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Block 31 Cardio-respiratory > wheezy cough and breathlessness > Flashcards

wheezy cough and breathlessness Flashcards

1
Q

what is bronchiectasis?

A
  • Abnormal and permanently dilated airways
  • Bronchial walls become inflamed, thickened and irreversibly damaged
  • Mucociliary transport mechanism is impaired and frequent bacterial infections occur
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2
Q

how is bronchiectasis characterised clinically?

A

productive cough with large amounts of discoloured sputum and dilated, thickened bronchi, detected on CT

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3
Q

what is the aetiology of bronchiectasis?

A

-Cystic fibrosis is the most common cause in developed countries. -Others: post infectious, immunodeficiency, genetic, aspiration or inhalation injury, connective tissue disorders, IBD, focal bronchial obstruction

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4
Q

what causes the dilation and thickening of the bronchi seen in bronchiectasis?

A

due to chronic inflammation elicited by the host response to micro-organisms colonising the airways

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5
Q

what is the result of the chronic inflammation seen in bronchiectasis?

A
  • bronchial wall oedema and increased mucus production
  • neutrophils, T cells, immune effector cells recruited and release cytokines, proteases, reactive oxygen mediators implicated in progressive destruction of airways
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6
Q

describe the viscous cycle seen in bronchiectasis?

A

initial insult to airways by primary infection leads to increased inflammation, causing bronchial damage, serves as nidus for subsequent colonisation. airways are predisposed to subsequent inflammatory reactions and progressive airway damage and recurrent infections

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7
Q

what are the clinical features of mild bronchiectasis?

A

only produce yellow or green sputum after an infection. Localised areas of the lung may be affected, depending on position sputum production with position

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8
Q

what are the clinical features of bronchiectasis as the condition worsens?

A

patients suffer persistent halitosis, recurrent febrile episodes with malaise and episodes of pneumonia. Clubbing occurs and course crackles heard over infected areas (lung bases).

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9
Q

what are the clinical features of severe bronchiectasis?

A

continuous production of foul smelling, thick, khaki coloured sputum. Haemoptysis can occur as blood strained sputum or as massive haemorrhage. Breathlessness due to airflow limitation

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10
Q

what investigations would be carried out for a patient with suspected bronchiectasis?

A
  • chest X-ray
  • CT
  • sputum
  • sinus X-rays
  • serum immunoglobulins
  • sweat electrolytes (suspect CF)
  • mucociliary clearance
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11
Q

what would be shown on CXR in a patient with bronchiectasis?

A

dilated bronchi with thickened bronchial walls and multiple cysts containing fluid, but can be normal

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12
Q

what would CT show in a patient with bronchiectasis?

A

scanning-reveals thickened, dilated bronchi and cysts at the end of the bronchioles. Characteristically the airways are larger than their associated blood vessels

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13
Q

what would a sputum test show for a patient with bronchiectasis?

A

examination and culture. Main pathogens are staph. Aureus, pseudomonas aeruginosa, H.influenzae and anaerobes

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14
Q

why would you do a sinus X-ray for a patient with bronchiectasis?

A

30% also have rhinosinusitis

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15
Q

what would serum immunoglobulins show in a patient with bronchiectasis?

A

upto 10% of adults with bronchiectasis have antibody class or subclass deficiency (IgA). Some have normal antibody class levels but fail to respond to respiratory pathogens. Response to pneumococcal and Hib vaccines may be impaired

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16
Q

how is mucociliary clearance measured?

A

nasal clearance of saccharin. Time to taste of a 1mm cube of saccharin measured (normally <30 minutes)

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17
Q

what are the treatment options for bronchiectasis?

A

postural drainage
antibiotics (ifCF)
bronchodilators (useful in patients with demonstratable airflow limitation)
anti-inflammatory agents (inhaled or oral steroids can decrease rate of progression)
surgery (rare for condition to be localised enough for resection to be practical)

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18
Q

what is postural drainage?

A

patients are trained by physiotherapists to tip themselves so that the affected lobes are uppermost at least 3 times a day for 10-20 minutes

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19
Q

What is type 1 respiratory failure?

