24A02: Exam Report

(a) Describe venous admixture and the sources contributing to it in an adult (60% of marks).
(b) Explain the effects of supplemental oxygen on arterial hypoxaemia (40% of marks).

43% of candidates passed this question.

  1. (a)  This part of the question required candidates to provide a definition of venous admixture and provide detail on the sources. This would include anatomical (including atelectasis/closing capacity) and V/Q Mismatch or Scatter. V/Q Scatter was commonly omitted from answers. The use of the verb “describe” implies that further details are required beyond a simple list of the sources (such as a description of their mechanism and relative importance).

  2. (b)  This part required the effect supplemental oxygen on the many causes of arterial hypoxaemia to be explained. This would require the effect that this has on areas of true shunt and different degrees of shunt fraction and also on V/Q scatter. Information for this can be found on Nunn’s Respiratory Physiology.

F6vi / 24A02: (a) Describe venous admixture and the sources contributing to it in an adult (60% of marks).
(b) Explain the effects of supplemental oxygen on arterial hypoxaemia (40% of marks).

Part A

Definition

Amount of mixed venous blood required to mix with pulmonary capillary blood to produce the observed alveolar- arterial PO2 difference. This can also be described as shunt.

Shunt may be physiological or pathological, accounting for any blood which has passed from the right to the left sided of the circulation without participating in gas exchange.

V/Q of 1 = optimal ventilation/ perfusion matching

There are 2 anatomical physiological sources of shunt

  1. Bronchial circulation – small amount drains directly into pulmonary veins (carrying oxygenated blood to left atrium)
  2. Thebesian veins – from walls of the left ventricle, drain directly into the left side of the heart before being ejected into the aorta

In addition, a Functional shunt occurs in low V/Q matched areas of the lung (0 < VQ
< 1)

            Ie a proportion of pulmonary capillary blood has passed through poorly ventilated lung regions, and so will not be fully oxygenated, overall lowering the expected PaO2 in comparison to the calculated PAO2 (as per the Alveolar Gas Equation).

Common causes for V/Q < 1

  • Atelectasis
  • Closing capacity (lung volume at end expiration when distal airways start to collapse, and the sum of RV and Closing volume)
    • Contributes when CC > FRC ie low FRC state (eg supine position) or increasing age.

In normal physiology the ratio VQ Ratios will vary along the distribution of lung units → this is KA “VQ Scatter”:

  • V/Q ratio = 1 (rib level #3)
  • V/Q of 3.3 found at the top of a lung (West Zone 1)
  • V/Q 0.6 typically located at the bottom of the lung (“West zone 3”)
Ventilation-perfusion ratio graph with apex and base values.

Attributed to heterogeneity and regional differences across a normal lung, including:

  • Uneven blood flow distribution secondary to gravity and hydrostatic pressure
  • posture (upright vs lateral vs supine position)
  • Uneven ventilation by lung’s own weight

Large V/Q mismatch = impaired gas exchange = hypoxaemia and/ or hypercapnea.

Ventilation- perfusion ratios down the upright lung

V/Q = 0

“True” shunt = V/Q of zero – complete lack of ventilation to a lung region which is still optimally perfused; the partial pressure of gases in these alveoli matches the mixed venous content of blood within pulmonary artery and providing supplementary O2 will not improve resultant hypoxaemia.

V/Q infinity (>3.3) – dead space ie no gas exchange)

Graph of lung ventilation-perfusion ratio curve
Ventilation-perfusion graph showing high and low ratios.

Pathological shunt associated with increased venous admixture can be split into:

  1. Intra cardiac shunt
    1. Congenital heart disease, with right- to- left shunting eg VSD, large AVM between pulmonary artery and vein.
  2. Intra pulmonary shunt – commonest cause
    1. Alveoli are perfused but poorly ventilated due to being fluid filled (eg oedema, pneumonia) or due to proximal airway occlusion (eg foreign body, single lung ventilation).
    2. Increased venous drainage eg from pulmonary neoplasms or infections.

