L8: Ventilation Flashcards
Pulmonary ventilation vs Alveolar ventilation vs Dead space ventilation
Pulmonary ventilation: amount of air moved in and out of lungs per minute (6L/min)
V= f x tidal volume
Alveolar Ventilation: amount of air reaching functioning alveoli per minute (4.2L/min)
Va = f x (tidal volume - dead space volume)
Dead space ventilation (physiological dead space): Pulmonary ventilation - Alveolar ventilation
PaCO2 - Va relationship (PaCO2: alveolar CO2)
VCO2 = Va x FaCO2 (VCO2: amount of CO2 exhaled per minute)
—> VCO2 = Va x PaCO2 x k1
—> PaCO2 = k2 x VCO2/Va
—> for constant level of CO2 production (PaCO2)
—> Va↑ —> PaCO2↓ (INVERSE relation)
—> shift along the PaCO2-Va curve (hyperventilation / hypoventilation)
- Hyperpnea
—> increased ventilation to meet metabolic demand
—> achieve same level of PaCO2 (stay along the iso-capnic line)
—> whole PaCO2-Va curve shift right
PaO2 - Va relationship (PaO2: alveolar O2)
VO2 = Va x (FiO2-FaO2) (VO2: amount of O2 uptake from alveoli per minute))
—> VO2 = Va x (PiO2-PaO2) x k1
—> PaO2 = PiO2 - (VO2/Va) x k2
—> for a constant level of O2 consumption (PaO2) and fixed level of inspired O2 (PiO2)
—> Va↑ —> PaO2↑ (DIRECT proportion)
—> shift along the PaO2-Va curve (hyperventilation / hypoventilation)
- Hyperpnea
—> increased ventilation to meet metabolic demand
—> achieve same level of PaO2 (stay along the iso-oxic line)
—> whole PaO2-Va curve shift to right
Alveolar gas equation
PaO2 = PiO2 - PaCO2 / R
PiO2: fixed 150mmHg
PaCO2: normal 40mmHg
R: normal 0.8
—> ideal PaO2 —> 100mmHg (assumed to be same as body PO2)
—> compared with actual measured ParterialO2
***R: respiratory quotient (VCO2 / VO2)
- since at steady state: CO2 exhaled = CO2 production, O2 uptake = O2 consumption
—> VCO2 = CO2 production by body; VO2 = O2 consumption by body
—> R: determined by body metabolism
-used to calculate ideal PaO2 (if no impairment of gas exchange)
—> measured against ParterialO2 —> see if difference
—> Alveolar-arterial O2 gradient (PaO2 - ParterialO2) (index for gas exchange function)
—> perfect gas exchange = 0mmHg
—> normal lungs: <10mg
—> increased for lungs with severe impaired gas exchange
Dead space volume and Bohr’s equation
Space where gas exchange cannot take place
- Anatomical dead space (airway: 150ml)
- Physiological dead space (anatomical dead space + space with no blood supply and excess ventilation)
—> use Bohr’s equation to estimate:
***Vd = TV (ParterialCO2 - PexpiredCO2) / ParterialCO2
—> ParterialCO2 and PexpiredCO2 measurable
—> PexpiredCO2↑ —> Vd↓
—> PexpiredCO2↓ (similar to inspired air)—> Vd↑
Ventilation capacity and factors affecting it
Maximal volume of air that can be taken into lungs per minute (normal: 200L/min)
Factors affecting ventilation capacity:
- Lung size (vital capacity - maximum stroke)
- Force available (muscle strength)
- Airway resistance (affects airflow)
- Respiratory frequency (optimal maximum: 80-90 breaths/min)
- Pathological conditions (obstructive: ↑Raw; restrictive: ↑lung stiffness)
Factors affecting Distribution of ventilation
- Alveolar compliance (larger compliance —> larger volume change)
**Gravity effect / Posture
- upright lung: pleural pressure ↓ up the lung (gravity扯lung向下)
- even though drop in pleural pressure is the same throughout the lungs during inspiration:
- More ventilation at Base:
Less negative pressure —> Lower initial volume (Higher compliance) —> Larger volume change —> steep slope of PV curve
- Less ventilation at Apex:
More negative pressure —> air filled up initially (一早扯開airway) —> Higher initial volume (Lower compliance) —> Less volume change (hard for further expansion) —> flat slope of PV curve - Alveolar time constant (time to fill up an alveolus): CL x Raw
- fast alveolus (faster to fill up): ↓CL + ↓Raw
- slow alveolus (slower to fill up): ↑CL + ↑Raw —> normal inspiration will not be adequate for gaseous exchange
**Pathological conditions
1. regional changes in elasticity
—> elastic wall —> ↓CL —> ↓filling time (easier to fill up alveoli)
- regional obstruction
—> ↑Raw —> ↑filling time (takes longer to fill up alveoli due to Raw) - regional check valve
—> ↑Raw (loss of radial traction) + ↑CL (loss of elasticity)—> ↑↑filling time - regional disturbance in expansion (oedema)
—> ↓CL —> ↓change in volume (little gaseous exchange) —> ↓filling time
Effect on increase in dead space on ventilation and alveolar ventilation
Increase in dead space
—> more air in dead space, less air to alveoli
—> alveolar ventilation decreases
—> if need to keep same metabolism
—> compensation to meet metabolic demand
—> increases pulmonary ventilation (push alveolar ventilation back up to normal)
Breath holding time is affected by
- Lung position
- Gas composition (amount of oxygen inside)
- Size of lungs
- Higher centre control (will/determination)
Hyperventilation syndrome
Prolonged hyperventilation —> ↓PCO2 —> less H in plasma —> free plasma protein bind Ca —> more free Na —> excitation of nerve and muscle —> tetanus
↓ cerebral blood flow —> faint (automatic shutdown) —> stop hyperventilation —> push back CO2 up
One treatment would be breathing in paper bag —> breathe in own CO2 —> push CO2 up