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respiration > Breathlessness and control of breathing > Flashcards

Breathlessness and control of breathing Flashcards

1
Q
  1. Is tidal expiration an active or passive process?
A

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

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2
Q
  1. State the equation for minute ventilation.
A

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

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

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

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4
Q
  1. What does VT/TI represent?
A

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

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5
Q
  1. What does TI/TTOT represent?
A

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

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

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

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

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

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

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

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

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

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

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

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11
Q
  1. What changes when we exercise?
A

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

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

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

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13
Q
  1. How is the metabolic controller reset in sleep?
A

The threshold for pCO2 activating breath is increased a bit

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

Between chest and shoulder

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

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

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16
Q
  1. Where are the peripheral chemoreceptors located?
A

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

17
Q
  1. Where are the pacemakers for respiratory breathing located?
A

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

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

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

19
Q
  1. What muscles are affected by respiratory augmenting?
A

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

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

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

21
Q
  1. Describe the carbon dioxide challenge and what it shows.
A

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

22
Q
  1. How does hypoxia affect the acute CO2 res ponse?
A

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

23
Q
  1. How does chronic metabolic acidosis affect the PCO2 threshold that gives a minimal drive to breathe?
A

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

24
Q
  1. Is the minimal drive to breathe present when asleep?
A

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

25
Q
  1. What can depress the ventilatory response to PCO2? Give a central and a peripheral example.
A

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

26
Q
  1. Describe the ventilatory response to a hypoxic challenge.
A

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

27
Q
  1. How does a high PCO2 affect the ventilatory response to hypoxia?
A

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

28
Q
  1. Why is this system bad at dealing with altitude where you experience hypoxic hyperventilation?
A

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

29
Q
  1. How is neural drive different in people with COPD?
A

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

30
Q
  1. How do people with obstructive disease maintain a normal minute ventilation despite breathing more shallowly?
A

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

31
Q
  1. How is the PCO2 in someone with bronchitis different to someone with emphysema?
A

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

32
Q
  1. What are the rapid and slow responses to respiratory acidosis?
A

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

33
Q
  1. How is metabolic acidosis different to respiratory acidosis?
A

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

34
Q
  1. What are the mechanisms for dealing with metabolic acidosis?
A

Ventilation stimulation to lower PaCO2

Exrete weak acid, keep Cl-

35
Q
  1. Give some central and peripheral causes of hypoventilation.
A

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

36
Q
  1. What are the three types of breathlessness?
A

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

37
Q
  1. What scale is used to measure breathlessness?
A

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

respiration (15 decks)

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