chapter 42 guyton Flashcards

1
Q

what is the respiratory centre composed of

A
  • several groups of neurons located bilaterally in medulla oblongata and pons of the brain stem
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2
Q

dorsal respiratory group location and function

A
  • dorsal portion of medulla
  • inspiration
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3
Q

ventral resp grp location and function

A
  • ventrolateral part of the medulla
  • expiration
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4
Q

pneumotaxic centre location and function

A
  • dorsally in superior portion of the pons
  • control of rate and depth of breathing
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5
Q

where are most neurons of dorsal resp grp found

A

nucleus of tractus solitarius NTS

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6
Q

role of NTS

A
  • 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
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7
Q

role of dorsal resp grp in rhythm

A
  • repetitive bursts of inspiratory neuronal action potentials; one neurone excites a second set which inhibits the first.
  • this then repeats
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8
Q

explain RAMP signal

A
  • 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
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9
Q

advantage of ramp signalling

A
  • causes steady increase in lung volume instead of inspiratory gasps
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10
Q

what 2 qualities of the ramp signal are controlled

A
  • 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
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11
Q

which nucleus is pneumotaxic centre located in

A

nucleus parabrachialis of upper pons

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12
Q

what does a strong pneumotaxic signal cause

A
  • limits inspiration, short as 0.5s
  • has secondary effect of increasing resp rate as it also shortens expiration
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13
Q

weak pneumotaxic signal causes what?

A
  • allows inspiration to continue for 5/more seconds
  • secondary effect of reducing rate of resp
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14
Q

which nucleus is ventral grp located in

A
  • nucleus ambiguus rostrally
  • nucleus retroambiguus caudally
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15
Q

how does ventral resp grp differ to dorsal

A
  1. totally inactive during normal quiet breathing
  2. dont ppt in rhythm
  3. 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
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16
Q

explain the hering-breuer inflation reflex

A
  • 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
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17
Q

what is the primary stimulus for the chemosensitive area

A

H+ concentration

18
Q

why does co2 have more effect on chemosensitive area than H+

A
  • 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
19
Q

explain attenuation of stimulatory effect of co2

A
  • 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
20
Q

where are carotid bodies located

A

bilaterally in the bifurcations of the common carotid arteries

21
Q

afferent nerve fibres of carotid bodies

A
  • pass through herings nerves to glossopharyngeal nerves and to dorsal respiratory grp
22
Q

aortic bodies location

A

arch of aorta

23
Q

afferent nerve fibres of aorta

A

pass through vagi ti dorsal respiratory grp

24
Q

arterial supply of carotid and aortic bodies

A
  • directly from adjacent arterial trunk, therefore exposed at all times to arterial blood
25
Q

mechanism of stimulation of peripheral chemoreceptors

A
  • 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
26
Q

what neurotransmitter is involved in peripheral chemoreceptors

A

ATP

27
Q

what levels stimulate peripheral chemoreceptors

A
  • o2 mainly
  • co2 and h+ – not as strong as central but more RAPID
28
Q

acute hypoxia vs chronic hypoxia responses

A
  • 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
29
Q

regulation of respiration during exercise

A
  • 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
30
Q

what are J lung receptors

A
  • 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
31
Q

effects of brain oedema on respiratory centre

A
  • depressed or inactivated by brain oedema resulting from concussion.
  • swelling of brain tissues compress cerebral arteries against cranial vault, blocking blood supply
32
Q

how are effects of brain oedema relieved

A
  • IV injection of hypertonic solution, eg highly concentrated mannitol solution, which osmotically remove some fluid of brain, relieving intracranial pressure and re establishing respiration
33
Q

effects of anaesthetics and narcotics overdosage on respiration

A
  • depresses respiratory centre
34
Q

cheyne stokes breathing

A
  • slow waxing and waning respiration occurring every 40-60 seconds
  • hyperventilation, then hypoventilation then apnea
  • cycle repeats
35
Q

causes of cheyne-stokes breathing

A
  • 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
36
Q

apnea definition

A

absence of spontaneous breathing

37
Q

sleep apnoea

A
  • frequency and duration of apneas greatly increased during sleep, lasting 10s or longer and occurring between 300-500 times a night
38
Q

obstructive sleep apnoea cause

A
  • blockage of airway; muscles of pharynx relax
  • narrow pharynx = complete blockage
  • elder obese people
  • large tongue
  • large tonsils
  • nasal obstruction
38
Q

treatment for obstructive sleep apnoea

A
  • surgery to:
  • remove excess fat tissue from throat
  • remove tonsils
  • create opening in trachea (tracheotomy)
  • nasal ventilation with CPAP
39
Q

central sleep apnoea causes

A
  • neural drive in respiratory centre is transiently abolished
  • caused by damage to the respiratory centre or insensitivity. treated with continuous positive airway pressure
40
Q

what is fvc + how to obtain

A

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

41
Q
A