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VENTILATION

Minute Ventilation (VE)

• What it is: Total air moving in and out of lungs per minute
• Formula: VE = VT × RR
• Normal values to memorize:
  • RR = 12-20 breaths/min
  • VT (tidal volume) = 500 mL/breath
  • VD (dead space) = 150 mL/breath
• Example: 500 × 15 = 7,500 mL/min

Alveolar Ventilation (VA)

• What it is: Air that actually reaches the alveoli and participates in gas exchange (more important than minute ventilation)
• Formula: VA = (VT - VD) × RR
• Why subtract VD? The 150 mL dead space (trachea, bronchi) never reaches alveoli - it just sits in the airway doing nothing
• Example: (500 - 150) × 15 = 5,250 mL/min

FCPS tip: If a patient takes slow, deep breaths vs. fast, shallow breaths, the VA is very different even if VE is the same. Deep breaths = better alveolar ventilation.

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LUNG AND CHEST WALL PROPERTIES

Hysteresis

• Simple concept: The pressure-volume curve during inflation is DIFFERENT from deflation
• Why? During inflation you must overcome surface tension (like blowing up a new balloon - harder at first)
• The graph (top right): Notice the lung volume and alveolar/intrapleural pressure waves during breathing
  • Intrapleural pressure swings between -6 and -10 cm H2O
  • It is always negative (keeps lungs from collapsing)

Elastic Recoil

• Lungs want to collapse inward (like a stretched rubber band wanting to snap back)
• Chest wall wants to spring outward
• At FRC (Functional Residual Capacity) these two forces balance each other perfectly
• At FRC: alveolar pressure = atmospheric (zero), intrapleural pressure is negative (-5 cm H2O)
• This negative intrapleural pressure is what prevents atelectasis (lung collapse)

Think of it like this: Lungs are a balloon inside a box. The balloon wants to shrink. The box wants to expand. FRC is where they reach a truce.

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COMPLIANCE

• Definition: How easily the lung stretches - change in volume per change in pressure (ΔV/ΔP)
• Inversely proportional to stiffness - stiff lung = low compliance
• Surfactant increases compliance (reduces surface tension, makes inflation easier)

The Compliance Graph (bottom right)

• X-axis: Airway pressure (cm H2O)
• Y-axis: Volume (L)
• Green curve (normal lung-chest wall): Sits between the individual curves
• Emphysema curve: Shifted UP and LEFT = high compliance (fills easily at low pressure)
• Fibrosis curve: Shifted DOWN and RIGHT = low compliance (needs more pressure to fill)
• FRC is marked on the Y-axis - this is where breathing starts at rest

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HIGH-YIELD EXAM MNEMONICS

• "ARDS, Fibrosis, Edema, Pneumonia" = all decrease compliance (stiff lungs)
• "Emphysema = Easy to fill, hard to empty" = increased compliance + air trapping
• Dead space = 150 mL = roughly 1 mL/lb body weight
• Negative intrapleural pressure = keeps lungs open at all times

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PULMONARY CIRCULATION

Key Characteristic

• Pulmonary circulation is low-resistance, high-compliance - opposite of systemic circulation
• It handles the same cardiac output as systemic but at much lower pressure

Hypoxic Vasoconstriction - THE BIG CONCEPT

• In the lungs: low O2 → vessels constrict (vasoconstriction)
• In systemic circulation: low O2 → vessels dilate (vasodilation)
• Why? To divert blood AWAY from poorly ventilated alveoli toward well-ventilated ones - smart matching of blood to air
• Chronic hypoxic vasoconstriction → pulmonary hypertension → cor pulmonale (right heart failure)

Memory trick: Lungs are "backwards" - low O2 constricts instead of dilating

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PERFUSION LIMITED vs DIFFUSION LIMITED

Perfusion Limited (Normal O2, CO2, N2O)

• Gas fully equilibrates (equalizes) between alveolar air and blood early along the capillary
• By the time blood reaches the end of the capillary, it already matches alveolar levels
• To get more gas exchange, you need more blood flow (more perfusion)
• Examples: O2 in normal health, CO2, N2O