A

a low level of oxygen in the blood (hypoxemia) with either a normal (normocapnia) or low (hypocapnia) level of carbon dioxide (PaCO2) but not an increased level (hypercapnia).

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20
Q

what is acute type 2 respiratory failure?

A

In a person withtype 2 acute respiratory failure, the lungs are not removing enough carbon dioxide. Thistypeofrespiratory failurecauses carbon dioxide levels to be high

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21
Q

what is acute on chronic type 2 respiratory failure?

A

Type 2(hypercapnic)respiratory failure: in which PaCO2 > 50 mmHg. Hypoxemia is common and it is due torespiratorypumpfailure. Alsorespiratory failureis classified according to its onset, course and duration intoacute,chronicandacuteon top ofchronic respiratory failure

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22
Q

in type 1 respiratory failure, what is…

  1. pH
  2. PaO2
  3. PaCO2
  4. Bicarbonate
A
  1. normal/high
  2. low
  3. normal/low
  4. normal
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23
Q

in acute type 2 respiratory failure, what is…

  1. pH
  2. PaO2
  3. PaCO2
  4. Bicarbonate
A
  1. normal/low
  2. low
  3. high
  4. normal/rising
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24
Q

in acute on chronic type 2 respiratory failure, what is…

  1. pH
  2. PaO2
  3. PaCO2
  4. Bicarbonate
A
  1. normal
  2. low
  3. high
  4. raised
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25
Q

what is the most common type of respiratory failure?

A

type 1

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26
Q

what is the usual underlying mechanism for type 1 respiratory failure?

A

ventilation perfusion mismatch

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27
Q

what are the common causes of type 1 respiratory failure?

A

severe acute asthma
pneumonia
pulmonary embolism
pulmonary oedema

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28
Q

what is the usual underlying mechanism of type 2 respiratory failure?

A

ventilatory failure
rise in PaCO2 not matched by increase in alveolar ventilation because of
-insufficient ventilatory drive
-excessive breathing
-inability of lungs to pump air in and out

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29
Q

what are the common causes of type 2 respiratory failure?

A

neuromuscular disorders
CNS depression
tension pneumothorax
commonest-acute COPD exacerbation

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30
Q

what is the management of type 2 respiratory failure?

A

-treat cause eg antibiotics for COPD exacerbation
-supportive care
-chemical or mechanical ventilation
-do not give high flow oxygen
check ABG after 20 mins

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31
Q

what is the initial management of type 1 respiratory failure?

A

give oxygen by facemask

assisted ventilation is PO2 <8kpa even with 0% O2

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32
Q

what is tidal volume?

A

amount of air inhaled during a normal breath

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33
Q

what is expiratory reserve volume?

A

amount of air that can be exhaled after a normal exhalation

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34
Q

what is inspiratory reserve volume?

A

amount of air that can be further inhaled after a normal inhalation

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35
Q

what is residual volume?

A

air left in the lungs after a forced exhalation

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36
Q

what is vital capacity?

A

maximum amount of air that can be moved in or out of the lungs in a single respiratory cycle

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37
Q

what is inspiratory capacity?

A

volume of air that can be inhaled in addition to a normal exhalation

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38
Q

what is functional residual capacity?

A

volume of air remaining after a normal exhlation

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39
Q

what is total lung capacity?

A

total volume of air in the lungs after maximal inspiration

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40
Q

what is forced respiratory volume (FEV1)?

A

how much air can be forced out of the lungs over a specific time period (1 second)

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41
Q

what is the 5 step approach to arterial blood gas interpretation?

A
  1. how is the patient
  2. is the patient hypoxaemic
  3. is the patient acidaemic or alkalaemic
  4. respiratory component (PaCO2)
  5. metabolic component (bicarbonate/base excess)
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42
Q

when interpretting the respiratory component what does a PaCO2>6kPa suggest?

A

respiratory acidosis

or respiratory compensation for metabolic acidosis

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43
Q

when interpretting the respiratory component what does a PaCO2<4.7kPa suggest?

A

respiratory alkalosis or respiratory compensation for metabolic acidosis

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44
Q

when interpretting the metabolic component what does bicarbonate <22mmol/l (or base excess

A

metabolic acidosis or renal compensation for respiratory alkalosis

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45
Q

when interpretting the metabolic component what does bicarbonate >26mmol/l (or base excess >+2mmol/l) suggest?

