West Zones

• Divided into zones based on relationship between Alveolar pressure (PA) Arterial pressure (Pa) Venous pressure (Pv) Interstitial pressure (Pi)
• West Zones 1,2,3: Due to changes in hydrostatic pressure when pumping to top of lung vs. bottom of lung

Vertical gradient of pleural pressure and alveoli

Inspiration

• Inspiratory muscle contraction → Overcomes resistance to insp flow → negative alveolae pressure -1cm H2O → VT 500ml
• Weight of lung on alveoli and pleura above:
  • causes gradient of pleural pressure: Apex (-10cmH2O) Base (-2.5cm H2O)
  • Apical alveoli larger
  • But compliance lesser (due to baseline distension)
  • Lesser ventilation for same pressure
• Apex and base on different part of compliance curve

Expiration:

• Gradient of pleural pressure smaller
  • Apex: -4cm H2O → on steeper part of compliance curve → ventilation better
  • Base +3.5cm H2O →airway closure → gas trapping & shunt

Ventilation, perfusion, V/Q matching

Vertical segments based on V and Q

• Both V and Q ↓ as you move from base to apex.
  • ↓ total number of alveoli → ↓ diffusive area → ↓ V
  • ↑ compression of intra-alveolar vessels → ↑ west zone 1 → ↓ Q
  • V ↓’s slower than Q

JC 2019

2021B 10: 47% of candidates passed this question.
This is a core aspect of respiratory physiology, and a detailed understanding of this topic is crucial to the daily practise of intensive care. As such the answers were expected to be detailed. Strong answers included precise descriptions of the zones of the lung as described by West and related these to the V/Q relationship in the upright lung. Generally, most candidates scored well in this section. Diagrams were of varying value. However, an impression from the examiners was that candidates spent too much time on this first section and ran out of time for a detailed answer in the second section. The answers to the second section seemed rushed and were often lacking in detail with many incorrect facts. This question highlights the importance of exam technique preparation in the lead up to the written paper.

Normal V/Q variation

• Both V and Q ↓ as you move from base to apex.
  • ↓ total number of alveoli → ↓ diffusive area → ↓ V
  • ↑ compression of intra-alveolar vessels → ↑ west zone 1 → ↓ Q
  • V ↓’s slower than Q
• The intersection of V/Q is at rib 3, here V/Q = 1
• V/Q = 3 at the apex
• V/Q = 0.67 at bases

Normal Variation in V/Q causes:

For PaO₂:

• Increased V/Q inequality causes:
  • Mild decrease in P_aO₂
  • At Apex
    • decrease in dissolved O2
    • Minimal decrease in Hb saturation due to flat part of OHDC
    • Thus overall decrease in C_aO₂
  • Base
    • P_AO₂ = P_vO₂ = 40
• Addition of a small quantity of poorly oxygenated shunted blood flow (PO₂ < PcO2) added to a large volume well-oxygenated PECB →  small fall in C_aO₂ BUT a LARGER fall in P_aO₂
• Because carrying capacity of blood to apex is decreased there is a decrease in P_aO₂

For PaCO₂:

Remembering that the relationship for the Alveolar gasses:

• Increased V/Q inequality causes:
  • Mild increase in P_aCO₂  which is rapidly compensated for due to Chemoreceptor reflexes
  • Apex to base
    • ↓P_ACO₂ towards the apices of the lungs
    • ↓gas transfer → ↑P_aCO₂ 
    • Sensed by chemoreceptors (sensitive to ±3mmHg) 
    • ↑RR and T_v as per the CO₂ dissociation curve
• Normal or slightly lower (after compensation) CO₂

Gladwin 2016

2017B 06: 48% of candidates passed this question.
Overall answers lacked sufficient detail on a core area of respiratory physiology. Answers expected included a description of V/Q ratios throughout the lungs and an explanation of how V/Q inequality lowers PaO2

2014B 05: 8% of candidates passed this question.
Very few candidates demonstrated understanding of this core topic. Candidates did not accurately define V/Q inequality and the physiological factors causing this phenomenon. V/Q scatter as well as true shunt (V/Q=0) and dead space (V/Q=∞) needed to be considered. The inability of high V/Q areas to compensate for low V/Q zones owing to the relatively small contribution of blood flow from these high V/Q units was not discussed. The differential effect of FiO2 on true shunt versus V/Q scatter was seldom explained. The shape of the oxy-Hb dissociation curve and CO2-dissociation curve were sometimes mentioned but their effect on arterial gas tensions not well explained.
Often graphs were reproduced inaccurately and contradictory statements made, leaving the impression that candidates did not understand the basic concepts. It is core knowledge for Intensive Care Specialists managing respiratory failure. A sophisticated knowledge based on the chapter in Nunn is a minimum standard expected for this topic.

