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Block 2 > Control Of Breathing > Flashcards

Control Of Breathing Flashcards

1
Q

Why must we have neural control over quiet respiration?

A

Because inhalation is active + the diaphragm will contract to bring air into lungs so impulses must be generated in phrenic nerves to trigger this + cease to facilitate exhalation

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2
Q

Where is the respiratory centre found? What happens if there is trauma near this centre?

A

Pons + medulla

If brainstem is sectioned above pons respiration continues normally but it will cease if the medulla is disconnected from the spinal cord

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3
Q

Why is the respiratory centre a robust system?

A

Many rhythm generating networks in parallel so it has lots of reserve + repetition

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4
Q

What neurons are present in the medulla for respiration?

A
  • Group contributing a pneumotaxic centre
  • Dorsal respiratory group containing inspiratory neurones
  • Ventral respiratory group containing both inspiratory + expiratory neurones
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5
Q

What is the function of the medulla in respiration?

A

Generates respiratory pattern

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6
Q

Explain the feedback cycle involved in respiration.

A

Sensors e.g. chemoreceptors, lung + other receptors -> input to central controller i.e. pons, medulla + other parts of brain -> output to effectors e.g. respiratory muscles -> back to beginning

Sensors will be continuously monitoring + feeding back so this system keeps cycling round

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7
Q

Input to the respiratory centre help modulate what part of respiration?

A

Normal eupneic rhythm

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8
Q

What 4 things input to the respiratory centre?

A
  1. Stretch receptors in lung
  2. Peripheral chemoreceptors (arterial pO2, pCO2 + pH)
  3. Higher centres (e.g. cerebral cortex in harder breathing)
  4. Central chemoreceptors (arterial pCO2 through pH of CSF)
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9
Q

What is the effector of the respiratory centre? Are these under voluntary or involuntary control?

A

Phrenic motor neurones (C3, 4 +5), vagus nerve etc. which effect the diaphragm, pharynx + other muscle groups

Under voluntary + involuntary non-rhythmic control (e.g. cough + swallowing)

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10
Q

What is the Hering Breuer reflex?

A

Stretch receptors in airways send signals through afferents in vagus nerve -> respiratory centre in medulla -> inhibition of inspiratory neurones -> end inspiratory effort permitting expiration

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11
Q

Is the Hering Breuer reflex important in humans?

A

Less important in humans than some mammals as the reflex is essential for normal RR + depth whereas it is not in humans although it is still present

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12
Q

What are the principal reflex regulators of respiration? Why?

A

Arterial blood gases (ABGs) because:

  • Need to provide tissues with O2 met by a hypoxic drive to respiration
  • Need to excrete CO2 met by respiratory responses to CO2
  • Need to defend acid-base balance means response to CO2 is more powerful than response to lack of O2
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13
Q

Why do ventilation and perfusion have to be matched?

A

Because if ventilation increases/decreases without change in usage of O2 or production of CO2 -> pO2 will increase + pCO2 will decrease/pO2 will decrease + pCO2 will increase respectively

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14
Q

Define hypercapnia.

A

Rise in arterial partial pressure of CO2 (paCO2)

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15
Q

Define hypocapnia.

A

Fall in arterial partial pressure of CO2 (paCO2)

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16
Q

Define hypoxia.

A

Fall in arterial partial pressure of oxygen (paO2)

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17
Q

What can the body do hypoventilation has made pO2 fall and pCO2 rise?

A

Increase pulmonary ventilation rate restoring alveolar pO2 + pCO2 (pAO2 + pACO2)

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18
Q

How is alveolar gas composition kept constant and how is this modified?

A

By respiration

Respiratory rhythm modified in response to changes in gas tensions in arterial blood

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19
Q

Why is it difficult to fix the respiratory systems when there is a ventilation-perfusion mismatch?

A

For example, pO2 may have fallen but pCO2 has not changed e.g. in high altitude so this is more difficult to correct because increased ventilation will correct hypoxia but cause hypocapnia

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20
Q

What pO2 will cause a substantial change in ventilation? Why?

A

pO2 < 8kPa

Ventilation rate rises a little with small changes in pAO2 but substantially if pO2 is below this value

At this point O2 has almost fully saturated Hb

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21
Q

What sensors sense changes in pO2? What do they do?

A

Peripheral chemoreceptors (carotid bodies) - receive blood supply at high rate so detect low O2 from external carotid artery

Respond rapidly (1-3 secs) sending impulses to respiratory centres in medulla in IXth CN

22
Q

What do the carotid bodies respond to?

A 
Principally hypoxia but also:
- paCO2
- Hypotension
Temperature
- Some chemicals
- pH
23
Q

How will the carotid bodies respond to hypoxia?

A

Sense hypoxia + send impulse in CNIX to respiratory centres -> increased ventilation rate i.e. rate + depth of respiration

= restored pAO2, increased BP + adrenal secretion (e.g. corticosteroids)

24
Q

What is the serum buffering system equation? How can it be reformulated?

A

H+ + HCO2- H2O + CO2

Can be reformulated to the Henderson-Hasselbalch (H-H) equation:
pH = pK + log10[HCO3-]/pCO2 x 0.23

25
Q

Why is [HCO3-] and pCO2 used in the serum buffering system?

A

HCO3-: maintained at high level by homeostatic mechanisms enabling it to maintain pH by buffering moderate increases in H+

CO2: weak acid as it reaches an equilibrium with its conjugate salt rather than fully ionise in solution like a strong acid e.g. HCl + CO2 produced can be rapidly excreted in lungs so production can continue w/o effecting pH much

26
Q

What determines the pH of body fluids?

