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Resp Flashcards

1
Q

Features of moderate acute asthma

A

Increasing symptoms
SpO2 ≥92%
PEF >50–75% best or predicted
No features of acute severe asthma

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2
Q

Features of acute severe asthma

A
  • PEF 33–50% best or predicted
  • respiratory rate ≥25/min
  • heart rate ≥110/min
  • inability to complete sentences in one breath
    • SpO2 ≥92%
    • Pulse ≥110 beats/min
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3
Q

Features of life-threatening

asthma

A 
PEF <33% best or predicted
SpO2 <92%
PaO2 <8 kPa
Altered conscious level
Exhaustion
Arrhythmia 
Hypotension 
Cyanosis
Silent chest
Poor respiratory effort
’normal’ PaCO2 (4.6–6.0 kPa)
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4
Q

Clinical features of patients with

severe asthma

A 
severe breathlessness (including too breathless to complete sentences in one breath),
tachypnoea, 
tachycardia, 
silent chest, 
cyanosis,
accessory muscle use, 
altered consciousness or collapse
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5
Q

What initial special test can you do to assess the severity of asthma

A

PEF or FEV1 are useful and valid measures of airway

calibre. PEF is more convenient in the acute situation

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6
Q

What do the BTS guidelines state with regards to oxygen therapy in acute asthma attacks?

A

Give controlled supplementary oxygen to all hypoxaemic patients with acute severe asthma titrated to maintain an SpO2 level of 94–98%. Do not delay oxygen administration in the absence of pulse oximetry but
commence monitoring of SpO2 as soon as it becomes available

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7
Q

What is the initial pharmacological therapy for a moderate asthma attack in the ED?

A

• Salbutamol 5mg nebulized with oxygen and give prednisolone 30mg PO.
• If PEF remains <75%, repeat salbutamol.
• Monitor oxygen saturation, heart rate, and respiratory rate.
(give one puff at a time; according to response, give another puff every 60 seconds up to maximum of 10 puffs)

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8
Q

Pharmacological management in acute severe asthma

A

Give β2 bronchodilator (salbutamol 5 mg) by oxygen-driven nebuliser

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9
Q

Immediate management of life threatening asthma

A

Obtain senior/ICU help now if any life-threatening features are present
IMMEDIATE MANAGEMENT
• Oxygen to maintain SpO2 94–98%
• β2 bronchodilator with ipratropium
- via nebuliser (preferably oxygen-driven), salbutamol
5 mg and ipratropium 0.5 mg

• Prednisolone 40–50 mg orally or IV hydrocortisone
100 mg

Measure arterial blood gases
Markers of severity:
• ‘Normal’ or raised PaCO2 (PaCO2>4.6 kPa; 35 mmHg)
• Severe hypoxia (PaO2 <8 kPa; 60 mmHg)
• Low pH (or high H+)
• Give/repeat salbutamol 5 mg with ipratropium 0.5 mg by oxygen-driven nebuliser after 15 minutes
• Consider continuous salbutamol nebuliser 5–10 mg/hr
• Consider IV magnesium sulphate 1.2–2 g over 20 minutes
• Correct fluid/electrolytes, especially K+ disturbances
• Chest X-ray
• Repeat ABG

THEN
ADMIT
Patient accompanied by a nurse or doctor at all times

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10
Q

What should you be doing at all times during an episode of acute asthma attack in the ED?

A

OBSERVE AND MONITOR
• SpO2
• heart rate
• respiratory rate

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11
Q

What is the next step after back to back nebs and pt is still not improving in moderate and acute severe asthma?

A

Repeat salbutamol 5 mg nebuliser

Give prednisolone 40–50 mg orally

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12
Q

DDx acute asthma

A
  • Acute infective exacerbation of COPD
  • Pulmonary oedema
  • Upper respiratory tract obstruction
  • Pulmonary embolus
  • Anaphylaxis
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13
Q

Hx acute asthma in ED

A
  • Ask about usual and recent treatment
  • Previous acute episodes and their severity
  • Best peak expiratory flow rate (PEF)
  • Have they been admitted to ICU?
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14
Q

Ix acute asthma

A
  • PEF—but may be too ill
  • Arterial blood gases if saturations <92%;
  • CXR (if suspicion of pneumothorax, infection or life-threatening attack)
  • FBC; U&E
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15
Q

Px acute asthma attack still not improving. Next steps?

A

• Discuss patient with senior clinician and ICU team
• Consider IV magnesium sulphate 1.2–2 g over 20 minutes (unless already given)
• Senior clinician may consider use of IV β2
bronchodilator or IV aminophylline or
progression to mechanical ventilation

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16
Q

What is treatment given if patient is improving within 15-30 minutes of life threatening asthma?

