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Respiratory > 9. Breathlessness & control of breathing in the awake state > Flashcards

9. Breathlessness & control of breathing in the awake state Flashcards

1
Q

List 4 functions of the respiratory muscles

A

Maintenance of arterial PO2, PCO2 and pH
Defence of airways and lungs: cough, sneeze, yawn
Exercise
Control of intrathoracic and intra-abdominal pressures

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2
Q

Describe a volume time graph for a single respiratory cucle

A

Upstroke= Inspiration
Downstroke= Expiration
Tidal volume= Peak

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3
Q

What is TTOT?

A

Duration of a single respiratory cycle (breath)

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4
Q

What is V.E

A

Minute ventilation

Ventilation on expiration

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5
Q

Equation for respiratory frequency

A

1 / TTOT

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6
Q

How do you calculate respiratory frequency per minute?

A

60 / TTOT

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7
Q

State the equation for minute ventilation.

A 
V.E = VT x 60/TTOT
V.E = Tidal volume X respiratory frequency (/min)
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8
Q

How can TTOT be split in 2?

A

Inspiratory: TI
Expiratory: TE

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9
Q

How can the equation for V.E be manipulated to include TI?

A

V.E = VT/TI x TI/TTOT

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10
Q

What does VT/TI represent?

A

Mean inspiratory flow (Neural drive)

how powerfully diaphragm contracts

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11
Q

What does TI/TTOT represent?

A

Inspiratory Duty Cycle

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

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12
Q

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

A

Increased ventilation required
INCREASE VT/TI
DECREASE TTOT (increase frequency of breaths)

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13
Q

How is TTOT decreased?

A

By a combination of reduction in TI and TE

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14
Q

What is the normal tidal volume and normal minute ventilation?

A

VT = 0.5 L
V.E = 6 L/min
Breathing Rate = 12 breaths per minute

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15
Q

What changes take place if you use a noseclip?

A

Breathe more DEEPLY: increase in VT
Breathe SLOWER: decrease in respiratory frequency
Ventilation remains the SAME as metabolic demands have not changed

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16
Q

What changes take place when artificial dead space is added? (i.e. a tube)

A 
V.E = INCREASES 
VT = INCREASES
Frequency = INCREASES 
VT/TI = INCREASES
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17
Q

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

A

Breathing is SHALLOWER and FASTER

shorter TTOT

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18
Q

What process is more difficult for those with COPD? Why?

A

Difficult to ventilate lungs more on expiration that inspiration
Because intrathoracic airways are narrowed
Have higher residual volume, which increases work of breathing

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19
Q

What changes when we exercise?

A 
Increases VT/TI (neural drive) and hence ventilation 
Increases frequency (decrease TTOT)
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20
Q

How does TI/TTOT change in normal people and those with obstructive lung disease when exercising?

A

Normal: TI/TTOT increases so more time for inspiration
COPD: TI/TTOT decreases so more time for expiration

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21
Q

Where is the voluntary and involuntary control of breathing located?

A

Voluntary (behavioural): Cerebral Cortex (suprapontine)

Involuntary (metabolic): Medulla (bulbo-pontine region)

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22
Q

Which control of breathing can override the other?

A

Metabolic will always override behavioural

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23
Q

What does the metabolic centre respond to? What does it determine (in part)?

A

Responds to metabolic demands for and production of CO2

Determines ‘set point’ for CO2

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24
Q

What does the behavioural centre of breathing allow?

A

Breath holding

Singing

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25
Q

What other factors may influence the metabolic centre?

A 
Limbic system (survival responses e.g. suffocation)
Frontal cortex (emotions)
Sensory inputs (startle)
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26
Q

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

A

H+ ION RECEPTORS found in the carotid bodies and in the metabolic centre itself

27
Q

Where are the peripheral chemoreceptors located?

A 
Carotid bodies 
(at the junction of the internal and external carotids)
28
Q

What is the function of peripheral chemoreceptors?

A

Rapid response system for detecting changes in arterial PCO2 and PO2
(If pCO2 was high, [H+ ion] would rise, H+ ion receptors would detect)

29
Q

Where are the pacemakers for respiratory breathing located?

A

~10 groups of neurones in the Medulla

30
Q

What is the main group of neurons that are essential for generating respiratory rhythm? What is this also termed?

A

Pre-Botzinger Complex

“Gasping centre”

31
Q

What muscles are affected by respiratory augmenting?

A

Inspiratory augmenting: Pharynx, larynx and airways

Expiratory augmenting: Expiratory muscles

32
Q

Describe the 3 cranial nerves involved in breathing reflexes

A 
Trigeminal nerve (V): irritant sensory info. from nose and face e.g. sneezing
Glossopharyngeal nerve (IX): irritant sensory info. from pharynx and larynx
Vagus nerve (X): irritant and stretch info. from bronchi and bronchioles
33
Q

What does activation of irritant receptors lead to?