A

metabolic alkalosis or renal compensation for respiratory acidosis

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46
Q

what does the acronym ROME stand for (with regards to arterial blood gas interpretation)?

A 
Respiratory=Opposite
-low pH + high PaCO2 (acidosis)
-high pH +low PaCO2 (alkalosis)
Metabolic=Equal
-low pH +low bicarb (acidosis)
-high pH+high bicarb (alkalosis)
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47
Q

when acid base homeostasis is disturbed and blood pH declines how is homeostasis restored?

A

Acidosis

  • brain and arterial receptors stimulated
  • increase resp rate
  • decrease blood CO2
  • decrease blood bicarb
  • increase pH
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48
Q

when acid base homeostasis is disturbed and blood pH increases how is homeostasis restored?

A

alkalosis

  • brain and arterial receptors stimulated
  • decrease resp rate
  • increase blood CO2
  • increase bicarb
  • decrease pH
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49
Q

what are the symptoms of acidosis?

A 
headache, sleepiness, confusion, loss of consciousness, coma
SOB, coughing
arrythmia, increased heart rate
seizures, weakness
nausea, vomiting, diarrhea
50
Q

what are the symptoms of alkalosis?

A

confusion, light headedness, stupor, coma
hand tremor, numbness/tingling in face, hands or feet
twitching, prologed spasms
nausea, vomiting

51
Q

When may pulse oximetry be used?

A
  • during or after surgery
  • test ability to handle increased activity
  • ensure ventilator is helping breathing
  • testing sleep apnea
52
Q

what does pulse oximetry measure?

A

haemoglobin saturation

53
Q

what are the types of oxygen delivery systems?

A

nasal canulas
simple face mask
non-rebreather mask
venturi system

54
Q

describe nasal cannulas?

A

flow rate=2-6L/min
dry nares if above 4L/min
oxygen reservoir=dead space of nasopharynx
enriches inspired air with oxygen

55
Q

describe a simple face mask?

A

flow rate=5-10L/min
50-60% oxygen
the initial method for acutely hypoxic patients

56
Q

describe a non-rebreather mask?

A

flow rate=12-15%

upto 90% conc oxygen

57
Q

describe the venturi system?

A

allows specific oxygen concentration (24, 28, 35, 40, 60)

58
Q

what are the common symptoms of asthma?

A

wheeze, chest tightness, cough, SOB, often worse at night

usually starts in early childhood

59
Q

what are the 3 characteristics of asthma?

A
  • airflow limitation
  • airway hyperresponsiveness
  • bronchial inflammation with T lymphocytes, mast cells, eosinophils with plasma exudation, oedema, smooth muscle hypertrophy, matrix depsition, mucus plugging and epithelial damage
60
Q

what may inflammation be accompanied by in chronic asthma?

A

irreversible airflow limitation as a result of airway remodelling that may involve large and small mucus impaction

61
Q

describe the prevelance of asthma?

A

increasing prevelance

more common in more developed countries

62
Q

what can asthma be classified into?

A

extrinsic asthma

intrinsic asthma

63
Q

what is extrinsic asthma?

A
  • mainly in atopic people
  • positive skin prick reactions to common inhalant allergen
  • childhood asthma accompanied by eczema
64
Q

what is intrinsic asthma?

A
  • often starts in middle age
  • non-atopic individuals develop asthma from extrinsic causes such as sensitisation to occupational agents, intolerance to NSAIDs
65
Q

how can bronchial hyperresponsiveness be demonstrated in a patient with asthma?

A

ask patient to inhale gradually and increase concentrations of histamine and methacholine
the severity can be graded according to provocation dose or concentration of the agonist that produces 20% fall in FEV1

66
Q

what type of asthma patients will respond to methacholine at low doses?

A

patients with clinical symptoms

67
Q

what type of asthma patients will respond to methacholine but only at higher doses?

A
  • asthma attacks on extreme exertion
  • wheezing or prolonged periods of coughing or viral infection
  • seasonal wheeze
  • allergic rhinitis
68
Q

what affects the degree of bronhial hyperresponsiveness in asthmatics?

