Breathlessness and control of breathing

Question 1

1. Is tidal expiration an active or passive process?

Answer 1

Breathing OUT is a passive process-elaticity of the wall does the trick SO most control is with inspiration

Question 2

2. State the equation for minute ventilation.

Answer 2

If Vt is the volume of tidal breath, and Vtot the length of a tidal breath
Then 1/Vtot is the frequency.
V.E is minute ventilation, equal to Ve=Vt1/Vtot=Vt60/Vtot

Question 3

3. How can this equation be manipulated to include TI?

Answer 3

Ttot can be split into Ti (inspiration) and Te (expiration). Multiplying the minute ventination by Ti/Ti, you get Ve=VT/TI*Ti/Ttot
Vt/Ti s the mean inspiratory flow-or how much muscle contract (how much air is driven in), which Ti/Ttot is the inspi duty cycle-how long inspiration is taking

Question 4

4. What does VT/TI represent?

Answer 4

Vt/Ti is the mean inspiratory flow, indicating how much muscle contract to let air in during Ti. This is called the neural drive

Question 5

5. What does TI/TTOT represent?

Answer 5

Ti/Ttot is the inspiratory duty cycle-time spend actively ventilating. If metabolic demand increases, Ti/Ttot increases as Ttot decreases-causing minute ventilation to increase

Question 6

6. How do these factors change when there is an increase in metabolic demand?

Answer 6

Vtot decreases and increase frequenct, V=Ti/Vtot increases AND Ti/Vt increases so Ve increases

Question 7

7. What is the normal tidal volume and normal minute ventilation?

Answer 7

VE is around 5.9 L/min, and Vt around 0.4 L

Question 8

8. What changes take place if you use a noseclip?

Answer 8

With a nose clide, Ve barely changes, but Frequency drops as Vtot increases. But Vt/Ti increases-more air taken per breath but less breaths taken-similar VE

Question 9

9. What changes take place when artificial dead space is added?

Answer 9

The extra dead space, like a snorkel, means Vt/Ti (L/s) increases a lot. Vt also rises to 0.5L. Frequency also rises. Deeper breaths and as often as normal-to clear the dead space-Ve increases to 7.4 L/min

Question 10

10. How is the breathing of someone with COPD different to a normal person?

Answer 10

With COPD, chronic bronchitis and emphyseama means intrathoracic airways are narrowed-need more effect on expiration and inspiration
Because of that, the breathing is shallower and faster (Smaller Vtot, also lower Vt)-but they don’t breath HARDER, as the ratio Vt/Ti is more or less the same-just less air in less time). Time spend expirating doesn’t increase either (takes same time to expire same volume, just has less), but Ti/Ttot increases to increase inspiration time

Question 11

11. What changes when we exercise?

Answer 11

Usually a near halving of Ttot, increasing frequency and Ve. Inspirational Ti times also takes up a bigger amount of time. But its reduced in people with obstruvtive disorber. Increase neural drive-Vt/Ti

Question 12

12. Where is the voluntary and involuntary control of breathing located?

Answer 12

Involuntary is in the brain stem, in bulbo pontine brain MEDULLA
The voluntary is in the motor area of cerebral cortex-but scattered throughout the brain
Metabolic (involuntary) always prevales over voluntary
Emotional response is also a factor, influencing the medulla. Other parts of cortex, such as pain, limbic system can also influence it
MAIN DRIVER is diaphragm, and main thing responding too is pCO2 and pH

Question 13

13. How is the metabolic controller reset in sleep?

Answer 13

The threshold for pCO2 activating breath is increased a bit

Question 14

14. Where, in the motor homunculus, is behavioural control of breathing located?

Answer 14

Between chest and shoulder

Question 15

15. Which receptors are involved in regulating the involuntary control of breathing?

Answer 15

Metabolic H+ receptor (about 60% of role) and peripheral (carotid body) H+ receptors, which reports back to metabolic center
They then impact Ti, Te, frequency through respiratory spinal motor neuron to Respiratory muscle to increase Ve

Question 16

16. Where are the peripheral chemoreceptors located?

Answer 16

Located to find well perfused carotid blood-at the junction of internal and external carotid in the neck

Question 17

17. Where are the pacemakers for respiratory breathing located?

Answer 17

All over the brainstem-innaccesible-near 10 groups around cranial nerves IX and X

Question 18

18. What is the main group of neurons that are involved in generating respiratory rhythm?

Answer 18

Pre-Botzinger comple, in medulla near 4th ventricle seems to generate the gaspin rythme (gasping center)-and it combines with other 6 groups of neurons to generate the actual breath
Main used nerve are 5th face, 9th pharynx and larynx and 10th bronchi and bronchiole

Question 19

19. What muscles are affected by respiratory augmenting?

Answer 19

Intercostal muscle-but mostly pharynx and larynx muscle which play a role in opening the airway

Question 20

20. Describe the Hering-breuer reflex. Which nerve is involved?

Answer 20

Another control of breath and size of it is the hering breuer effect-reflex from stretch receptor located in the lungs-react to the lengthening and shortening. WEAK IN HUMANS. Activation can inhbiti medullar input to terminate inspiration

