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ESA 3 > Resp 5 > Flashcards

Resp 5 Flashcards

1
Q

Define the term hyperventilation

What affect will this have on partial pressures of respiratory gases in the alveoli?

A

Ventilation increase with no change in metabolism

pCO2 falls

pO2 rises

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2
Q

Define hypoventilation

What affect will this have on alveolar gases partial pressure?

A

Ventilation decrease with no change in metabolism

pCO2 rises

pO2 falls

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3
Q

In what situations can changes in ventilation rate not correct imbalance in respiratory gases partial pressure?

A

If pCO2 or pO2 change without an opposite reaction from the other gas such as in the case of hypo/hyper-ventilation then the system cannot be controlled by change in ventilation

In these cases one gases partial pressure is prioritised for control

E.g. If pO2 falls without change in pCO2 then increase in ventilation will correct hypoxia but produce hypocapnia

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4
Q

What is hypoxia?

When does it become significant?

A

Fall in pO2 in arterial blood below 8kPa

Fall of pO2 below 8kPa significantly reduces saturation of Hb

Further falls lead to large reduction in O2 transport

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5
Q

What is the link between pCO2 and plasma pH?

A

pCO2 affects plasma pH

pH = pK + Log10 ([HCO3-] / (pCO2 x 0.23))

At constant HCO3-

pCO2 fall leads to rise in pH and vise versa

Small changes in pCO2 lead to large changes in Plasma pH

Ratio of [HCO3-] and pCO2 determine plasma pH

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6
Q

What are the effects of significantly increased or decreased plasma pH?

A

Plasma pH below 7.0:

Lethally denatured enzymes

Plasma pH above 7.6:

Free [Ca2+] increase

Tetany

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7
Q

Describe the effects of hyper/hypo-ventilation on plasma pH

A

Hyperventialtion:

pCO2 falls

pH rises

Causes respiratory alkalosis

Hypoventialtion:

Leads to rise in pCO2

pH falls

Causes repiratory acidosis

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8
Q

Describe the role of the kidneys in plasma pH control

A

Changes in pCO2 can be compensated for by changes in [HCO3-] (which is controlled by the kidneys)

Respiratory alkalosis is compensated for by increase in [HCO3-]

Respiratory acidosis is compensated for by decrease in [HCO3-]

Takes 2-3 days

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9
Q

Describe the involvement of other body tissues on the plasma pH

A

Metabolic acidosis:

Tissue metabolism produces H+ and CO2

this reacts with HCO3- and increases CO2

Fall in pH results

Can be compensated for by increased ventilation (lowers pCO2)

Metabolic alkalosis:

Plasma HCO3- rise

Plasma pH rises

Can be compensated for by decreasing ventilation (to a degree)

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10
Q

What might cause rise in plasma HCO3-?

A

Vomiting

Stomach acid must be replaced

H20 + CO2 = HCO3- + H+

H+ enters stomach and HCO3- is expelled into blood

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11
Q

Describe Peripheral chemoreceptors

Hint: Functions and locations

A

Found in the carotid bodies and aortic bodies

Monitor arterial pO2:

Large falls in pO2 stimulate:

    • increased ventialtion rate*
    • changes in heart rate*
    • diversion of blood flow to brain*

Hence they couteract and protect against the effects of hypoxia

Monitor arterial pCO2:

Detect changes in pCO2 but are very insensitive, this function is largely ignored

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12
Q

What are the functions of central chemoreceptors?

Where are they found?

A

Functions:

Detect small changes in pCO2 in the CSF

Will increase or decrease ventilation to compensate for changes in pCO2

Negative feedback control of breathing

Found:

Medulla

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13
Q

What structures control the pH of the CSF?

A

Blood brain barrier:

Allows free movement of CO2 therefore CSF pCO2 determined by arterial pCO2

Impermeable to HCO3-

Choroid plexus cells in blood brain barrier:

Control [HCO3-] in CSF

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14
Q

Describe short term control of CSF pH

A

[HCO3-] fixed in short term

Fall or rise in pCO2 of arterial blood and hence CSF leads to change in CSF pH

Change in pH detected by central chemoreceptors

Leads to change in vntialtion drive which in turn corrects pCO2

pH returns to normal and ventilation drive is changed accordingly

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15
Q

Describe longer term regulation of the CSF pH

A

Persistent change in pCO2 and hence CSF pH lead to change of [HCO3-] by the Choroid plexus cells

CSF [HCO3-] determines the pCO2 set points that are associated with ‘normal’ CSF pH

