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Control of Breathing

Physiology and Pharmacology

QuestionAnswer
What is controlled Plotting Po2 and Pco2 against rate of breathing show the harder you breathe the lower the pco2 and higher the Po2 These are derived by considering CO2 production and O2 consumption - alveolar gas equations These curves are hyperbolas
Effects of inspired gas and metabolic rates of alveolar gas equation Varying inspired gas - vary asymptotes (normally 0 for Pco2 and 20 KPa for Po2) Varying metabolic rate - vary area constant
Considerations when controlling ventilation Want to breathe enough to ensure Hb gets close to full saturation Dont want to breathe more than necessary - waste of effort Want to regulate CO2 carefully as variations in CO2 vary pH which alter physiological function
Effects of ventilation on pH Double Ve causes arterial pH to rise from 7.4 to >7.6 Halve Ve causes arterial pH to fall from 7.4 to <7.2 Normal = 7.35-7.45
Types of chemoreceptors Central chemoreceptors Peripheral chemoreceptors
Central chemoreceptors Lie within 0.3 mm of anterior surface of medulla - close to surface of brain Rostral zone Intermediate zone - mainly neurons Caudal zone Generate 80% of Ve response to CO2 Relatively slow response as highly buffered
What to central chemoreceptors respond to Brain extracellular pH and not Pco2 Determined by composition of blood and CSF due to proximity to medulla BBB is not permeable to H+, so brain pH is determined by blood Pco2 not pH
Types of peripheral chemoreceptor Carotid bodies Aortic bodies - mainly vascular so not needed in respiration
Anatomy of carotid bodies Lie close to baroreceptors near carotid artery bifurcation Innervated by sinus nerve - branch of glossopharyngeal Small - 10mg Very high blood supply - 200ml per 100g per min Means environment of cells is close to arterial -small a-v difference Rapid
What to carotid bodies respond to Decrease in Po2 and a rise in H+/CO2 Not known how receptor works Fall in Po2/rise in H+ cause an increase in intracellular Ca in type 1 cells - triggers transmitter release
Response to hypoxia/hypercapnia At low CO2, dont really notice low O2 At high CO2, a large response to low O2 is seen In high O2, good CO2 response via central chemoreceptors In normal/low O2, larger response to low CO"
Response to sustained isocapnic hypoxia Acute response via peripheral Decreases at onset of hypoxia See a progressive rise over time Mechanism is unknown - modifications of reflex sensitivity??
CNS respiratory structures Localised at pons and medulla by sectioning the CNS - between medulla and spinal cord stops breathing Nucleus parabrachialis medialis Dorsal respiratory group - mainly afferent Ventral respiratory group - mainly efferent
Slowly adapting stretch receptors Between smooth muscle cells in large airways Large myelinated fibres in vagus Respond mainly to stretch, with slow adaptation Reflex effects are - inhibition of inspiration (Hering-Breuer reflex and bronchodilation)
Rapidly adapting stretch receptors Between epithelial cells in large airways Small myelinated fibres in vagus Respond to stretch with rapid activations Also to irritants within airway Reflex effects - cough, bronchoconstriction and tachypnoea
J receptors Receptors by alveoli and capillaries Unmyelinated C fibres in vagus Stimulated by oedema in interstitium of lung - visceral pain receptor Reflex effect - rapid shallow breathing
Loss of peripheral chemoreceptors Removal of carotid bodies in asthma, or lost following vascular surgery Probably settle at Pco2 0.5KPa higher No sensitivity to hypoxia Animals without carotid bodies at altitude become sick and die
Loss of all chemoreceptors Have wildly varying Pco2 values as normal 2.5-7.5 KPa Still breathe adequately when awake Need to be ventilated during sleep
Loss of lung receptors Lung transplants lose all afferents - no receptors Remarkably few consequences
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