Alveolar gases, ventilation and perfusion

Question 1

Alveolar gases and ventilation

Answer 1

• Alveolar partial pressure determined by alveolar ventilation (V) ̇and partial pressures of gases in blood which has mixed venous blood coming back from right side of heart (which has a small pO2 and high pCO2)
• During breathing and ventilation, high pO2 is brought in, alveolar ventilation is adding O2 to alveolar gas, losing O2 from alveolar gas to blood (taken away around body = perfusion for metabolism)
• Blood flowing through lung = cardiac output from right side of heart = CO left side, CO pumped around body is related to O2 consumption = metabolic rate
• Perfusion (Q) is a proxy for metabolism: ↑ metabolism and O2 consumption, ↑ CO and flow through lung in a minute
• Alveolar ventilation is around 4L/min-1 at rest (cardiac output is around 5L/min-1) at alveolar ventilation of 4L/min-1, PO2 and PCO2 is set at certain level (oxygen alveolar partial pressure = 13kPa, carbon dioxide = 5kPa)
• Increased metabolism: curve of pO2 moves down, curve for pCO2 moves up as ventilation ↑ matches to metabolism ↑ and PAO2 = inversely related to PACO2
• Matching metabolism to ventilation means diffusion kept between alveoli and blood
• Small fluctuations in PO2 on breath by breath basis (dynamic situation)
• Ventilation not the same in all parts of lung, there are different gas compositions in different parts, change in ventilation measured through radioactivity of different regions due to distending pressure being different (from apex to base, ↑ ventilation)
• Different gas compositions = blood equilibrates at different pO2/pCO2

Question 2

What is the effect of gravity on perfusion?

Answer 2

• Systemic circulation: standing up, pressure in feet > shoulder due to vertical difference, also vertical difference between top-bottom of lung when upright, effect of pressure between apex and base
• Flow: dependent on pressure gradient from arterial side to venous side, ↑ pressure in base of lung will impact blood flow
• Property of pulmonary blood vessels: lower pressure in pulmonary circulation = blood vessels do not have much vascular smooth muscle, thin walls = easy to distend/expand also collapsible so outside alveolar pressure needs to be considered
• In zone 3 of lung = continuous flow, with a pressure gradient going from 10 to 0 in blood vessel, so, arterial to venous pressure gradient for flow, but pressure inside > pressure outside always, causing positive distending pressure → blood vessel always open (zone 4 has greater flow, walls are further distended, bigger pressure gradient of +20 at arterial to +10 at venous)
• Higher in lungs: reduced pressure in arterial side, towards venous pressure outside vessel > pressure inside vessel → vessel collapses
• If lungs were higher, pressure outside would continue to drop at arterial end so pressure outside > pressure inside always → no flow at all
• No flow seen in people with haemorrhage → blood pressure falls substantially, might lower hydrostatic pressure, regions of zone 1 no flow so no gas exchange can occur
• As blood pressure ↑, vessels distend and resistance ↓ causing an ↑ blood flow
• ↑ perfusion pressure (increased CO) opens some closed capillaries recruits vessels higher up lungs, perfusing vessels higher up = ↑ surface area for gas exchange
• Alveoli size ↑, can pinch blood vessels in between to affect flow
• Control of pulmonary capillary flow include: recruitment & distension, mechanical effects, and vasoactive factors

Question 3

Effects of regional V/Q on gas exchange

Answer 3

• From top to bottom of the lung, 2 ½ increase in ventilation (straight line increase) 6 fold increase in perfusion (straight line but steeper increase)
  * VQ ratio: ventilation/perfusion (produces curve)
• Middle of curve (two lines cross over), ventilation equals perfusion, VQ ratio is 1, blood is bypassing gas exchange regions so no gas exchange will occur (shunt)
• Right side of curve (top of lungs) ventilation > perfusion (VQ>1) ventilation of perfusion insufficient → hypoperfusion, left side (bottom of lung), ventilation < perfusion (VQ<1), ventilation is sufficient for level of metabolism → hypoventilation
• Area where there is ventilation but no perfusion = dead space (V/Q ratio of infinity)
• Physiological shunts: some blood flow bypassing gas exchange region but normal in its physiology (thebesian veins and bronchial circulation), right/left shunt (extreme cases) alveolar gas composition equilibrates to venous blood
• VQ ratio of individual alveoli (or small region of lung) determines blood gas composition leaving that area
• VQ ratio of infinity then in extreme cases ultimately by ventilating that space, gas in that space = gas in atmosphere being brought in
• Blood coming back together towards left side of heart, different VQ ratio areas will have different alveolar gas compositions to give different partial pressures, but by mixing them → ultimate partial pressure depends on number of high and low pressures
• High V/Q: alveolar PaCO2 (bronchoconstriction) reduces, ↓ ventilation and PaO2 ↑ (vasodilation), ↑ perfusion, both will lead to decrease in region V/Q
• Low V/Q: PACO2 ↑ (bronchodilation), PAO2 ↓(vasoconstriction), both ↑ regional V/Q
• Changes in alveolar/airway pCO2 directly effects airway smooth muscle to alter ventilation, changes in blood pO2 directly effects pulmonary vascular smooth muscle to alter perfusion, together these local intrinsic mechanisms help ↓ changes in V/Q
• Final V/Q ratio determines gas exchange in that region of lung