A. List the normal values for mixed venous blood gases and briefly explain the factors determining mixed venous oxygen tension.(1996)
B. Briefly describe the factors that influence the partial pressure of oxygen in mixed venous blood (00A2)
C. What factors influence the mixed venous CO2 tension. Briefly explain how these factors exert their influence. (1993)
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.
Has 3 major component:
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.
PO2 from IVC is normally higher (SO2 77%) than from SVC (SO2 71%)
=> because kidney takes 25% of cardiac output but use only 7-8% of body's O2 consumption
=> IVC receives blood more oxygen rich.
With severe haemorrhage,
=> PO2 from SVC may be higher because of renal vasoconstriction.
Typical value: 40mmHg or 75% oxygen saturation
NB: 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.
Typical value: 46mmHg or 52mLs of CO2 per 100mL blood
=> (assuming SvO2 of 75%)
If SvO2 is 97%,
=> at PvCO2 of 46mmHg, CvCO2 = 50mLs/100mL
=> due to Haldane effect
NB. Arterial PaCO2 = 40mmHg
NB. Arterial CaCO2 = 48mLs/100mL
"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"
=> VO2 = Q (CaO2 - CvO2)
From Fick equation,
=> CaO2 - CvO2 = VO2 / Q
=> CvO2 = CaO2 - VO2/Q
O2 Concentration = 1.39 x [Hb] (g/100mL) x Sat% + 0.003 x PO2 (mmHg)
Thus, 1.39 x Hbg x SvO2 = 1.39 x Hb x SaO2 - VO2/Q [ignoring effectos of dissolved O2]
=> SvO2 = SaO2 - VO2/(Qx1.39x[Hb])
NB: Different from examiner's comment.
NB: SvO2 is derived so O2 dissociation curve (which is SpO2 vs PO2) can be used.
SvO2 = SaO2 - VO2/(Qx1.39x[Hb])
SvO2 is increased when:
As SvO2 increase, PO2 is increased.
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.
When ODC moves, given the same SvO2, PvO2 will increase.
=> PvO2 increase when ODC moves to the right due to:
Bohr effect - 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)
Similar to Fick's principle
Production of CO2 = Elimination of CO2
VCO2 = Q (CaCO2-CvCO2)
=> CvCO2 = CaCO2 - VCO2/Q
CvCO2 is increased when
NB. CO2 output and production are the same in steady state, but different in dynamic state because much of CO2 produced is diverted into body stores.
When CO2 dissociation curve moves, given the same SvCO2, PvCO2 will increase
=> PvCO2 increase when dissociation curve moves to right due to:
Mixed venous O2 tension is increased by:
O2 is carried in blood in two forms:
Dissolved O2 follows Henry's Law
=> amount dissolved is proportional to partial pressure
For each mmHg of PAO2, 0.003 mL of O2 is dissolved in 100 mL of blood
O2 capacity = maximum amount of O2 that can be bound to Hb
=> 1g of Hb can combine with 1.39mL of O2
(per West. Alternative values are 1.34 or 1.36mL)
(per Nunn 1.31mL of O2 per gram of Hb)
=> =1.39 x [Hb] (g/100mL)
Normal blood has 15grams of Hb per 100mL
=> O2 capacity = 20.85mL O2 per 100mL blood
O2 saturation (%) = O2 combined with Hb / O2 capacity
=> = (O2 content - dissolved O2)/O2 capacity
NB. West defined O2 capacity as maximum O2 bound to Hb, thus doesn't include dissolved O2.
NB. Nunn includes dissolved O2 in its definition of O2 capacity.
Functional saturation = [HbO2]/([HbO2]+[DeoxyHb])
Fractional saturation = [HbO2]/[Total Hb]
Total Hb include HbO2, DeoxyHb, MetHb, COHb
Pulse oximeter measures HbO2 and deoxyHb, but may be calibrated to allow for MetHb and COHb
O2 concentration (mL/100mL)
= 1.39 x [Hb](g/100mL)x Sat(%) + 0.003x PO2(mmHg)
Remember this is NOT content.
Unit for O2 concentration is mL of O2 per 100mL of blood.
Once the volume of blood is known, then the content of O2 can be calculated.
Sigmoid shaped.
[Assuming temp = 37C, pH = 7.40, Base excess = 0]
[See diagram 20050305(1) - Oxygen dissociation curve]
In adult, P50 = 27mmHg
With foetal haemoglobin, P50 is lower at about 18mmHg
=> due to reduced binding of 2,3 DPG
Two portions:
Fall in alveolar PO2
=> little change in O2 sats.
As peripheral tissues extract O2
=> drop in PO2 is not too great
=> maintains O2 diffusion gradient
NB. positive cooperativity - when one of the 4 globin chains in Hb binds with O2, it causes structural changes which increase O2 affinity of the haem of the remaining chains => cause the sigmoid shape
Two effects
Carboxyhaemoglobin dissociation curve is extremely left-shifted and is a rectangular hyperbola.
Question about the correctness of the formula in examiner's comment.
? effects of carbon monoxide
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Updated | 20050305 |
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