Control of breathing
- Central controller(normally brain stem control, cortex can over ride when req)–> effectors(resp muscles)–> chemoreceptors and other receptors –> feedback to central controller.
- Central control
- respiratory centre – baseline resp rhytm
- Pneumotaxic centre – increases resp rate (in upper pons actually)
- Exp area – for forced expiration
- Chemo receptors
- Central chemoreceptors are the most important in minute-minute ventilation
- Respond to increased H+ in CSF (from arterial CO2 diffusing out)–> ventilation
- CSF ph changes more for a given concentration of CO2 than blood ph
- CSF also compensates (renally) faster for any prolonged change in its pH.
- Peripheral chemoreceptor – in carotid bodies at bifurcation of common carotid and aortic bodies in arch of aorta.
- Carotid body responds rapidly to arterial hypoxia, acidosis and hypercarbia –> non linear- only really starts to fire up rapidly once O2 is below 100mmHg. This is KEY for hypoxic ventilatory drive. They respond rapidly to hypoxia and ph drop. Co2 control is more central change, but change is amplified if Po2 is low too.
- Important in high altitude and chronic hypoxia(cos central CO2 stimulus has desensitised).
- Lung receptor
- Stretch receptors in airway smooth muscle- increased lung volume –> stretch –> increase vagal tone –> slow RR –> this shows little adaptation. (Hering Breuer reflex)
- Irritant receptors – stimulated by noxious gases, smoking, dusts, cold air –> vagus–> bronchoconstriction, hyperpnoea
○ J receptors stimulated by chemicals in pulmonary circulation –> vagus–> rapid shallow breathing.
- Nose, upper airway receptors – sneeze, cough, bronchospasm
- Joint/muscle receptors – eg early exercise
- Arterial baroreceptors – largely unkown how it works but hypotension –> hyperventilation and vice versa
- Young person can increase ventilation 15x from normal
- Ventilation 4L/min to ventilation 120L/min
- Increase O2 consumption from 300ml/min –> 3000ml/min
- CO2 out put from 240ml/min –> 3000ml/min
- Resp quotient goes from 0.8–>1
- VO2 increases linearly with work but at a point it levels out VO2max –> after this an increase in work –> anaerobic glycolysis
- Increase 3x diffusion capacity- recruitment and distension of capillaries
Hypoxia – low O2 in body; Hypoxaemia – low O2 in blood (Important).
Causes of hypoxaemia
- Hypoxia and hypercarbia always, hypoxaemia easily reversed with O2, normal A-a gradient
- Chest wall pain, decreased drive eg opioid OD, fatigue in resp muscles, motor neuron disease
- R to L Shunt
- Responds poorly to added inspired O2
- A-a gradient increased
- Congenital abnormality, pneumonia, pulm oedema
- Diffusion impairment
- Thickening of alveolar membrane
- PaCO2 is normal, A-a usually normal at rest but can increase with exercise
- Pulmonary fibrosis, interstitial lung disease
- V/Q mismatch
- Hypoxia and PCO2 usually normal
- A-a gradient increased
- Increased ventilation can correct the hypercarbia but not the hypoxia
- Can be assess using A-a gradient using arterial O2 to calculate ideal alveolar O2 then find the difference between the 2.
- PE, pneumothorax
- Low inspired O2
- A-a gradient normal
- PCO2 decreased(hyperventilation)
- Blue or purple discolouration of skin due to hypoxic tissue near the skin surface
- Sea level 760mmHg
- Hyperventilation – most important. It reduces PCO2. Acclimatisation stops the central chemoreceptors resisting the hypoxic vent drive of the peripheral chemoreceptors.
- Polycythemia – from hypoxic stimulation of erythropoietin from kidney
- Initially at slightly higher altitude the O2 disociation curve shift right (23 DPG increase) then it shifts Left to help O2 loading in lungs.
- Acute mountain sickness – headache, fatigue, dizzy, palpitations, insomnia, nausea, loss of appetite.
O2 treatment / toxicity.
- O2 therapy can cause damage through free radical formation and inflammation
- Especially a concern in neonates where resuscitation with air is first line
- An abnormal pattern of breathing where respirations vary between hyperpnoea and then slower deeper breaths followed by a period of apnoea. This cycle follows a crecendo-dimniuendo pattern due to variations in serum oxygen and CO2.
- Tell me about the control of breathing (a very popular question).
- Where are the centres for respiratory drive ?
- What different stimuli affect respiratory drive ?
- Tell me about the ventilatory response to exercise.
- What do you understand by the term “oxygen debt” ?
- What factors operate to increase tissue oxygen offloading during exercise ?
- What is cyanosis?
- What forms of hypoxia are you aware of?
- Tell me about the respiratory effects of ascending to altitude.
- Tell me about the compensatory mechanisms which mediate acclimatisation to altitude.
- Tell me about V/Q mismatch.
- Tell me about O2 toxicity.
- How are Cheyne-Stokes respirations produced ?
- Tell me about decompression sickness.
- Pressure increases by 1atm for every 10m
- Divers should exhale on the ascent so they don’t over inflate and rupture the lungs
- WOB increases the deeper you dive –> may cause CO2 retention.
- High partial pressure of N2 on diving forces it into solution, if you ascend too quickly they form N2 bubbles which can give joint pains (bends), in severe case –> deafness, impaired vision. Can reduce this by using a helium-O2 breathing gas. Also by slow staged ascent.
- Treatment – recompression in a chamber