Ventilation, perfusion & dead space

Why this matters to the anaesthetist

Hypoxaemia under anaesthesia is almost always a V/Q story: atelectasis (low V/Q and shunt), tube malposition, pulmonary embolism (high V/Q dead space), low cardiac output amplifying venous admixture, or HPV failure during one-lung ventilation. Primary candidates must define V/Q, draw the spectrum from shunt to dead space, write the shunt and Bohr equations, list the five causes of hypoxaemia, and explain why 100% oxygen distinguishes true shunt from low V/Q. [1]

The V/Q ratio

For the whole lung at rest: alveolar ventilation VA ≈ 4 L/min, cardiac output Qt ≈ 5 L/min, so overall V/Q ≈ 0.8. Individual units range from 0 (perfused but unventilated = shunt) to infinity (ventilated but unperfused = dead space). Ideal units sit near 1. Arterial blood is the flow-weighted mixture of end-capillary contents from all units; expired gas is the ventilation-weighted mixture of alveolar gases. [1]

Regional distribution — West zones and gravity

In the upright lung: [1]

• Blood flow increases from apex to base (gravity, recruitment/distension of vessels).
• Ventilation also increases from apex to base, but less steeply.
• Therefore apex: high V/Q (relatively over-ventilated), base: low V/Q (relatively over-perfused). [1]

West zones (exam classic): [1]

Under anaesthesia in the supine patient the vertical gradient shrinks but still exists (dependent lung). Lateral position and OLV exaggerate inequalities. PEEP can convert zone 3 toward zone 1/2 if alveolar pressure rises above pulmonary arterial pressure — raising alveolar dead space. [1]

The V/Q spectrum and gas exchange

Low V/Q units: alveolar gas approaches mixed venous gas — low PO2, high PCO2. They contribute disproportionately to arterial hypoxaemia because the O2 dissociation curve is flat at high saturation: well-ventilated units cannot fully compensate by carrying extra O2 once Hb is nearly full. CO2 is different — the CO2 content curve is steeper/near-linear, so high-V/Q units can excrete extra CO2 and largely compensate for low-V/Q units' CO2 retention. Result: V/Q mismatch causes hypoxaemia more readily than hypercapnia; hypercapnia appears when total VA is inadequate or dead space is extreme. [1]

High V/Q units: waste ventilation (like dead space), raise the work of breathing for a given CO2 elimination, increase PaCO2–EtCO2 gradient. [1]

Shunt — true shunt and venous admixture

True shunt (Qs): blood bypasses ventilated alveoli entirely (V/Q = 0). Causes: anatomical (bronchial veins, Thebesian veins — normal 2–5%), intracardiac R→L, pulmonary AVMs, consolidated/collapsed lung. [1]

Venous admixture: the calculated shunt that would produce the observed CaO2 if all admixture were true shunt — includes true shunt plus contribution of low-V/Q units. [1]

Shunt equation: Qs/Qt = (Cc′O2 − CaO2) / (Cc′O2 − CvO2) [1]

Cc′O2 is ideal end-capillary content from PAO2 via alveolar gas equation. On FiO2 1.0, nitrogen is gone and the calculated shunt approximates true shunt more closely. [1]

Critical property: hypoxaemia from true shunt is not abolished by 100% oxygen (though PaO2 may rise somewhat as dissolved O2 in non-shunt blood increases). Hypoxaemia from low V/Q usually is largely correctable with oxygen because PAO2 in low-V/Q units rises. [1]

Dead space — anatomic, alveolar, physiologic

Anatomic dead space (VD anat): conducting airways ~2 mL/kg (~150 mL). Fowler method (N2 washout) measures it. [1]

Alveolar dead space (VD alv): ventilated alveoli with no (or inadequate) perfusion — PE, low CO, zone 1 from high PEEP, emphysema. [1]

Physiologic dead space (VD phys) = VD anat + VD alv [1]

Bohr equation: VD/VT = (PaCO2 − PECO2) / PaCO2 [1]

