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A. MIXED VENOUS BLOOD
Mixed venous blood - mixture of all the systemic
venous blood draining from all the tissue capillary
beds of the body, excluding shunted blood (i.e.
central or peripheral shunt). Pulmonary venous
blood is not included.
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A. List the normal values for mixed venous blood gases and briefly
explain the factors determining mixed venous oxygen tension?
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It Has 3 major component: SVC ;IVC ;coronary
sinus.
Sustained tissue hypoxia is one of the most
important cofactors in the development of
multiorgan failure
Oxygen delivery – tissue demand mismatch can
be measured by venous oximetry.
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Oxygen Delivery (DO2) =
Cardiac Output (HR X Stroke Volume) X Oxygen Content (Hb X SaO2)
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First Compensation: Cardiac Output increases
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Second Compensation: Tissue oxygen
extraction increases. (decreased SvO2).
Third Compensation: Anaerobic Metabolism
iIncreases:Prolonged anaerobic metabolism leads
to energy depletion and metabolic acidosis.
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If SvO2 decreases, it indicates that the tissues are
extracting a higher o2.
In otherwords, a decreased SvO2 indicates that the
cardiac output is not high enough to meet tissue
oxygen needs.
A rise in SvO2 demonstrates a decrease in oxygen
extraction
A return of the SvO2 to normal suggests patient
improvement.
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Why
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A rise in SvO2 in the presence of a rising lactate
= anaerobic metabolism (third compensation)
should have evidence of a high cardiac output
and increased extraction. This is an ominous
finding, suggesting that the tissues are unable to
extract. It can be seen in late septic shock, or in
cell poisoning such as cyanide.(Desoxyia)
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Measuring SvO2 before and after a change can
assist in determining whether the therapy made
the patient better or worse.SvO2 can also be
useful when evaluating changes to ventilator
therapy, especially in unstable patients.
The "best" PEEP is the level that improves the
SaO2 without causing the SvO2 to fall.(PEEP
affect COP)
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VO2 (Oxygen Consumption) = Cardiac Output X Hb X
(SaO2 - SvO2)
There are 4 fundamental causes for a drop in SvO2:
1. The cardiac output is not high enough to meet tissue
oxygen needs
2. The Hb is too low
3. The SaO2 is too low
4. The oxygen consumption has increased without an
increase in oxgyen delivery(ERO2)
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Pathophysiology of mixed venous oxygensaturation and central venous oxygen saturation
In healthy individuals, anerobic metabolism may occur when SvO2 drops below its normal value of 75% to 30–40%
Normal oxygen extraction is 25–30% corresponding to a ScvO2
>65%
< 65% = Impaired tissue oxygenation
>80% = High PaO2; or suspect:
1-Cytotoxic dysoxia (e.g. cyanide poisoning, mitochrondial
disease, severe sepsis)
2-Microcirculatory shunting (e.g. severe sepsis, liver failure,
hyperthyroidism)
3-Left to right shunts
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To measure venous oxygen saturation
Central venous oxygen saturation (ScvO2)
Mixed venous oxygen saturation (SvO2)
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Mixed venous blood is best taken from
pulmonary artery as adequate mixing has
occurred. Sometimes right ventricle can be
used. In right atrium, the bloods are not
adequately mixed.
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Patients with injury suggestive of blood loss.
HR, BP, Urine output, CVP and SCVO2 measured.
Blood loss estimated.
SCVO2 most sensitive indicator blood loss
SCVO2 <65% associated with increased injury,
blood loss and transfusion requirements.
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SCVO2 Monitoring in Trauma
In severe sepsis and septic shock
In a retrospective study, Varpula et al. showed
the most important hemodynamic variables
relevant to outcome are mean arterial
pressure and lactate levels in the first 6 h and
mean arterial pressure, SvO2, and central
venous pressure in the first 48 h.
1-In patients with severe sepsis or septic shock a goal of
70% for central venous oxygen saturation corresponds to
a mixed venous oxygen saturation between 60 and
65% !!!
2-Reflecting the balance between oxygen delivery (DO2)
and consumption (VO2).
3-May have a role in the management of postoperative
patients
Difference between SvO2 and ScvO2
ScvO2 is usually less
than SvO2 by about 2–
3%
In septic shock ScvO2
often exceeds SvO2 by
about 8%.