2008A 06: No candidates (0%) passed this question.
The main points expected for a pass were:

• Range, regional pulmonary differences and gradients of V/Q ratios.
• Definitions of shunt (V/Q = 0) and dead space (V/Q = ∞).
• Explanation of why and how V/Q mismatch lowers arterial P_aO₂ (majority of pulmonary blood flow being from basal regions, shape of haemoglobin disassociation curve).
• Explanation of why and how V/Q mismatch lowers arterial P_aCO₂ (majority of pulmonary blood flow being from basal regions, predominately linear shape of CO₂ disassociation curve within the physiological range of P_aCO₂ values).

Again, the use of illustrations would be very useful aids as part of a good answer.
Candidates often failed to frame their answer to the question that was asked and deviated to areas not directly sought after by the question. This resulted in wasted time and opportunities for marks.
Syllabus B1g
Reference Nunn 4th edition page 165-187

Dead space

• Ventilated lung volume in which no gas exchange occurs
• Anatomical dead space
  • Dead space volume of conducting airways
    • Oropharynx, nasopharynx and first 16 divisions of the tracheobronchial tree
    • Approx 2ml/kg
  • Measured by fowlers method (N₂ washout)
• Alveolar dead space
  • Dead space volume of parts of the respiratory airways that are ventilated but not perfused
    • West Zone 1 (P_A > P_a)
      • Low cardiac output
      • Positive pressure ventilation
      • Posture
    • Disease states
      • Pulmonary Embolism
  • Measured by subtracting anatomical deadspace from physiological dead space
• Physiological dead space
  • Alveolar + anatomical dead space
  • Calculated from Bohr equation
  • Normal arterial to end-tidal CO₂ gradient is approx 5mmHg
    • Increases if increased dead space
• Apparatus dead space
  • Dead space contributed by artificial airway devices (endotracheal tubes, LMA, HME filters)
  • Usually reduces anatomical deadspace (due to bypass of oropharynx)

Calculation / Measurement of Dead Space

Bohr’s Method

• Bohr’s Equation:

• Based on the principle that all CO₂ exhaled must come from ventilated alveoli

• PĒ_CO2 is mixed-expired CO2 in an expired tidal breath
• Alveolar PCO2 is difficult to measure, so the Enghoff modification is used
  • which assumes P_ACO₂ = P_aCO₂

Fowler’s Method

Single-breath nitrogen washout test

• Single Vital Capacity Breath – 100% O2 → Exhales to Residual volume
• Expired Nitrogen concentration and volume is measured
• Plot of concentration by volume generated
  • Phase I: Pure dead space. No Nitrogen present.
  • Phase II: Midpoint is volume of Anatomical dead space.
  • Phase III: Expired N2 plateaus
  • Phase IV: Closing capacity. Sudden Increase in Nitrogen.

Consequences of increasing dead space

• Alveolar ventilation
  • RR x (tidal volume – dead space)
  • Therefore, as dead space approaches tidal volume, alveolar ventilation approaches zero, and cannot be compensated by increasing respiratory rate
• P_aCO₂ is inversely proportional to alveolar ventilation → P_aCO₂ increases as alveolar ventilation decreases
  • Decreased pH
  • Increased central and peripheral stimulation of ventilation → Reduction in P_aCO₂
    • Central chemoreceptors activate medullary vasomotor centre → increased sympathetic discharge
  • If P_aCO₂ increases, alveolar CO₂ in non-dead space alveoli will increase
    • P_AO₂ will decrease according to alveolar gas equation

Sakurai / JC 2016

2018A 03: 59% of candidates passed this question.
Some candidates failed to provide a correct definition of dead space. An outline of anatomical, alveolar and physiological dead space was expected. The Bohr equation was commonly incorrect, and many did not comment on how to measure the components of the Bohr equation. Fowler’s method was generally well described though some plotted the axes incorrectly. The impact of increased dead space was not often well explained. Very few people stated the major impact of increased dead space is reduced minute ventilation and how this would affect CO2.

