Control of Respiration Flashcards
1
Q
What are the 2 types of control in respiration?
A
Neural and chemical
2
Q
What is the rhythm of respiration?
A
Inspiration followed by expiration
3
Q
What is the major neural rhythm generator?
A
The medulla
4
Q
What neurones is the breathing rhythm generated by?
A
Pre-Botzinger complex
5
Q
Where is the Pre-Botzinger complex located?
A
Upper end of the medullary respiratory centre
6
Q
What is rhythm of inspiration generated by?
A
Pre-Botzinger complex
7
Q
How is the rhythm of inspiration generated by the Pre-Botzinger complex?
A
- Excites dorsal respiratory group neurones (inspiratory)
- Fire in bursts
- Firing leads to contraction of inspiratory muscles - inspiration
8
Q
What happens when firing of dorsal respiratory group neurones stops?
A
Passive expiration
9
Q
Where is the medulla located?
A
Between the pons and spinal cord
10
Q
How is active expiration induced during hyperventilation?
A
- Increased firing of dorsal neurones excites a second group - ventral respiratory group neurones
- Excites internal intercostals, abdominals etc - resting in forceful (active) expiration
11
Q
Are ventral respiratory group neurones stimulated in normal breathing?
A
No, in normal quiet breathing ventral neurones do not activate expiratory muscles
12
Q
What can the rhythm generated in the medulla be modified by?
A
Neurones in the pons
13
Q
How is inspiration inhibited by neurones in the pons?
A
- Stimulation of the pneumotaxic centre (PC) by firing of dorsal respiratory neurones
- Stimulation terminates inspiration
- Inspiration inhibited
14
Q
What would happen if there was no pneumotaxic centre?
A
Apneusis - breathing would be prolonged inspiratory gasps with brief expiration
15
Q
What is apneusis?
A
Breathing is prolonged inspiratory gasps with brief expiration
16
Q
What causes apneusis?
A
If pneumotaxic centre is non-functioning
17
Q
What other centre involve din respiration (other than the PC) is present in the pons?
A
Apneustic centre
18
Q
What 2 respiratory centres are present in the medulla?
A
Dorsal and ventral respiratory group neurones
19
Q
What 2 respiratory centres are present in the pons?
A
Pneumotaxic and apneustic centre
20
Q
What is the role of the apneustic centre?
A
Prolongs inspiration
21
Q
How does the apneustic centre prolong inspiration?
A
- Impulses from bpneustic centre excite inspiratory area of medulla
- Prolong inspiration
22
Q
Where is respiratory rhythm generated?
A
Medulla
23
Q
Where can respiratory rhythm be modified?
A
In the pons
24
Q
What stimuli are respiratory centres influenced by?
A
- Higher brain centres e.g. cerebral cortex, limbic system, hypothalamus
- Stretch receptors in the walls of bronchi and bronchioles - Hering-Breur reflex, guards against hyperinflation
- Juxtapulmonary (J) receptors - stimulated by pulmonary capillary congestion, pulmonary oedema (caused by e.g. left heart failure), and pulmonary emboli
Joint receptors – stimulated by joint movement
Baroreceptors: increased ventilation rate in response to decreased blood pressure - Central chemoreceptors
- Peripheral chemoreceptors (involved in chemical control of respiration)
25
How does stimulation of juxtapulmonary receptors by pulmonary emboli affect breathing?
Rapid shallow breathing
26
What are examples of involuntary modifications of breathing?
* Pulmonary stretch receptors - Hering-Bruer Reflex
* Joint Receptors Reflex in Exercise
* Stimulation of Respiratory Centre by temperature,
adrenaline, or impulses from cerebral cortex
* Cough reflex
27
How do pulmonary stretch receptors modify breathing?
* Activated during inspiration, afferent discharge inhibits inspiration (Hering-Breuer reflex)
28
Do pulmonary stretch receptors switch off inspiration during normal respiratory cycle?
No - only activated at large (> 1 litre) tidal volumes
29
When is Hering-Breuer reflex important?
* In newborn babies
| * May prevent over-inflation of the lungs during hard exercise
30
How do joint receptors modify breathing?
Impulses from moving limbs reflexly increase breathing
31
How do joint receptors contribute in exercise?
Contribute to ventilation during exercise
32
What are factors that increase ventilation during exercise?
* Reflexes originating from body movement (joint receptors)
* Adrenaline release
* Impulses from the cerebral complex
* Increase in body temperature
* Accumulation of CO2 and H+ generated by active muscles
33
What is the ventilatory response to exercise?
Rapid increase in ventilation followed by gradual increase in ventilation
34
What causes the initial rapid increase in ventilation during exercise?
* Joint receptors
| * Cerebral cortex
35
What causes the gradual increase in ventilation during exercise?
Chemical changes
36
What causes the recovery of normal ventilation after exercise?
Removal of neural/chemical stimuli
37
What is the cough reflex?
Vital part of body defence mechanisms - helps clear airways of dust, dirt or excessive secretions
38
When is cough reflex activated?
