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Semester 3 > Resp Session 5 > Flashcards

Resp Session 5 Flashcards

1
Q

What are changes in blood pH called before HCO3- becomes involved?

A

Alkalaemia/acidaemia

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2
Q

What happens in to pO2 and pCO2 in exercise?

A

Metabolism increases –> decreased pO2 and increased pCO2 –> breathing alters to restore partial pressures

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3
Q

What happens to pO2 and pCO2 in hyperventilation?

A

Ventilation increases but metabolism stays constant so pO2 increases and pCO2 decreases

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4
Q

What happens to pO2 and pCO2 in hypoventilation?

A

Ventilation decreases but metabolism stays constant –> decreased pO2 and increased pCO2

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5
Q

What happens if pO2 decreases without a change in pCO2?

A

Correction of decreased pO2 by increasing RR leads to hypocapnia

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6
Q

Why do small pCO2 changes cause big pH changes?

A

Logarithmic function in the relationship

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7
Q

What happens in respiratory acidosis?

A

Hypoventilation –> increased pCO2 –> hypercapnia –> decreased pH

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8
Q

How is respiratory acidosis compensated?

A

Kidneys increase [HCO3-] by reducing excretion over 2-3 days

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9
Q

What happens in metabolic acidosis?

A

Tissues produce acid –> acid reacts with HCO3- –> decreased [HCO3-] and increased CO2 –> decreased pH

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10
Q

How is metabolic acidosis compensated?

A

Increase ventilation to decreased pCO2

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11
Q

What happens in respiratory alkalosis?

A

Hyperventilation –> decreased pCO2 –> hypocapnia –> increased pH

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12
Q

How is respiratory alkalosis compensated?

A

Kidneys decrease [HCO3-] by increasing excretion over 2-3 days

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13
Q

What happens in metabolic alkalosis?

A

Loss of H+ –> decreased HCO3- –> increased pH

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14
Q

How is metabolis alkalosis compensated?

A

Decreasing ventilation but this is limited by hypoxia risk

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15
Q

What sensors have inputs into the respiratory control sensors?

A

Central chemoreceptors
Peripheral chemoreceptors
Pulmonary receptors
Joint and muscle receptors

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16
Q

What do central chemoreceptors detect?

A

H+

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17
Q

What do peripheral chemoreceptors detect?

A

O2, CO2, H+

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18
Q

What do pulmonary receptors detect?

A

Stretch

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19
Q

What do joint and muscle receptors detect to send signals to the respiratory control centre?

A

Stretch and tension

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20
Q

What are the effectors of the respiratory control centre?

A

Diaphragm
Inspiration: external intercostals and accessory muscles
Expiration: internal intercostals and abdominal muscles

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21
Q

What partial pressure can pO2 decrease down to before sats markedly affected as shown by the plateau on the Hb dissociation curve?

A

8 kPa

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22
Q

Where are peripheral chemoreceptors located?

A

Carotid and aortic bodies

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23
Q

How do peripheral chemoreceptors signal respiratory changes?

A

Have highest bloodflow of any tissue so signal large decrease in pO2 when their metabolic demands are not met

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24
Q

Why are peripheral chemoreceptors relatively insensitive to pO2 changes?

A

Have low metabolic demands

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25
Q

What might cause peripheral chemoreceptors to respond to normal pO2?

A

Circulatory problems impacting bloodflow

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26
Q

What do peripheral chemoreceptors stimulates?

A

Increased breathing
Change in heart rate
Change in bloodflow distribution to protect more vulnerable tissues

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27
Q

Are peripheral chemoreceptors sensitive to pCO2?

A

No, relatively insensitive

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28
Q

Where are central chemoreceptors found?

A

Ventral surface of brainstem in the medulla very close to effector neurones

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29
Q

What do central chemoreceptors respond to changes in?

A

[H+] in CSF

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30
Q

What causes changes in [H+] in the CSF?

A

Production from CO2 moving across blood-brain barrier and undergoing carbonic anhydrase activity in the CSF

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31
Q

What do small variations in pCO2 detected by central chemoreceptors stimulate?

A

Increase –> increased ventilation

Decrease –> decreases ventilation

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32
Q

What controls CSF composition?

A

Choroid plexus cells

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33
Q

What is the result of the blood-brain barrier being impermeable to HCO3-?

