Resp 8 - Breathlessness and control of breathing Flashcards

1
Q

Is tidal expiration an active or passive process?

A

Passive - due to the natural recoil of the lungs

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2
Q

State the equation for minute ventilation (VE)

A
VE = VT x Frequency 
Frequency = 60/TTOT (if you want it per minute) or 1/TTOT for frequency 
TTOT = duration of one inspiration
VT = tidal volume
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3
Q

How can this equation be manipulated to include TI?

A
VE = VT/TI x TI/TTOT
TI is the Inspiratory time 
TE is the expiratory time 
TTOT = TE + TI 
VT/TI mean inspiratory flow
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4
Q

What does VT/TI represent?

A

Neural Drive - mean inspiratory flow (volume over time gives flow)
How powerfully the muscles contract. It is the slope of the upstroke.

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5
Q

What does TI/TTOT represent?

A

Inspiratory Duty Cycle

Proportion of the cycle spent actively ventilating (i.e. breathing in)

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6
Q

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

A

Increased metabolic demand —> increased ventilation
VT/TI = INCREASE
TTOT = DECREASE (increase frequency)
TTOT is decreased by a combination of reduction in TI and TE

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7
Q

What is the normal tidal volume, normal minute ventilation, breathing rate, TI/TTOT?

A

Tidal Volume = 0.5 L
Minute Ventilation = 6 L/min
Breathing Rate = 12 breaths per minute
TI/TTOT = 40%

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8
Q

What changes take place if you use a noseclip?

A

Breathe more DEEPLY - increase in VT
Breathe SLOWER - decrease in frequency
Ventilation remains the SAME

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9
Q

What changes take place when artificial dead space is added?

A
Compared to with mouthpiece only:
Minute ventilation = INCREASE
VT = INCREASE
Frequency = INCREASE 
VT/TI (neural drive)= INCREASE - to satisfy need for more ventilation
TI/TOTT UNALTERED
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10
Q

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

A

Breathing is SHALLOWER and FASTER
Difficulty more on expiration
Neural drive is the same - do not breathe harder

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11
Q

What changes when we exercise?

A
Increases neural drive and hence ventilation 
Increases frequency (halving TTOT)
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12
Q

Where is the voluntary and involuntary control of breathing located?

A
Voluntary = Cerebral Cortex 
Involuntary = Medulla
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13
Q

How is the metabolic controller reset in sleep?

A

PCO2 rises

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14
Q

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

A

Between the hip and the trunk

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15
Q

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

A

HYDROGEN ION RECEPTORS found in the carotid bodies and in the metabolic centre itself

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16
Q

Where are the peripheral chemoreceptors located?

A

Carotid bodies (at the junction of the internal and external carotids, supplied by pharyngeal nerve)

17
Q

Where are the pacemakers for respiratory breathing located?

A

Many pacemakers close together in the brain stem. Inaccessible.
10 groups of neurons in medulla

18
Q

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

A

The pre-Botzinger complex situated near 4th ventricle

called the ‘gasping centre’

19
Q

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

A

10th nerve
Pulmonary stretch receptors sense lengthening and shortening and terminates inspiration and expiration.
Basically feedback from lung helps terminate inspiration.

20
Q

What are the two parts of the metabolic controller?

A
  • central part in the medullla responding to [H+] in the EC fluid -> SLOW response
  • peripheral part at the carotid bifurcation (carotid sinus) - H receptors -> FAST
    Fast and slow responses due to the fact that change of H+ is rapidly sensed in hyperperfused carotid bodies but not in EC fluid
21
Q

Describe the carbon dioxide challenge and what it shows.

A

Testes the sensitivity of the metabolic respiratory centre to H ions.
Ventilation measured against PCO2.
Changes in PCO2 induced by breathing in and out of 6L bag with 7% CO2.

The slope of the curves obtained indicate the chemosensitivity. Arterial PCO2 rises at a constant rate of about 1 pKa per minute. This causes a rise in minute per ventilation - 30L/min per pKa.

22
Q

How does hypoxia affect the acute CO2 response?

A

Hypoxia increases the sensitivity (so the slope is greater) of the acute CO2 response. mediated through carotid bodies

23
Q

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

A

Increases the threshold (shifts the intercept with the x on the left) but does not alter sensitivity (gradient is the same as in hypoxia). Chronic metabolic alkalosis has the opposite effect.

24
Q

Is the minimal drive to breathe present when asleep?

A

No it is attributed to wakefulness. In sleep, ventilation would drop to 0 but continuing CO2 production means that in 10-60 seconds, arterial PCO2 has risen sufficiently above the apnoeic point to restant breathing.

25
Q

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

A

Depress ventilatory response to CO2 means a flattening of the slope and rised set point.

This is caused by disease affecting metabolic control (tumour, congenital) but more commonly suppressed by drugs - opioid/anaesthetics
Peripheral cause - respiratory muscle weakness
COPD

26
Q

Describe the ventilatory response to a hypoxic challenge.

A

It increases when alveolar PO2 decreases - the relationship is hyperbolic.
And increases when oxygen saturation decreases - a linear relationship.
There is a 30L/min increase in minute ventilation for a 7kPa change in arterial PO2 –> a similar change of 30L/min would be brought about by 1kPa change in arterial PCO2.

27
Q

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

A

Altitude = a fall in PaO2 and PaCO2 together.
System is good at dealing like this: fall in ventilation –> fall in PaO2 and rise in PaCO2
The fall in PaCO2 increases sensitivity of carotid bodies to PaCO2 and H+ therefore ventilation is increased and PaO2 increased.

Altitude lowers PCO2 and inhibits the ventilatory response because no rise in PaCO2 but a fall.
So the body needs several days of acclimatisation before metabolic centres adjust.

28
Q

How is neural drive different in people with COPD?

A

It is the same

29
Q

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

A

Their frequency increases

30
Q

What are the rapid and slow responses to respiratory acidosis?

A

Rapid - fall in ventilation leads to rise in PCO2 and H+ which stimulates metabolic controls to increase breathing
Slow - renal excretion and retention of weak acids as an important backup if the lungs can’t compensate fully

31
Q

How is metabolic acidosis different to respiratory acidosis?

A

When the excess H+ comes from metabolism rather than inadequate ventilation.
Example of ause: diabetic ketoacidosis

32
Q

What are the mechanisms for dealing with metabolic acidosis?

A

Compensatory mechanisms: ventilatory stimulation - hyperventilation, renal excretion of weak acids, renal retention of chloride to reduce strong ion difference
Metabolic alkalosis would be the opposite.

33
Q

Give some central and peripheral causes of hypoventilation.

A

Central
Anaesthetics, drugs - acute - metabolic centre poisoning
chronic:
Disease of metabolic centre, congenital central hypoventilation syndrome, obesity hypoventilation syndrome, chronic mountain sickness

Peripheral
Acute
Muscle relaxant drugs, myasthenia gravis
Chronic
Neuromuscular with respiratory muscle weakness
34
Q

What are the three types of breathlessness?

A
  • tightness
  • increased work and effort
  • air hunger
35
Q

What scale is used to measure breathlessness?

A

Borg scale