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 Venous admixture

اذهب الى الأسفل 
كاتب الموضوعرسالة
الصقر الجارح
المدير العام عمرو محمد
المدير العام عمرو محمد
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ذكر
القوس
عدد المساهمات : 3025
سمعة المساهمه : 35405
تاريخ الميلاد : 30/11/1996
تاريخ التسجيل : 25/04/2009
العمر : 21

مُساهمةموضوع: Venous admixture    الإثنين فبراير 13, 2012 12:29 pm

Venous admixture

Define 'Venous Admixture'. Briefly explain how venous admixture influences arterial O2 tension and how an increase in inspired O2 concentration may affect this. (02A3) (95B1)
Definition of venous admixture
Nunn: the degree of admixture of mixed venous blood with pulmonary end-capillary blood, that would be required to produce the observed difference between the arterial and the pulmonary end-capillary PO2.
Brandis: the amount of mixed venous blood that would have to be added to pulmonary end-capillary blood to produce the observed drop in arterial PO2 (PaO2) from the PO2 in the end-capillary blood (Pc'O2).
Venous admixture is a theoretical/calculated amount, not an actual amount.
assumption: pulmonary end capillary blood (Pc'O2) is taken as the "ideal" alveolar PaO2.
assumption: all blood either go past areas of normal V/Q, or completely shunted.
assumption: all shunted blood have the same PO2 as mixed venous blood.
PO2 in true shunts differs from PO2 in mixed venous blood.
PO2 in blood from low V/Q area also differ from PO2 in mixed venous blood.
Components of venous admixture
1. Anatomical shunt (aka true shunt, extra-pulmonary shunt)
Blood which enters the arterial system without passing through ventilated areas of the lung.
1.1. Physiological
Coronary blood enters LV via the thebesian veins
Some bronchial artery blood enters the pulmonary veins
Blood from these sources is NOT mixed venous blood and thus would have different PO2 from PvO2.
1.2. Pathological
These blood may be of mixed venous bloods.
Congenital heart disease with R->L shunt
Perfusion of non-ventilated alveoli (V/Q=0)
(atelectasis, bronchial obstruction)
Pulmonary arterio-venous shunts (haemangioma)
2. Regions of low V/Q (lower than N=0.86)
2.1. Physiological
Normal scatter of V/Q ratios
Changes with posture
2.2. Pathological
Abnormal scatter of V/Q ratios
Alveolar-capillary block
Measurement of venous admixture
QT x CaO2 = (QT-QS) x Cc'O2 + QS x CvO2
=> QS x (Cc'O2 - CvO2) = QT x (Cc'O2 - CaO2)
=> QS/QT = (Cc'O2 - CaO2) / (Cc'O2 - CvO2)
QS = blood flow through the shunt
QT = total blood flow
CaO2 = concentration of O2 in arterial blood
Cc'O2 = concentration of O2 in pulmonary end-capillary blood
CvO2 = mixed venous blood
[See diagram 20050224(1) - Venous admixture]
Shunt Equation:
QS/QT = (Cc'O2-CaO2) / (Cc'O2 - CvO2)
Normally cardiac output is used for QT.
=> QS/QT = 2-3%
CaO2 - measured by ABG
Cc'O2 - derived from the "ideal" alveolar PAO2 (using the alveloar gas equation)
(assuming Pc'O2 = ideal PAO2)
CvO2 - measured from RV or pulmonary artery
NB. IVC and SVC PO2 are different, and at RA these blood remain separate.
Shunt vs V/Q inequality
Shunt refers to blood which enters the arterial system without passing through ventilated areas of the lung.
Shunt includes:
some bronchial blood flow
thebesian circulation
atelectasis, bronchial obstruction, congenital heart disease with R to L shunt
Shunt excludes blood draining any alveoli with a V/Q ratio >0.
V/Q inequality excludes shunts.
Effects of venous admixture on arterial PaO2 and PaCO2
Venous admixture reduces the arterial O2 content and increases the arterial CO2 content.
Because PaO2 is usually on the flat part of the haemoglobin dissociation curve,
=> small reduction in O2 content leads to large drop in PaO2
=> increased A-a gradient
Because CO2 dissociation curve is usually steep and more linear,
=> increases in CO2 content don't lead to large increase in PaCO2
In clinical settings, venous admixture
=> reduced PaO2
=> compensatory hyperventilation
=> more than enough to offset the small increase in PaCO2
=> PaCO2 often reduced rather than increased
Increases in PaCO2 are seldom caused by venous admixture.
Distinction between effects of shunt and effects of V/Q inequality
It usually is impossible to say to what extent the calculated venous admixture is due to a true shunt or to perfusion of alveoli with low V/Q.
If FIO2 is increased, the effect on PaO2 depends on the cause of the venous admixture.
If oxygenation is impaired by true shunt, increases in FIO2 will lead to increases in the PaO2 as per iso-shunt diagram.
10% shunt requires FIO2 30% to restore normal PaO2
20% shunt requires FIO2 57% to restore normal PaO2
30% shunt requires FIO2 97% to restore normal PaO2
40% shunt - normal PaO2 cannot be restored
50% shunt - increasing FIO2 has almost no effect on PaO2
[See diagram 20050224(3) - Iso-shunt diagram Nunn p190]
If oxygenation is impaired by V/Q scatter, increases in FIO2 will cause the PaO2 to approach the normal PaO2 value for that particular FIO2.
