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Medicine block (Y3) > Week 3: Respiratory medicine (3) (common conditions, PFTs, ABG) > Flashcards

Week 3: Respiratory medicine (3) (common conditions, PFTs, ABG) Flashcards

1
Q

forced vital capacity

A

volume of air that can be forcibly expelled from the lungs from a position of maximal inspiration

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2
Q

forced expiratory volume 1

A

volume of air forcibly expelled from lungs in the first second- following maximal inspiration

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3
Q

how to do spirometry

A

• Blow
– As hard
– As fast
– As long as possible

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4
Q

obstructive vs restrictive patterns on spirometry

A
  • Obstructive = FEV1/FVC <70%

- Restrictive = FEV1/FVC >70%

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5
Q

obstructive lung disease

A

COPD and Asthma

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6
Q

restrictive lung disease

A

ILD and conditons like muscular dystophy

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7
Q

how are lung volumes measured

A 
–	Plethysmography
•	Long, expensive, patients don’t like as much
•	Less error
–	Helium dilution
•	More error (in disease)
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8
Q

Lung volumes

A

More detailed than spirometry and help differentiate underlying pathologies e.g. which ling disease and which therapy.

• Measures
– Total Lung Capacity (TLC)
– Functional residual capacity (FRC)
– Residual volume (RV)

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9
Q

Flow- volume loops

A 
•	Breath in, out and in
–	Patient breathes in to TLC
–	Forced expiration to RV
–	Finally breathe back in to TLV
•	Detail of flows
–	Useful for obstruction
•	Headache inducing for doctors (especially MRCP)
–	Pattern recognition
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10
Q

Respiratory muscle function

A 
•	Postural changes in VC
•	Serial VC measures
–	Acutely GBS (Guillain barre syndrome)
•	Mouth pressures
•	Nasal pressures
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11
Q

Measures of oxygenation

A 
-	Blood gases (capillary)
o	Resting hypoxaemia
	Long term oxygen therapy
o	Exercise desat
	Ambulatory oxygen
-	Fitness to fly assessment
–	If SpO2 <95%
–	Breath at FiO2= 0.15 (15%) for 20 mins
–	In flight O2 if pO2 < 6.6 (KPa) or SpO2 <85%
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12
Q

example 1

A

Example 1- Asthma

  • FEV1/FVC ratio = 1.05/2.15= 0.49
    o Below 70%- obstructive
  • Reversibility with SABA
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13
Q

example 2

A

Example 2a COPD

-	FEV1/FVC =56%
•	Obstructive spirometry
–	Again by definition (GOLD criteria)
–	No reversibility
•	RV commonly elevated
•	TLC raised
–	False low TLC with helium dilution
•	TLCO/KCO
–	Normal in chronic bronchitis
–	Low in emphysema
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14
Q

example 3

A

Example 3- Pulmonary fibrosis

•	Restrictive Spirometry
–	Stiffness of lungs
•	Low TLC/VC
–	Early sign
•	Reduced TLCO/KCO
–	Thickened alveolar-capillary membrane
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15
Q

four causes of low PaO2

A
  • hypoventilation
  • diffusion impairment
  • shunt
  • V/Q mismatch
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16
Q

hypoventilation example

A

unconscious

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17
Q

diffusion impairment

A
  • ILD e.g. pulmonary fibrosis

* Emphysema

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18
Q

shunt

A

persistent hypoxaemia despite 100% oxygen inhalation- passage of deoxygenated blood from the right side of the heart to the left without participation in gas exchange in pulmonary capillaries
• Pneumonia e.g. when alveoli filled with fluid causing parts of the lungs to be unventilated although they are still perfused
• ARDs
• Alveolar collapse

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19
Q

V/Q mismatch

A 
when parts of the lungs receives oxygen without blood flow or blood flow without oxygen 
•	Asthma
•	COPD
•	Bronchiectasis
•	CF
•	ILD
•	Pulmonary hypertension
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20
Q

Persistent hypoxaemia causes

A

pulmonary hypertension which can cause cor pulmonale -> right sided heart failure

