*Physiology 5 (lecture 6) Flashcards Preview

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Flashcards in *Physiology 5 (lecture 6) Deck (52)
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1
Q

What 2 factors control respiration?

A

Neural

Hormonal

2
Q

What control the rhythmicity (inspiration followed by expiration) of breathing?

A

Neural control

3
Q

What are the 3 parts of the brainstem?

A

The midbrain
Pons
Medulla oblongata

4
Q

What part of the brain is the major rhythm generator?

A

Medulla

5
Q

What are the respiratory centres of the pons? (2)

A

Pneumotaxic centre

Apneustic centre

6
Q

What are the respiratory centres of the medulla? (3)

A

Pre-Botzinger complex
Dorsal respiratory group
Ventral respiratory group

7
Q

What 2 parts of the brain stem have respiratory control centres in them?

A

Pons respiratory centres

Medullary respiratory centres

8
Q

What network of neurones generates the breathing rhythm?

A

Pre-botzinger complex

9
Q

What are pacemakers?

A

a group of cells or a body part (as the sinoatrial node of the heart) that serves to establish and maintain a rhythmic activity e.g. the neurones of the pre-botzinger complex display pacemaker activity

10
Q

What does the Pre-botzinger complex do with the rhythm it generates?
What does this cause?

A

Excites dorsal respiratory group neurones which fire in bursts leading to contraction of inspiratory muscles = inspiration

11
Q

What causes passive expiration?

A

When the firing from dorsal respiratory group neurones stops

12
Q

Is the dorsal respiratory group neurones concerned with inspiration or expiration?

A

Inspiration

13
Q

What causes “active” expiration during hyperventilation?

A

Increased firing of dorsal neurones excites the ventral respiratory group neurones
These excite internal intercostal muscles and muscles in the abdominal wall causing forceful expiration

14
Q

What are the major muscles of inspiration? (contract every inspiration; relaxation causes passive expiration)

A

External intercostal muscles

Diaphragm

15
Q

Accessory muscles of inspiration? (contract only during forceful inspiration)

A

Scalenus

Sternocleidomastoid

16
Q

What ar the muscles of active expiration (contract only during active expiration)?

A

Internal intercostal muscles

Abdominal muscles

17
Q

What is the purpose of the pons respiratory centres?

A

To modify the rhythm generated in the medulla

18
Q

What does stimulation of the pneumotaxic centre do?

When is the PC stimulated?

A

Terminates inspiration

When dorsal respiratory neurones fire

19
Q

What is breathing like without a functioning pneumotaxic centre?

A

Prolonged inspiratory gasps with brief expiration called apneusis

20
Q

What is the purpose of the apneustic centre?

A

To excite inspiratory area of medulla prolonging inspiration

21
Q

What are some examples of stimuli influencing the respiratory centre? (7)

A

Higher brain centres e.g. cerebral cortex, limbic centre
Stretch receptors in the wall of bronchi and bronchioles
Juxtapulmonary (J) receptors
Joint receptors
Baroreceptors
Central chemoreceptors
Peripheral chemoreceptors

22
Q

What is an example of a reflex due to the stretch receptors in the walls of the bronchi and bronchioles?
What does this protect against?

A

The inflation Hering-Breuer reflex
Guards against hyperinflation
(involuntary modification of breathing)

23
Q

What stimulates juxtapulmonary (J) receptors? (3)

What does this cause?

A

Stimulated by pulmonary capillary congestion, pulmonary oedema and PE
Causes rapid shallow breathing

24
Q

what stimulates joint receptors?

What is this important in?

A

Joint movement increases breathing reflexly
Exercise
(involuntary modification of breathing)

25
Q

What does stimulation of baroreceptors cause?

A

Increased ventilatory rate in response to decreased blood pressure

26
Q

What 4 factors cause involuntary increase in ventilation during exercise?

A
Reflexes originating from body movement
Adrenaline release
Impulses from the cerebral cortex
Increase in body temperature
Later accumulation of CO2 and H+ generated by active muscles
27
Q

Is the cough reflex a voluntary or involuntary modification of breathing?

A

Involuntary

28
Q

How does the Hering-breur reflex work?

When is this activated?