A

[HCO3-]

[CO2]

27
Q

What can happen to pCO2, if [HCO3-] is constant in different respiratory states?

A

Hypoventilation: pCO2 rise -> pH falls = respiratory acidosis

Hyperventilation: pCO2 fall -> pH rise = respiratory alkalosis

28
Q

__ changes in pCO2 lead to large changes in pH.

A

Small

29
Q

What are the normal values of H-H equation?

A

pH = pK + log10[HCO3-]/pCO2 x 0.23

pH = 7.4
pK = 6.1
[HCO3-] = 24mmol/L
[CO2] = 1.2mmol/L
0.23 = constant to change units to kPa
30
Q

What is the normal pH range?

A

7.35-7.45

31
Q

What pH indicates an acidosis? What are the 2 different causes of this?

A

pH < 7.35

Metabolic: low HCO3-
Respiratory: high paCO2

32
Q

What pH indicates an alkalosis? What are the 2 different causes of this?

A

pH > 7.45

Metabolic: high HCO3-
Respiratory: low paCO2

33
Q

What happens in respiratory acidosis?

A

Hypoventilation (e.g. opioid OD or COPD) -> paCO2 rises (hypercapnia) but [HCO3-] stays the same -> plasma pH falls = acidosis

HCO3- can increase to compensate

34
Q

What happens in respiratory alkalosis?

A

Hyperventilation (e.g. anxiety) -> pCO2 falls (hypocapnia) but [HCO3-] stays the same -> plasma pH rises = alkalosis

HCO3- can fall to compensate

35
Q

Where and how is pCO2 sensed?

A

On ventral surface of medulla the area is chemosensitive; central chemoreceptors respond to pCO2 generated changes in the pH of the CSF -> send information to medullary centre regulating ventilation rates

36
Q

Why does CSF give an indication of pCO2?

A

CSF is a secretion of the choroid plexus, is protein free + pH determined by [HCO3-] + [CO2] as [HCO3-] determined exclusively by choroid plexus CO2 readily diffuses across BBB so pCO2 is same in arterial blood + CSF

37
Q

What else influences the central chemoreceptors response to arterial and thus, CSF pCO2?

A

Levels of O2 + exercise

Diverse receptors, CNS centres, effector organs + their connecting nerves function as an integrated system that is not yet clarified

38
Q

How are metabolic acids produced in the body?

A

Via normal metabolism e.g. lactic acid

Acids then dissociate producing H+

39
Q

Where is HCO3- generated in the body when it is used in the buffer system?

A

Kidneys

40
Q

Why is the serum buffer system limited? What does this mean for the pH of the body?

A

Reaction reaches equilibrium in tissues = [H+] and pH will still change

41
Q

What happens in a metabolic acidosis?

A

Ingestion/production of acids (e.g. diabetic ketoacidosis, lactic acidosis or renal failure) -> overwhelms buffering capacity of HCO3- i.e. kidney cannot regenerate it as quickly as its utilised -> [HCO3-] falls -> limits removal of H+ -> [H+] increases = pH falls

42
Q

What is the respiratory response to metabolic acidosis i.e. compensation?

A

RR increases (hyperventilation) excreting more CO2 to reduce paCO2 -> ratio of [HCO3-]/[CO2] restored to near normal -> [H+] + pH restored to low/normal value

BUT [HCO3-] + [CO2] are lower than normal physiological values

43
Q

Why does overcompensation not occur?

A

pH driven RR changes cease once the pH normalises i.e. once the [HCO3-]/[CO2] ratio normalises, not the physiological values

44
Q

What happens in metabolic alkalosis?

A

E.G. prolonged vomiting causes excessive loss of H+ -> shift in equilibrium -> increase in [HCO3-] = pH increases

45
Q

What is the respiratory response to a metabolic alkalosis i.e. compensation?

A

RR decreases (hypoventilation) by decreasing minute volume + increasing pCO2 above normal physiological levels restoring pH as ratio of [HCO3-]/[CO2] is restored

BUT both [HCO3-] and [CO2] higher than normal

46
Q

What are the key players of respiratory compensation?

A

Central chemoreceptors

47
Q

What do blood gas results include?

A 
FiO2
pH 
PaO2
PaCO2
HCO3-
Base excess
Serum lactate
48
Q

How should you analyse a blood gas result in a step-by-step fashion?

A
  1. Is there hypoxia (PaO2 < 8 KpA)?
  2. Direction of pH change
  3. Magnitude of pH change
  4. Is there compensation?
49
Q

How can you tell if a acidosis/alkalosis is compensated for or uncompensated for?

A

Uncompensated/partially compensated: pH outside normal range

Fully compensated: pH is just within normal range (OR acidosis/alkalosis may not be severe enough yet to cause a significant pH change)

50
Q

How do you tell the difference between a compensated acidosis/alkalosis or a mixed abnormality?

A

Compensated: system not involved in primary abnormality abnormal in direction OPPOSITE to pH change

Mixed abnormality: abnormal in SAME direction as ph change

51
Q

Define base excess (BE).

A

Amount of strong acid (i.e. HCO3-) that must be added (or removed) for each litre of fully oxygenated blood to return the pH to 7.40 at a temperature of 37 degrees + a pCO2 of 5.3 kPa SO by correcting for respiratory component, BE represents the metabolic component

-ve BE = metabolic acidosis
+ve BE = metabolic alkalosis

52
Q

What are the 5 causes of metabolic acidosis?

A
  1. Lactic acidosis
  2. Ketoacidosis
  3. Acute renal failure
  4. Excessive loss of HCO3- (= raised plasma chloride)
  5. All of the other causes (poisons) e.g. aspirin, methanol

Block 2 (45 decks)

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