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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
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

Semester 3 (50 decks)

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