control of breathing - awake Flashcards
control of breathing
intrinsic breathing controlled in the lower part of the brainstem
muscles are striated
we have voluntary control
this si because it is an evoluntionary advantage to communicate with sound ie speech
functions of the respiratory muscles - unconscious
maintenance of PO2, PCO2, pH
defence of airways - cough, sneeze yawn
exercise- fight and flight
speech
functions of the resp muscles - voluntary
midbrain/cortical
sing, blow
laugh cry emotions
control of intrathoracic and intrabdominal pressures - defecation, belch, vomiting
determinants of tidal breath
minute ventilation expiration = tidal vol * frequency
60/Ttot = respiratory frequency per minute
Ttot = duration of breath
brain certain rate discharge to respiratory muscles - makes flow
vT/TI = mean inspiratory flow - how rapidly diaphragm contract, how hard muscles are driven
minute ventilation expiration = VT/TI * TI/Ttot
TI/Ttot = timing - proportion of breath spent inspiring
what increases breathing
have nose clip, more breathing than normal
extra dead space - mimics exercise = higher metabolic demand - increases te discharge rate to muscles
when conscious of breathing, breath slower and deeper - metabolic demand is the same though so total air in is the same
tidal volume increases because the increase in flow is greater than the decrease in TI
people with emphysema - more difficulty breathing out than breathing in - airway narrowing on expiration
airflow limitation - breathe faster and more shallow, inspiration and changes in exercise the same as normal though
Brain and breathing
automatic bulbopontine controller - brainstem, hind brain - close to pons
behavioural suprapontine control - widely distributed in mid and upper brain, motor cortex
metabolic will override the behavioural
emotional responses influence the metabolic centre
sleep via reticular formation influences the metabolic centre
actions of the metabolic and behavioural parts of the brain
metabolic responds to changes in demand for and production of CO2 - and determines the set point for CO2, generally monitored as PaCO2
behavioural centre is in the higher brain - controls breath holding and singing
limbic system - survival responses eg suffocation, hunger and thirst - emotions, sensory inputs can influence the metabolic centre
communication involves relationship between vocalisation part of the motor cortex, including the larynx, and the diaphragm
diaphragm is the ultimate controller with respect to the motor cortex
the organisation of breathing control
the H+ ion in the fluid surrounds the control centre - determines the impulse frequency
increase in H+ - equivalent to increase in CO2 - cause increase in impulse to respiratory muscles, switches on inspiration and expiration
phrenic nerve = contraction of the diaphragm and increased volume of the chest
stretch and irritant receptors send signals back to the brain about the levels of distension
carotid body H+ receptor sends chemical info from blood to the controller - signal amplified if hypoxia
upper airway muscle sunder the action of the controller - dilate on inspiration and contract on expiration - sop inspiration and expiration being jerky
behavioural controller can temporarily override
The peripheral chemoreceptor
carotid body ‘tastes’ arterial blood
lies at the junction of internal and external carotid arteries
rapid response system for detecting change in PCO2 and PO2
responsible for 40% controller for CO2
central coordination for breathing
group pacemaker from 10 groups of neurons in the medulla near nuclei 9 and 10 cranial nerves
pre-botzinger complex - in-ventroctranial medulla - near the 4th ventricle - essential for generating the respiratory rhythm - gasping centre
coordination of this is needed with other controllers toi generate an orderly and responsive respiratory rhythm
discrete groups of neurons in medulla discharge at different phases of the respiratory cycle and have different functions
early inspiratory initiates inspiratory flow via respiratory muscles
inspiratory augmenting may dilate the larynx pharynx and airways
late inspiratory end inspiration - break start of expiration
expiratory decrementing may break passive expiration by adducting larynx and pharynx
expiratory augmenting - activate expiratory muscles when ventilation increase on exercise
late expiratory - signal end of exp and dilate pharynx - start of insp
peripheral reflex control
5th nerve - afferents from nose and face - irritants
9th nerve - from pharynx and larynx - irritant
10th nerve - bronchi and bronchioles - irritant and stretch
irritant receptors are defensive - none deeper in lung where GE takes place
stretch receptors - feedback info about expansion
Hering-Breuer reflex - from pul stretch receptors senses lengthening and shortening and terminates insp and exp - weak in human - more responsive to stretch in the chest wall
thoracic spinal cord - from chest wall and resp muscles
what is being controlled
the control of H+ is more significant than the control of O2
HH+ mirror PCO2 - fast for carotid body, slow for the medulla
PO2 - increase from birth, decrease >40yrs
PCO2 constant - defended more than O2
SaO2 is defended
fall in ventilation causes a fall in PaO2 - increase sensitivity of carotids to PaCO2 - so ventilation and PaO2 increase and PaCO2 decreases by -ve feedback
when PaCO2 and PaO2 fall together -because high alitiude - detract from ventilation stimulus - system resets for the lower CO2 levels
primarily the acid-base status of blood and tissues is what is being controlled - slowly by kidney, quickly by the lung
if lung damage response will be slow
metabolic acidosis/alkalosis
H+ conc determined by balance between strong cation and weak anions
body produce/lose too much acid/gain too much bicarb
respiratory acidosis/alkalosis
H+ offset caused by the lungs
metabolic acidosis
excess production H+
caused - diabetic ketoacidosis, salicylate overdose, renal tubular defects
compensations: vent stil lowers PaCO2 and H+, renal secretion of keto and lactate (weak) acids, renel retention of cl to reduce strong ion difference
voluntary control of breathing
signal from motor cortex between shoulder and diaphragm
hyperventilate there is a hot spot of activity here
neuroimaging of the brain help us understand this
override the automatic centre in the brainstem
Automatic control of breathing
preBotzinger complex - area of the brain that generates resp rhythm
network of cells that receprically inhibit each other
on the ventrolateral surface of the medulla
detect pH in cerebrospinal fluid
cells on rostroventrolateral region of medulla connect to the preBotz - tell it to go quicker or slower
Metabolic alkalosis
loss of h+ = high HCO3-
cause vomiting, diuretics and dehydration
compensation: hypovent = higher PaCO2 and H+. renal retention of lactate and keto (weak) acids, renal excretion of chloride to increase strong ion difference
respiratory acidosis
Is a stimulation for hyperventilation
where fail to breath enough = lungs cant cope = lung fail to excrete CO2 from metabolic processes
Acute respiratory acidosis
hypovent = PaO2 decrease, H+ and PaCO2 increase
stimulate metabolic centre and carotid body to increase minute vent
restore blood gas and H+ levels
Chronic respiratory acidosis
vent compensation inadequate for PaCO2
so renal excreation of weak acids (lactate and keto) and retention of chloride (reduce strong ion difference) return H+ to normal even though PaCO2 still high and PaO2 low
H+ conc maintained at expense of chronically high chloride and bicarbonate `
Acute hypoventilation
metabolic centre stop functioning properly
drugs eg opiates or anesthetic
Chronic hypoventilation
vascular/neoplastic disease of metabolic centre - rare because small area
congenital hypoventilation syndrome = low Ve - enough normally, if have trigger - cant cope = hiagh PaCO2 and low PaO2 because have insensitive trigger at end of curve
obesity hypoventilation syndrome - sluggish resp centre = high PaCO2 unless lose weight
chronic mountain sickness = sluggish resp centre = secondary polycythemia - response to low PO2 - make more erythropoietin
Peripheral hypoventilation conditions
resp centre give signals but muscles not responding
acute - muscle relaxant drug, myasthenia gravis
chronic - resp neuromuscular weakness = inadequate ventilation - mainly at night when PCO2 increased - need nocturnal vent