Change in the [HCO3-] leads to a change in these set points

E.g. Long term increase in pCO2 in CSF leads to a rise in [HCO3-] in CSF and therefore a rise in pH, this stops the response of the central chemoreceptors to the rise pCO2 by correcting/raising pH without correcting pCO2

As a result, the central chemoreceptors are reset to act around this new set point of pCO2 (which although is raised is now seen as normal by the central chemoreceptors)

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16
Q

List the oxygen and CO2 transport chains

A

O2:

Air - Airways - Alveoli - Alveolar membrane - Arterial blood - Regional arteries - Capillary blood - Tissues

CO2:

Tissues - Regional veins - Venous blood - Alveolar membrane - Alveoli - Airways - Air

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17
Q

What are the typical pCO2 and pO2 in the:

    • Air*
    • Alveolar air*
    • Venous blood*
    • Arterial blood*
A

Air:

p02 - 21kPa

pCO2 - 0.03kPa

Alveolar Air:

p02 - 13.3kPa

pCO2 - 5.3kPa

Venous Blood:

p02 - 5.3kPa

pCO2 - 6.1kPa

Arterial Blood:

p02 - 13.3kPa

pCO2 - 5.3kPa

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18
Q

What is the ideal ventilation/perfusion ratio?

What is the V/P ratio at the lung apex and base?

A

Ideal:

V/P = 1 (l/min)

Apex:

Alveolar ventilation - 0.24l/min

Blood flow - 0.07l/min

Ratio = 3.3

Base:

Alveolar ventilation - 0.82l/min

Blood flow - 1.29l/min

Ratio = 0.63

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19
Q

What is the effect of fibrotic lung disease on alveolar exchange and hence the arterial blood?

A

Exchange surface is thickened

Arterial pO2 = Low

Arterial pCO2 = Normal (CO2 diffuses easier than O2)

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20
Q

What is the effect of Pulmonary Oedema on alveolar exchange and hence the arterial blood?

A

Exchange surface is normal but there is increased perfusion distance

Arterial pO2 = Lower

Arterial pCO2 = Normal (CO2 more soluble than O2)

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21
Q

What is the effect of Emphysema on alveolar exchange and hence the arterial blood?

A

Exchange surface area is decreased

Arterial pO2 = Low

Arterial pCO2 = Normal (Diffuses easier than O2)

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22
Q

What is the broad definition of respiratory failure?

A

Not enough oxygen enters the blood or not enough Co2 leaves the blood

Doesn’t necessarily occur together

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23
Q

What is type 1 resp failure?

A

Not enough O2 enters blood

CO2 removal not compromised

pO2 of arterial blood = Low

pCO2 of arterial blood = Normal of slightly low

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24
Q

What is type 2 resp failure?

A

Not enough O2 enters blood

Not enough CO2 leaves blood

Arterial pO2 = Low

Arterial pCO2 = High

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25
Q

What is ‘Oxygen saturation’?

How is it measured?

What is the ideal measurement?

A

O2 saturation of Hb in arterial blood (SaO2)

Measured with a pulse oximeter and expressed as a %

Ideally >95%

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26
Q

What is arterial blood gas analysis?

A

Arterial blood obtained (usually from radial artery)

Blood is heparinised and put in cold water (prevents clotting)

Sample put through a blood gas analyser

Normally reads pCO2, pO2 and pH

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27
Q

What would be the results of an ABG, pulse oximetry and resp rate observation in a patient with type 1 resp failure?

A

Low pH

Hypoxic

Normal CO2

Low Hb saturation (<95%)

High resp rate

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28
Q

What are the 2 categories of Type 1 Resp failure?

Give examples of conditions in each category

A

Some alveoli poorly ventilated:

Pulmonary embolism

Pneumonia

Consolidation

Early stages of acute asthma

Most alveoli poorly ventilated:

Pulmonary Oedema

Fibrosis

    • Fibrosing alveolitis*
    • Extrinsic allergic alveolitis*
    • Pneumoconiosis*
    • Asbestosis*
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29
Q

What are the common features of a patient with type 1 resp failure?

A

Breathlessness

Exercise intolerance

Central cyanosis

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30
Q

What are the typical findings of an ABG, Pulse oximetry and observation of resp rate in a patient with type 2 resp failure?

