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Flashcards in Resp Session 5 Deck (88):
1

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

Alkalaemia/acidaemia

2

What happens in to pO2 and pCO2 in exercise?

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

3

What happens to pO2 and pCO2 in hyperventilation?

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

4

What happens to pO2 and pCO2 in hypoventilation?

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

5

What happens if pO2 decreases without a change in pCO2?

Correction of decreased pO2 by increasing RR leads to hypocapnia

6

Why do small pCO2 changes cause big pH changes?

Logarithmic function in the relationship

7

What happens in respiratory acidosis?

Hypoventilation --> increased pCO2 --> hypercapnia --> decreased pH

8

How is respiratory acidosis compensated?

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

9

What happens in metabolic acidosis?

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

10

How is metabolic acidosis compensated?

Increase ventilation to decreased pCO2

11

What happens in respiratory alkalosis?

Hyperventilation --> decreased pCO2 --> hypocapnia --> increased pH

12

How is respiratory alkalosis compensated?

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

13

What happens in metabolic alkalosis?

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

14

How is metabolis alkalosis compensated?

Decreasing ventilation but this is limited by hypoxia risk

15

What sensors have inputs into the respiratory control sensors?

Central chemoreceptors
Peripheral chemoreceptors
Pulmonary receptors
Joint and muscle receptors

16

What do central chemoreceptors detect?

H+

17

What do peripheral chemoreceptors detect?

O2, CO2, H+

18

What do pulmonary receptors detect?

Stretch

19

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

Stretch and tension

20

What are the effectors of the respiratory control centre?

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

21

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

8 kPa

22

Where are peripheral chemoreceptors located?

Carotid and aortic bodies

23

How do peripheral chemoreceptors signal respiratory changes?

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

24

Why are peripheral chemoreceptors relatively insensitive to pO2 changes?

Have low metabolic demands

25

What might cause peripheral chemoreceptors to respond to normal pO2?

Circulatory problems impacting bloodflow

26

What do peripheral chemoreceptors stimulates?

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

27

Are peripheral chemoreceptors sensitive to pCO2?

No, relatively insensitive

28

Where are central chemoreceptors found?

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

29

What do central chemoreceptors respond to changes in?

[H+] in CSF

30

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

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

31

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

Increase --> increased ventilation
Decrease --> decreases ventilation

32

What controls CSF composition?

Choroid plexus cells

33

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

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

34

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

Selectively add H+ or HCO3- to alter CSF composition

35

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

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

36

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

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

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

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

What are the four types of hypoxia?

Hypoxaemic/respiratory
Anaemic
Stagnanct/circulatory
Cytotoxic

39

What's is stagnant/circulatory hypoxia?

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

40

What is cytotoxic hypoxia?

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

41

What is respiratory failure?

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

42

What is type I respiratory failure?

Decreased oxygen entry but CO2 is not compromised
O2 sats

43

What causes type I respiratory failure?

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

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

Hypoxia stimulates hyperventilation

45

What is type II respiratory failure?

Decreased oxygen entry and decreased CO2 exit causing pO2

46

What causes type II respiratory failure?

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

Why is TB usually seen at the apex of lungs?

Higher pO2 for mycobacteria

48

How does the V/Q vary across the lung?

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

49

How is respiratory failure managed?

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

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

Exercise intolerance
Tachypnoea
Confusion
Central cyanosis

51

What visible changes occur in a pt with sats

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

52

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

Increased EPO increases Hb levels by causing polycythaemia
2,3-DPG increased to aid tissue oxygenation

53

What leads to cor pulmonale in chronic hypoxia?

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

54

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

Can be either

55

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

COPD

56

What happens in chronic type II respiratory failure?

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

57

What drives respiration in chronic type II respiratory failure?

Hypoxia via peripheral chemoreceptors

58

How is chronic type II respiratory failure treated?

Titrated O2 therapy which needs close monitoring

59

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

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

60

What environmental cause can lead to chronic hypoxia?

High altitude

61

What is asthma characterised by?

Reversible airflow obstruction
Airway wall inflammation and remodelling
Increased airway responsiveness

62

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

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

63

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

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

64

What mediates airway wall remodelling in development of asthma?

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

65

What can trigger airway smooth muscle contraction?

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

66

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

Decreases by 35%

67

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

Decreases by 50%

68

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

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

69

Describe the aetiology of asthma.

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

70

What is aspirin sensitive asthma?

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

71

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

No

72

How does viral-induced wheeze compare to asthma?

Children

73

What is the immediate response in allergic asthma?

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

74

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

Type I hypersensitivity

75

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

~20 mins

76

What happens in the late phase response of allergic asthma?

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

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

Type IV hypersensitivity

78

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

3-12 hrs

79

What features lead to a clinical diagnosis of asthma?

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

80

What is a wheeze?

Variable intensity and tonicity expiratory sound originating from vocal cords

81

What lung function tests can be used in asthma diagnosis?

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

82

How is asthma managed?

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

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

Have no visible effects

84

What is the classification of mild acute asthma?

>92% sats in air
HR75% predicted

85

What is the classification of moderate acute asthma?

Same as mild but with PEFR 75-50% predicted

86

What is the classification of severe acute asthma?

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

87

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

Type I

88

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

Type II