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HOSAM M ATEF

HOSAM

VSO2(venous oximetry) Mixed Venous O2 Sat

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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

Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med 2001

Changes in central venous saturation after major association with outcomesurgery

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

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