Respiration

Transpulmonary Pressure + Intrapleural Pressure

Pressure is inversely proportional to volume

The stretchability of the lungs, determining the ease of breathing
Volume change/Pressure change
Main factors are the amount of elastic tissue (1/3) and surface tension (2/3), large amounts of both causing a decrease in compliance

ST is due to attractive forces between water molecules
Pressure = 2x ST/Radius
Prem babies born before 36 weeks have infant respiratory distress syndrome and can die of exhaustion due to a lack of surfactant

The amount of air entering all of the conducting and respiratory zones in one minute
Tidal Volume x Respiratory Rate

Volume of air entering respiratory zones each minutes
(Tidal Volume x Resp Rate) – (Dead space x Resp Rate)
VA = VE – VD

Amout of air entering all of the conducting zones each minute
Dead Space volume x Respiratory Rate
Volume of dead space is roughly equal to a person’s weight in pounds

In tissues PO2 is low so less oxygen bound to Hb so O2 will move into cells
When exercising more O2 dissociates at lower PO2 – curve shifts down and right

- Dissolved in the plasma (7-10%)
- Carried as bicarbonate ions (70%)
- Attached to proteins, forming carbamino compounds (20-23%)

CO2 + H20 H2CO3 HCO3- + H+
Conversion of CO2 and H20 to H2CO3 is catalysed by carbonic anhydrase
Occurs on Hb
Equation only works with catalyst and also the removal of the products – HCO3- by diffusion into the blood and H+ by chloride shift

After bicarbonate is produced it diffused into the blood and H+ stays bounds to Hb
Cl- moves onto Hb to balance out the +ve charge

Medulla oblongata – rhythmic neurone activity acts like a pacemaker
Has an inspiratory and expiratory centre
The inspiratory centre stims the active process of inspiration and also inhibits expiratory centre
Quiet exhalation is passive, but in exercise the inspiratory centre is inhibited by an active expiratory centre

The cerebral cortex – it can override the spontaneous centre

Hypoventilation
Also causes hypoxaemia

Hyperoxaemia and hypocapnia

Increased ventilation to meet increased demand

- Determines acid/base balance
- Controls calibre of cerebral blood vessels
- Indicates adequacy and alveolar ventilation

(Volume of air inhaled x Fraction of oxygen in the inspired air) - (Volume of air exhaled x Fraction of oxygen in expired air)

CO2 given out/O2 absorbed
Generally about 0.8

Caused by any decrease in the rate of diffusion
e.g. emphysema

Blood spends about 0.75s in pulmonary capillaries at rest and around 0.25s during exercise
O2 equilibriates after 0.25s so in exercise O2 only just has time
CO2 can cross membrane in under 0.1s so alveolar diffusion defects cause hypoxaemia and by hypercapnia

Mechanism PaO2 PaCO2
Alveolar hypo Low High
Alveolar hyper High Low
Diffusion defect Low Normal
V'A:Q'C mismatch Low Normal
Shunt Low Normal

pH>7.4 [H]<40nM

pH<7.4 [H]>40nM

- Increased [H] decreases heart contractility because hydrogen competes with Ca for troponin bindind sites
- Increased [H] decreases Ca binding to plasma proteins
- Increased [H] slows glycolysis as phosphofructokinase, the enzyme for the rate determining step F-6-P to F-1,6-biP is [H] sensitive

VA:QC = 0
A blockage in an air or blood channel
Apex has a high ratio, decreasing down the body to about 0.7 near the base

A low ventilation:perfusion ratio decreases local PO2, which leads to a constriction of SM of arterioles supplying excessively perfused alveoli

AKA pulmonary heart disease
Chronic ventilation failure leading to RHF
Continued hypoventilation decreases PO2 and eventually hypertrophies SM

An alternate channel
Best examples are in the foetus: the foramen ovale and the ductus ateriosus (which transfers anything that doesn't pass through the foramen ovale from the RV to the aorta)

Anything blocking and air or blood channel
Breathing O2 does not improve patients with a shunt, unlike a mismatch where there is an improvement