Resp 7 - Breathlessness and control of breathing (awake) Flashcards Preview

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Flashcards in Resp 7 - Breathlessness and control of breathing (awake) Deck (49)
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1
Q

Name 5 functions of the respiratory muscles

A
  1. Maintain arterial pO2, pCO2, and pH (pH most important)
  2. Defence of airways
  3. Exercise
  4. Speech
  5. Control of intrathoracic and infra-abdominal pressures
2
Q

Does arterial pCO2 change at all during life?

What about arterial pO2?

A

Arterial pCO2 doesn’t change.

Arterial pO2 is lower neonatally and in old age than years between.

3
Q

What does minute ventilation equal?

A

VE = VT x f

4
Q

What is TTOT?

A

Duration of single respiratory cycle

Can be split into Inspiratory (TI) and Expiratory (TE)

5
Q

What nerve supplies the diaphragm?

A

Phrenic Nerve

6
Q

What is normal ventilation rate?

A

6L / min

7
Q

What is normal tidal volume?

A

0.5L

8
Q

What does adding dead space do ?

A

It increases neural drive.

VT/TI (neural drive) increases to clear the extra space.

9
Q

What happens in patients with chronic bronchitis and emphysema?

Shorter VTs and TTOTS but similar gradients to normal people

A
  1. These patients struggle more on expiration.
  2. They have higher residual volume than normal people - increasing chest stiffness and the work of breathing.
  3. They have much shorter TTOTs - shallower and faster breathing
  4. VT/TI is roughly similar - so these patients don’t breathe harder
  5. Exercising increases neural drive and ventilation. It also halves TTOT (doubling frequency)
10
Q

What is the difference between people with COPD and normal people when exercising, with regard to TI/TTOT.

A

Normal = longer TI/TTOT - more time for inspiration

COPD = shorter TI/TTOT - gives more time for expiration

11
Q

People with obstructive disease have difficulty expiring

A

T. This is key

12
Q

Where is the involuntary centre which controls breathing (aka metabolic centre)

What about the voluntary centre (aka behavioural centre)

A

Medulla = involuntary/metabolic

Motor area of cerebral cortex = voluntary/behavioural

13
Q

Name involuntarily controlled parts of the cortex which influence metabolic centre

A

Emotional responses

14
Q

Name an influencer of the metabolic centre.

A

Sleep via reticular formation

15
Q

What happens to pCO2 during sleep?

A

It rises a little

16
Q

What does the metabolic centre respond to?

A

Metabolic demands for CO2 production (VCO2), and also determines the set point of CO2 (usually measured as PaCO2)

17
Q

Name 3 things that may influence the metabolic centre.

A
  1. Limbic system (survival)
  2. Frontal cortex (emotions)
  3. Sensory inputs (pain)
18
Q

Where is the metabolic centre of the brain?

A

In the brainstem - automatic bulbopontine region

19
Q

Describe how the metabolic controller works.

A
  1. H+ ion receptor in metabolic controller.
  2. It regulates the phrenic nerves - activates muscles in chest wall and lungs
  3. Chemoreceptors in carotid bodies in the neck sense H+ levels in the blood and feedback to controller.
  4. The controller itself has H+ receptors too.
  5. Information (secondary) also received from lungs and respiratory muscles.
  6. Upper airway muscles also controlled by controller.
20
Q

Where does the (peripheral) carotid body chemoreceptor lie?

A

At the junction of the internal and external carotid arteries.

This is the fast response as it is hyperperfused

21
Q

Unlike the heart, breathing has many pacemakers that are close together in the brain stem and are inaccessible. How many groups of nerves are there and where are they located?

A

10 groups and in the medulla - near the nuclei of cranial nerves 9 and 10.

22
Q

What is special about the pre-Botzinger complex?

A

Essential for generating respiratory rhythm - aka the “gasping centre”.

The pre-botzinger complex must be coordinated with other controllers to convert gasping into an orderly rhythm.

Disease affecting control centres in the brain are rare.

23
Q

What is the important role of pharyngeal and laryngeal muscles?

A

They open up the airways and act as a brake in breathing

24
Q

Which 3 nerves regulate reflex control of breathing (sneezing, coughing, etc)

A

5th nerve - afferent from nose and face (irritant)

9th nerve - from pharynx and larynx (irritant)

10th nerve - from bronchi and bronchioles (irritant and stretch)

25
Q

Hering-Breur reflex is a cut off signal. How?