At FIO2 of 100%, V/Q scatter has almost no effect on PaO2.
[See diagram 20050224(2) - Shunt vs V/Q inequality]
Quantification of V/Q scatter can be measured by the alveolar-arterial PN2 difference.
<= because PN2 difference is not affect by shunt at all.
Effects of cardiac output on venous admixture
Reduction in CO produces two opposing effect:
Reduction in CO
=> reduction in mixed venous O2 content
=> greater reduction in PaO2 (provided shunt fraction is the same)
Reduction in CO
=> reduction in the shunt fraction (except for atelectasis)
(maybe due to pulmonary vasoconstriction secondary to reduced PvO2)
Overall, the effect of reduced CO is
reduced shunt
more desaturated mixed venous blood
roughly unchanged PaO2, and thus A-a gradient
Isoshunt
Where venous admixture is low, an increased PIO2 could improve the observed level of PaO2 and compensate for the V/Q mismatch and shunt that is present. However, due to the shape of the oxygen dissociation curve, such compensation by increased PIO2 is only to limited extent. Where venous admixture is high, PaO2 will remain low despite increased PaO2.
However, if there is an great increase in barometric pressure and the amount of dissolved O2 becomes significant, then increased PIO2 can compensate better.
Additional notes
Other versions of the alveolar gas equation
Rossier, Mean
PAO2 = PIO2 - (PaCO2/R)
Riley
PAO2 = PIO2 - (PaCO2/R) x [1-FIO2(1-R)]
Selkurt
PAO2 = PIO2 - PaCO2 x [FIO2 + (1-FIO2)/R]
Filley, MacIntosh, & Wright
PAO2 = PIO2 - PaCO2 x [(PIO2-PEO2)/PECO2]
=> alllows for disequilibrium of inert gases
Effect of V/Q inequality on PaO2
V/Q inequality lowers PaO2 because
more blood come from areas of low V/Q
shape of oxygen dissociation curve
Alveoli with high V/Q ratio are on the flatter part of the haemoglobin dissociation curve than alveoli with a low V/Q.
=> the beneficial effect of high V/Q on oxygen content is not enough to compensate for the adverse effect of low V/Q on oxygen content.
Alveolar-arterial PO2 gradient (A-a gradient)
Normal gradient < 15mmHg (2 kPa)
+3 mmHg each decade over 30y.o.
Increased A-a gradient can be caused by
pulmonary collapse/consolidation
neoplasm
infection
alveolar destruction
drugs
- vasodilators
- volatile anaesthetics
hormones
- pregnancy and progesterone
- hepatic failure
extrapulmonary shunting
Increased A-a gradient is the most common cause of arterial hypoxemia
Factors influencing A-a gradient
Magnitude of venous admixture
=> with small shunts, the magnitude of venous admixture is proportional to A-a gradient
=> with larger shunts, the relationship is lost.
V/Q scatter
Actual alveolar PO2 (PAO2)
=> due to the non-linear shape of the oxygen dissociation curve, with everything else being equal
=> the greater the PAO2, the greater the A-a gradient
Cardiac output
=> cardiac output is inversely proportional to alveolar/arterial O2 content difference, given the same venous admixture
BUT, venous admixture also decrease with reduced CO
=> PaO2 is relatively unchanged (see above)
Hb concentration
=> [Hb] does not influence pulmonary end-capillary/arterial oxgen content difference
But increase in [Hb] would cause small decrease in the tension difference
Alveolar ventilation
=> increased ventilation increase both PAO2 and A-a gradient.
When venous admixture <3%, PaO2 will always increase.
When venous admixture >3% AND ventilation >1.5L/min, the higher the shunt/ventilation,
=> lower PCO2
=> lower CO
=> greater alveolar/arterial O2 content difference
=> A-a gradient is greater than the increase in PAO2
=> PaO2 can actually decrease with higher ventilation
Cardiac output and shunt
Decrease in cardiac output
--> Decrease mixed venous O2 concent
--> Greater reduction in PaO2 if shunt fraction is constant
But
Decrease in cradiac ouput
--> Approximately proportional reduction in the shunt FRACTION
* Except in atelectasis
Overall, two changes cancel each other out
--> Little change in PaO2
Examiner's comment
According to examiner's comment, need to have:
An adequate definition
A brief discussion of shunt and V/Q inequality, both physiological and pathological
A brief discussion of the contribution of V/Q inequality and shunt to changes in PaO2
A differentiation between true shunt and V/Q inequality
An explanation of the effect of cardiac output on venous admixture
An explanation of the effects of increased FiO2 on true shunt and on venous admixture due to V/Q inequality
(extra mark) sources of physiological and pathological shunt and V/Q inequality
(extra mark) effect of the shape of Hb saturation curve on the response to increasing FiO2
(extra mark) extra-pulmonary shunts (normal and abnormal)
(extra mark) iso-shunt diagram
(extra mark) shunt equation
(common mistake) incorrect labelling of isoshunt diagram
normal value




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Venous admixture
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