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21
Q

5- step approach to ABG

A
  1. How is the patient?
    – Will provide useful clues to help with interpretation of the results
  2. Assess oxygenation
    – Is the patient hypoxaemic?
    – The PaO2 should be > 10 kPa (75 mmHg) breathing air and about 10 kPa less than the % inspired concentration
  3. Determine the pH (or H+ concentration)
    – Is the patient acidaemic; pH < 7.35 (H+ > 45 nmol l-1)
    – Is the patient alkalaemic; pH > 7.45 (H+ < 35 nmol l-1)
  4. Determine the respiratory component
    – If the pH < 7.35, is the PaCO2 > 6.0 kPa (45 mmHg) – respiratory acidosis
    – If the pH > 7.45, is the PaCO2 < 4.7 kPa (35 mmHg) – respiratory alkalosis
  5. Determine the metabolic component
    – If the pH < 7.35, is the HCO3- < 22 mmol l-1 (base excess < -2 mmol l-1) – metabolic acidosis
    – If the pH > 7.45, is the HCO3- > 26 mmol l-1 (base excess > +2 mmol l-1) – metabolic alkalosis
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22
Q

oxygen dissociation curve

A
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23
Q

acid base balance

A

H+ + HCO3- ↔ H2CO3 ↔H2O + CO2

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24
Q

An arterial blood gases (ABG) test is done to:

A
  • Check for severe breathing problems and lung diseases, such as asthma, cystic fibrosis, or chronic obstructive pulmonary disease (COPD).
  • See how well treatment for lung diseases is working.
  • Find out if you need extra oxygen or help with breathing (mechanical ventilation).
25
Q

acid-base disturbance summary

A
26
Q

respiratory failure summary

A
27
Q

type 1 resp failure

A

Type 1 - (hypoxemic) respiratory failure has a PaO2 < 60 mmHg with normal or subnormal PaCO2.

In this type, the gas exchange is impaired at the level of aveolo-capillary membrane.

Examples of type I respiratory failures are carcinogenic or non-cardiogenic pulmonary edemaa, ARDs, COVID-19 and severe pneumonia.

28
Q

Type 2 resp failure

A

Type 2 - (hypercapnic) respiratory failure has a PaCO2 > 50 mmHg. Hypoxemia is common, and it is due to respiratory pump failure.
• RF a major cause of mortality and morbidity and mortality rates increase with age and presence of co-morbidities.

29
Q

alveolar gas equation

A
30
Q

The A-a gradient,

A

or the alveolar-arterial gradient, measures the difference between the oxygen concentration in the alveoli and arterial system. The A-a gradient has important clinical utility as it can help narrow the differential diagnosis for hypoxemia.

31
Q
A
  • PAO2 = Alveolar partial pressure of oxygen 
  • PIO2 = Room air (approx. 20 kPa)
  • PACO2 is virtually the same as arterial partial pressure of carbon dioxide (PaCO2)
32
Q

A-a gradient in young healthy people should be

A

less than 2 kPa, and less than 4 kPa in older people

>4 kPa implies lung pathology

33
Q

Case 1 – a 26 year old female nurse thought to be hyperventilating

A
  • On air pH7.56, pCO2 2.7, PO2 11.5, B.E. -2, HCO3 23
  • PAO2 = PIO2 – PaCO2/0.8 = 20 – 2.7/0.8 = 20-3.4 = 16.6 kPa
  • PA-aO2= 16.6-11.5 = 5.1 kPa
  • THEREFORE PROBLEM WITH THE LUNGS – NOT JUST HYPERVENTILATION !!!
34
Q

Case 2 – the Hepatology consultant from the liver unit refers a 31 year old man with liver failure and new hypoxia. On examination – jaundice, ascites.

