Control Of Breathing 6 Notes

CONTROL OF BREATHING

Generation of breathing rhythm within the brainstem

-the breathing rhythm is determined by the central pattern generator and it depends on the tonic drive from the central and peripheral chemoreceptors which monitor arterial blood gases

-the periodic nature of inspiration and expiration is controlled by neurons in the pons and medulla – respiratory centres found by sectioning the CNS at varying levels in anaesthetised animals

-Medullary respiratory centre- has a dorsal respiratory group that is associated with inspiration and a ventral respiratory group for expiration

-neurons of the inspiratory area pattern generator have intrinsic periodic firing- basic rhythm of ventilation- the pattern starts with a latent period where there is no activity, action potentials then begin to appear, increase in crescendo

- the impulses stimulate the phrenic nerve – innervates diaphragm and intercostals nerves- as the frequency of impulses from the pattern generator increases inspiratory muscle activity stronger- ramp type pattern – inspiratory action potentials cease- inspiratory muscle tone falls back to preinspiratory level and the lungs and the chest wall return to original postion due to elastic recoil

-output from the inspiratory cells is further modulated by the vagal and glossopharyngeal nerves

-the expiratory area is inactive during normal quiet breathing- more forceful breathing expiration becomes active

Apneustic centre: lower pons, impulses from this centre have an excitatory effect on inspiratory area of medulla- the impulses prolong the ramp action potentials by delaying the switch of signal

Pneumotaxic centre: upper pons- this area switches off inspiration – demonstrated experimentally in animals by direct stimulation of pneumotaxic centre – inspiration shortens and breathing rate is increased

LUNG RECEPTORS

Pulmonary stretch receptors:

-slowly adapting pulmonary stretch receptors- lie within the airway smooth muscle

-they discharge inresponse to distension of the lung and their activity is sustained with lung inflation – they show little adaption

-impulses travel in the vagus nerve via large myelinated fibres- main reflex effect inhibiting the apneustic centre is a slowing of respiratory frequency due to an increase in expiratory time

Hering Breuer inflation reflex: shown in rabbit preparation where diaphragm has a slip of muscle from which recording are taken- inflation of lungs inhibits further inspiratory muscle activity. When there is deflation of lungs inspiratory activity is initiated (deflation reflex)

Paralysed and artificially ventilated animal, prevention of lung inflation led to prolonged phrenic nerve output han if the animal were not paralysed. Inflation of lungs produces feedbac that shortens the duration f the inspiratory activity

The initiation reflex- plays a major role in ventilation- information from these stretch receptors are used to modulate the switching off mechanism in the medulla. Removal of these stretch receptors causes slow deep breathing

-prevents the overinflation of the lung, maintains constant alveolar ventilation

CORTEX

-Cortex can override the function of the brainstem within limits

RELATIONSHIP BETWEEN VENTILATION AND PARTIAL PRESSURE OF OXYGEN AND CO2

Metabolic Hyperbola

-the rate of breathing is mostly controlled by the concentration of co2 in the arterial blood

-alveolar partial pressure of c02 = C02 production/ Alveolar ventilation , this equation forms a metabolic hyperbola

-as ventilation increases the partial pressure of C02 decreases

-the metabolic hyperbola for oxygen, as ventilation increases the partial pressure of oxygen for the alveoli increases

SENSORS

-chemoreceptors respond to change in the chemical composition of blood or fluid around it

Central chemoreceptors

-most important receptors are found in the ventral surface of the medulla- control breathing rate according to the metabolic activity of the body- determined by partial pressure of C02 – control the minute to minute ventilation

- local application of H+ / CO2 stimulates central chemoreceptors and triggers impulses to the central pattern generator nerves – innervate respiratory muscles– increase in breathing

-central chemoreceptors are surrounded by brain extracellular fluid –The composition of the extracellular fluid is controlled by the cerebrospinal fluid, local blood fow, local metabolism

-cerebrospinal fluid- separated from the blood by the blood brain barrier- the barrier is relatively impermeable to H+ , HC03- but C02 diffuses into the CSF – right handed shift in the equilibrium so more H+ liberated- it is the increase in H+ ion concentration stimulate chemoreceptors which increases ventilation NOT co2. The CSF pH is the proxy for blood C02 concentration- so a change in blood c02 takes time for central chemoreceptors to respond through change in H+

-normal CSF ph is 7.32, CSF contains much less protein than blood so has a lower buffering capacity- so a change in CSF ph for a given change in pH is greater than in blood

-central chemoreceptors- pH sensitive neurones- inhibitory neurons are inhibited by the decrease in pH so decrease in inhibition of brathing- excitatory serotonergic neurons are stimulated by acidosis- increase in breathing rate

-the central chemoreceptors is important in respiratory acidosis- decreased in ventilation- increase in arterial pc02

-if ph is displaced for long period of time central chemoreceptors are unable to respond to elevated arterial pc02- initial decrease in pH in ECF and CSF is corrected by the active transport of bicarbonate ions from the blood- so blood pH returns to normal and chemoreceptor activity decreases

-The central chemoreceptors are insensitive to metabolic acidosis which is...

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