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
functions of respiratory muscles linked to control
maintenance of arterial PO2, PCO2, pH; defence of airways and lung; during exercise; communcation (under voluntary control)
determinants of a tidal breath
minute ventilation = volume difference (tidal volume) x frequency (60/duration of breath (TTot))
calculating TTot
inspiratory volume + expiratory volume
minute ventilation calculation
VT/TI (mean inspiratory flow - neural drive) x TI/TTot (timing)
features of tidal breath in disease (chronic bronchitis and emphysema)
more difficulty breathing out than in, airflow limitation so breathe faster and more shallowly
involuntary (metabolic) and voluntrary (behavioural) breathing controllers in brain: location and function
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
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
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
other influencers over breathing
emotions, pain, sleep
3 chemoreceptors: location and detection
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
features group pacemaker activity for pace of breathing
complex, subtle and specialised; about 10 groups of neurones in medulla
early inspiratory
initiates inspiratory flow via respiratory muscles
inspiratory augmenting
dilate pharnyx, larynx, airways
late inspiratory
brake start of expiration
expiratory decrementing
brake passive expiration by adducting larynx and pharynx
expiratory augmenting
activate expiratory muscles
late expiratory
signal end of expiration and onset of inspiration
reflex control: V, IX and X
V: afferents from nose and face (irritants); IX: from pharynx and larynx (irritant); X: from bronchi and bronchioles (irritant and stretch)
what is the Hering-Breuer reflex (mechanism and purpose)
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
what are CO2 responses potentiated by
acidosis and hypoxia; apneic threshold sensitive to acid-base status in sleep
O2 sensitivity at high PCO2
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
when do PaO2 and PaCO2 fall together
at high altitude, as body becomes more sensitive to PaCO2
compensatory mechanisms for too much acid or alkali
lung (fast) and kidney (slow)
causes of acidosis and alkalosis
metabolic and respiratory
determining [H+]
constant x PaCO2/HCO3-; strong ion difference: [Na+ + H+] - Cl-; pH = -log[H+]
respiratory acidosis: cause and outcome
lung failing to excrete CO2 produced by metabolic processes, so high PaCO2
acute respiratory acidosis: cause, outcome and response
hypoventilation causes low PaO2 and high PaCO2 and H+; stimulates metabolic centre to increase minute ventilation and restore blood gas and H+ levels
chronic respiratory acidosis: outcome and response
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
central causes of acute respiratory acidosis
metabolic centre poisoning
central causes of chronic respiratory acidosis
vascular, neoplastic disease of metabolic centre, congenital central hypoventilation syndrome, obesity hypoventilation syndrome, chronic mountain sickness
peripheral causes of acute respiratory acidosis
muscle relaxant drugs, myasthenia gravis
peripheral causes of chronic respiratory acidosis
neuromuscular with respiratory muscle weakness
respiratory alkalosis: feature and outcome
ventilation in excess of metabolic needs, lowering PaCO2 and raising blood pH
causes of respiratory alkalosis
chronic hypoxaemia, excess HCO3- (metabolic causes), pulmonary vascular disease, chronic anxiety
normal pH range
7.35-7.45, to allow enzyme and protein function
dissociation of H2CO3 and locations
(lungs) CO2 + H20 H2CO3 H+ + HCO3- (kidney)
arterial blood gas measurements
pH, pO2, pCO2, base excees
what is base excess
+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)
ROME
respiratory opposite, metabolic equal
diagram of ROME
diagram (HCO3- mops up H+)
what do opiods effect
repress respiratory centre, causing pin-point pupils
what does hyperventilation cause
respiratory alkalosis as loss of CO2 so increase in pH
what does diarrhoea cause
metabolic acidosis as loss of HCO3-, decreasing pH
what does vomiting cause
metabolic alkalosis as loss of HCl from stomach, increasing pH
if issue is respiratory, what compensates
metabolic (and vice versa; lungs respond quicker)
define hypoxia
PaO2 <10
define hypoxia with respiratory failure
PaO2 <8
2 types of respiratory failure
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