A

allergic mechanisms, pathogenesis, mode of inheritance, combination of airway inflammation and tissue remodelling

69
Q

what type of compounds can cause occupational asthma?

A
  • low molecular weight (non IgE related)

- high molecular wright (IgE related)

70
Q

what affect does smoking have on the risk of developing occupational asthma?

A

smokers have an increased risk

71
Q

give examples on nonspecific stimuli that can cause bronchial hyper responsiveness in asthmatics?

A
  • cold air and exercise (histamine etc release)
  • atmospheric pollution and irritant dusts, vapours and fumes
  • diet (fruit and veg protective)
  • emotion
  • drugs (NSAIDs/selective beta 1 antagonists)
  • allergen induced
72
Q

give examples of low molecular weight causes of occupational asthma?

A 
isocyanates (paints etc)
colophony fumes (welder/electricians)
wood dust
bleaches and dyes
complex metal salts
73
Q

give examples of high molecular weight causes of occupational asthma?

A
  • animals and insect allergens
  • antibiotics (nurses)
  • latex (health workers)
  • proteolytic enzymes (manufacture of biological washing powders)
  • complex salts of platinum
  • acid anhydrides and polyamine hardening agents (industrial coatings)
74
Q

give examples of different types of asthmatic reactions following interaction with allergen?

A
  • immediate asthma
  • isolated late reaction
  • dual asthmatic response
  • recurrent asthmatic reactions
75
Q

describe the inflammatory component involved in the pathogenesis of asthma?

A

driven by Th2 type T lymphocytes facilitating IgE synthesis by production of IL-4 and eosinophilic inflammation via IL-5.
in more severe and chronic disease it loses sensitivity to steroids so greater Th1 response and release of mediators such as TNF alpha and tissue damage, mucous metaplasia and aberrant epithelial and mesenchymal repair

76
Q

describe the role of mast cells in asthmatic inflammation?

A
  • increased in epithelium, smooth muscle and mucous glands in asthma
  • relese mediators acting on smooth muscle, small blood vessels and mucus secreting cells
  • histamine, tryptase, PGD2, cysteinyl leukotrienes causing immediate asthmaticreaction
  • mast cells inhibited by sodium cromoglycate and beta 2 agonists
  • they release cytokines, chemokines and growth factors leading to late asthmatic response
77
Q

describe the role of eosinophils in asthma?

A
  • in large numbers in bronchial walls and asthmatic secretions
  • attracted to airways by cytokines, IL-3, IL-5 and GM-CSF and chemokines
  • enhanced mediator secretion
  • when activated release LTC4 and basic proteins which are toxic to epithelial cells
  • the number and activation is decreased by steroids
78
Q

what inflammatory cells are involved in asthma?

A

mast cells
eosinophils
dendritic cells
lymphocytes

79
Q

what are the causes and triggers of asthma? (9)

A
  • allergen exposure (pollen, pets)
  • viruses (rhinovirus, parainfluenza, RSV)
  • cold air
  • emotion
  • irritant dusts, vapours and fumes
  • genetic factors
  • drugs (NSIAIDs, beta blockers)
  • atmospheric pollution (sulfur dioxide, ozone)
  • occupational sensitisers
80
Q

what are the features of atopy?

A
  • athma and hayfever
  • runs in families
  • wealing skin to common allergens
  • circulating allergen specific antibodies
81
Q

give examples of genes that can influence development of asthma?

A
  • cytokine production genes (these affect mast cell, eosinophil and IgE production)
  • polymorphic variation in proteins along IL-4/IL13 pathway
  • PHF11 on chromosome 2 (SETDB2, RCBTB1)
  • ADAM 33
82
Q

what environmental factors can contribute to development of asthma?

A
  • early childhood exposure to allergens and maternal smoking

- hygiene hypothesis

83
Q

what are the signs and symptoms of COPD?

A
  • easily fatigued
  • frequent respiratory infections
  • use of accessory muscles
  • orthopneic
  • cor pulmonale (late)
  • thin
  • wheeze
  • pursed lip
  • chronic cough
  • barrel chest
  • dyspnoea
  • prolonged expiratory time
  • bronchitis (increased sputum)
  • digital clubbing
84
Q

how can COPD severity be assessed?