Activated by irritation of airways or tight airways (e.g. asthma)
39
Describe the mechanisms of the cough reflex
* Afferent discharge stimulates short intake of breath
* Closure of the larynx
* Contraction of abdominal muscles (increases intra-alveolar pressure)
* Opening of the larynx and expulsion of air at a high speed
40
Why is coughing a symptom of asthma?
Due to tight airways that stimulate cough reflex
41
What is chemical control of respiration?
A negative feedback control system
42
What are the controlled variables in chemical control of respiration?
Blood gas tensions - especially CO2
43
What is the sensor for gas tensions?
Chemoreceptors
44
Wha are the 2 types of chemoreceptors?
* Peripheral
| * Central
45
What do peripheral chemoreceptors do?
Sense tension of oxygen, CO2 and H+ in the blood
46
Where are central chemoreceptors located?
Near the surface of the medulla
47
What do central chemoreceptors do?
Respond to the H+ concentration of the cerebrospinal fluid (CSF)
48
What separates the CSF and blood?
Blood-brain barrier
49
Describe the permeability of the blood-brain barrier
* Relatively impermeable to H+ and HCO3
| * CO2 diffuses readily
50
How can central chemoreceptors respond to the H+ concentration in the CSF if the blood-brain barrier is impermeable to H*?
* CO2 readily diffuses into CSF and reacts with water to form H2CO3
* CSF is less buffered than blood, so results in increased H+ as H2CO3 dissociates
* H+ can then be sensed by central chemoreceptors
(They really respond to arterial PCO2 as arterial H+ cannot cross blood-brain barrier)
51
Why is CSF less buffered than blood?
Less protein than blood
52
Is the system more sensitive to O2 than CO2?
No - system is very sensitive to PCO2 (hypercapnia) than PO2 (hypoxia)
53
Why is the system less sensitive to PO2 than PCO2?
Decrease in oxygen in blood - peripheral chemoreceptors are not stimulated until PO2 drops below 8.0 kPa
54
What happens if PO2 continues to drop to critical levels?
Depresses neurones in CNS - depresses ventilation
55
What receptors are involved in hypoxic drive of respiration?
Peripheral chemoreceptors
56
When are peripheral chemoreceptors activated by hypoxia?
Stimulated only when arterial PO2 falls to low levels (<8.0 kPa)
57
Is hypoxic drive of respiration important in normal respiration?
No, PO2 does not fall below 8.0 kPa in normal respiration
58
When is hypoxic drive of respiration important?
* In patients with chronic CO2 retention (e.g. patients with COPD)
* Important at high altitudes
59
What does partial pressure of inspired oxygen depend on?
* Total pressure (e.g. atmospheric pressure)
| * Proportion of oxygen in gas mixture (about 21% in atmosphere)
60
What happens to atmospheric pressure as altitude increases?
It decreases, meaning PO2 in the body decreases
61
What is hypoxia at high altitudes caused by?
Decreased partial pressure of inspired oxygen (PiO2)
62
What is the acute response to hypoxia at high altitudes?
* Hyperventilation
| * Increased cardiac output
63
What are symptoms of acute mountain sickness?
* Headache
* Fatigue
* Nausea
* Tachycardia
* Dizziness
* Sleep disturbance
* Exhaustion
* Shortness of breath
* Unconsciousness
64
What are chronic adaptations to high altitude hypoxia?
* Increased RBC production (polycythaemia) - increases O2 carrying capacity of blood
* Increased 2,3-Biphosphoglycerate produced in RBCs - O2 offloaded more easily into tissues
* Increase in number of capillaries - blood diffuses more easily
* Increase in number of mitochondria - O2 can be used more effectively
* Kidneys conserve acid - decreases arterial pH
65
What receptors play a role in the (non-carbonic acid) H+ drive of respiration?
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Peripheral chemoreceptors
(H+ doesn't really cross blood-brain barrier but CO2 does)
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66
What does H+ drive of respiration by peripheral chemoreceptors play a major role in?
Adjusting for acidosis caused by addition of non-carbonic acid H+ to the blood
67
What are causes of acidosis?
* Lactic acid during exercise
| * Diabetic ketoacidosis
68
How do peripheral chemoreceptors counteract acidosis?
Stimulation by H+ causes hyperventilation and increases elimination of CO2 from the body (CO2 can generate H+ - its increased elimination helps reduce H+ in the body)
69
What is H+ drive of respiration important in?
Acid-base balance
70
What is the effect of arterial PCO2 (H+ in brain CSF) on peripheral and central chemoreceptors?
* Peripheral chemoreceptors - weak stimulation
| * Central chemoreceptors - strong stimulation (dominant control of ventilation)
71
What is the effect of arterial PO2 on peripheral and central chemoreceptors?
* Peripheral chemoreceptors - only become important if PO2 falls to <8 kPa
* Central chemoreceptors - severe hypoxia depresses respiratory centre
72
What is the effect of arterial H+ on peripheral and central chemoreceptors?
* Peripheral chemoreceptors - stimulation (important in acid-base balance)
* Central chemoreceptors - H+ cannot cross the blood-brain barrier