A

Low pH

Hypoxia

Hypercapnia

<95% Hb saturation

High resp rate

31
Q

Give some examples of causes of type 2 resp failure

A

Ineffective respiratory effort:

Poor resp effort

    • Resp depression (narcotics)*
    • Muscle weakness (upper or lower motor neurone disease)*

Chest wall problems

    • Scoliosis/Kyphosis*
    • Trauma*
    • Pneumothorax*

Hard to ventilate lungs

- High airway resistance (bronchitis, asthma)

Emphysema

32
Q

Describe the causes and effects of emphysema

A

Cause:

Alpha1 - antitrypsin deficiency (genetic or smoking)

Effects:

Increased lung compliance (Barrel chest)

Airway obstruction (bronchiole collapse during expiration)

V/P mismatch

Reduced O2 absorption

Type 1 failure initially

Progresses to type 2 as CO2 transport impaired

33
Q

Describe how the body reacts to acute hypoxia

A

pO2 falls below 8kPa

Peripheral chemoreceptors sense this and increase respiratory drive

This leads to correction of hypoxia but causes hypocapnia

Leads to rise in CSF pH causing an attempted reduction in respiratory drive

34
Q

How does the body react to acute hypoxia?

A

Increased ventilation causes hypocapnia

Renal correction of acid base balance in blood (decrease in HCO3- in blood corrects pH)

Increased ventilation persists due to continued action of peripheral chemoreceptors

35
Q

What are the acute effects of type 2 resp failure?

A

pCO2 rises, pO2 falls

Central chemoreceptors increase respiratory drive

Breathlessness is felt and respiration rate increases

This provides some respiratory compensation

However poor ventilation (due to disease) prevents full compensation

36
Q

What are the chonic effects of type 2 resp failure?

A

CO2 retention:

CSF rise in pCO2 corrected by choroid plexus

Central chemoreceptors are reset to higher CO2 level

Hypoxia persists

Reduction in respiratory drive (which is now driven by peripheral chemoreceptors (hypoxia)

Pulmonary circulation:

Hypoxia causes pulmonary hypertension

leads to right heart failure (cor pulmonale)

Hypoxia:

Increased Hb (polycythaemia)

2,3 BPG release

Increased respiratory effort:

Increased work required for breathing

Severely disabling

37
Q

Define Asthma

A

A chronic disorder characterised by:

    • Chronic inflammation leading to Airway wall remodelling*
    • Reversible, variable airflow reduction*
    • Increase in airway response to variety of stimuli (Airway hyper-responsiveness)*
    • Susceptibility to infection*
38
Q

Compare airway remodelling in Asthma with other weezing disorders

A

Asthma:

Increased acellular membrane thickness

Damaged epithelium

Thickened reticular basement membrane

Smokers or premature lungs:

As in asthma

+ Loss of alveolar septa

39
Q

Describe the initial cellular reaction to allergen exposure in asthma

A

Th2 lymphocytes are activated by macrophages which have absorbed and processed the antigen

Th 2 cells release cytokines which attract and activate mast cells and eosinophils also B cells, which produce IgE

2 phase response results

Immediate response phase(0-20 minutes):

Interaction of allergen and specific IgE leads to mast cell degranulation and mediator release (Histamine, tryptase, prostaglandins and leukotriene)

This leads to bronchial smooth cell contraction/bronchoconstriction

Late phase response (3-12 hours later):

Complex array of inflammatory cells, mediators and cytokines that causes airway inflammation

Eosinophils release leukotriene C4 which causes shedding of epithelial cells

40
Q

What cells/mediators are involved in airway remodelling in asthma?

What is the process called that leads to this airway remodelling?

A

Cellular:

Neutrophils

Eosinophils

Mast cells

Soluble mediators:

Cytokines (TNF-a)

Leukotrienes

Growth factor (involved in repair)

Process:

Chronic inflammation

41
Q

In what ways do airway inflammation reduce airway diameter?

A

Mucosal oedema due to vascular leak

Thickening of bronchial walls due to infiltration of inflammatory cells

Mucus overproduction (thich, tenacious, slow moving, Doesnt come up in dry cough)

Smooth muscle contraction

Hyperresponsiveness of airways

Airway remodelling:

    • Hypertrophy and hyperplasia of smooth muscle*
    • Hypertrophy of mucus glands*
    • Thickening of basement membrane*
42
Q

What are the effects of airway narrowing in asthma?

A

Wheeze and other clincal features of asthma

Obstructive pattern on spirometry (decreased FEV1/FVC ratio and obstructive flow volume loop)

Air trapping increases residual volume

43
Q

Describe the effects of asthma on the ventilation/perfusion ratio and the concequences of this

A

Airway narrowing leads to reduced ventilation

Hyperventilation cannot compensate for reduced O2 but can compensate for CO2 retention by increasing breathed out CO2

Mild to moderate attack:

Reduced pCO2 and pO2

Type 1 resp failure

Severe attacks:

More extensive airway involvement + exhaustion due to hyperventilation leads to further gas exchange impairment and the loss of CO2 compensation

Reduced pO2 and Increasing pCO2

Type 2 resp failure

Can be life threatening

44
Q

Why do small smooth muscle contractions in the airway have such a large effect on breathing?