A

GOLD stage (global initiative for obstructive lung disease)

85
Q

what is GOLD stage 1?

A

mild

FEV1>80% predicted

86
Q

what is GOLD stage 2?

A

moderate

50%

87
Q

what is GOLD stage 3?

A

severe

30% FEV1<50% predicted

88
Q

what is GOLD stage 4?

A

very severe

FEV1<30% predicted

89
Q

what condition is associated with ‘blue bloater’?

A

chronic bronchitis

90
Q

what condition is associated with ‘pink puffer’?

A

emphysema

91
Q

what are the symptoms of chronic bronchitis (blue bloaters)?

A
  • chronic productive cough
  • purulent sputum
  • haemoptysis
  • mild dyspnoea
  • cyanosis
  • peripheral oedema (cor pulmonale)
  • crackles, wheezes
  • prolonged expiration
  • obese
92
Q

what are the complications of chronic bronchitis (blue bloater)?

A
  • secondary polycythemia vera due to hypoxaemia
  • pulmonary hypertension due to reactive vasoconstriction from hypoxemia
  • cor pulmonale from chronic pulmonary hypertension
93
Q

what are the symptoms of emphysema (pink puffer)?

A
  • dyspnoea
  • minimal cough
  • increased minute ventilation
  • pink skin, pursed lip breathing
  • accessory muscle use
  • cachexia
  • hyperinflation, barrel chest
  • decreased breath sounds
  • tachypnea
94
Q

what are the complications of emphysema (pink puffer)?

A
  • pneumothorax due to bullae

- weight loss due to work of breathing

95
Q

what is an acute exacerbation of COPD?

A
  • Sudden worsening of COPD symptoms such as SOB, quantity and colour of phlegm typically lasting for several days
  • It can be triggered by infection with bacteria or viruses or by environmental pollutants
  • 75% of COPD symptoms due to infections
  • Classified as either mild, moderate and severe. as COPD progresses exacerbations become more frequent
96
Q

what are the signs and symptoms of an acute exacerbation of COPD?

A
  • Increased severity and frequency of coughing
  • Worsened chest congestion and discomfort
  • SOB and wheezing
  • Increased sputum and change in its appearance
  • Rupture of airways in lungs which could cause spontaneous pneumothorax
  • If due to infection- weakness, fever and chills. If bacterial infection sputum may be slightly streaked with blood or coloured yellow or green
97
Q

what are the causes of an acute exacerbation of COPD?

A
  • respiratory infections
  • allergens
  • toxins
  • air pollution
  • failing to follow drug therapy
98
Q

what common respiratory infections cause acute exacerbations of COPD?

A
  • haemophilus influenzae
  • streptococcus pneumoniae
  • Moraxella catarrhalis.

Pathogens commonly seen in patients with impaired lung function -haemophilus parainfluenzae

  • mycoplasma pneumoniae
  • gram negative, opportunistic pathogens
99
Q

what can be used to prevent acute exacerbations of COPD?

A
  • LABAs, long acting anticholinergics, inhaled corticosteroids, low dose theophylline
  • Smoking cessation
  • Flu and pneumooccal vaccination
  • Exercise
  • Avoiding infected people
  • Fluid intake
100
Q

what is the treatment for a mild exacerbation of COPD?

A

SABA

101
Q

what is the treatment for a moderate exacerbation of COPD?

A

SABA + antibiotic or oral corticosteroid

102
Q

what is the treatment for a severe exacerbation of COPD?

A

emergency hospital treatment

poor prognosis

103
Q

what other medical intervention is given to patients with an exacerbation of COPD?

A

oxygen-88-92%
medications
mechanical ventilation (endotracheal intubation, continuous positive airway pressure, bilevel positive airway pressure)

104
Q

what inhaled bronchodilators are used for COPD acute exacerbations?

A
  • beta agonists (salbutamol/terbutaline)

- anticholinergic (ipratropium)-via inhaler or nebuliser

105
Q

what medications are used in acute exacerbations of COPD?

A
  • inhaled bronchodilators
  • corticosteroids
  • antibiotics
106
Q

describe antibiotic choices for patients with an acute exacerbation of COPD?