Enghoff modification uses PaCO2 as a surrogate for ideal alveolar PCO2. Normal VD/VT ≈ 0.2–0.35. Raised VD/VT → need higher VE to keep PaCO2 normal; EtCO2 underestimates PaCO2 (widened a–ET gradient). [1]

West & Wagner concepts: high V/Q units contribute to alveolar dead-space-like behaviour. [1]

The five causes of hypoxaemia (must list)

1. Low inspired PO2 (altitude, hypoxic mixture) — A–a normal
2. Hypoventilation — A–a normal; high PaCO2
3. Diffusion impairment — A–a raised; uncommon sole cause at rest
4. Shunt — A–a raised; poor response to O2
5. V/Q mismatch — A–a raised; usually responds to O2 [1]

(Some lists add low mixed venous O2 as an amplifier rather than a primary cause.) [1]

Hypoxic pulmonary vasoconstriction as V/Q defender

HPV diverts blood from hypoxic alveoli, narrowing the scatter of V/Q ratios and protecting PaO2. Inhibitors (volatiles, vasodilators) widen scatter and worsen venous admixture — link to the oxygen-cascade/HPV topic. [1]

Shunt versus low V/Q — the oxygen test

Atelectasis under anaesthesia often behaves as shunt (compression, absorption atelectasis with high FiO2). [1]

Equations toolkit

• PAO2 = FiO2(Patm − 47) − PaCO2/R
• A–a = PAO2 − PaO2
• Qs/Qt = (Cc′O2 − CaO2)/(Cc′O2 − CvO2)
• VD/VT = (PaCO2 − PECO2)/PaCO2
• VA = VE × (1 − VD/VT)
• PaCO2 ∝ V̇CO2 / VA [1]

Anaesthetic relevance

• GA + supine + high FiO2: FRC falls, dependent atelectasis → shunt-like fractions; PEEP and recruitment help.
• PE: sudden rise in VD/VT, fall in EtCO2, rise in a–ET CO2 gradient, hypoxaemia, RV strain.
• Low cardiac output: lower PvO2 → any given shunt fraction produces lower PaO2; also more zone 1 if PA high.
• OLV: intentional extreme V/Q inequality; HPV and positional blood flow determine PaO2.
• COPD: high VD/VT and low V/Q regions coexist; oxygen careful titration. [1]

[1] [1] [1] [1]

Graph descriptions for the viva

1. O2–CO2 diagram (Rahn–Fenn): plot PACO2 vs PAO2 for units from shunt point (mixed venous gas) to inspired gas point; ideal alveolar point on the R line.
2. Multiple inert gas elimination technique (MIGET) concept: distribution of perfusion and ventilation against V/Q ratio — bimodal distributions in ARDS/COPD.
3. Iso-shunt diagrams: PaO2 vs FiO2 for different shunt fractions — shows limited benefit of high FiO2 once Qs/Qt is large. [1]

Viva traps

1. Overall V/Q is 0.8 not 1 — remember VA 4 vs Q 5.
2. Anatomic shunt of 2–5% is normal — zero calculated shunt is not expected.
3. Dead space fraction uses PaCO2 and mixed expired CO2 — not EtCO2 alone in the classic Bohr form (though EtCO2 approximates end-tidal alveolar gas for trends).
4. Zone 1 is not normal in healthy spontaneous breathing at rest — if present extensively, dead space is pathological.
5. Hypercapnia is not required for the diagnosis of V/Q mismatch. [1]

Additional depth — absorption atelectasis

When FiO2 is high, nitrogen's splinting effect in poorly ventilated units disappears; ongoing gas uptake collapses the unit → conversion of low V/Q to shunt. This is why 100% oxygen for long periods promotes atelectasis and why a balance exists between preoxygenation safety and absorption collapse — recruitment and modest PEEP mitigate. [1]

Additional depth — position and blood flow

Upright → base-predominant flow. Supine → caudal-dependent. Prone in ARDS → more uniform dorsal expansion and improved matching (clinical ARDS application of V/Q physiology). Lateral decubitus for thoracic surgery: dependent lung receives more blood but is compressed; HPV and surgical manipulation alter distribution minute to minute. [1]