A

SM contraction lead to narrowing of airways

Flow is greatly impeded even by seemingly small contraction

There is also a large increase in the work required to breath

E.g. A 20% reduction in airway diameter leads to 60% reduced airflow and greatly increased work in breathing

45
Q

What are some of the direct triggers to Airway smooth muscle (ASM) contractions?

A

Muscarinic antagonists (E.g. Ach)

Histamine

Cold air

Arachadonic acid metabolites (Prostaglandins, Leukotrienes)

46
Q

What is airway hyper-responsiveness?

What is its relevance to asthma?

A

Where a larger % reduction in FEV1 is seen in response to increasing histamine levels than would be normally expected

AHR is a feature of asthma, however many non-asthmatics have AHR

47
Q

You recieve the flow/volume loop of a patient showing airway obstruction, Suspected diagnoses based on other elements of the history are COPD or Asthma

How do you differentiate?

A

Airway obstruction in asthma is reversible:

>15% improvement spontaneously or on administration of bronchodilators or steroids

COPD airway obstruction is not:

<15% improvement with treatment

48
Q

What are some of the causes of asthma?

A

Hereditary

Sensitisation to airborn allergens:

Air pollution

Tobacco smoke (pre/post-natal or direct)

Fungal spores (Damp housing)

Hygiene hypothesis:

Excess hygiene in childhood leads to derangement of normal immune development

49
Q

Give examples of atopic and non-atopic asthma

A

Atopic (Type 1 hypersensitivity)

Allergic asthma

Viral induced wheeze (Classified as asthma in under 5s)

Non-atopic (not type 1 hypersensitivity associated):

Aspirin sensitive asthma

Occupational asthma (Farmers, Bakers, Welders)

50
Q

How is an asthma diagnoses made?

A

Clinical diagnoses only, non standard definitions for type, severity, findings on investigation etc.

Includes 1 or more of these reccurent symptoms:

Wheeze

Breathlessness

Chest tightness

Cough

Variable airflow obstruction

AHR and airway inflammation assessment

51
Q

Describe an asthmatic wheeze

A

Wheeze:

High pitched, expiratory, musical

Originates in airways which have been narrowed by compression or obstruction

In asthma:

Variable intensity and tone

Bilateral

52
Q

Describe an asthmatic cough

A

Often worse at night

Exercise induced

Dry (wet indicates infection/COPD etc)

53
Q

Describe the pattern of breathing difficulty experienced by asthma patients

A

Often with exercise

During acute exacerbations

Assessment might find:

    • Tachypnoea*
    • Intercostal Recession (negative pressures draw intercostal muscles inward)*
    • Tracheal tug (movement of the trachea and thyroid cartilages downwards)*

A prolonged expiratory phase is with or without wheeze is a common marker of asthma

54
Q

What are the features of a history in a patient with suspected asthma?

A

Onset and pattern of symptoms:

Symptoms

Disturbance to life

Precipitating factors

Past medical history:

Hayfever, eczema

Prenatal smoke exposure

Family history:

Asthma, smoking

Occupational history:

Farms, Woods, Coal fires

Non-asthma drug history

Pets

55
Q

When performing an examination on a patient with suspected asthma what might you expect to find?

A

Inspection:

Chest:

    • Scars or deformities*
    • Hyperexpansion (barrel chest)*

General:

    • Hayfever*
    • Eczema*
    • Lethargy*
    • Can they talk?*

Room:

    • Meds*
    • Charts*

Percussion:

Hyperresonant

Ascultation:

Polyphonic wheeze

56
Q

Give examples of common and uncommon chest wall deformities in asthma

A

Common:

Harrison’s Sulcus (indrawing of costal cartilages in children

Uncommon:

Sternal (pectus) deformities

57
Q

How is PEFR measured?

A

With a peak flow meter:

Check flow meter is at zero, sit the patient upright

Hold device horizontal ask the patient to take a deep breath, firmly seal lips around the mouthpiece and exhale as hard as possible

58
Q

What are PEFR reading taken with a peak flow meter used for?

What are the limitations?

A

Usage:

Better used for monitoring as opposed to diagnosis

Limitations:

Wide range of normal values

No correction for ethnicity

Less reproducible than FEV1

Effort dependent

59
Q

How is spirometry performed?