A
  • On air pH 7.35, PO2 7.2, PCO2 8.6, HCO3 35, Sats 87%
  • PAO2 – PaO2 = 2.1kPa, i.e. NORMAL lungs.
  • There is under ventilation secondary to drugs, encephalopathy, or just ascites.
35
Q

asthma background

A
  • Asthma is a chronic inflammatory disease of the airways
  • Airway obstruction that is reversible (but not completely so in some subjects), either spontaneously or with treatment
  • FEV/FVC ratio below <70% - reversible
  • Increased airway responsiveness (airway narrowing) to a variety of stimuli
36
Q

risk factors of asthma

A
  • Parent with asthma
  • Severe childhood resp infection
  • Atopic
    Chemical/industrial irritants in work place
37
Q

signs and symptoms of asthma

A
  • Coughing, especially at night
  • Wheezing (can be heard through auscultation on exhalation)
  • Shortness of breath
  • Chest tightness, pain, or pressure
38
Q

Asthma Pathophysiology

A
  1. Airway epithelial damage – shedding and subepithelial fibrosis, basement membrane thickening
  2. An inflammatory reaction characterised by eosinophils, T-lymphocytes (Th2) and mast cells. Inflammatory mediators released include histamine, leukotrienes, and prostaglandins
  3. Cytokines amplify inflammatory response
  4. Increased numbers of mucus secreting goblet cells and smooth muscle hyperplasia and hypertrophy
  5. Mucus plugging in fatal and severe asthma
39
Q

wheeze differentials

A

o Acute Asthma Exacerbation
o Bronchitis – viral or bacterial

-	Other causes of wheeze less likely: 
o	Pulmonary oedema 
o	PE 
o	Vocal cord dysfunction 
o	Gastro-oesophageal reflux 
o	Foreign body 
o	Allergy 
o	Hyperventilation / psychosocial 
o	Cardiac disease 
o	Vasculitides – Churg-Strauss syndrome, polyarteritis nodosa, Granulomatosis with Polyangiitis (Wegener’s granulomatosis)
40
Q

Asthma Trigger Factors

A
  • Smoking
  • Upper respiratory tract infections – mainly viral
  • Allergens – pollen, house dust mite, pets
  • Exercise – also cold air
  • Occupational irritants
  • Pollution
  • Drugs – aspirin, beta blockers (including eye drops)
  • Food and drink – dairy produce, alcohol, orange juice
  • Stress
  • Severe asthma – consider inhaled heroin, pre-menstrual, psychosocial aspects
41
Q

Acute Asthma Management:

A

• ABCDE
• Aim for SpO2 94-98% with oxygen as needed, ABG if
sats <92%
• 5mg nebulised Salbutamol (can repeat after 15 mins)
• 40mg oral Prednisolone STAT (IV Hydrocortisone if
PO not possible)

If severe:
• Nebulised Ipratropium Bromide 500 micrograms
• Consider back to back Salbutamol

If life threatening or near fatal:
• Urgent ITU or anaesthetist assessment
• Urgent portable CXR
• IV Aminophylline
• Consider IV Salbutamol if nebulised route ineffective

42
Q

eosinophilia in asthma

A

Some patients with asthma have eosinophilic inflammation which typically responds to steroids. However, there are several differentials of eosinophilia:

  • Airways inflammation (asthma or COPD)
  • Hayfever / allergies
  • Allergic Bronchopulmonary Aspergillosis
  • Multiple courses of antibiotics for chronic infections
  • Eosinophilic Granulomatosis with Polyangiiitis
  • Eosinophilic Pneumonia
  • Parasites e.g. Hookworm
  • Lymphoma
  • SLE
  • Hypereosinophilic syndrome
43
Q

Criteria for safe asthma discharge after exacerbation

A
  • PEFR >75%
  • Stop regular nebulisers for 24 hours prior to discharge
  • Inpatient asthma nurse review to reassess inhaler technique and adherence
  • Provide PEFR meter and written asthma action plan
  • At least 5 days oral prednisolone
  • GP follow up within 2 working days
  • Respiratory Clinic follow up within 4 weeks
  • For severe or worse, consider psychosocial factors
44
Q

management of chronic asthma

A
  • Use the BTS stepwise management guidelines
  • Assess and teach Inhaler Technique
  • Use Self Management Plans
  • Avoid trigger factors
45
Q

