Viva F6(v, vi)

What is shunt?

• "Vascular connection between circulatory pathways so that venous blood is diverted into vessels containing arterialized blood"
• "blood that enters the arterial system without going through ventilated areas of the lung"

What is venous admixture, and how is it different from shunt?

• "venous admixture" is the calculated estimate of how much hypoxic blood would be required to produce the measured arterial oxygen results, for a given cardiac output.
• It is a calculated volume of deoxygenated blood from the venous circulation which appears to have bypassed the lungs, not participating in any gas exchange. 
• True" intrapulmonary shunt, in contrast, is the volume of venous blood which actually bypassed the aerated alveoli, and returned deoxygenated blood to the left heart via the pulmonary circulation. 
• True" shunt does not integrate the contribution of Thebesian veins and alveolar regions with V/Q ratios between 0 and 1.0, or any other added sources of extra venous blood contributing to the systemic circulation (like intracardiac right-to-left shunts) 
• Therefore the calculated venous admixture volume will usually be larger. 
• It is actually impossible to measure "true" shunt, so we resort to using venous admixture as a surrogate for shunt, and report it as "shunt fraction", or Fshunt

What are the sources of hypoxic blood that contribute to venous admixture?

• "True" shunt through useless lung: 
  • blood passing through lung with V/Q ratio of 0 (i.e. no V, all Q). This blood will exchange no gas. 
• "V/Q scatter": 
  • Lung regions which have a V/Q ratio less than 1 will have inefficient gas exchange, and will return pulmonary venous blood which is incompletely oxygenated. 
• Thebesian veins,
  • flow contributes 0.12% to 0.43% of the total aortic flow.
  • Oxygen content within these veins is probably very low, and the impact on the A-a difference is not trivial.
• Bronchial veins 
  • 1% of total cardiac output.
  • in patients with bronchiectasis or COPD this contribution could be considerable - as much as 10% of the cardiac output.
• Congenital heart disease 
  • right-to-left shunting: right heart ejects into the left circulation, bypassing the lungs.
• Intrapulmonary arteriovenous connection,
  • eg. AVM or fistula, would do exactly the same thing as the intracardiac shunt
• Intrapulmonary sources of poorly oxygenated blood
  • eg. lung tumour, or portopulmonary shunts in liver disease
• Virtual shunt 
  •  When one's measurement of shunt is performed without a mixed venous blood sample, the resulting shunt is referred to as virtual.
  • This is  "the shunt which would explain the relationship between arterial PO2 and inspired oxygen concentration if the arterial-to-mixed venous oxygen concentration difference was 5 vol %".
  • As far as one can tell, this terminology is unique to works published by, or about, Nunn (see Lawler & Nunn, 1984).

How much shunt is normal?

• Different sources say different things
• Venous admixture, as measured in normal subjects breathing room air, is usually about 3%.
• True shunt should be 0% in healthy people

How do you measure shunt?

• The shunt equation, otherwise known as the Berggren equation, is used to calculate the shunt fraction:

Qs/Qt = (Cc_O2 - Ca_O2) / (Cc_O2 - Cv_O2)
where
    Qs/Qt = shunt fraction (shunt flow divided by total cardiac output)
    Cc_O2 = pulmonary end-capillary O₂ content, same as alveolar O₂ content
    Ca_O2 = arterial O₂ content
    Cv_O2 = mixed venous O₂ content

• A criticism of all shunt calculations is the fact that they use a two-compartment model.
• If the FShunt is 25%, the equation leads one to believe that in a two-compartment lung, 25% of the blood is travelling through the non-ventilated compartment.
• In reality, the lung is a mixture of heterogeneous units, each with a different V/Q ratio. The shunt equation is therefore a very gross estimate of oxygenation defects.

How do you measure "true" shunt?

• Using 100% FiO₂:
• As the FiO₂ increases, areas of low V/Q ratio would suddenly find themselves ventilated with a higher oxygen concentration.
• Even small increases in oxygen concentration here will yield substantial increases if endcapillary oxygenation, because of the steepness of the oxygen-haemoglobin dissociation curve.
• Thus, the difference between endcapillary blood and arterial blood would diminish, such that at 100% FiO₂ the contribution of V/Q scatter would be minimal.
• Sure, there would still be lung units with an extremely low V/Q ratio (less than 0.10), but these are usually few, and the amount of blood passing through them would be minimal (ergo their contribution to arterial blood would also be small).
• However, for lung units with "true" shunt, V/Q = 0, and no amount of extra inspired oxygen is going to improve their oxygenation. 
• As a consequence of this, breathing a high FiO₂ essentially eliminates the contribution of V/Q scatter to the total shunt fraction, and what is left over is the "true" shunt.

What are the effects of shunt on oxygenation?

• Venous admixture gives rise to systemic hypoxemia.
• The degree of hypoxemia is generally said to be roughly proportional to the shunt fraction.
• At a shunt of 50%, the arterial oxygen tension at 21% FiO₂ is somewhere in the order of 53 mmHg.
• A shunt fraction of 25% is enough to drop one's oxygen saturation into the low 90s.

What are the effects of increasing inspired oxygen on shunt?

• lung regions with true shunt (V/Q = 0) are not expected to increase their endcapillary oxygen content in response to an increase in alveolar oxygen.
• as the shunt fraction increases, so the increase of FiO₂ should yield smaller and smaller benefits, ultimately becoming pointless

What are the effects of shunt on CO₂ clearance?

• Shunt does not make much of a difference to CO₂ clearance, and in fact CO₂ clearance may increase in the presence of a massive shunt. 
• The main reason is the increase in alveolar ventilation associated with hypercapnia
• In patients who are unable to increase their alveolar ventilation, PaCO₂ may increase slightly (eg. by up to 15-30% with a shunt fraction of 50%)
• Low cardiac output and metabolic acidosis increase the effect of shunt on PaCO₂