A

Stand or sit patient in upright position

Incentivise patients that are children to put in maximum effort (visual cues or trained professional)

2-3 tidal breaths are taken with lips around spirometer

Deep breath taken to TLC and then blow out as hard as possible

Repeat 3 more times to achieve maximum of 5% variaion from largest FVC

Can then be repeated post bronchodilator to test obstructive reversibility

60
Q

Describe the findings of spirometry that might indicate asthma

A

May be normal or show lower airway obstruction on a flow/volume graph

Normal or reduced FEV1 and FVC do not exclude asthma

Reversibility must be checked

Typical profile:

Low PEFR

Low FEV1/FVC ratio

Remember normal profile doesn’t exclude and to check reversibility

61
Q

How is Airway hyperresponsiveness commonly tested?

A

Checking for exercise induced bronchoconstriction with an exercise stress test and spirometry

Spiro is done pre-exercise

6-8 mins of exercise monitoring SaO2 and HR

Perfore post-exercise spiro after 1, 5, 10 and 15 minutes

Repeat spiro post bronchodilator

62
Q

What is an Exhaled NO test

How is it performed?

A

Exhaled NO testing (FeNO) is a test of exhaled levels of Nitric oxide, which is a biomarker for chronic inflammation and is found in higher levels with people with chronic inflammation of the airways, such as in asthma

Procedure:

Lungs are emptied as far as possible

Inhaled to Vital capacity through device filter

Ehale steadily into device

63
Q

What are the limitations of FeNO and when is it performed?

A

Limitations:

Not specific to asthma

Normal result doesn’t exclude asthma

Uses:

In someone judged as intermediate risk of asthma after initial clinical examination can be tested (in conjuction with other tests) to aid diagnoses

64
Q

Other than the tests described in previous cards, what are some investigations that could be performed in clinic to test or monitor asthma?

A

Skin prick allergy test

Blood IgE levels in response to specific allergens

Test for exercise induced asthma

Chest X-rays (exclude other disease such as pneumothorax in acute exacerbations)

65
Q

When educating patients and professionals about asthma, what are the important topics?

A

Patients:

Correct recognition of symptoms

Timely use of medication

Appropriate use of health services

Personal asthma action plan

Professionals:

Appropriate medication

Concordance with treatment plans

66
Q

List methods for primary prevention of asthma

A

Stop smoking

Remove wood/laminate flooring from house (Questionable)

Cleaning (Questionable)

Fresh air

Breast feeding

Exposure to allergen/triggers

Weight loss

Diet (Questionable)

67
Q

What are the two main types of pharmacological treatment?

Give the drug types and examples of drugs for each

A

Reliever therapy:

B2 agonists

Muscarinic antagonists

Theophylline/Aminophylline

Preventer therapy:

Corticsteroids

Leukotriene receptor antagonist

68
Q

What are the effects of Corticosteroids on someone with asthma?

A

Decrease secretion and number of eosinophils

Decrease cytokines released from T lymphocytes

Decrease mast cell numbers

Decrease macrophage numbers and cytokine secretion

Decrease epithelial cell cytokine release

Decrease mucos secretion from mucus glands

Decrease the leak of endothelial cells

69
Q

What are the BTS treament guidelines for asthma?

A

Start treatment at step most appropriate to initial severity

Acheive early control

Maintain control by stepping up or down as necessary

70
Q

Outline some of the key features of treatment for mild, modeate and severe asthma

A

Mild:

Inhaled short acting B2 agonist as needed

Moderate:

Add inhaled steroid daily

May add inhaled long action B2 agonists

Severe:

Consider increasing steroid dose and adding further drugs (E.g. theophylline)

Finally add daily steroid tablet

71
Q

What are some of the clinical features of mild, moderate and severe acute asthma exacerbations?

A

Mild:

SaO2 >92% in air

HR <110

RR <25

Speech normal

Minimal wheeze

PEFR >75% predicted

Moderate:

As above however

Increased wheeze

PEFR 50-75% predicted

Severe:

SaO2 <92% in air

HR >110

RR >25

Cant complete sentences

No wheeze

PEFR 35-50% predicted

72
Q

Outline the clinical features of life threatening asthma

A

SaO2 <92% in O2

Silent chest, Poor respiratory effort

Altered onciousness/hyper-aggressive

Exhaustion

PEFR <35% predicted

Rising or ‘normal’ pCO2

73
Q

What is the treatment plan for acute severe asthma attacks?

A

GET HELP

A - Oxygen

B- Continuous salbutamol and iptatropium nebs

C - IV access (Salbutamol, Mg Sulphate, Aminophylline)

Intubate and ventilate

Short course of oral prednisilone may also be required

Increase through steps as required until symptoms resolve

ESA 3 (54 decks)

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