A
  • given if suspect bacterial infection
  • lipid soluble (macrolides, tetracyclines, fluroquinolones) penetrate lung tissue well.
  • simple COPD <65 - less than 4 exacerbations are year-amoxicilin (beta lactam)
  • complicated >65, more than 4 exacerbations a year, FEV1/FVC <50%-aim tratment at gram negative bacteria (cefuroxime or co-amoxiclav)
107
Q

describe the pathway of inhaled therapies used for COPD?

A
  • SABA or short acting muscarinic antagonist (as required)
    NEXT:
    -FEV1>50% = LABA or long acting muscarinic antagonist (+corticosteroid if needed)
    -FEV1<50% = LABA +inhaled corticosteroid or long acting muscarinic antagonist
    NEXT
    -long acting muscarininc antagonist + LABA + inhaled corticosteroid
    in combination inhaler
108
Q

describe the technique for inhaler use?

A
  • remove cap
  • shake inhaler
  • breathe out gently
  • place mouthpiece between lips
  • actuate inhaler and breathe in slowly and deeply
  • hold breath for 5-10 secs then breath out
  • wait a few secs then repeat
  • replace inhaler cap
109
Q

when should an asthmatic seek emergency help?

A
  • hard to talk
  • nose opens wide when breathing
  • skin is pulled in around ribs and neck when breathing
  • HR or pulse is fast
  • hard to walk
  • lips or fingernails turn grey or blue
110
Q

what is the BTS guidelines for asthma treatment?

A
  1. inhaled SABA
    • inhaled steroid (200-800ug)
  3. +LABA
  4. increase steroid, +leukotriene
  5. daily oral steroid +refer
111
Q

what are the features of acute severe asthma?

A
  • PEF 33-50% of predicted
  • can’t complete sentences in one breath
  • resp rate >25
  • pulse >110
112
Q

what are the features of life threatening asthma?

A
  • PEF <33% predicted
  • O2 sats <92%
  • silent chest, cyanosis, poor respiratory effort
  • arrythmia or hypotension
  • exhaustion, altered consciousness
113
Q

if a patient has features of life threatening asthma what investigation would be needed?

A

arterial blood gas

114
Q

what are the features of near fatal asthma?

A
  • raised PaCO2

- need mechanical ventilation with raised inflation pressures

115
Q

what is the immediate management for a patient with acute asthma?

A
  • oxygen
  • salbutamol 5mg (nebulised)
  • ipratropium bromide 5mg (nebuliser)
  • prednisolone tablet 40-50mg OR IV hydrocortisone 100mg
  • no sedatives
  • CXR if suspect needs mechanical ventilation
116
Q

what is the treatment for acute asthma if life threatening features are present?

A
  • senior clinician
  • IV magnesium sulphate 1.2-2g infusion over 20 mins
  • nebulised salbutamol more frequently
117
Q

what is the subsequent management for a patient with acute asthma if they are improving?

A
  • oxygen
  • prednisolone daily or IV hydrocortisone
  • nebulised beta bronchodilator with ipratropium
118
Q

what is the subsequent management for a patient with acute asthma if they are not improving after 15-30 mins?

A

-oxygen and steroids
-continuous nebulisation of salbutamol
-continue ipratropium
IF STILL NO IMPROVEMENT
-senior clinician
-IV magnesium sulphate

119
Q

how should you monitor a patient with acute asthma?

A
  • PEF every 15-30 mins
  • SpO2
  • blood gases
  • PEF before and after beta bronchodilator
120
Q

when should a patient with acute asthma be transferred to ICU?

A
  • deteriorating PEF, worsening or persisting hypoxia or hypercapnia
  • exhaustion, altered consiousness
  • poor respiratory effort or respiratory arrest
121
Q

after hospital admission for acute asthma patients should have what on discharge?

A
  • been on discharge medication for 12-24 hours with inhaler technique checked
  • PEF >75% of predicted and PEF diurnal variability <25%
  • oral steroids for at least 5 days and inhaled steriods
  • own PEF meter and athma action plan
  • GP within 2 days
  • resp clinic follow up in 4 weeks

Block 31 Cardio-respiratory (15 decks)

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