L32, L33 – Control of Breathing Flashcards Preview

MBBS I CPRS > L32, L33 – Control of Breathing > Flashcards

Flashcards in L32, L33 – Control of Breathing Deck (100):
1

What are 3 basic elements in respiratory control system?

Central controller - brain
Effectors - respiratory muscles
Sensors

2

Name the motor centers and coordinating centers.

Motor centers: Inspiratory center & Expiratory center

Coordinating centers: Pneumotaxic center and Apneustic center

3

Where are motor centers?

medulla oblongata

4

Where are coordinating centers?

pons

1. Pneumotaxic center (upper pons)

2. Apneustic center (middle and lower pons)

5

Roles of motor centers?

primary regulation:
1. Inspiratory center: for inspiration
2. Expiratory center: for expiration

6

Roles of coordinating centers?

modifies level / pattern of breathing:

1. Pneumotaxic center: quickens transition from inspiration to expiration (shorten inspiratory phase > increase breathing frequency)

2. Apneustic center: Inhibits transition from inspiration to expiration > prolong inspiratory phase

7

What are the 2 neural pathways for control of breathing?

Vagal feedback (Hering Breur Reflex)

Pneumotaxic feedback

8

What is Neurogenic control of breathing?

Maintain regular, rhythmic
breathing pattern

9

What neural pathways are stimulated in Inspiration?

Inspiration = Active process

Lung stretch receptor > Stimulate Apneustic centre > Stimulate Inspiratory centre > Inhibit Expiratory centre & Stimulate Lung inspiration (via spinal cord)

10

What neural pathways are stimulated in Expiration? (2 components- vagal and pneumotaxic feedback)

Passive process

1) Stop discharge of Inspiratory centre:
Lung stretch receptors from lung inspiration inhibit Apneustic centre > decrease stimulation to inspiratory centre via VAGAL FEEDBACK


2) For Passive lung deflation
Inspiratory centre then stimulates Pneumotaxic center > Inhibit Apneustic center> decrease stimulation to Inspiratory centre via PNEUMOTAXIC FEEDBACK

inspiratory muscles relax > passive lung deflation

11

During lung inspiration, what center is stimulated?

Expiratory center via vagal nerves

12

During lung expiration, what center is stimulated?

Inspiratory center AND Apneustic center

13

What is the neural pathway to begin inspiration after expiration?

Lung expiration > Stretch receptors stimulate
1) Inspiratory center
2) Apneustic center > Stimulate Inspiratory center

> both pathways Stimulate Lung Inspiration via spinal cord

14

Relationship between Higher centers and Pneumotaxic centers?

Stimulate or Inhibit

15

Deduce the change in breathing if the neural organisation is cut at: Cut between higher centers and pneumotaxic center?

breathe normally

16

Deduce the change in breathing if the neural organisation is cut at: Cut between pneumotaxic center and apneustic center?

still have vagal feedback between lung Inspiration stretch receptors and apneustic center > breathe normally

17

Deduce the change in breathing if the neural organisation is cut at: Cut between apneustic center and inspiratory/expiratory centers? e.g.Vagotomy

Cut link between Apnuestic center and Inspiratory center > change in breathing pattern

18

Deduce the change in breathing if the neural organisation is cut at: Cut between inspiratory/expiratory centers and lungs ? (e.g. spinal cord or vagus cut)

no breathing > die

19

What receptor type is most important in chemical / metabolic control of breathing (minute to minute control) ?

 Chemoreceptors

20

What are the two types of chemoreceptors?

1. Peripheral chemoreceptors

2. Central chemoreceptors

21

Name locations of the 2 types of chemoreceptors?

Peripheral chemoreceptors:
 Aortic arch
 Carotid body (at bifurcation of common carotid artery)

Central chemoreceptors:
 In medulla oblongata, close to motor centers

22

Explain action of Peripheral chemoreceptors on increasing ventilation?

Increase chemo-sensitive cell activity

Stimulated by:
Decrease pO2, pH, blood flow

Increase pCO2, temperature, drugs

Increase ventilation by increasing frequency and Tidal volume

23

Explain action of Peripheral chemoreceptors on decreasing ventilation?

Decrease chemo-sensitive cell activity

Stimulated by:
Increase pO2, pH, blood flow

Decrease pCO2, temperature, drugs

Decrease ventilation by decreasing frequency and Tidal volume

24

Explain action of Central chemoreceptors on decreasing ventilation?

Exactly the same as peripheral chemoreceptor
except the action of pO2


Decrease chemo-sensitive cell activity

Stimulated by:
Increase pH, blood flow

Decrease pCO2, temperature, drugs

Decrease ventilation by decreasing frequency and Tidal volume

25

Explain action of Central chemoreceptors on Increasing ventilation?