A

Changes in pCO2 controlled by changes in ventilation cause changes in CSF pH

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34
Q

What can choroid plexus cells do to tolerate a persistent change in pCO2?

A

Selectively add H+ or HCO3- to alter CSF composition

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35
Q

What is the response of choroid plexus cells to persisting hypoxia as seen in early lung disease?

A

Hypoxia detected by peripheral chemoreceptors –> increased ventilation –> pCO2 decreases –> CSF changes composition to accept new pCO2 as normal

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36
Q

What is the action of choroid plexus cells in persisting hypercapnia as seen in progression of lung disease?

A

Hypoxia and hypercapnia –> respiratory acidosis –> decreased pH of CSF –> peripheral and central chemoreceptors increase breathing –> acidic pH bad for neurones -> choroid plexus add HCO3- to CSF to accept high pCO2

37
Q

Give the stages in transport of oxygen from the air to tissues.

A

Air -> airways -> alveoli -> diffusion across alveolar capillary membrane -> binds to Hb in pulmonary capillary -> pulmonary veins -> L atrium -> L ventricle -> CO -> aorta -> regional arteries -> capillary blood -> tissues

38
Q

What are the four types of hypoxia?

A

Hypoxaemic/respiratory
Anaemic
Stagnanct/circulatory
Cytotoxic

39
Q

What’s is stagnant/circulatory hypoxia?

A

Reduced delivery of oxygen due to poor perfusion which can be global (shock) or local (peripheral vascular disease)

40
Q

What is cytotoxic hypoxia?

A

Where tissues can’t utilise delivered oxygen e.g. cyanide poisoning

41
Q

What is respiratory failure?

A

Not enough oxygen enters the blood +/- not enough CO2 leaves

42
Q

What is type I respiratory failure?

A

Decreased oxygen entry but CO2 is not compromised

O2 sats

43
Q

What causes type I respiratory failure?

A

Diffusion defects such as fibrotic lung disease, pulmonary oedema or emphysema which affect oxygen exchange more due to its lower solubility
V/Q mismatch

44
Q

Why is pCO2 normal or low in type I respiratory failure?

A

Hypoxia stimulates hyperventilation

45
Q

What is type II respiratory failure?

A

Decreased oxygen entry and decreased CO2 exit causing pO2

46
Q

What causes type II respiratory failure?

A

Ventilatory failure which can be due to suppression of the respiratory centre, muscle weakness, chest wall problems, very severe fibrosis or increased airway resistance

47
Q

Why is TB usually seen at the apex of lungs?

A

Higher pO2 for mycobacteria

48
Q

How does the V/Q vary across the lung?

A

Apex: V/Q>1
Most of lung = 1
Base: V/Q

49
Q

How is respiratory failure managed?

A

Test cause
Type I: O2 therapy to improve gradient for diffusion and O2 uptake in V/Q mismatch
Type II: hypercapnia may need assisted ventilation

50
Q

What are some clinical fractures of hypoxia which are common to both type I and II respiratory failure?

A

Exercise intolerance
Tachypnoea
Confusion
Central cyanosis

51
Q

What visible changes occur in a pt with sats

A

Central cyanosis with concomitant peripheral cyanosis due to arrival of already desaturated blood to peripheries

52
Q

How does the body respond to the gradual development of chronic hypoxia in COPD?

A

Increased EPO increases Hb levels by causing polycythaemia

2,3-DPG increased to aid tissue oxygenation

53
Q

What leads to cor pulmonale in chronic hypoxia?

A

Hypoxic vasoconstriction of pulmonary arterioles eventually –> pulmonary hypertension –> RH failure

54
Q

Is chronic hypoxia seen in type I or II respiratory failure?

A

Can be either

55
Q

What is the commonest cause of chronic type II respiratory failure?

A

COPD

56
Q

What happens in chronic type II respiratory failure?

A

CO2 retention in some pts –> central chemoreceptors reset -> increased tolerance of high pCO2 acts on CNS –> warm hands and flapping tremors

57
Q

What drives respiration in chronic type II respiratory failure?

A

Hypoxia via peripheral chemoreceptors

58
Q

How is chronic type II respiratory failure treated?

A

Titrated O2 therapy which needs close monitoring

59
Q

Why does O2 therapy need to be closely monitored when treating COPD pts with chronic type II respiratory failure?

A

Can worsen hypercapnia by reducing respiratory drive and shunting hypoxic vasoconstriction in place to improve V/Q mismatch

60
Q

What environmental cause can lead to chronic hypoxia?