SAQ: five causes of hypoxaemia with A–a gradient

1. Low inspired oxygen — normal A–a
2. Hypoventilation — normal A–a, high PaCO2
3. Diffusion limitation — raised A–a
4. Shunt — raised A–a, poor O2 response
5. V/Q mismatch — raised A–a, usually good O2 response [1]

Dead space versus shunt clinical contrast table in prose

Shunt makes blood that never saw alveolar gas; dead space makes gas that never saw blood. Shunt hurts oxygenation more than CO2 elimination; dead space hurts CO2 elimination efficiency and widens a–ET CO2 gradients. Both can coexist in ARDS: flooded units shunt while overdistended units act as dead space, especially with high PEEP. [1]

MIGET conceptual paragraph

The multiple inert gas elimination technique infuses dissolved inert gases of different solubilities and measures arterial and expired retention/excretion to recover a distribution of ventilation and perfusion against V/Q. Normal lung shows a unimodal distribution near V/Q 1; disease produces low and high V/Q modes. You will not perform MIGET in theatre, but describing the concept scores marks for depth. [1]

West zone manipulation by the ventilator

High alveolar pressure from PEEP or dynamic hyperinflation can create West zone 1 conditions at non-dependent regions: ventilation without perfusion, raised physiologic dead space, falling EtCO2, rising PaCO2, and wasted work. Reducing overdistension can improve CO2 elimination without increasing set minute ventilation — applied V/Q thinking. [1]

Primary exam expansion

Mathematical identities you must write under pressure

VA = f × (VT − VD) PaCO2 = K × V̇CO2 / VA Qs/Qt = (Cc′O2 − CaO2)/(Cc′O2 − CvO2) VD/VT = (PaCO2 − PECO2)/PaCO2 A−a gradient = [FiO2(Patm − 47) − PaCO2/R] − PaO2 [1]

Why 100% oxygen cannot fully correct true shunt

Blood traversing true shunt has content ≈ CvO2. Non-shunt blood can carry at most ~1.34×Hb + 0.003×PAO2. Dissolved oxygen adds only ~2 mL/dL even at PAO2 ~660 mmHg — not enough to offset a large admixture of venous blood. Hence SpO2 remains depressed when Qs/Qt is large. [1]

Atelectasis types under anaesthesia

Compression atelectasis (dependent lung, reduced FRC), absorption atelectasis (high FiO2 in closed units), and surfactant impairment. All create low V/Q or shunt. Recruitment manoeuvres reopen units; PEEP keeps them open; both reshape the V/Q distribution toward normal. [1]

Pulmonary embolism as a dead-space prototype

Sudden rise in alveolar dead space: EtCO2 falls, PaCO2 may rise or stay same if VE increases, a–ET gradient widens, VD/VT rises, hypoxaemia from mechanisms above, RV afterload rises. Capnography is a continuous dead-space monitor in this setting. [1]

COPD V/Q pattern

Broadened distribution with both low and high V/Q regions; high VD/VT; chronic HPV and vascular remodelling; oxygen carefully titrated because removing hypoxic stimulus can increase blood flow to low V/Q regions (worse venous admixture) and reduce ventilation slightly in retainers. [1]

Prone positioning physiology

In ARDS, dorsal lung is often poorly ventilated but still perfused (shunt). Prone positioning improves dorsal expansion, homogenises transpulmonary pressures, and improves matching — an applied V/Q intervention proven to affect outcomes in severe ARDS when done properly. [1]

Exam graph: iso-shunt diagram

Describe PaO2 on the y-axis versus FiO2 on the x-axis with curves for Qs/Qt of 0%, 10%, 20%, 30%, 50%. As shunt fraction rises, the curve flattens: increasing FiO2 buys less and less PaO2. This picture explains refractory hypoxaemia. [1]