Exactly the same as peripheral receptor except action of pO2

Increase chemo-sensitive cell activity

Stimulated by:
Decrease pH, blood flow

Increase pCO2, temperature, drugs

Increase ventilation by increasing frequency and Tidal volume

26

What is the main difference between peripheral and central chemoreceptors in their stimulation?

PO2 has effect only in peripheral but not in central chemoreceptors

27

Why does PO2 has effect only in peripheral but not in central chemoreceptors?

Brain cell activity is not sensitive to oxygen level due to depressive effect.

otherwise hypoxia suppresses central chemoreceptor activity, cannot react to compensate low O2

28

Are baroreceptors normally employed for control of breathing?

No

29

What are baroreceptors? Where are they located depending on function??

mechanical receptors in CVS

 Carotid sinus, aortic arch: high blood pressure
 Pulmonary artery, great veins: low blood pressure

30

What do the different baroreceptors detect/ monitor?

High BP baroreceptors @ Carotid sinus, aortic arch > monitor systemic arterial pressure

Low BP baroreceptors @ Pulmonary artery, great veins> monitor pulmonary arterial and venous pressure

31

Explain the action of systemic arterial pressure on ventilation.

Increase BP > Decrease ventilation

Decrease BP > Increase ventilation

32

Explain the action of Pulmonary arterial pressure on ventilation.

Increase pulmonary arterial or venous pressure > Increase ventilation

Decrease pulmonary arterial or venous pressure > Decrease ventilation

33

How does Left Heart failure cause change to Ventilation?

2 pathways:

1) LHF cause decrease systemic pressure > stimulate baroreceptors at carotid sinus/ aortic arch > Increase Ventilation

2) LHF cause blood congestion in pulmonary circulation (or RHF cause increase venous pressure) > increase pulmonary arterial pressure >Increase ventilation

34

Effect of breathing on venous return?

Inspiration changes pleural pressure >

negative thoracic pressure and positive abdominal pressure > distend vena cava and increase lumen diameter > acts as RESPIRATORY PUMP on venous return to propel blood > increase venous return

35

Aortic arch has which receptors?

High BP baroreceptors and peripheral chemoreceptors

36

Where are thermoreceptors located?

 Central (hypothalamus)
 Peripheral (skin)

37

Explain action of thermoreceptors on ventilation?

Increase Temp. > Increase ventilation

Decrease temp > decrease ventilation

38

How does fever OR exercise change ventilation?

Increase temp.> increase ventilation
 Remove CO2, take in O2
 Remove heat to the environment

39

Where are Ergoreceptors?

in muscles

40

How do ergoreceptors stimulate change in ventilation?

Increase muscle contraction (e.g. exercise) > detected by ergoreceptors > stimulate increase in ventilation > prepare for metabolic change in muscle

41

Name the 3 types of pulmonary receptors.

1. Irritant receptors
2. Stretch receptors
3. Type J receptors
(juxtapulmonary capillary)




42

name location of the three pulmonary receptors.

Irritant = Epithelium of airways

Stretch = Smooth muscles of airways

Type J = juxtapulmonary capillary in alveolar wall

43

What are irritant receptors' action on breathing?

rapid, shallow breathing pattern in Lung and airway diseases

44

What are stretch receptors' action on breathing?

Maintain regular breathing pattern by Vagal feedback neurological control

45

What are Type J receptors' action on breathing?

Rapid, shallow breathing pattern in lung diseases

46

What are the stimuli of irritant receptors?

Chemical and mechanical irritations (Pneumothorax, Pulmonary congestion, Asthma)

47

What are the stimuli of stretch receptors?

Δ lung volume (e.g. inflation,
deflation)

Δ transpulmonary pressure
(TPP increase = lung size increase)

48

What are the stimuli of Type J receptors?

Increase Interstitial volume
Chemical injury
Pathological conditions (e.g. fibrosis, emphysema)

49

What are the changes in ventilation in irritant receptor and Type J receptor activation?

Rapid, shallow breathing, increased ventilation by:

Increase frequency
Decrease tidal volume

50

What system compensates for airway obstruction diseases?

Gamma system

Act on muscle spindles (intercostalis, diaphragm) > increase muscle contraction to overcome muscle elongation caused by airway obstruction

51

What and Where are the upper airway receptors?

Upper airway receptors = irritant receptors in nose, nasopharynx, larynx

52

What is the function of upper airway receptors?

Mechanical or chemical irritation > receptor stimulate Sneezing, coughing, bronchoconstriction

prevents further entry of foreign substances / irritants into system

53

What blood gas regulates ventilation?

