# Breathlessness and Control of Breathing (awake) Flashcards Preview

## LSS 1 - Resp > Breathlessness and Control of Breathing (awake) > Flashcards

Flashcards in Breathlessness and Control of Breathing (awake) Deck (37)
1
Q

Is tidal expiration an active or passive process?

A

Passive - due to the natural recoil of the lungs

2
Q

State the equation for minute ventilation.

A
```VE = VT x Frequency
Frequency = 60/TTOT (if you want it per minute)```
3
Q

How can this equation be manipulated to include TI?

A

VE = VT/TI x TI/TTOT

4
Q

What does VT/TI represent?

A

Neural Drive - mean inspiratory flow

5
Q

What does TI/TTOT represent?

A

Inspiratory Duty Cycle

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

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

7
Q

What is the normal tidal volume and normal minute ventilation?

A

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

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

9
Q

A
```Compared to with mouthpiece only:
Minute ventilation = INCREASE
VT = INCREASE
Frequency = INCREASE
VT/TI = INCREASE```
10
Q

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

A

Breathing is SHALLOWER and FASTER

11
Q

What changes when we exercise?

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

Where is the voluntary and involuntary control of breathing located?

A
```Voluntary = Cerebral Cortex
Involuntary = Medulla```
13
Q

How is the metabolic controller reset in sleep?

A

PCO2 rises

14
Q

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

A

Between the hip and the trunk

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

16
Q

Where are the peripheral chemoreceptors located?

A

Carotid bodies (at the junction of the internal and external carotids)

17
Q

Where are the pacemakers for respiratory breathing located?

A

Medulla

18
Q

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

A

Pre-Botzinger Complex

19
Q

What muscles are affected by respiratory augmenting?

A

Pharynx, larynx and airways = inspiratory augmenting

Expiratory muscles = expiratory augmenting

20
Q

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

A
```Vagus Nerve (cranial nerve X)
Pulmonary stretch receptors are activated by large airway/lung inflation leading to a CUT OFF signal for inspiration
IMPORTANT: changes in proton concentration mirrors changes in PCO2.```
21
Q

Describe the carbon dioxide challenge and what it shows.

A

Changes in arterial PCO2 are induced by asking a subject to breathe in and out of a bag with a fixed volume of oxygen and primed with 7% CO2.
Re-breathing means that arterial PCO2 rises at a constant rate
The rise in PCO2 is accompanied by a pronounced rise in minute ventilation

22
Q

How does hypoxia affect the acute CO2 response?

A

Hypoxia increases the sensitivity of the acute CO2 response.

With hypoxia, there is an even GREATER rise in minute ventilation per 1 kPa rise in PCO2.

23
Q

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

A

Chronic metabolic acidosis shifts the line to the left - a lower PCO2 is needed to cause an increase in minute ventilation
Chronic metabolic alkalosis does the opposite

24
Q

Is the minimal drive to breathe present when asleep?

A

No - in sleep, ventilation will drop down to the zero but then the arterial PCO2 will rise rapidly to exceed the apnoeic threshold and cause breathing.

25
Q

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

A

Central - disease affecting the metabolic centre or DRUGS (e.g. opioids and anaesthetics)
Peripheral - respiratory muscle weakness

26
Q

Describe the ventilatory response to a hypoxic challenge.

A

You get a 30 L/min change in minute ventilation for every 7 kPa change in PO2
So the system is MUCH LESS SENSITIVE TO PO2

27
Q

How does a high PCO2 affect the ventilatory respone to hypoxia?

A

Increased PCO2 increases the sensitivity of the response to hypoxia.
But usually it is the PCO2 that has a greater effect on control of ventilation.

28
Q

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

A

Hypoxic hyperventilation —> fall in PCO2 —> inhibits the ventilatory response (effect of PCO2 in increasing ventilation)

29
Q

How is neural drive different in people with COPD?

A

VT/TI seems to indicate that their neural drive is normal but, in fact, they have a MUCH HIGHER NEURAL DRIVE (if you measure diaphragm activity).
They have to try much harder to maintain the same VT/TI as normal healthy people.
This is partly because of the airway narrowing and because the hyperinflated lungs are pressing down on the diaphragm meaning that the diaphragm fibres are shorter and don’t contract as efficiently.

30
Q

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

A

Increase frequency - breathe faster

31
Q

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

A

Bronchitis would cause V/Q mismatch because they are breathing SHALLOWER so their PCO2 will be HIGHER
Emphysema - reduced efficiency of gas exchange - PCO2 is LOWER than bronchitis

32
Q

What are the rapid and slow responses to respiratory acidosis?

A

RAPID - ventilation changes when pH changes (alters the removal of CO2 by the lungs)
SLOW - renal compensation (kidneys can excrete weak acids e.g. lactate and keto acids)

33
Q

How is metabolic acidosis different to respiratory acidosis?

A

Source of excess H+ comes from metabolism rather than from inadequate ventilation (not due to high PCO2)

34
Q

What are the mechanisms for dealing with metabolic acidosis?

A

Increase in ventilation
Renal excretion of weak acids
Renal retention of Cl- to reduce the strong ion difference

35
Q

Give some central and peripheral causes of hypoventilation.

A

Metabolic centre poisoning - anaesthetics, drugs, chronic mountain sickness
Peripheral - muscle relaxant drugs, myasthenia gravis

36
Q

What are the three types of breathlessness?

A

Air Hunger
Increased Work and Effort
Tightness

37
Q

What scale is used to measure breathlessness?

A

Modified Borg Scale