Gas Exchange in the Lungs Flashcards
what does efficient gas transfer require
large surface area of contact between air (alveoli) and blood (capillaries)
what forms the ideal lung
extensive branching in both bronchial and arterial anatomy
blood vessels branch more than bronchi so have bigger airspaces with smaller vessels
what feature of alveoli and capillaries allows for gas transfer
thin walls
equilibrium of partial pressure
PP of gas in solution = PP of gas above air
what happens to most oxygen
carried by haemoglobin rather than dissolved
features of haemoglobin
a tetramer - 2 alpha and 2 beta subunits
each subunit has a haem group - a porphyrin with a central ferrous atom which binds o2
combines loosely with oxygen
combination alters shape and charge
allosteric effect
affinity of binding o2 increases with each successively bound o2 molecule
what happens once o2 is bound to hb
number of factor can change ability of hb to take up and liberate oxygen
what does right shift o2/hb dissociation mean
less affinity for o2
gives up oxygen more readily
hb liberates o2 in tissue
what causes a right o2/hb dissociation
increase co2
increase H+
increase temp
increase 2,3-DPG
what does a left o2/hb dissociation result in
hb takes up o2 in lung
partial pressure of oxygen pO2 (kPa)
gas exchange driven by PP
PP of o2 in alveolus = PP in blood draining alveolus
partial pressure when considering lung as complete unit
no apparent equilibrium
PP of o2 in arterial blood lower than PP of alveolus
due to shunting and dead space
what is shunting
to move something from one place to another, usually because that thing is not wanted, without considering any unpleasant effects
anatomical shunts
small amount of arterial blood doesnt come from lung - thebesian veins
small amount of blood goes through without seeing gas
physiological shunts (decrease V) and alveolar dead space (decrease Q)
not all lung units have same ratio of ventilation (V) to blood flow (Q)
V/Q mismatch
what accounts for lower pO2 of arterial blood than expected
anatomical shunts
physiological stunts and alveolar dead space
physiological dead space
anatomical dead space represents the conducting airways where no gas exchange takes place
alveolar dead space represents areas of insufficient blood supply for gas exchange and is practically non-existant in health young but appears with old age
physiological dead space = anatomical dead space + alveolar dead space
ventilation and perfusion ration
V/Q
if ventilation = perfusion then will get perfect gas exchange (shunting aside)
in the lung naturally have V/Q mismatch with less blood and air going to top of the lung
‘normal’ v/q mismatch
less airflow and blood flow at the top of the lung but v>q = increased v/q, higher pO2
middle of lung v/q normal
bottom of lung more ventilation and more blood flow but v<q so decreased v/q, lower pO2
physiological v/q mismatch
in healthy lungs physiological v/q mismatch generally cancels itself out
v/q mismatch in lung disease
mismatch becomes more apparent with disease
lung diseases cause additional mismatch leading to gas exchange problems
why do patients become hypoxaemic
hypoventilation
ventilation-perfusion (v/q) mismatch (pathological vs physiological)
combination of both
hypoventilation as a cause of low oxygen levels
not enough oxygen being provided for gas exchange
what causes hypoventilation
CNS - decreased central respiratory drive
airway - potential difficult airway, obstructive sleep apnoea
cardiovascular - coronary artery disease, congestive heart failure
respiratory - restrictive chest physiology, pulmonary hypertension, hypoxaemia/hypercapnia
others - difficult vascular acccess, difficult positioning
failure of ventilatory pump
wont breathe - control failure
- brain failure to command e.g. drug overdose
cant breathe - broken peripheral mechanism
- nerves not working e.g. spinal injury
- muscles not working e.g. muscular dystrophy
- chest cant move e.g. severe scoliosis
- gas cant get in and out e.g. asthma, copd
hypoventilation and co2
oxygen levels decrease in hypoventilation
normal ventilation - co2 diffuses out blood into alveolus following partial pressure gradient
co2 mostly dissolved in blood rather than bound to haemoglobin
lower ventilation - co2 accumulates in alveolar space meaning less can be removed from blood
v/q mismatch as cause of low oxygen
not enough oxygen encountering blood to allow adequate gas exchange
what causes v/q mismatch
conditions thickening alveolar wall or narrow and block small airways
lung infections e.g. pneumonia
bronchial narrowing such as asthma and copd - can progress to hypoventilation and type 2 resp failure
interstitial lung disease
acute lung injury
v/q mismatch in pneumonia
pneumonia causes inflammation and damage in small airways and alveoli
hypoxaemia is because blood does not come into contact with adequate o2
co2 will also decrease but doesnt impact overall co2 levels in blood
what happens to arterial o2 in v/q mismatch
blood leaving areas of low v/q ratio has low PaO2 and high PaCO2
high PaCO2 stimulates ventilation
extra ventilation goes to areas of normal lung and areas with high v/q ratio
extra ventilation cant push o2 content much higher than normal
blood from both areas mix but cant overcome low o2 level
what happens to arterial co2 in v/q mismatch
blood leaving areas of low v/q ratio has low PaO2 and high PaCO2
high PaCO2 stimulates ventilation
extra ventilation goes to areas of normal lung and areas with high v/q ratio so get blood with low co2
blood from both areas mix so overall co2 is normal
v/q mismatch due to perfusion problems
pulmonary embolism
can range from small PTE causing no problems with gas exchange to massive PE with hypoxia
emboli effectively cause areas of dead space with ventilation but no perfusion causing hypoxia
massive emboli can cause circulatory failure and death
respiratory failure - PaO2 lower than expected
v/q mismatch or hypoventilation
diagnosing resp failure
PaO2 is low - patient has resp failure
if PaCO2 high - type 2 resp failure - ventilatory failure (hypoventilation)
if PaCO2 not high - type 2 resp failure - v/q mismatch
type 1 resp failure
decrease in po2
normal pco2
common causes in hospital - pneumonia, PE, acute severe asthma, copd
due to vq mismatch as main problem
type 2 resp failure
decrease in po2
increase in pco2
common causes in hospital - opiate toxicity, severe copd (acute or chronic), acute sever asthma, pulmonary oedema in acute left ventricular failure
due to hypoventilation as main feature
type 1 resp failure treatment
give oxygen - short term life saving measure
fundamental problem inadequate gas exchange
improve gas exchange by treating underlying cause
some cases - mechanical ventilation required
type 2 resp failure treatment
give oxygen - controlled in copd patients with chronic resp failure
treat underlying cause to reverse hypoventilation e.g. bronchodilators for acute asthma or opiate antagonists for overdose
support ventilation - either non-invasive or invasive
oxygen therapy - masks
variable performance - cheap, exact inspired o2 concentration not known
fixed function - constant, known inspired concentration
reservoir mask - high inspired o2 concentration
pre mixed gases - venturi mask
venturi principle uses negative pressure zone
velocity increase - increased kinetic energy
uses specifically designed plastic jet system to deliver oxygen
controlled oxygen therapy - venturi mask
aims to supply oxygen at faster rate than patient can breathe
reservoir masks
supplies maximum amount of oxygen
stores during expiration
delivers during inspiration
nasal high flow oxygen
reduces anatomical dead space
gives close to 100% oxygen
comfortable
cpap
either a mask or a helmet
provides positive pressure as well as high flow oxygen
increases alveolar surface area and improves vq mismatch
invasive ventilation
required for severe resp failure not responding to o2 therapy
not suitable for all patients
provided in intensive therapy units
non invasive ventilation for type 2 resp failure
common treatment for copd exacerbations with type 2 resp failure
tight fitting mask, no need to sedate and intubate
increases ventilation efficiency
also useful in neuromuscular disease and thoracic wall disease