A

Pulmonary stretch receptors that lie in airway smooth muscle are activated by lung inflation and inhibit medullary inspiratory neurons.

26
Q

For every 1kPa rise in arterial pCO2, what is the rise in minute ventilation?

A

30 L/min

27
Q

What does hypoxic breathing do to the acute CO2 response?

A

It increases the sensitivity

28
Q

What happens during sleep?

A

Ventilation drops to 0, but continuing CO2 production means that arterial pCO2 rises above apnoeic point which restarts breathing.

29
Q

What could be a cause of reduction in sensitivity to arterial pCO2?

A

Respiratory muscle weakness

30
Q

For every 7kPa decrease in arterial pO2, there is a 30 L/min rise in minute ventilation.

What conclusion can be drawn?

A

The system is much more sensitive to pCO2 than pO2.

31
Q

Which is better defended: oxygen saturation or arterial pO2.

A

Oxygen saturation (due to oxygen binding to Hb and ODC)

32
Q

How does a fall in ventilation get corrected.

A
  1. Fall in ventilation = fall in pO2 = rise in pCO2.
  2. Fall in pO2 increases sensitivity of carotid body to pCO2 and H+.
  3. Ventilation therefore increases and pO2 increases.
  4. pCO2 falls by negative feedback.
33
Q

Why is the human not so well equipped for fall in pO2 caused by altitude?

A
  1. Hypoxic hyperventilation lowers pCO2. This inhibits the ventilatory response.
  2. Therefore, several days of acclimatisation are required to adjust to a lower pO2 set point.
34
Q

What are the 2 responders to acid-base problems?

A

Lung (fast responder) and kidney (slow responder)

35
Q

What are the 2 types of acidosis and alkalosis?

A
  1. Metabolic

2. Respiratory

36
Q

Describe metabolic acidosis.

A

When source of H+ comes from metabolism rather than ventilation.
Causes = diabetic ketoacidosis, salicylate overdose, renal tubular defects.

37
Q

What are the compensatory mechanisms for metabolic ketoacidosis?

A
  1. Ventilation to lower pCO2 and H+
  2. Renal excretion of weak acids
  3. Renal retention of chloride - reduces strong ion difference
38
Q

Describe metabolic alkalosis.

A
  1. Loss of H+ leads to excess HCO3-.

2. Causes = vomiting, diuretics, dehydration

39
Q

What are the compensatory mechanisms for metabolic alkalosis?

A
  1. Hypoventilation raises pCO2 and H+
  2. Renal retention of weak acids
  3. Renal excretion of chloride to increase strong ion difference
40
Q

Describe respiratory acidosis

A

Lungs fail to excrete CO2 produced by metabolic processes (hypoventilation)

41
Q

What determines the H+ ion concentration in the blood?

A

The pCO2:bicarbonate ratio

42
Q

What are central hypoventilation conditions?

A

Acute - metabolic centre poisoning

Chronic - vascular or neoplastic disease of metabolic centre, Obesity Hypoventilation syndrome, etc

43
Q

What are peripheral hypoventilation conditions?

A

Acute - muscle relaxant drugs

Chronic - Neuromuscular with respiratory muscle weakness

44
Q

What is respiratory alkalosis?

A

Ventilation in excess of metabolic needs

Causes = chronic hyperaemia, excess H+, pulmonary vascular disease, chronic anxiety

45
Q

What is the difference between dyspnea at rest and exercise?

A

Rest - implies difficulty in expiration or inspiration

Exercise - excessive breathing for the task

46
Q

What are the 3 types of breathlessness?

A
  1. Tightness - difficulty inspiring due to airway narrowing
  2. Increased work and effort - breathing normally/high minute ventilation but HIGH lung volume (or against inspiratory/expiratory resistance)
  3. Air hunger - sensation of a powerful urge to breathe (worst)
47
Q

Mismatch between VE demand and VE achieved in air hunger. What 2 inputs does the cerebral cortex compare?

A

Demand and output

48
Q

How can breathlessness be scored?

A

BORG scale (out of 10).

49
Q

What does Breath Holding Time do?

A

Tests strength of behavioural vs metabolic controller.

Breakpoint can be prolonged by increasing lung volume, lowering pCO2, taking an isoxic/isocapnic breath near break point.