CO2

regulate concentration of CO2 throughout the body

54

What is the slope of Ventilation / PACO2 graph?

Response coefficient to PACO2

55

How does response coef. change at Low PACO2?

Lower (<40 mmHg) : Response coef. > 0
Ventilation is INDEPENDENT of PCO2

56

How is PACO2 controlled during sleep?

At low PACO2 during sleep (e.g. sleep apnea):

Higher brain centers activate tonic discharge, WAKEFULLNESS DRIVE, to PREVENT BREATHING CESSATION

57

How does response coef. change at Normal PACO2?

High response coef.
(3 L/min/mmHg)



58

How does response coef. change at High PACO2?

Response ceof. decreases (flatter slope)

59

What is the effect of very high PACO2 on ventilation?

Central depression (brain sensitive to PCO2 so brain activity becomes depressed)

Ventilation decrease to zero > death

60

Can CO2 in blood directly stimulate CO2?

No, has to diffuse to receptor and then dissociate for H+ to act on receptors

61

Acute CO2 inhalation:
Compare the speed of action between CO2 in blood and in CSF on stimulating receptors? Why?

In blood (within a second)

In CSF (latency = 20-30 seconds; steady response in 5-10 min)

In CSF, CO2 has to cross blood-brain-barrier, takes time

62

Acute CO2 inhalation:
Compare the responses induced by blood CO2 vs CSF CO2 on receptors?

Blood CO2 on peripheral chemoreceptors induces smaller response than CSF CO2 on central chemoreceptors

63

Acute CO2 inhalation:
Why is amplitude of peripheral chemoreceptor response lower than central chemoreceptor response?

PROTEIN BUFFERS IN BLOOD buffer the increase in H+ from CO2, so ventilatory change is lower > (1/3) of total response

No protein buffers in CSF > (2/3) of total response

64

Chronic CO2 inhalation:
Explain pathway for compensation to restore normal pH

Chronic CO2 inhalation (e.g. obstructive lung disease) > respiratory acidosis > pH drop compensated by increased HCO3- production > more HCO3- in blood and CSF

65

How does HCO3- concentration change ventilation?

More HCO3- = more H+ buffered = less H+ reach chemoreceptors (peripheral or central) = decrease stimulation of increase ventilation

66

Where is HCO3- in blood and CSF circulation produced? What is the overall effect of HCO3- production on ventilation?

HCO3 in blood : made by kidneys, affect peripheral chemoreceptors

HCO3 in CSF: made by Choroid plexus and brain cells, affect central chemoreceptors

More HCO3 in blood and CSF = LESS VENTILATION

67

What is the effect of raised CSF HCO3- over long time on chemoreceptors response to pCO2 change?

reset, acclimatize central chemoreceptors towards a higher PCO2 level > CO2 less stimulatory on pH/ need more CO2 to induce change in ventilation


CO2 no longer acts as a potent ventilator stimulus (e.g. in COPD patients)

68

How is acclimatization to low pCO2 in CSF achieved? (not the effect of prolonged low pCO2)

Decrease CSF HCO3-
Reset central chemoreceptors to lower pCO2

Lack of O2 becomes important ventilator stimulus

69

How does PAO2 affect ventilation?

Only at lower than 60mmHg > stimulate Ventilation

Normal O2 levels does not affect ventilation

70

Why does PAO2 only affect ventilation at lower than 60mmHg?

Sigmoid shape of O2 dissociation curve > decreasing PAO2 only
stimulate when PAO2 < 60 mmHg
60 mmHg = intersection of steep and flat sections of O2 dissociation curve

71

What is the response coefficient of ventilation to O2? Why is it so low?

low response coefficient (0.25 L/min/mmHg) compared to CO2: 3 L/min/mmHg


Braking effects of accompanying hypocapnia
(at low pCO2 and high pO2, effect of CO2 on ventilation decreases to zero)

72

Is pO2 important in physiological control of ventilation then?

No

73

Explain the action of Hypoxia in blood on ventilation?

Low pO2 > chemoreceptors stimulated > initially ventilation increases > Due to accompanying decrease in pCO2 and H+ (braking effect of accompanying hypocapnia) > LESSEN INITIAL INCREASE in Ventilation

74

Explain the action of accompanying hypocapnia (after hypoxia) on CSF.

Low pCO2 > decrease H+ to stimulate central chemoreceptors > Lessen initial increase in ventilation

Overall, acute hypoxia causes small increase in ventilation

75

How is prolonged hypoxia compensated?

Hypoxia induces respiratory alkalosis:

Compensate by decrease HCO3- in blood and CSF > increase H+ stimulation on chemoreceptors > gradual increase ventilation

76

Explain acclimatization to low PCO2 (e.g. high altitude).

