Control of ventilation Flashcards
What are the lungs controlled by
Neural control (brain stem, lung receptors and other inputs), Chemical control (response to changes in PCO2 and PO2 and pH, central chemoreceptors, peripheral chemoreceptors)
Draw and label brain stem:
Label pneumotaxic=inhibits inspiratory phase, apneustic=prolongs inspiration, euponea, apneusis, gasping, apnoea
Name 4 nucleoi in medulla and its locations
Dorsal respiratory group is within Nucleus tractus solitarius
Ventral contains Nucleus ambiguus and Nucleus retroambigualis. Pre-botzinger and botzinger complex located near the nucleus rectofacialis
What does DRG include and what is it responsible for
Inspiratory neurones that fire before and during inspiration. Increases steadily, rate of increase and termination points controlled, receives input from chemoreceptors and lung mechanoreceptors (CNIX and X and spinal cord), DRG inhibitory neurones inhibit expiratory neurones in VRG and Pontine respiratory group
Draw flow charts of pons, medulla, respiratory muscles
ref. notes
Basic control system in cyclic breathing
Draw flowchart
Stretch receptors where and function
smooth muscle of bronchial walls, make inspiration shorter/shallower, delays next inspiratory cycle
Used in -ve feedback: Hering-Breuer inflation reflex=inflation inhibits inspiration (only when v close to vital capacity.
Deflation reflex=deflation augments inspiration (exhalation helps next breath in)
Juxtapulmonary receptor where, function, stimulated by
Site: alveolar/bronchial walls close to capillary
Function: causes apnoea and rapid shallow breathing, fall in heart rate and BP, laryngeal constriction, relaxation of skeletal muscles
Stimulated by: increased alveolar wall fluid, oedema, pulmonary congestion, microembolism, inflammatory mediators e.g. histamine
Irritant receptors where, function, stimulated by
Site: throughout airways between epithelial cells
Function: receptors in trachea lead to cough, hyperpnoea in lower airways, reflexx bronchial and laryngeal constriction
Stimulated by: irritant gases, smoke and dust, inflammation, rapid large inflations and deflations, pulmonary congestion
Responsible for deep augmented breaths to reverse slow collapse of lungs
Proprioceptive afferents
Site: respiratory muscles
stimulated by: shortening and load of respiratory muscles (but not diaphragm). Helps cope with increased load and optimal tidal volume and frequency.
Other receptors
Pain receptors: often cause brief apnoea followed by increased breathing
Trigeminal region and larynx: apnoea or spasm, heart rate
Nasal trigeminal nerve endings-ssneeze reflex
Arterial baroreceptors-stimulation inhibits breathing
How rate of metabolism estimated
CO2 producttion: estimated from PCO2
O2 cconsumption-estimated from PO2
H+ production-estimated from pH
Plot graph of PACO2 against ventilation
ref. notes
Negative feedback of ventilatory response to CO2
PACO2 is proportional to rate of CO2 production/Alveolar ventilation. So as alveolar ventilation halves, PaCO2 doubles
Effect of change in pH in PACO2 vs ventilation graph
Acidosis-lines shifts to left, ventilation increases becausse blow off CO2 to normalise
Alkalosis-line shifts to right. Ventilation reduced because retain,volatile acid, normalise pH
Plot graph for PqAO2 angainst ventilation and comment
ref.. notes
where are the central chemoreceptors on brain stem
ventrolateral surface of medulla, near the exit of CIX and X
Draw CSF, interstitium and blood compartments and what substances go to and from each
ref. notes. NB interstitial pH governed by diffusion of CO2 ffroom blood and HCO3- from CSF
What is {H+] proportional to
Blood PCO2/CSF {HCO3-] As blood CO2 increases, interstitial fluid around chemoreceptor becomes more acidotic. Central chemoreceptors primarily affected by changes in raterial pCO3 not arterial pH
What does the lack of proteins in CSF mean
little buffering of pH. Small change in pCO2 causses large change in pH
central chemoreceptors do not respond to
Oxygen
What happens to responsse to pCO2 after peripheral chemoreceptor removed
80% response remains as central chemoreceptor responsible for 80% hypercapnic ventilatory response
Speed of central chemoreceptor response
Slow, around 20 seconds
Central chemoreceptor adaptation to prolonged hypercapnia and altitude
Prolonged hypercapnia: CSF pH returns to normal, ventilatory drive decreases, e.g. chronic respiratory disease
Altitude: CSF initially alkaline due to hypoxic drive but CSF returns to normal and drive increases to level appropriate for hypoxia
Where are peripheral chemoreceptors located
Aortic bodies above aorta, carotid body at thee bifucation of common carotid artery
Carotid body size and blood flow
very small, high blood flow;A-V PO2 difference very small
Peripheral chemoreceptors types of cell
Type 1/glomus cellss=rich in neurotransmitteres;contact axons
Type 2/sheath cells=partly enclose part 1 cells
Draw carotid bodies surrounded by sinusoidal capillaries
ref. ntoes
Function of peripheral chemoreceptors
Increase in PCCo2 or H+ increases discharge
Decrease in PO2 increase discharge
very fast response so responds to oscillations in blood
NB responds to PO2 not O2 content
Breathing disorders:
Loss of CO2 drive (chronic hypercapnia, adaptation)
Chyne-Stokes respiration (heart failure, stroke, altitudde sickness)
Central sleep apnoea
can’t breathe=neuromauscular disease llike muscular dystrophy, phrenic nerve damage
won’t breathe==brain stem damage/disease like ccurse of ondine