During anesthesia,
ScvO2 may exceed
SvO2 by up to 6%
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1• Coronary Sinus
The heart has a High O2 extraction ratio (55-65%) The PO2
of coronary sinus blood is thus Typically low > 20mmHg
Increase in myocardial oxygen consumption can only be
met by increasing coronary blood flow
2• PO2 of SVC is higher than IVC
PO2 of SVC and IVC: PO2 from IVC is normally higher (SO2
77%) than from SVC (SO2 71%)
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2. FACTORS AFFECTING PO2 OF MIXED VENOUS BLOOD
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because kidney takes 25% of cardiac output but use
only 7-8% of body's O2 consumption
; IVC receives blood more oxygen rich.
Important
With severe haemorrhage,PO2 from SVC may be
higher because of renal vasoconstriction.
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The PvO2 and SvO2 of mixed venous blood has a
typical value of 40mmHg or 75% oxygen saturation
This mixed venous blood point does NOT lie on the
standard oxygen dissociation curve because at
mixed venous blood level, the curve is right-shifted
because of increased PvCO2 and decreased
pH(CvO2 = 15mL/100mL)
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Why does PvO2 not lie on the Standard Oxygen Dissociation Curve ?
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Typical value: 46mmHg O2 per 100mL blood
(assuming SvO2 of 75%)
If SvO2 is 97%, > at PvCO2 of 46mmHg, CvCO2 =
50mLs/100mL > due to Haldane effect
NB
PaCO2 = 40mmHg
CaCO2 = 48mLs/100mL
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.PvCO2 and SvCO2 of mixed venous blood
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"It is the Amount of O2 extracted from respired gases equals
the amount added to the blood that flows through the lung"
i.e. "O2 consumption per unit time = O2 taken up by
pulmonary blood flow per unit time"
Fick equation VO2 = Q (CaO2 - CvO2)
VO2 = O2 consumption per minute (mL O2/time)
Q = pulmonary blood flow (mL/time)
CaO2 = O2 concentration in blood leaving lung (mL/100mL)
CvO2 = O2 concentration in mixed venous blood (mL/100mL)
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What is Fick's principle?
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Factors affecting mixed venous O2 tension
From Fick equation
VO2 = Q x (CaO2 - CvO2)
CvO2 = CaO2 - VO2/Q
SvO2 = SaO2 - VO2/(Q x 1.34 x [Hb])
NB:SvO2 is derived so O2 dissociation curve (which
is SpO2 vs PO2) can be used
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Firstly When O2 dissociation curve is fixed:
SvO2 = SaO2 - VO2/(Qx1.34x[Hb])
SvO2 is increased when:
• SaO2 is increased
• O2 consumption (VO2) is decreased
• cardiac output (Q) is increased
• Hb concentration is increased
As SvO2 increase, PO2 is increased.
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What happens when Oxygen Dissociation Curve is Shifted To The Right?
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However, at mixed venous blood level of PO2
(40mmHg), changes in SvO2 doesn't have as great
an effect on PvO2 as it would at higher level of
PO2.
PvO2 will increase when ODC moves to the right
due to:• increased PvCO2;• increased [H+] (i.e.
drop in pH);• increased temperature;increased red
cell 2,3 DPGH
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The Bohr effect denotes CO2 loading assisting in
O2 unloading from Hb (for comparison, Haldane
effect is when O2 unloading from Hb helps with
CO2 loading)
Majority of Bohr effect is due to pH change caused
by changes in PO2)
What are the Factors affecting mixed CO2 tension?
According to Fick's principle
Production of CO2 = Elimination of CO2
VCO2 = Q (CaCO2-CvCO2) CvCO2 = CaCO2 - VCO2/Q
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What is the Bohr effect ?
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Mixed venous O2 tension is increased by:
increased SaO2
decreased O2 consumption
increased cardiac output
increased Hb concentration
right shift in ODC, due to:
* increased PvCO2
* increased [H+]
* increased temperature
* increased red cell 2,3DPG
SUMMARY
Take Home Message
Difference between SvO2 and ScvO2
Early goal-directed therapy in the treatment of
severe sepsis and septic shock is important to
reduce mortality and morbidity.
In major surgery, whether reductions in ScvO2
are independently associated with post-operative
complications still needs a large interventional
multi-center study
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ScvO2 and SvO2 are superior to
conventional hemodynamic monitoring
parameters in the assessment of the
adequacy of global tissue oxygenation
Continuous monitoring of ScvO2 and SvO2 in
the framework of hemodynamic goals and
treatment algorithms have resulted im
improved patient outcome H
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ScvO2 closely parallels SvO2 saturation
In patients with shock ScvO2 is 7 – 10% (mean) higher
than SvO2
These differences between ScvO2 and SvO2 saturation
result from changes in the regional blood flow and
oxygen supply/demand ratio
Normal or high ScvO2 and SvO2 do not rule out tissue
hypoxia on the organ or regional level