Shunt equation allows calculation of the proportion of CO that is shunted from the venous to the arterial system, expressed as a fraction or “shunt ratio”.

Shunt equation for blood flow and oxygen content variables.

Shunt equation uses both the Oxygen content equation and the AGE to derive its shunt fraction.

Oxygen content equations in blood analysis.
Explanation of the alveolar gas equation components.

R typically 0.8 for Western diet

Part B

Effects of supplemental oxygen on arterial hypoxaemia

Definition

Hypoxia = inability for tissues to undergo aerobic metabolism

Hypoxaemia = a reduced PaO2 (< 60 mmHg)

Causes of Hypoxaemic Hypoxia by aetiology (where low PaO2 causes reduced Hb saturation and O2 – carrying capacity)

  1. Hypoventilation
  2. Diffusion limitation
  3. V/Q mismatch
  4. Shunt

1. Hypoventilation

  • Hypoxaemia is a consequence of hypercapnea in hypoventilation, as per AGE and inverse relationship between alveolar ventilation and PaCO2.
  • Supplemental oxygen will need to increase PiO2 substantially more than the effect of a high PaCO2 (as per AGE), to improve hypoxaemia.
PACO2 formula relation to ventilation.

2. Diffusion limitation

An uncommon cause of hypoxaemia, unless there is:

  1. Severe disruption/ thickening to the alveolar- capillary barrier eg pulmonary fibrosis
  2. Low inspired O2 tension eg high altitude
  3. Exercise, particularly if the above already present.

Supplemental oxygen will improve hypoxaemia depending on underlying aetiology.

3. V/Q mismatch

Ideally ventilation (L/min) and perfusion (L/min) will be matched, for a V/Q of 1.

If either V or Q are reduced, this causes a mismatch

Types of V/Q mismatch

High V/Q mismatch ratio > 1  ie intact ventilation with relatively reduced perfusion.

  • → Leads to increased WOB as wasted ventilation does not allow for efficient gas exchange and CO2 clearance ie alveolar ventilation rises. As seen with hypoventilation, supplemental O2 will improve hypoxaemia caused by hypercapnic respiratory failure (similar to hypoventilatory hypoxaemia)

Low V/Q mismatch ratio  <1 ie intact perfusion with relatively low ventilation

  • → Pulmonary capillary blood will transit though non ventilated alveoli, to different degrees. By causing venous admixture, this will reduce arterial O2 concentration and cause hypoxaemia.  

A small degree of mismatch is expected in healthy, heterogenous lungs as noted by a normal A-a gradient of 5- 15 mmHg.

(A-a gradient is the difference between alveolar and arterial O2 concentration, and will increase by 1 mmHg for every decade of age). Any of the above causes of hypoxaemia will increase an individual’s A-a gradient. 

Ie Supplemental oxygen will improve a small low V/Q mismatch, but not a large one (as approaches V/Q of zero, aka “true shunt”).

4. Shunt

In true pathological shunt, supplemental oxygen will not improve hypoxaemia, as by definition, perfused alveoli are not being ventilated (regardless of inspired FiO2).

A minor improvement may be seen purely from slight increase in additional O2 in dissolved blood.

From Alveolar Gas Equation alone  giving supplemental oxygen will increase the inspired FiO2 (PiO2), which increases the O2 pressure gradient across the alveolar- capillary gradient.

As per Fick’s Law of Diffusion, the increased concentration gradient enhances O2 diffusion across to capillary blood, and this in turn increases arterial oxygen tension.

Calculating the “shunt ratio” using central venous and arterial oxygen analysis can assist in determining the effects of supplemental oxygen on PaO2 based on severity of shunt fraction. As expected, as shunt fraction increases (ie severe V/Q mismatch), the lower of an impact on PaO2 supplemental O2 will have.

The effect of FiO2 on PaO2 at different shunt

(Chambers)

Graph of arterial PO2 vs. inspired O2 fraction.

References

  • Chambers
  • V/Q Diagram – West youtube lectures
  • Power and Kam – PO2 – PCO2 DIAGRAM

Author: Ines Vaz