chapter 42 guyton Flashcards
what is the respiratory centre composed of
- several groups of neurons located bilaterally in medulla oblongata and pons of the brain stem
dorsal respiratory group location and function
- dorsal portion of medulla
- inspiration
ventral resp grp location and function
- ventrolateral part of the medulla
- expiration
pneumotaxic centre location and function
- dorsally in superior portion of the pons
- control of rate and depth of breathing
where are most neurons of dorsal resp grp found
nucleus of tractus solitarius NTS
role of NTS
- sensory termination of vagal and glossopharyngeal nerves, transmits sensory signals into the respiratory centre from:
1. peripheral chemoreceptors
2. baroreceptors
3. receptors in the liver, pancreas and multiple parts of the git
4. several types of receptors in the lungs
role of dorsal resp grp in rhythm
- repetitive bursts of inspiratory neuronal action potentials; one neurone excites a second set which inhibits the first.
- this then repeats
explain RAMP signal
- nervous signal transmitted to diaphragm is not instantaneous;
- rather increases steadily in ramp manner for 2 seconds
- ceases abruptly, turns off excitation for the next 3 seconds
- allows elastic recoil of lungs and chest wall to cause expiration
- inspiratory signal repeats again for another cycle
advantage of ramp signalling
- causes steady increase in lung volume instead of inspiratory gasps
what 2 qualities of the ramp signal are controlled
- control of the rate of increase of the ramp signal; heavy resp ramp increases rapidly
- control of limiting point at which ramp suddenly ceases ; ceases earlier = shorter inspiration=shorter exp= increased frequency
which nucleus is pneumotaxic centre located in
nucleus parabrachialis of upper pons
what does a strong pneumotaxic signal cause
- limits inspiration, short as 0.5s
- has secondary effect of increasing resp rate as it also shortens expiration
weak pneumotaxic signal causes what?
- allows inspiration to continue for 5/more seconds
- secondary effect of reducing rate of resp
which nucleus is ventral grp located in
- nucleus ambiguus rostrally
- nucleus retroambiguus caudally
how does ventral resp grp differ to dorsal
- totally inactive during normal quiet breathing
- dont ppt in rhythm
- involved in inspiration and expiration. especially imp in powerful expiratory signals to diaphragm during heavy expiration.
- therefore functions as overdrive mechanism when increased pulmonary ventilation is req eg during exercise
explain the hering-breuer inflation reflex
- stretch receptors in muscular portion of bronchi and bronchioles transmit signals through vagi into dorsal resp grp when overstretched
- function in same way as pneumotaxic centre; switches off the inspiratory ramp, stops further inspiration
- inc rate of resp
- not activated until tidal volumes is 3x normal, so more of a protective mechanism to prevent excess lung inflation
what is the primary stimulus for the chemosensitive area
H+ concentration
why does co2 have more effect on chemosensitive area than H+
- H+ cannot easily cross BBB
- co2 passes very easily through BBB
- reacts with water to form carbonic acid
- dissociates into HCO3- and H+
- H+ then have potent direct stimulatory effect on chemosensitive area
explain attenuation of stimulatory effect of co2
- co2 effect gradually declines after 1 or 2 days
1. renal adjustment; increasing HCO3- in cerebrospinal fluid which binds with h+
2. HCO3- slowly diffuses across BBB and binds with H+ - therefore CO2 has potent acute effect but weak chronic effect
where are carotid bodies located
bilaterally in the bifurcations of the common carotid arteries
afferent nerve fibres of carotid bodies
- pass through herings nerves to glossopharyngeal nerves and to dorsal respiratory grp
aortic bodies location
arch of aorta
afferent nerve fibres of aorta
pass through vagi ti dorsal respiratory grp
arterial supply of carotid and aortic bodies
- directly from adjacent arterial trunk, therefore exposed at all times to arterial blood
mechanism of stimulation of peripheral chemoreceptors
- glomus cells have 02-sensitive K+ channels
- inactivation of channels = depolarise
- opens voltage gated ca2+ channels
- inc in intracellular ca2+ ions
- stimulate release of neurotransmitter
- activates afferent neurons - send signals to CNS and stimulate respiration
what neurotransmitter is involved in peripheral chemoreceptors
ATP
what levels stimulate peripheral chemoreceptors
- o2 mainly
- co2 and h+ – not as strong as central but more RAPID
acute hypoxia vs chronic hypoxia responses
- acute hypoxia: peripheral chemoreceptors increase ventilation, but central still sensitive to pco2 and ph
- chronic hypoxia: central chemoreceptors lose sensitivity, peripheral increase ventilation greatly to compensate
regulation of respiration during exercise
- po2, pco2 and ph levels remain almost exactly same
- when brain transmits impulses to exercising muscles, also transmits collateral signals to brain stem to excite respiratory centre
- this allows for almost adequate o2 levels
- chemical factors make the final adjustments
what are J lung receptors
- sensory nerve endings in alveolar walls in juxtaposition to pulmonary capillaries
- stimulated when capillaries become engorged w/ blood or due to pulmonary oedema
- excitation may give feeling of dyspnea
effects of brain oedema on respiratory centre
- depressed or inactivated by brain oedema resulting from concussion.
- swelling of brain tissues compress cerebral arteries against cranial vault, blocking blood supply
how are effects of brain oedema relieved
- IV injection of hypertonic solution, eg highly concentrated mannitol solution, which osmotically remove some fluid of brain, relieving intracranial pressure and re establishing respiration
effects of anaesthetics and narcotics overdosage on respiration
- depresses respiratory centre
cheyne stokes breathing
- slow waxing and waning respiration occurring every 40-60 seconds
- hyperventilation, then hypoventilation then apnea
- cycle repeats
causes of cheyne-stokes breathing
- severe cardiac failure: causes slow blood flow, delays transport of gases from lungs to brain
- damage to respiratory centres causing increased negative feedback gain; brain damage switches off respiratory centre for a few seconds and low co2 levels switch it back on with force. often prelude to death from brain malfunction
apnea definition
absence of spontaneous breathing
sleep apnoea
- frequency and duration of apneas greatly increased during sleep, lasting 10s or longer and occurring between 300-500 times a night
obstructive sleep apnoea cause
- blockage of airway; muscles of pharynx relax
- narrow pharynx = complete blockage
- elder obese people
- large tongue
- large tonsils
- nasal obstruction
treatment for obstructive sleep apnoea
- surgery to:
- remove excess fat tissue from throat
- remove tonsils
- create opening in trachea (tracheotomy)
- nasal ventilation with CPAP
central sleep apnoea causes
- neural drive in respiratory centre is transiently abolished
- caused by damage to the respiratory centre or insensitivity. treated with continuous positive airway pressure
what is fvc + how to obtain
forced expiratory vital capacity
- pt inspires maximally to TLC then exhales rapidly + w/ max expiratory effort
- represented by total distance of downslope of lung volume