Decrease CSF HCO3- > reset central chemoreceptros to lower PCO2 threshold > pCO2 becomes more stimulatory to ventilation > increase ventilation in low CO2 environment > further increase in ventilation

77

In summary what gas controls ventilation in normal vs COPD patients?

Normal = CO2
COPD = chronic hypercapnia = O2

78

Is ventilation more sensitive to CO2 or pH change?

less sensitive to pH change than to PCO2 change (probably due to braking effect of hypocapnia)

79

How does pH change ventilation?

Lower pH = increase ventilation

Higher pH = decrease ventilation

80

Summarize the effect of respiratory acidosis/ acute hypercapnia on ventilation

In blood: increase CO2 = increase H+ > due to buffer effect on peripheral chemoreceptors is 1/3 of total response

In CSF: more H+ > no buffer means effect on central chemoreceptors is 2/3 total response

Overal tremendous increase in ventilation

81

Summarize the effect of metabolic acidosis/ acute hypoxia on ventilation.

In blood: accumulation of non-CO2 acid > increase ventilation via peripheral chemoreceptors > accompanying hypocapnia and decrease in H+ cause braking effect > lessen initial increase in ventilation

In CSF: Hypoxia cause accompanying hypocapnia > decrease CO2 and H+ cause braking effect on central chemoreceptors > Lessen initial increase in ventilation

Overall small increase in ventilation

82

Overall, ventilation response to respiratory acidosis is higher or lower than response to metabolic acidosis?

Respiratory acidosis response is higher (Response to hypercapnia is much larger than response to hypoxia/ accompnaying hypercapnia)

83

How does Hypercapnia change the response coef. to O2 lack?

Increase Co2 = decrease O2 lack threshold = increase response coef. to O2 lack > easier to initiate response to change in pO2 at high pCO2

84

How does Hypoxia change response coef. to CO2?

Low pO2 > decrease CO2 threshold > Increase response coef. to CO2 (accompanying hypocapnia)

85

How does CO2 response coef. change with pH?

Decrease in pH (e.g. prolong hypercapnia) causes decrease in CO2 threshold but the response coef. remains the same

86

How can ventilation be depressed in sleep via wakefullness drive?

Inhibit higher centers to stimulate medullary centers by Wakefullness Drive

(During wake- tonic discharge from ascending reticular formation to brain stem and midbrain stimulate medullary centers)

87

How can ventilatory response be changed to cause depressed ventilation in sleep?

Depress O2 and CO2 ventilatory responses + shift CO2 response curve to right = harder to stimulate

88

How can upper airway lead to depressed ventilation in sleep?

Sleep > depressed tonic activity in upper airway muscles > tongue fall back > upper airway obstruction

89

Control of breathing:
During non-REM sleep? (4 stages)

Stage 1 & 2 = control by wakefullness drive and metabolic

Stage 3 & 4 = control by metabolic only

90

REM sleep control of breathing? (tonic and phasic)

Tonic = Wakefulness drive and metabolic

Phasic = Behavioral

91

Awake control of breathing?

Rest = wakefulness drive and metabolic

Activity = behavioral

92

Compare the breathing patterns of stages of non REM sleep?

Stage 1 & 2 = periodic

Stage 3 & 4 = regular

93

Compare breathing pattern of REM sleep?

Tonic = regular

Phasic = irregular

94

Compare breathing pattern of awake ?

At rest = regular

Exercise = irregular

95

Periodic breathing occurs in Stage 1 & 2 (light) of Non-REM sleep. (** ask first **)

(await questions)

96

What is sleep apnea?

Pathological condition
Periods of apnea (10-90sec) recurring AT LEAST 11 times per sleeping hour

(<5-10 episodes per sleeping hour is normal)

97

What are the 3 types of sleep apnea?

 Central apnea (loss of ventilatory effort: Decreased drive from brain; or Skeletal muscles do not contract)

 Obstructive apnea (upper airway obstruction)

 Mixed apnea (central + obstructive) – more common

98

What are some consequences of sleep apnea?

1) Snoring (partial upper airway obstruction)

2) Daytime sleepiness (interrupted sleep at night >need to compensate)

3) polycythemia, pulmonary constriction, right heart failure

4) systemic hypertension

99

Explain polycythemia and how pulmonary constriction can lead to RHF in sleep apnea?

1) Hypoxia > produce erythropoietin > polycythemia (more RBC) > blood more viscous and harder to pump

2) Repeated hypoxic episodes > pulmonary constriction > increase resistance

Right Heart hypertrophy > Failure

100

How can sleep apnea cause systemic hypertension?

Frequent cerebral arousals > repeated sympathetic activation > higher BP

Decks in MBBS I CPRS Class (78):