Positioning and one-lung anaesthesia V/Q

Lateral decubitus: dependent lung better perfused; non-dependent better ventilated if both lungs open — relative mismatch. When non-dependent lung is collapsed for surgery, its ventilation goes to zero while residual perfusion becomes shunt until HPV and surgical ligation reduce flow. [1]

Extended viva dialogue

Examiner: Define the ventilation–perfusion ratio and give the normal whole-lung value. [1]

Candidate: V/Q is alveolar ventilation divided by blood flow for a lung unit or the lung as a whole. Whole-lung alveolar ventilation is about 4 L/min and cardiac output about 5 L/min, so overall V/Q is about 0.8. Individual units range from zero (shunt) to infinity (dead space). [1]

Examiner: Why does V/Q mismatch cause hypoxaemia more than hypercapnia? [1]

Candidate: The oxygen dissociation curve is flat at high saturation, so high-V/Q units cannot carry much extra oxygen to compensate for desaturated blood from low-V/Q units. The carbon dioxide content curve is steeper and more linear, so high-V/Q units can eliminate extra CO2 and largely compensate. Therefore arterial hypoxaemia appears first; hypercapnia implies inadequate total alveolar ventilation or extreme dead space. [1]

Examiner: Write the shunt and Bohr equations and state when 100% oxygen distinguishes shunt from low V/Q. [1]

Candidate: Qs/Qt equals (Cc-prime-O2 minus CaO2) divided by (Cc-prime-O2 minus CvO2). VD/VT equals (PaCO2 minus mixed expired PCO2) divided by PaCO2. True shunt hypoxaemia is not abolished by pure oxygen because shunted blood never contacts alveolar gas; low-V/Q hypoxaemia usually improves substantially as alveolar PO2 rises in poorly ventilated units. [1]

Examiner: Describe West zones and how PEEP can create dead space. [1]

Candidate: Zone 1 has alveolar pressure greater than arterial and venous pressures so vessels collapse and act as alveolar dead space. Zone 2 has intermittent flow, zone 3 continuous flow. High PEEP raises alveolar pressure and can expand zone-1-like conditions, raising physiologic dead space, widening the arterial-to-end-tidal CO2 gradient, and lowering cardiac output via venous return effects. [1]

Clinical synthesis: Intraoperative desaturation algorithms are V/Q algorithms: tube position (mainstem creates massive low V/Q/shunt), recruitment, FiO2, cardiac output (mixed venous oxygen), and embolism (dead space). Speak in those terms and you sound like a consultant. [1]

Red flags

• True shunt hypoxaemia is not abolished by 100% oxygen; low-V/Q usually is improved — the distinguishing test.
• A–a gradient separates hypoventilation/low PIO2 (normal A–a) from shunt/mismatch/diffusion (raised A–a).
• Apex high V/Q, base low V/Q in the upright lung.
• PE is the classic acute alveolar dead-space state — wasted ventilation, raised a–ET gradient.
• HPV defends matching and is impaired by volatiles and many vasodilators. [1]

References

1. [1]Coppola S, et al. Lung Imaging in Acute Hypoxemic Respiratory Failure: From Physics to Bedside Applications J Clin Med, 2026.PMID 42279206
2. [2]Baino B, et al. Eisenmenger Syndrome: The Pulmonology Perspective Chest, 2026.PMID 42341977
3. [3]Ramidi SR, et al. Refractory Hypoxemia Secondary to Patent Foramen Ovale Presenting With Platypnea-Orthodeoxia Syndrome Cureus, 2026.PMID 42333279
4. [4]Evans B, et al. Quantitative perfusion imaging from non-contrast micro-ct for pulmonary embolism evaluation in preclinical models Phys Med Biol, 2026.PMID 42335950
5. [5]Lacoste-Palasset T, et al. Impact of Pulmonary Arterial Hypertension Therapies on Gas Exchange in Portopulmonary Hypertension Chest, 2026.PMID 42066896
6. [6]Hoecker RN. Partial Pressure of Oxygen 2026.PMID 29630271