Control of ventilation

Question 1

What are the lungs controlled by

Answer 1

Neural control (brain stem, lung receptors and other inputs), Chemical control (response to changes in PCO2 and PO2 and pH, central chemoreceptors, peripheral chemoreceptors)

Question 2

Draw and label brain stem:

Answer 2

Label pneumotaxic=inhibits inspiratory phase, apneustic=prolongs inspiration, euponea, apneusis, gasping, apnoea

Question 3

Name 4 nucleoi in medulla and its locations

Answer 3

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

Question 4

What does DRG include and what is it responsible for

Answer 4

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

Question 5

Draw flow charts of pons, medulla, respiratory muscles

Answer 5

ref. notes

Question 6

Basic control system in cyclic breathing

Answer 6

Draw flowchart

Question 7

Stretch receptors where and function

Answer 7

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)

Question 8

Juxtapulmonary receptor where, function, stimulated by

Answer 8

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

Question 9

Irritant receptors where, function, stimulated by

Answer 9

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

Question 10

Proprioceptive afferents

Answer 10

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.

Question 11

Other receptors

Answer 11

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

Question 12

How rate of metabolism estimated

Answer 12

CO2 producttion: estimated from PCO2
O2 cconsumption-estimated from PO2
H+ production-estimated from pH

Question 13

Plot graph of PACO2 against ventilation

Answer 13

ref. notes

Question 14

Negative feedback of ventilatory response to CO2

Answer 14

PACO2 is proportional to rate of CO2 production/Alveolar ventilation. So as alveolar ventilation halves, PaCO2 doubles

Question 15

Effect of change in pH in PACO2 vs ventilation graph

Answer 15

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

Question 16

Plot graph for PqAO2 angainst ventilation and comment

Answer 16

ref.. notes

Question 17

where are the central chemoreceptors on brain stem

Answer 17

ventrolateral surface of medulla, near the exit of CIX and X

Question 18

Draw CSF, interstitium and blood compartments and what substances go to and from each

Answer 18

ref. notes. NB interstitial pH governed by diffusion of CO2 ffroom blood and HCO3- from CSF

Question 19

What is {H+] proportional to

Answer 19

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

Question 20

What does the lack of proteins in CSF mean

Answer 20

little buffering of pH. Small change in pCO2 causses large change in pH

Question 21

central chemoreceptors do not respond to

Answer 21

Oxygen

Question 22

What happens to responsse to pCO2 after peripheral chemoreceptor removed

Answer 22

80% response remains as central chemoreceptor responsible for 80% hypercapnic ventilatory response

Question 23

Speed of central chemoreceptor response

Answer 23

Slow, around 20 seconds

Question 24

Central chemoreceptor adaptation to prolonged hypercapnia and altitude

Answer 24

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

Question 25

Where are peripheral chemoreceptors located

Answer 25

Aortic bodies above aorta, carotid body at thee bifucation of common carotid artery

Question 26

Carotid body size and blood flow

Answer 26

very small, high blood flow;A-V PO2 difference very small

Question 27

Peripheral chemoreceptors types of cell

Answer 27

Type 1/glomus cellss=rich in neurotransmitteres;contact axons
Type 2/sheath cells=partly enclose part 1 cells

Question 28

Draw carotid bodies surrounded by sinusoidal capillaries

Answer 28

ref. ntoes

Question 29

Function of peripheral chemoreceptors

Answer 29

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

Question 30

Breathing disorders:

Answer 30

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