2010A 19: (50%) of candidates passed this question
A definition of dead space incorporating subtypes (anatomical, apparatus, alveolar, physiological) was expected. Explanation of measurement methods attracted additional marks. Changes to End-tidal CO2 relative to PaCO2 were relevant to the question. The Bohr equation was stated and variables defined in better answers. Causes of an increased dead space should have been described including hypoperfusion and increased alveolar pressure. Increased dead space primarily results in CO2 retention, unless minute ventilation is increased commensurately. The physiological effects of
increased PaCO2, increased respiratory rate and work of breathing are central to the question. Many candidates predicted severe hypoxemia; however the alveolar gas equation was not stated to explain this observation. Hypoxemia is a relatively late effect of significant hypo-ventilation, especially if the patient is breathing supplemental O2.
Syllabus: B1e 2c Reference: Nunn’s Applied Respiratory Physiology p310-311.
Principles of Physiology for the Anaesthetist, Power & Kam p84-87 5

Venous admixture

“Theoretical volume of mixed venous blood added to pulmonary end-capillary blood to produce the observed C_aO₂ “

Causes of venous admixture

Shunt

• Physiological
  • Thebesian vessels – drain venous blood from coronary circulation directly into cardiac chambers (including L ventricle)
  • Bronchial circulation – Fracture of blood from bronchial circulation drains into pulmonary veins
• Pathological
  Blood from pulmonary capillaries supplying unventilated alveoli (V/Q = 0)
  • Obstruction within bronchial tree
  • Atelectasis
  • Usually mitigated by hypoxic pulmonary vasoconstriction

V/Q mismatch

• Variation in ventilation and perfusion within the lung
  • V/Q > 1 – Areas of lung with high relative ventilation to perfusion
    • West Zone 1
    • Lung apices
    • In pathology
      • Positive pressure ventilation
      • Shock and hypoperfusion
      • PE
  • V/Q < 1 – Areas of lung with low relative ventilation to perfusion
    • Lung bases
    • West zone 4
    • In pathology: Left heart failure, Pulmonary oedema
• Areas of high V/Q cannot compensate for areas of low V/Q due to the shape of the oxyHb dissociation curve and the sharp desaturation of deoxygenated blood. Also there may be decreased flow through the highly ventilated areas of lung
• V/Q mismatch in pathology
  • Obstructive lung diseases: Asthma, COPD
  • Restrictive lung diseases: ILD, ARDS

Sakurai 2016

Diagnosis of venous admixture

Estimated using A-a gradient using alveolar gas equation

R – Respiratory quotient, usually 0.8

Normal A-a gradient = 2.5 + (0.21 x Age)

Quantification of venous admixture

Shunt equation

Where

• Q_t = Total cardiac output
• Q_ns = Flow through non-shunt areas
• Q_s = Flow through shunt
• C_aO₂ = arterial content of O₂
• C_cO₂ = pulmonary end-capillary O₂ (presumed 100% SpO₂)
• C_mvO₂ = mixed venous content of O₂
  • Blood sampled from R atrium

V/A quantification

• MIGET (Multiple inert gas elimination technique)
  • IV injection of a volume of liquid with known quantities of 6 inert gases
  • V/Q calculated from the elimination spectra of these gases
• PET
  • Xe¹³³ gas and Tc⁹⁹ labelled RBC
• MRI

Sakurai 2016

Effects of Supplemental Oxygen

2024A 02: 43% of candidates passed this question.
(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).
(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.

2009B 06: 5 (56%) of candidates passed this question
This question related to an area of basic respiratory physiology. A good answer necessitated the precise meaning of venous admixture, being that amount of mixed venous blood which would have to be added to ideal pulmonary end-capillary blood to explain the observed pulmonary end-capillary to arterial PO2 difference. Diagnosis required the candidate to mention, a demonstrated increased in the Aa-DO2, what are normal values. For quantification mention and description of the shunt equation was required.
Candidates lacked a definition for venous admixture, were inaccurate with their description of the shunt equation and often overlooked mentioning calculation of arterial and mixed venous blood oxygen content.