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LSS 2- Respiration > Breathlessness and control of breathing > Flashcards

Breathlessness and control of breathing Flashcards

1
Q

what contributes to respiration

A

Breathing in

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2
Q

what is the equation to work out minute ventilation

A

VE= Vt x f

Upstroke= inspiration
VT= tidal volume
TTOT= Duration of a single respiratory cycle
V.E= Minute ventilation
Frequency= 1/TTOT
60/TTOT= converts to respiratory frequency per minute
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3
Q

what is minute ventilation

A

minute ventilation= tidal volume x frequency

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4
Q

what can TTOT be split into?

A

-Inspiratory (TI)

Expiratory ( TE)

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5
Q

Is tidal expiration an active or passive process?

A

Passive - due to the natural recoil of the lungs

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6
Q

State the equation for minute ventilation.

A 
VE = VT x Frequency 
Frequency = 60/TTOT (if you want it per minute)
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7
Q

How can this equation be manipulated to include TI?

A

VE = VT/TI x TI/TTOT

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8
Q

What does VT/TI represent?

A

Neural Drive - mean inspiratory flow. This is how powerfully the muscles contract

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9
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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10
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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11
Q

What is the normal tidal volume and normal minute ventilation?

A

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

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12
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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13
Q

What changes take place when artificial dead space is added?

A

Compared to with mouthpiece only:
Minute ventilation = INCREASE
VT = INCREASE
Frequency = INCREASES
TTOT= DECREASES
VT/TI = INCREASE, to satisfy the need for more ventilation.
-the inspiratory duty cycle ( TI/TOT) is essentially unaltered.

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14
Q

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

A

Breathing is:

  • shallower
  • faster (shorter TTOT)
  • However, breathing is not any harder (VT/TI is similar)
  • People with COPD have expiratory airway obstruction but the proportion of time used for expiration in patients with COPD does not change
  • Hence, the gradient of the downward slope is the same
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15
Q

What changes when we exercise?

A
  • Increases neural drive and hence ventilation
  • Increases frequency (doubles since TTOT is halved)
  • Inspiratory duty cycle (TI/TTOT) increases a little to give more time for inspiration
  • In people with airway obstruction, TI/TTOT decreases a little to give more time for expiration as people with obstructive lung disease have difficulty expiring
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16
Q

Where is the voluntary and involuntary control of breathing located?

A

Voluntary or behavioural = motor area of Cerebral Cortex

Involuntary or metabolic = Medulla

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17
Q

How is the metabolic controller reset in sleep?

A

PCO2 rises

18
Q

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

A

Between the hip and the trunk

19
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

20
Q

Where are the peripheral chemoreceptors located?

A

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

21
Q

Where are the pacemakers for respiratory breathing located?

A

Medulla

22
Q

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

A

Pre-Botzinger Complex

23
Q

What are the 6 groups of neurons in the medulla and brainstem and what muscles do they affect?

A
  1. Early inspiratory
    - initiates inspiratory flow via the respiratory muscles
  2. Inspiratory augmenting
    - may also dilate pharynx, larynx, and airways
  3. Late inspiratory
    - may signal the end of inspiration, and ‘brake’ the start of expiration
  4. Expiratory decrementing
    - may ‘brake’ passive expiration by adducting the larynx and pharynx
  5. Expiratory augmenting
    - may activate expiratory muscles when ventilation increases on exercise (internal intercostal and abdominal muscles)
  6. Late expiratory
    - may sign the end of expiration and onset of inspiration, and may dilate the pharynx in preparation for inspiration
24
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
- Stretch receptors in the airways and intercostal muscles send afferent signals to the medulla via the vagus nerve.
- These signals dampen down respiratory centre activity.
- This leads to decreased firing of the phrenic nerve -> decreased respiratory rate.

IMPORTANT: changes in proton concentration mirrors changes in PCO2.

25
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

*There is a 30 L/min rise in minute ventilation for every 1 kPa rise in arterial PCO2

26
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.

27
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

28
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.

29
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

30
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 MUCHMORE SENSITIVE TO PO2

31
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.

32
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)

33
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.

34
Q

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

A

Increase frequency - breathe faster

35
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

36
Q

What are the rapid and slow responses to respiratory acidosis?

A

ACIDOSIS
RAPID (lungs) - fall in ventilation will lead to a rise in PCO2
SLOW (kidneys) - renal compensation as the kidneys retain bicarbonate (compensatory metabolic alkalosis)

ALKALOSIS (e.g. due to panic attacks, COPD, heart attack)
RAPID - hyperventilation removes CO2
SLOW - excrete bicarbonate, retain acid

37
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)

38
Q

How is metabolic acidosis different to respiratory acidosis?
Source of excess H+ comes from metabolism rather than from inadequate ventilation (not due to high PCO2)
What are the mechanisms for dealing with metabolic acidosis and alkalosis?

A

ACIDOSIS (due to diabetic ketoacidosis= production of acid, kidney failure= kidney failure)
Lungs - Acidic blood stimulates metabolic controller to increase breathing (compensatory respiratory alkalosis)
Kidneys - increase in ventilation, renal excretion of weak acids, renal retention of Cl- to reduce the strong ion difference

ALKALOSIS (due to vomitting= acid loss, excessive gaviscon= alkali gain)
Lungs - alkaline blood reduces stimulation of metabolic centre, hypoventilation to raise PCO2, compensatory respiratory acidosis
Kidneys: retain weak acids (e.g. lactate, ketones)

39
Q

Give some central and peripheral causes of hypoventilation.

A

Central
Acute: metabolic centre poisoning e.g.drugs
Chronic: vascular/neoplastic disease, congenital central hypoventilation syndrome, obesity hypoventilation syndrome, chronic mountain sickness

Peripheral
Acute: muscle relaxant drugs, myasthenia gravis
Chronic: neuromuscular with respiratory muscle weakness

40
Q

What are the three types of breathlessness?

A
  1. Air Hunger: a powerful urge to breathe e.g. breath holding during exercise or breathing hypoxic air
  2. Increased Work and Effort: breathing against increased resistance or at higher lung volumes e.g. COPD or heart failure leading to pulmonary oedema
  3. Tightness: difficulty in expanding the thorax, generally associated with airway narrowing
41
Q

What scale is used to measure breathlessness?

A

Modified Borg Scale

  • Breathlessness can be scored on the 10-point borg scale
  • Subjects score themselves during a task

Breath holding time

  • Tests behavioral versus metabolic controller
  • Break point is an expression of air hunger
  • Can be prolonged by increasing lung volume, lowering PaCO2
  • Acute thoracic muscle paralysis does not prolong BHT
42
Q

what effects the metabolic centre and how?

A
  • there are other parts of the cortex that are not under voluntary control e.g. emotional responses
  • sleep via the reticular formation also influences the metabolic centre
  • Limbic system ( survival responses e.g. suffocation, hunger) and
  • frontal cortex ( emotions) and sensory inputs ( pain, startle) may influence the metabolic centre

LSS 2- Respiration (17 decks)

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