A

High altitude

61
Q

What is asthma characterised by?

A

Reversible airflow obstruction
Airway wall inflammation and remodelling
Increased airway responsiveness

62
Q

What is the function of airways smooth muscle in utero and in the adult?

A

In utero: airway persistalsis to create a mechanical stimulus for growth
In adult: no function - have no resting tone

63
Q

What differences are seen in the structure of the asthmatic airway wall?

A

Increased airway smooth muscle thickness
Damaged epithelium
Thickened basement membrane
Same number of alveolar attachments

64
Q

What mediates airway wall remodelling in development of asthma?

A

Cells and soluble mediators of chronic inflammation - cytokines, neutrophils, mast cells and growth factor

65
Q

What can trigger airway smooth muscle contraction?

A

Muscarinic agonists
Histamine
Cold air
Arachadonic acid metabolites e.g. prostaglandins

66
Q

What effect does a 10% decrease of effective radius in the airways have on flow?

A

Decreases by 35%

67
Q

What effect does a 20% decrease of effective radius in the airways have on flow?

A

Decreases by 50%

68
Q

How can triggers of airway smooth muscle contraction be used to assess FEV1 in asthma diagnosis?

A

Most healthy people can tolerate toxic doses of these without any contraction but asthma pts will experience contraction (airway hyper-responsiveness)

69
Q

Describe the aetiology of asthma.

A 
FHx due to genetics
Sensitisation to airborne allergens
Pre/post natal/active exposure to tobacco smoke
Aspirin sensitive asthma
Occupational
Viral induced wheeze
70
Q

What is aspirin sensitive asthma?

A

Over production of pro-inflammatory leukotrienes due to anomaly in arachidonic acid metabolism seen only in adults

71
Q

Are asthma symptoms experienced outside of the working environment in occupational asthma?

A

No

72
Q

How does viral-induced wheeze compare to asthma?

A

Children

73
Q

What is the immediate response in allergic asthma?

A

Allergen and specific IgE antibodies –> mast cell degranulation –> mediator release –> bronchoconstriction

74
Q

What is the immediate response in allergic asthma an example of?

A

Type I hypersensitivity

75
Q

How long after exposure to an allergen does the immediate response peak in allergic asthma?

A

~20 mins

76
Q

What happens in the late phase response of allergic asthma?

A

Full spectrum of inflammatory cells infiltrate and thicken bronchial walls
Release of mediators and cytokines –> oedema in mucosa due to vascular leak
Abnormal mucus over-production
ASM contraction
Shedding of epithelium due to toxic cytokines

77
Q

What is the late phase response in allergic asthma am example of?

A

Type IV hypersensitivity

78
Q

How long after exposure to an allergen is the late phase response seen in allergic asthma?

A

3-12 hrs

79
Q

What features lead to a clinical diagnosis of asthma?

A 
Recurrent wheeze
Recurrent breathlessness
Recurrent chest tightness
Recurrent cough which is non productive with diurnal pattern
Variable airflow obstruction
80
Q

What is a wheeze?

A

Variable intensity and tonicity expiratory sound originating from vocal cords

81
Q

What lung function tests can be used in asthma diagnosis?

A 
PEFR - often shows diurnal pattern
Spirometry
Exercise induced bronchoconstriction 
Exhaled NO 
Allergy testing 
CXR
82
Q

How is asthma managed?

A

Education: recognise symptoms, how to use medication
Primary prevention: stop smoking, exposure to allergens, fresh air
Pharmacology: airway relaxants to provide relief e.g. beta agonists, antimuscarinics, anti inflammatory agents for prevention e.g. corticosteroids, leukotriene receptor antagonists

83
Q

Why do preventer pharmacological interventions used in asthma have poor compliance?

A

Have no visible effects

84
Q

What is the classification of mild acute asthma?

A

> 92% sats in air

HR75% predicted

85
Q

What is the classification of moderate acute asthma?

A

Same as mild but with PEFR 75-50% predicted

86
Q

What is the classification of severe acute asthma?

A 
110
RR>25
Can't complete sentences
No wheeze due to lack of air
PEFR 35-50% of predicted
87
Q

What type of respiratory failure do mild/moderate acute asthma pts experience?

A

Type I

88
Q

What type of respiratory failure do severe acute asthma pts experience?

A

Type II

Semester 3 (50 decks)

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