A

Pulmonary stretch receptors are activated during inspiration
Afferent discharge inhibits inspiration through the hearing-breur reflex
At tidal volumes&raquo_space;1L meaning they don’t tend to switch off respiration during the normal respiratory cycle
May prevent over inflation of the lungs during hard exercise or in new born babies

29
Q

What activates the cough reflex? (2)

A

Irritation of airways or tight airways e.g. in asthma

30
Q

Where is the centre that controls coughing located?

A

In the medulla

31
Q

What type of control system is the chemical control of respiration?

A

Negative feedback system

32
Q

What are the controlled variables in the chemical control of respiration?
What senses the values of these?

A

Blood gas tensions (especially CO2)

Chemoreceptors

33
Q

Where are the peripheral chemoreceptors located?

What do these sense?

A

Carotid bodies
Aortic bodies
Tension of O2, CO2 and [H+] in the blood - mainly O2 levels

34
Q

Where are the central chemoreceptors located?

What do these sense?

A

Near the surface of the medulla in the brainstem

[H+] of the cerebrospinal fluid (CSF) - CO2 levels

35
Q

What separates CSF from blood?

What is this impermeable to?

A

Blood brain barrier

Impermeable to H+ and HCO3- (CO2 diffuses readily)

36
Q

Is the CSF more or less buffered than blood?

A

Less as it contains less proteins

37
Q

What is hypercapnia?

A

An abnormally high level of CO2 in the blood

38
Q

Why can you not raise your breath for a long period of time?

A

The system is very sensitive to PCO2 meaning CO2 will rise and diffuse into the CSF causing the [H+] to rise leading to the stimulation of central chemoreceptors = increased respiratory rate

39
Q

What happens to ventilation rate when hypoxia is extremely severe?

A

Neurons will be depressed meaning ventilation rate decreases

40
Q

When can your peripheral chemoreceptors be stimulated?

A

When PO2 is less than 8.0kPa

41
Q

Is changes in our respiratory rate normally based on our O2 or CO2 concentration?

A

Changes in our CO2 concentration (detected by our central chemoreceptors) - increase in CO2 = increase in rate and depth of breathing

42
Q

What happens to the control of respiratory rate in patients with conditions such as COPD?

A

Over time the central chemoreceptors become insensitive to the chronically high levels of CO2. This therefore leads to the peripheral chemoreceptors controlling ventilation rate through the levels of O2

43
Q

What is hypoxia?

A

Deficiency in the amount of O2 reaching the tissues

44
Q

What is the hypoxic drive?

A

A type of respiratory drive in which the body uses oxygen (peripheral) chemoreceptors instead of CO2 receptors (central chemoreceptors) to regulate the respiratory cycle

45
Q

When is hypoxic drive stimulated?

A

When arterial PO2 falls below 8.0kPa

46
Q

Apart from in COPD patients with chronic CO2 retention, when else is the hypoxic drive important?

A

In high altitudes

47
Q

What is hypoxia at high altitudes caused by?

A

Decreased partial pressure of inspired oxygen (PiO2)

48
Q

What is the acute response to hypoxia at high altitudes?

A

Hyperventilation (due to the hypoxic drive) and increased cardiac output

49
Q

What are the symptoms of acute mountain sickness?

A
Headache 
fatigue
nausea
Tachycardia
dizziness
sleep disturbance
exhaustion
SOB
unconsciousness
(all due to a lack of O2)
50
Q

What are some chronic adaptions to high altitude hypoxia? (5)

A

RBC production (polycythaemia) - O2 carrying capacity of the blood is increased
2,3 BPG produced within RBCs - O2offloaded more easily into tissues
Increased number of capillaries - blood diffuses more easily
Increased number of mitochondria = O2 can be used more efficiently
Kidneys conserve acid - arterial pH increases

51
Q

Does H+ move readily across the blood brain barrier

A

No - CO2 does

52
Q

What is the [H+] respiratory drive?

A

When there is acidosis caused by the addition of non-carbonic acid H+ to the blood e.g. lactic acid or diabetic ketoacidosis, peripheral chemoreceptors cause hyperventilation increasing elimination from the body (central chemoreceptors do not do this as H+ doesn’t diffuse across the blood brain barrier - CO2 does)