sepsis)
• histotoxic hypoxia (e.g. cyanide poisoning)
• abnormalities in distribution of blood flow
•

17. Problems
• Recent data showing that lactate clearance in sepsis is non-
inferior to continuous ScVO2 monitoring (Jones, JAMA, 2010)
• Titration of end of resuscitation to ScvO2 may not be required
(ICU Monitor, 2010 – summary of Jones, JAMA, 2010)
• ScvO2 does not reflect myocardial perfusion (upstream from the
opening of the coronary venous sinus)

18. COMPLICATIONS
• Same as those associated with central line insertion & PAC
• Equipment failure
• CeVox can block a CVC lumen completely and is prone to drift
• Potential misinterpretation of the measured values if devices are
incorrectly calibrated or malpositioned

19. Clinical application

20. Clinical application

22. Thank You
Taking the earth as the individual and its satellite the moon as the relative, moonlight
can be seen as what can still shed light during the night of an unconscious state

23. • Shunt fraction=Q˙S/Q˙T=(CcO2−CaO2)/(CcO2−CvO2),Shunt
fraction=Q˙S/Q˙T=(CcO2−CaO2)/(CcO2−CvO2),(Eq.7)where Cco2 is
the oxygen concentration in maximally saturated pulmonary end-
capillary blood (i.e., Sco2 = 1). Ignoring dissolved oxygen, this can be
simplified to:Shunt fraction=(1 − SaO2)/(1 − SvO2).Shunt
fraction=(1 − SaO2)/(1 − SvO2).
• For example, when pulse oximeter oxygen saturation is 90% and
Sv−v−O2 is 60%, the shunt fraction is (1 − 0.9)/(1 − 0.6) = 25%, or
when pulse oximeter oxygen saturation is 85% and Sv¯O2 Sv¯O2 is
70%, the shunt fraction is (1 − 0.85)/(1 − 0.7) = 50%. With this
simple equation in mind, bedside estimates of the clinical effect of
diuresis, PEEP, and other treatment strategies on shunt fraction
becomes very straightforward.