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30 Cards in this Set

  • Front
  • Back
Alveolar pressure
Transpulmonary Pressure + Intrapleural Pressure
Boyle's Law
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
What is the role of surfactant? (w/ equation)
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
Pulmonary Ventilaiton (VE)
The amount of air entering all of the conducting and respiratory zones in one minute
Tidal Volume x Respiratory Rate
Alveolar Ventilation (VA)
Volume of air entering respiratory zones each minutes
(Tidal Volume x Resp Rate) – (Dead space x Resp Rate)
VA = VE – VD
Dead Space Ventilation (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
Oxygen-Haemoglobin dissociation curve
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
How can CO2 be transported in the plasma?
- Dissolved in the plasma (7-10%)
- Carried as bicarbonate ions (70%)
- Attached to proteins, forming carbamino compounds (20-23%)
Bicarbonate equation
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
What is 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
Where is the origin of spontaneous respiration in the brain?
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
Where is the origin of voluntary respiration in the brain?
The cerebral cortex – it can override the spontaneous centre
What is the only way you can become hypercapnic?
Also causes hypoxaemia
How does hyperventilation affect levels of O2 and CO2?
Hyperoxaemia and hypocapnia
Increased ventilation to meet increased demand
Roles of PCO2
- Determines acid/base balance
- Controls calibre of cerebral blood vessels
- Indicates adequacy and alveolar ventilation
Volume of O2 (or CO2) uptake (equation)
(Volume of air inhaled x Fraction of oxygen in the inspired air) - (Volume of air exhaled x Fraction of oxygen in expired air)
Respiratory Exchange Ratio
CO2 given out/O2 absorbed
Generally about 0.8
Arterial Hypoxaemia
Caused by any decrease in the rate of diffusion
e.g. emphysema
Rates of alveolar diffusion
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
Effects of respiratory diseases
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
Hydrogen ion's effect on the body
- 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
Hypoxic pulmonary vasoconstriction
A low ventilation:perfusion ratio decreases local PO2, which leads to a constriction of SM of arterioles supplying excessively perfused alveoli
Cor pulmonale
AKA pulmonary heart disease
Chronic ventilation failure leading to RHF
Continued hypoventilation decreases PO2 and eventually hypertrophies SM
Extrapulmonary shunt
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)
Intrapulmonary shunt
Anything blocking and air or blood channel
Breathing O2 does not improve patients with a shunt, unlike a mismatch where there is an improvement