control of breathing Flashcards

central control of breathing: explain the central organisation of breathing, and recall the principle inputs and outputs, including sensitivity to carbon dioxide and hypoxia

1
Q

functions of respiratory muscles linked to control

A

maintenance of arterial PO2, PCO2, pH; defence of airways and lung; during exercise; communcation (under voluntary control)

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2
Q

determinants of a tidal breath

A

minute ventilation = volume difference (tidal volume) x frequency (60/duration of breath (TTot))

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3
Q

calculating TTot

A

inspiratory volume + expiratory volume

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4
Q

minute ventilation calculation

A

VT/TI (mean inspiratory flow - neural drive) x TI/TTot (timing)

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5
Q

features of tidal breath in disease (chronic bronchitis and emphysema)

A

more difficulty breathing out than in, airflow limitation so breathe faster and more shallowly

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6
Q

involuntary (metabolic) and voluntrary (behavioural) breathing controllers in brain: location and function

A

automatic bubopontine controller (brainstem) - adjusts ventilation rate in response to pH in blood; behaviour suprapontine control (widely distributed but mainly in motor cortex) - controls breath holding, singing, talking etc. and can be overridden by involuntary; reflex in limbic system and CNS

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7
Q

metabolic centre: mechanism of automatic bubopontine controller (medulla brainstem); where is distension and chemical information sent from and to in response to change to confirm (in)adequacy of response

A

H+ receptor in carotid bodies detects H+ in EC fluid → glossopharyngeal nerve firing to medulla → impulse frequency affects phrenic nerve, contracting diaphragm → repeat to switch on inspiration, then expiration, to clear CO2 (example of metabolic acidosis cleared by respiratory compensation); upper airway muscles also dilate and narrow to ensure smooth inspiration and expiration; distension info sent back from lung and respiratory muscles to brain; chemical info sent back from carotid bodies to brain

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8
Q

other influencers over breathing

A

emotions, pain, sleep

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9
Q

3 chemoreceptors: location and detection

A

central (slow): ventrolateral surface of medulla to detect ECF pH; aortic: detect oxygen and CO2; carotid body (fast): at junction of external and internal carotid arteries in neck for pH, CO2 and oxygen

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10
Q

features group pacemaker activity for pace of breathing

A

complex, subtle and specialised; about 10 groups of neurones in medulla

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11
Q

early inspiratory

A

initiates inspiratory flow via respiratory muscles

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12
Q

inspiratory augmenting

A

dilate pharnyx, larynx, airways

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13
Q

late inspiratory

A

brake start of expiration

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14
Q

expiratory decrementing

A

brake passive expiration by adducting larynx and pharynx

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15
Q

expiratory augmenting

A

activate expiratory muscles

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16
Q

late expiratory

A

signal end of expiration and onset of inspiration

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17
Q

reflex control: V, IX and X

A

V: afferents from nose and face (irritants); IX: from pharynx and larynx (irritant); X: from bronchi and bronchioles (irritant and stretch)

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18
Q

what is the Hering-Breuer reflex (mechanism and purpose)

A

pulmonary stretch receptors (mechanoreceptors) in bronchi and pleura detect stretch → signal to medulla pons via Vagus nerve → terminates inspiration (phrenic to diaphragm) to prevent overinflation (pneumotaxic centre of pons inhibits apneustic centre, stopping inspiration); weak in humans; continuous as then lower minute ventilation so hypoxaemia develops, so must increase minute ventilation again

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19
Q

what are CO2 responses potentiated by

A

acidosis and hypoxia; apneic threshold sensitive to acid-base status in sleep

20
Q

O2 sensitivity at high PCO2

A

at high PCO2, more sensitive to smaller changes in PO2; SaO2 defended, as decreased PO2 will increase sensitivity of carotid bodies to PCO2 to increase breathing and correct hypoxia

21
Q

when do PaO2 and PaCO2 fall together

A

at high altitude, as body becomes more sensitive to PaCO2

22
Q

compensatory mechanisms for too much acid or alkali

A

lung (fast) and kidney (slow)

23
Q

causes of acidosis and alkalosis

A

metabolic and respiratory

24
Q

determining [H+]

A

constant x PaCO2/HCO3-; strong ion difference: [Na+ + H+] - Cl-; pH = -log[H+]

25
Q

respiratory acidosis: cause and outcome

A

lung failing to excrete CO2 produced by metabolic processes, so high PaCO2

26
Q

acute respiratory acidosis: cause, outcome and response

A

hypoventilation causes low PaO2 and high PaCO2 and H+; stimulates metabolic centre to increase minute ventilation and restore blood gas and H+ levels

27
Q

chronic respiratory acidosis: outcome and response

A

ventilatory compensation inadequate for PaCO2 homeostasis, but renal excretion of weak acids and renal retention of Cl- return H+ to normal, even though PaCO2 remains high and PaO2 low

28
Q

central causes of acute respiratory acidosis

A

metabolic centre poisoning

29
Q

central causes of chronic respiratory acidosis

A

vascular, neoplastic disease of metabolic centre, congenital central hypoventilation syndrome, obesity hypoventilation syndrome, chronic mountain sickness

30
Q

peripheral causes of acute respiratory acidosis

A

muscle relaxant drugs, myasthenia gravis

31
Q

peripheral causes of chronic respiratory acidosis

A

neuromuscular with respiratory muscle weakness

32
Q

respiratory alkalosis: feature and outcome

A

ventilation in excess of metabolic needs, lowering PaCO2 and raising blood pH

33
Q

causes of respiratory alkalosis

A

chronic hypoxaemia, excess HCO3- (metabolic causes), pulmonary vascular disease, chronic anxiety

34
Q

normal pH range

A

7.35-7.45, to allow enzyme and protein function

35
Q

dissociation of H2CO3 and locations

A

(lungs) CO2 + H20 H2CO3 H+ + HCO3- (kidney)

36
Q

arterial blood gas measurements

A

pH, pO2, pCO2, base excees

37
Q

what is base excess

A

+ve or -ve difference depending on how much base is present (if +ve, noo much alkali, so body decreases pH to restore base excess to normal level)

38
Q

ROME

A

respiratory opposite, metabolic equal

39
Q

diagram of ROME

A

diagram (HCO3- mops up H+)

40
Q

what do opiods effect

A

repress respiratory centre, causing pin-point pupils

41
Q

what does hyperventilation cause

A

respiratory alkalosis as loss of CO2 so increase in pH

42
Q

what does diarrhoea cause

A

metabolic acidosis as loss of HCO3-, decreasing pH

43
Q

what does vomiting cause

A

metabolic alkalosis as loss of HCl from stomach, increasing pH

44
Q

if issue is respiratory, what compensates

A

metabolic (and vice versa; lungs respond quicker)

45
Q

define hypoxia

A

PaO2 <10

46
Q

define hypoxia with respiratory failure

A

PaO2 <8

47
Q

2 types of respiratory failure

A

type 1: low O2, normal CO2 (PaCO2<6), caused by V/Q mismatch e.g. pulmonary embolism; type 2: low O2, high CO2 (PaCO2>6), caused by chronic COPD e.g. alveolar hypoventilation