BTS stepwise management of asthma

A

offered SABA PRN when diagnosed

1) regular preventer (low-dose ICS) if SABA used >3/week
2) initial add on therapy- inhaled LABA to low-dose ICS (don’t give LABA without ICS)

3) Additional controller therapies
- increasing ICS to medium dose or
- adding LTRA

4) specialist therapy

46
Q

COPD is an umbrella term for

A

emphysema
chronic bronchitis

COPD is characterised by airflow obstruction. The airflow obstruction is usually progressive, not fully reversible and does not change markedly over several months. The disease is predominantly caused by smoking.
- FEV1/FVC ratio is below <70% - non reversible with bronchodilators

47
Q

RF for COPD

A
  • Smoking
  • Exposure to air pollution.
  • Breathing secondhand smoke.
  • Working with chemicals, dust and fumes.
  • Alpha-1 deficiency.
  • Childhood respiratory infection.
48
Q

signs and symptoms of COPD

A
  • Chronic cough w or without sputum
  • Shortness of breath during activity
  • Wheezing
  • Ankle oedema
    o Cor pulmonale
49
Q

outline emphysema

A
  • Damage to walls of alveoli
  • Rather than lots of small alveoli, they breakdown forming larger alveoli  unable to support bronchioles
    o Bronchioles collapse and trap air inside the lungs
  • Changes in emphysema are irreversible
    Causes
  • Smoking (must stop smoking to stop it getting worse)
  • Alpha 1- antitrypsin deficiency
50
Q

outline chronic bronchitis

A
  1. Chronic inflammation of the bronchioles
  2. Inflammatory changes like asthma
  3. Instead of responding to allergen, it responds to irritants like cigarette smoke
    • Not T1 hypersensitivity
  4. Non-reversible
  5. Increased mucus and inflammation that causes narrowing of the airway  not bronchoconstriction

Symptoms :Chronic productive cough

51
Q

diagnosis of COPD

A

o Spirometry
 Will show obstructive airway pattern- reduced FEV: FVC ratio
 Poor bronchodilator reversibility (not caused by bronchoconstriction)
o CXR
 Can see bigger alveoli air trapping shows up as hyperdense
 Hyperinflated chest – how many ribs can you seen

52
Q

severity of COPD based on

A

o Based on decreased FEV1

o MRC dyspnoea scale (symptomatic test)

53
Q

COPD and long term therapy

A

Long Term Oxygen Therapy  oxygen reduction
• Extended periods of hypoxia cause renal and cardiac damage – can be prevented by LTOT
• LTOT to be used at least 16 hours/day for a survival benefit
• LTOT offered if pO2 consistently below 7.3 kPa, or below 8 kPa with cor pulmonale
• Patients must be non-smokers and not retain high levels of CO2
• O2 needs should be balanced with loss of independence and reduced activity which may occur
• Note: oxygen is not a treatment for breathlessness; it is a treatment to help prevent organ hypoxia

ankle oedema sign that LTOT needs commencing

54
Q

why controlled oxygen therapy in COPD

A

stop CO2 retention

55
Q

Outpatient COPD Management

A
  • ‘COPD Care Bundle’
  • SMOKING CESSATION
  • Pulmonary Rehabilitation
  • Increase exercise tolerance
  • Anxiety management
  • Breathing techniques
  • Bronchodilators
  • Antimuscarinics
  • Steroids
  • Mucolytics
  • Diet
  • LTOT if appropriate
  • LUNG VOLUME REDUCTION if appropriate
56
Q

Core pulmonale in COPD

A

increased pressure In the right ventricles due to pulmonary hypertension due to chronic hypoxia–> blood flow back to the RA reduced- ankle oedema

57
Q

MRC dyspnoea scale - used to quantify pt breathlessness

A
58
Q

pulmonary rehab for COPD

A

• Many COPD patients with COPD avoid exercise and physical activity because of breathlessness

  • This may lead to a vicious cycle of increasing social isolation and inactivity leading to worsening of symptoms
  • Pulmonary Rehabilitation aims to break this cycle – an MDT 6-12 week programme of supervised exercise, unsupervised home exercise, nutritional advice, and disease education

Medicine block (Y3) (38 decks)

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