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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
What other factors may influence the metabolic centre?
``` Limbic system (survival responses e.g. suffocation) Frontal cortex (emotions) Sensory inputs (startle) ```
26
Which receptors are involved in regulating the involuntary control of breathing?
H+ ION RECEPTORS found in the carotid bodies and in the metabolic centre itself
27
Where are the peripheral chemoreceptors located?
``` Carotid bodies (at the junction of the internal and external carotids) ```
28
What is the function of peripheral chemoreceptors?
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
Where are the pacemakers for respiratory breathing located?
~10 groups of neurones in the Medulla
30
What is the main group of neurons that are essential for generating respiratory rhythm? What is this also termed?
Pre-Botzinger Complex | "Gasping centre"
31
What muscles are affected by respiratory augmenting?
Inspiratory augmenting: Pharynx, larynx and airways | Expiratory augmenting: Expiratory muscles
32
Describe the 3 cranial nerves involved in breathing reflexes
``` 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
What does activation of irritant receptors lead to?
Coughing and sneezing | defensive
34
Describe the Hering-breuer reflex. Which nerve is involved?
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
Which cranial nerve receives afferent fibres from the carotid body?
Glossopharyngeal nerve
36
What does the central component of the metabolic controller in the medulla respond to?
H+ ion concentration of extracellular fluid
37
What does the peripheral component of the metabolic controller in the carotid bodies respond to?
H+ ion concentration in the blood
38
Which component of the metabolic controller responds more quickly?
Peripheral component: carotid bodies | As these are hyperperfused
39
Describe the carbon dioxide challenge and what it shows.
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
How does hypoxia affect the acute CO2 response?
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
How does chronic metabolic acidosis affect the PCO2 threshold that gives a minimal drive to breathe?
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
Is the minimal drive to breathe present when asleep?
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
What can depress the ventilatory response to PCO2? | Give a central and a peripheral example.
Central: disease affecting the metabolic centre e.g. tumour or drugs e.g. opioids Peripheral: respiratory muscle weakness
44
What changes in the line of a depressed ventilatory response to PCO2?
Flattening of the slope (decrease in sensitivity) | Rise in the set point (resting arterial PCO2)
45
Describe the ventilatory response to a hypoxic challenge.
30 L/min change in minute ventilation for every 7 kPa change in PO2 So the system is MUCH LESS SENSITIVE TO PO2
46
How does a high PCO2 affect the ventilatory respone to hypoxia?
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
Why are breathing control systems bad at dealing with altitude where you experience hypoxic hyperventilation?
Hypoxic hyperventilation Lowers PCO2 Inhibits the ventilatory response
48
Describe the control of PaO2
PaO2 is NOT as tightly controlled as PaCO2 and H+
49
What organs have compensatory mechanisms for too much acid or alkali?
Lung (FAST responder) | Kidney (SLOW responder)
50
What is metabolic acidosis caused by?
Excess production of H+ | Diabetic ketoacidosis, Salicylate overdose, Renal tubular defects
51
What are the compensatory mechanisms for metabolic acidosis?
Ventilatory stimulation lowers PaCO2 and H+ Renal excretion of weak (lactate and keto) acids Renal retention of chloride to reduce strong ion difference
52
What determines H+ concentration?
H+ PaCO2/ HCO3- Strong ion difference
53
What is metabolic alkalosis caused by?
Loss of H+ leads to excess HCO3- | Vomiting, Diuretics, Dehydration
54
What are the compensatory mechanisms for metabolic alkalosis?
Hypoventilation raises PaCO2 and H+ Renal retention of weak (lactate and keto) acids Renal excretion of chloride to increase strong ion difference
55
What is respiratory acidosis caused by?
lung fails to excrete the CO2 produced by metabolic processes
56
Response to acute respiratory acidosis
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
Response to chronic respiratory acidosis
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
List 1 acute and 2 chronic central causes of hypoventilation.
Acute: Metabolic centre poisoning (anaesthetics) Chronic: Vascular/ neoplastic disease of metabolic centre, Chronic mountain sickness
59
List 2 acute and 1 chronic peripheral causes of hypoventilation.
Acute: Muscle relaxant drugs, Myasthenia gravis Chronic: Neuromuscular with respiratory muscle weakness
60
Mechanism causing respiratory alkalosis
Ventilation in excess of metabolic needs
61
List 4 causes of respiratory alkalosis
Chronic hypoxaemia Excess H+ (metabolic causes) Pulmonary vascular disease Chronic anxiety (psychogenic)
62
What are the 3 types of breathlessness?
Air Hunger (powerful urge to breath) Increased Work and Effort Tightness (due to airway narrowing)
63
Describe increased work and effort of breathing
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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