Question 21

22. Describe the carbon dioxide challenge and what it shows.

Answer 21

Patient is asked to breath in a bag with 7% CO2 (6L)-rises pCO2 by 1KPa every minute as breathing and rebreathing increases pCO2. Found nearly 30L/min increase in Ve per 1kpa of CO2
Hypoxic breathing increases the gradient of this-bigger increase of Ve per pCO2 Kpa
Alkalosis (chronic metabolic) results in the curve X intercept moving up (starts at higher kPa) but doesn’t affect the gradient vs Normal. In chronic acidosis, gradient ressembles hypoxia, but shifted X intercept to start at lower pCO2
If arterial pCO2 DROPS to 0 (below resting level-5.3kPa), still breath to a minimum

Question 22

23. How does hypoxia affect the acute CO2 res ponse?

Answer 22

It increases the gradient of the curve-meaning the increase of Ve per KPa is higher

Question 23

24. How does chronic metabolic acidosis affect the PCO2 threshold that gives a minimal drive to breathe?

Answer 23

It shifts the gradient along the X axis-increases the threshold for PCo2 but doesn’t change the sensitivity (gradient)

Question 24

25. Is the minimal drive to breathe present when asleep?

Answer 24

Ventilation would drop but production of CO2 causes the arterial CO2 pressure to reach the apnoeic point and start breathing again-repeat cycle every 10-60s

Question 25

26. What can depress the ventilatory response to PCO2? Give a central and a peripheral example.

Answer 25

Peripheral reduction of sensitivity would be muscle weakness-same pCO2 is sensed, but the response isn’t quite good enough Central response failure lead to flattening of cuve (loss of sensitivity), and rise in arterial CO2-could be due to disease in metabolic center (tumour, lesion, congenital) or drug sedation

Question 26

27. Describe the ventilatory response to a hypoxic challenge.

Answer 26

Hypoxia increases the sensitivity to CO2, and decreases the threshold. The curves are hyperbolic at different pCO2 for alveolar pO2 vs Ve because it follows linearly the oxygen saturation-and oxygen saturation and pO2 have a sigmoid relation A 7kPa change of pO2 only increases Ve by 30/L while 1kPa of CO2 was enough for same response. Oxygen saturation is much better defended (linear relation

Question 27

28. How does a high PCO2 affect the ventilatory response to hypoxia?

Answer 27

At high CO2, failure in ventilation, also causes decrease O2. PaO2 down increases the carotid body sensitivity, meaning it increases the Ve, increasing PO2. PCO2 then falls by negative feedback

Question 28

29. Why is this system bad at dealing with altitude where you experience hypoxic hyperventilation?

Answer 28

The change is O2 due to alitutude takes a while to adapt to-hypersensitive for a wile causing altitude sickness

Question 29

30. How is neural drive different in people with COPD?

Answer 29

The breathing is shallower and shorter-Ve is the same, but Vt/Ti is also considerably increased-neural drive is higher. Diapgram is working much harder to achieve same Vt/Ti. This is because narrower airways means the lungs are hyperinflated and press of the diaphragm Emphyseama measn pCO2 is lower as air exchange is impaired

Question 30

31. How do people with obstructive disease maintain a normal minute ventilation despite breathing more shallowly?

Answer 30

They breath much more often-increase frequency and also the diaphgragm works much harder-this is because hyper inflated lungs press on it

Question 31

32. How is the PCO2 in someone with bronchitis different to someone with emphysema?

Answer 31

With emphyseama, arterial CO2 is lower because of damaged impaired gas exchange. People with bronchitis have naturaly higher pCO2 than empyseama

Question 32

33. What are the rapid and slow responses to respiratory acidosis?

Answer 32

Increase CO2 causes a direct and rapid increase of beathing to return to normal But also a slower response (hours), where kidneys act on renal exrection of weak acids (lactate and keto) as a blood buffer, but also keep Chloride to increase strong ion difference. The acidosis is controlled by the pCO2/bicarbonate ratio-one controlled by lungs other by kindeys Opposite with alkalosis

Question 33

34. How is metabolic acidosis different to respiratory acidosis?

Answer 33

Its caused by excess hydrogen ions from metabolism-not respiratory-so opposite response-ventialtion lowers PaCO2 and H+, and kidney keeps weak acids as buffer and secrete Chloride Exact opposite in alkalosis

Question 34

35. What are the mechanisms for dealing with metabolic acidosis?

Answer 34

Ventilation stimulation to lower PaCO2 | Exrete weak acid, keep Cl-

Question 35

36. Give some central and peripheral causes of hypoventilation.

Answer 35

Central-acute-poisoning, chronic-vascular/neoplastic disease of metabolic centre, congenital hyperventialer, obesity, chonric mountain sickness Peripheral-acute-muscle relaxant drugs, myasthenia gravis Chronic-neuromuscllar with muscle weakness

Question 36

37. What are the three types of breathlessness?

Answer 36

Tightness-difficulty inspiring due to airway narrowing Increases work and effort-breathing at high lung volume, against inspiratory resistant Air hunger-powerful urge to breathe-mismatch between Ve demand and achieved Ve Demand

Question 37

38. What scale is used to measure breathlessness?

Answer 37

Borg Scale-10 point. Breath holding time also measured, which measured strength of metabolic vs behavioral