Diffusion Limited (O2 in emphysema/fibrosis, CO)

• Gas never fully equilibrates by the time blood reaches the end of the capillary
• The barrier itself is the problem, not blood flow
• Examples:
  • O2 in emphysema/fibrosis
  • CO - always diffusion limited (that's why CO is used to test diffusion capacity)

Understanding the Graph

FCPS tip: Diseases causing diffusion limitation (fibrosis) cause hypoxia BEFORE hypercapnia because CO2 diffuses 20x faster than O2 across membranes

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FICK'S LAW OF DIFFUSION

• Emphysema → ↓ A (alveolar walls destroyed = less surface area)
• Pulmonary fibrosis → ↑ Δx (thickened membrane = harder to cross)

DLCO (Diffusion Capacity for CO)

• Measures how well CO passes from alveoli into blood
• CO is used because it is always diffusion limited - perfect test of membrane function
• ↓ DLCO in fibrosis, emphysema, pulmonary edema
• ↑ DLCO in polycythemia, pulmonary hemorrhage (more hemoglobin available to bind CO)

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PULMONARY VASCULAR RESISTANCE (PVR)

Formula

Poiseuille's Law for Resistance

The r⁴ rule: Doubling the radius decreases resistance by 16 times (2⁴ = 16). This is why small changes in vessel diameter have massive effects on resistance.

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HIGH-YIELD EXAM SUMMARY

Diffusion Limited Gas Exchange - Elaborated

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First, understand the normal journey of O2

Alveolus
─────────────────────────────────────────
  ↑↑↑ O2 crosses here    | no more needed
─────────────────────────────────────────
Capillary start -----> Capillary end
  [low O2]    equilibrates    [= alveolar O2]

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What goes wrong in Fibrosis?

• O2 has to fight through a much thicker wall
• It diffuses slowly
• By the time blood reaches the end of the capillary, O2 has still NOT fully equilibrated
• Blood leaves the lung with lower O2 than the alveolus - this is hypoxia

FIBROSIS:
Alveolus
━━━━━━━━━━━━━━━━━━━━━━ (thick wall)
  ↑ O2 crossing slowly...still going...still going...
─────────────────────────────────────────────────────
Capillary start ──────────────────────────> end
  [low O2]                              [still low O2]
                                         ❌ never equilibrated

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What about Emphysema?

• In emphysema, alveolar walls are destroyed
• This means less surface area for diffusion
• Less area = less O2 can cross per unit time
• Again, blood leaves without fully equilibrating

Think of it like trying to exchange heat through a tiny window vs. a large window. Emphysema = very small window.

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Why is CO Always Diffusion Limited?

• CO binds hemoglobin almost instantly and completely
• Almost zero CO remains dissolved in plasma
• So the partial pressure of CO in blood stays near zero throughout the entire capillary length
• The pressure gradient from alveolus to blood is maintained at maximum the whole time
• CO keeps diffusing at full speed from start to end of capillary - but still never equilibrates because hemoglobin just keeps grabbing it

CO situation in capillary:
Alveolus CO pressure = 0.3 mmHg (stays constant)
Blood CO pressure    ≈ 0       (stays near zero because Hb grabs it all)

Gradient stays maximum → CO diffuses constantly
BUT still never equilibrates → always diffusion limited

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So why use CO to test diffusion capacity (DLCO)?

1. Its transfer is limited ONLY by the membrane - not by blood flow
2. So DLCO tells you purely about the membrane's ability to transfer gas
3. If DLCO is low → membrane is damaged (fibrosis, edema) OR surface area is reduced (emphysema)

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One-line Summary for Exam

Diffusion limited = the membrane or surface area is the bottleneck. O2 becomes diffusion limited when the membrane thickens (fibrosis) or surface area shrinks (emphysema). CO is ALWAYS diffusion limited because hemoglobin grabs it so tightly that no free CO ever builds up in blood, so the gradient never disappears.

