HOSAM M ATEF

HOSAM 1

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.

H 2

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.

H 3

Oxygen Delivery (DO2) =

Cardiac Output (HR X Stroke

Volume)

X

Oxygen Content (Hb X SaO2)

H 4

Second Compensation: Tissue oxygen extraction

increases. (decreased SvO2).

Third Compensation: Anaerobic Metabolism

iIncreases:Prolonged anaerobic metabolism leads

to energy depletion and metabolic acidosis.

H 5

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.

H 7

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)

H 8

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)

H 9

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)

H 10

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

12

Central venous oxygen saturation (ScvO2)

Mixed venous oxygen saturation (SvO2)

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.

H 14

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.

H 15

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

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%

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%)

H 21

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.

H 22

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)

H 23

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

H 24

"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)

H 25

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

H 26

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.

H 27

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 DPG

H 28

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)H 29

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

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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

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 32

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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