A

Coughing and sneezing

defensive

34
Q

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

A

Vagus Nerve (X)
Pulmonary stretch receptors send afferent signals to medulla via vagus nerve on inspiration leading to a dampening of respiratory centre activity
Leads to decreased firing of phrenic nerve and decreased respiratory rate

35
Q

Which cranial nerve receives afferent fibres from the carotid body?

A

Glossopharyngeal nerve

36
Q

What does the central component of the metabolic controller in the medulla respond to?

A

H+ ion concentration of extracellular fluid

37
Q

What does the peripheral component of the metabolic controller in the carotid bodies respond to?

A

H+ ion concentration in the blood

38
Q

Which component of the metabolic controller responds more quickly?

A

Peripheral component: carotid bodies

As these are hyperperfused

39
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 O2, 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

40
Q

How does hypoxia affect the acute CO2 response?

A

Hypoxia increases the sensitivity (gradient of line) of the acute CO2 response- this effect is mediated through the carotid body.
With hypoxia, there is an even GREATER rise in minute ventilation per 1 kPa rise in PCO2.

41
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 axis to the left)
Does NOT alter sensitivity (gradient of line)

Chronic metabolic alkalosis does the opposite (shifts to right)

42
Q

Is the minimal drive to breathe present when asleep?

A

No: in sleep, ventilation would drop down to 0 but continuing CO2 production means arterial PCO2 rises rapidly to exceed the apnoeic threshold and cause breathing.

43
Q

What can depress the ventilatory response to PCO2?

Give a central and a peripheral example.

A

Central: disease affecting the metabolic centre e.g. tumour or drugs e.g. opioids
Peripheral: respiratory muscle weakness

44
Q

What changes in the line of a depressed ventilatory response to PCO2?

A

Flattening of the slope (decrease in sensitivity)

Rise in the set point (resting arterial PCO2)

45
Q

Describe the ventilatory response to a hypoxic challenge.

A

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

46
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.

47
Q

Why are breathing control systems bad at dealing with altitude where you experience hypoxic hyperventilation?

A

Hypoxic hyperventilation
Lowers PCO2
Inhibits the ventilatory response

48
Q

Describe the control of PaO2

A

PaO2 is NOT as tightly controlled as PaCO2 and H+

49
Q

What organs have compensatory mechanisms for too much acid or alkali?

A

Lung (FAST responder)

Kidney (SLOW responder)

50
Q

What is metabolic acidosis caused by?

A

Excess production of H+

Diabetic ketoacidosis, Salicylate overdose, Renal tubular defects

51
Q

What are the compensatory mechanisms for metabolic acidosis?

A

Ventilatory stimulation lowers PaCO2 and H+
Renal excretion of weak (lactate and keto) acids
Renal retention of chloride to reduce strong ion difference

52
Q

What determines H+ concentration?

A

H+
PaCO2/ HCO3-
Strong ion difference

53
Q

What is metabolic alkalosis caused by?

A

Loss of H+ leads to excess HCO3-

Vomiting, Diuretics, Dehydration

54
Q

What are the compensatory mechanisms for metabolic alkalosis?

A

Hypoventilation raises PaCO2 and H+
Renal retention of weak (lactate and keto) acids
Renal excretion of chloride to increase strong ion difference

55
Q

What is respiratory acidosis caused by?

A

lung fails to excrete the CO2 produced by metabolic processes

56
Q

Response to acute respiratory acidosis

A

Hypoventilation causes decrease in PaO2 and increase in PaCO2 & H+
This stimulates metabolic centre (and carotid body) to increase minute ventilation, restore blood gas and H+ levels.

57
Q

Response to chronic respiratory acidosis

A

Ventilatory compensation inadequate so need:
Renal excretion of weak acids
Renal retention of chloride to reduce strong ion difference This returns H+ to normal, even though PaCO2 remains high and PaO2 low

58
Q

List 1 acute and 2 chronic central causes of hypoventilation.

A

Acute: Metabolic centre poisoning (anaesthetics)
Chronic: Vascular/ neoplastic disease of metabolic centre, Chronic mountain sickness

59
Q

List 2 acute and 1 chronic peripheral causes of hypoventilation.

A

Acute: Muscle relaxant drugs, Myasthenia gravis
Chronic: Neuromuscular with respiratory muscle weakness

60
Q

Mechanism causing respiratory alkalosis

A

Ventilation in excess of metabolic needs

61
Q

List 4 causes of respiratory alkalosis

A

Chronic hypoxaemia
Excess H+ (metabolic causes)
Pulmonary vascular disease
Chronic anxiety (psychogenic)

62
Q

What are the 3 types of breathlessness?

A

Air Hunger (powerful urge to breath)
Increased Work and Effort
Tightness (due to airway narrowing)

63
Q

Describe increased work and effort of breathing

A

High minute ventilation,

or at a normal minute ventilation but at a high lung volume, or against an inspiratory/ expiratory resistance

Respiratory (21 decks)

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