V/Q MISMATCH & ALVEOLAR GAS EQUATION - FCPS Part 1

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PART 1: V/Q RATIO (Ventilation/Perfusion)

The Basic Concept

• Perfect V/Q = 1 → perfect gas exchange
• In reality, the lung is not uniform - different regions have different V/Q ratios

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The Three Lung Zones - MOST TESTED

• PA = alveolar pressure (air pressure inside alveolus)
• Pa = arterial pressure (blood coming IN to capillary)
• Pv = venous pressure (blood leaving capillary)

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ZONE 1 - Apex (Top of lung)

• Alveolar pressure is so HIGH it squeezes the capillary
• Blood flow is minimal (vessels compressed by air pressure)
• Ventilation is present but perfusion is poor
• V/Q is HIGH (= 3) → "wasted ventilation" - air comes in but no blood to exchange with
• In normal people, Zone 1 is nearly non-existent
• Zone 1 expands in: hemorrhage, hypotension (Pa drops), positive pressure ventilation (PA rises)
• TB loves the apex because high O2 + low blood flow = ideal for TB bacteria

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ZONE 2 - Middle of lung

• Arterial pressure exceeds alveolar pressure
• Blood flow is moderate and variable
• V/Q ≈ 1 → best matching of air and blood
• This is the ideal zone

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ZONE 3 - Base (Bottom of lung)

• Gravity pulls blood down → base has the MOST blood flow
• Alveolar pressure is lowest here so vessels stay wide open
• Perfusion is excellent but ventilation is relatively less
• V/Q is LOW (= 0.6) → "wasted perfusion" - lots of blood but relatively less air
• Blood leaves slightly under-oxygenated

APEX  → high V/Q (3) → more air than blood → wasted ventilation
MIDDLE → V/Q ≈ 1    → perfect match
BASE  → low V/Q (0.6) → more blood than air → wasted perfusion

Memory trick: "Apex = Air dominates. Base = Blood dominates."

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The Two Extremes - V/Q = 0 and V/Q = ∞

V/Q = 0 → SHUNT

• Zero ventilation, perfusion is present
• Airway is completely blocked (foreign body aspiration, mucus plug, consolidated lung)
• Blood flows past the alveolus but picks up NO oxygen
• 100% O2 does NOT improve PaO2 - because no air reaches the alveolus at all
• The deoxygenated blood just mixes back into circulation

Blocked airway → No air → blood passes through → still deoxygenated
Giving 100% O2 is useless because O2 can't reach the blocked alveolus

V/Q = ∞ → DEAD SPACE

• Zero perfusion, ventilation is present
• Blood flow is blocked (pulmonary embolism)
• Air reaches the alveolus but no blood comes to pick up O2
• 100% O2 DOES improve PaO2 (slightly) - because other normal alveoli can compensate
• The ventilated alveolus is "wasted" - physiological dead space

PE → No blood → air sits in alveolus doing nothing → dead space
Giving 100% O2 helps via other normal alveoli

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Exercise and V/Q

• Exercise increases cardiac output → apical capillaries dilate and recruit
• V/Q at apex approaches 1
• Overall lung V/Q becomes more uniform → more efficient gas exchange

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PART 2: ALVEOLAR GAS EQUATION

Formula

Breaking Down Each Part

Why subtract PaCO2/RQ? Because CO2 from blood is constantly entering the alveolus and "diluting" the O2 space. More CO2 in = less room for O2.

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The A-a Gradient - VERY HIGH YIELD

• Normal alveolar O2 ≈ 100 mmHg
• Normal arterial O2 ≈ 95 mmHg
• So there is always a small normal gradient

• For a 40-year-old: (40/4) + 4 = 14 mmHg
• For a 20-year-old: (20/4) + 4 = 9 mmHg

Why does the A-a gradient matter?

Key rule: Normal A-a gradient = problem is OUTSIDE the lung (hypoventilation, altitude). Increased A-a gradient = problem is INSIDE the lung (V/Q mismatch, shunt, diffusion issue).

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EXAM SUMMARY TABLE