A
  • Oxygen to maintain SpO2 94–98%
  • Prednisolone 40–50mg daily or IV hydrocortisone 100 mg 6 hourly
  • Nebulised β2 bronchodilator with ipratropium 4–6 hourly
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17
Q

Side effects of salbutamol

A

tachycardia, arrhythmias, tremor, K+ reduced

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18
Q

What drug class do Hydrocortisone and prednisolone belong do? What do they do?

A

Steroids, reduce inflammation.

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19
Q

ACUTE ASTHMA: IF PATIENT NOT IMPROVING AFTER 15–30 MINUTES?

A

• Continue oxygen and steroids
• Use continuous nebulisation of salbutamol at 5–10 mg/hour if an appropriate nebuliser is available. Otherwise give nebulised salbutamol 5 mg every 15–30
minutes
• Continue ipratropium 0.5 mg 4–6 hourly until patient is improving

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20
Q

How must a patient with acute asthma be monitored?

A

Repeat measurement of PEF 15–30 minutes after starting treatment
• Oximetry: maintain SpO2 >94–98%
• Repeat blood gas measurements within 1 hour of starting treatment if:
- initial PaO2 <8 kPa (60 mmHg) unless subsequent SpO2
>92% or
- PaCO2 normal or raised or
- patient deteriorates
• Chart PEF before and after giving β2 bronchodilator and at least 4 times daily throughout hospital stay

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21
Q

What must you ensure before discharging patients from hospital?

A

Been on discharge medication for 12–24 hours and have had inhaler technique
checked and recorded
• PEF >75% of best or predicted and PEF diurnal variability <25% unless discharge is
agreed with respiratory physician
• Treatment with oral steroids (prednisolone 40–50 mg until recovery - minimum 5
days) and inhaled steroids in addition to bronchodilators
• Own PEF meter and written asthma action plan
• GP follow up arranged within 2 working days
• Follow-up appointment in respiratory clinic within 4 weeks

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22
Q

In acute asthma when do you transfer a patient to ICU?

A

Transfer to ICU accompanied by a doctor prepared to intubate if:
• Deteriorating PEF, worsening or persisting hypoxia, or hypercapnia
• Exhaustion, altered consciousness
• Poor respiratory effort or respiratory arrest

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23
Q

What is the only Ix you need for the immediate management of a px with life threatening asthma?

A

ABG

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24
Q

What are the blood gas markers of a life threatening attack?

A 
• ‘Normal’ (4.6–6 kPa, 35–45 mmHg) PaCO2
• Severe hypoxia: PaO2 <8 kPa
(60 mmHg) irrespective of treatment with
oxygen
• A low pH (or high H+)
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25
Q

Acute exacerbation of COPD: Ix

A

obtain a chest X-ray

measure arterial blood gas tensions and record the inspired oxygen concentration

record an ECG (to exclude comorbidities)

perform a full blood count and measure urea and electrolyte concentrations

measure a theophylline level on admission in people who are taking theophylline therapy

send a sputum sample for microscopy and culture if the sputum is purulent

take blood cultures if the person has pyrexia

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26
Q

What is the first choice oral antibiotic in px with (infective) COPD exacerbation?

A

First-choice oral antibiotics (empirical treatment or guided by most recent sputum culture and susceptibilities)

Amoxicillin-500 mg TDS 5 days
or
Doxycycline 200 mg first day  then 100 mg OD for 5‑day course in total 
or
Clarithromycin 500 mg BD
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27
Q

What is the first choice IV antibiotic in px with (infective) COPD exacerbation?

A 
Amoxicillin 500 mg TDS
or
Co-amoxiclav 1.2 g TDS
or
Clarithromycin 500 mg BD
or
Co-trimoxazole 960 mg BD
or
Piperacillin with tazobactam 4.5 g TDS
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28
Q

What is the Oral second line (if no improvement after at least 2 to 3 days) in acute exacerbation of COPD?

A

Use a first line antibacterial from a different class to the antibacterial used previously.
Alternative if at high risk of treatment failure:
co-amoxiclav 500/125 mg TDS for 5 days
or
levofloxacin 500 mg OD for 5 days-(with specialist advice if co-amoxiclav or co-trimoxazole cannot be used; consider safety issues)
or
co-trimoxazole 960 mg BD for 5 days (only when sensitivities are available and there is good reason to use co-trimoxazole over single antibacterials).

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29
Q

When should IV abx be reviewed?

A

Review intravenous antibiotics by 48 hours and consider stepping down to oral antibiotics where possible.

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30
Q

Causes of pneumothorax

A

• Spontaneous (especially in young thin men) due to rupture of a subpleural bulla
• Chronic lung disease: asthma; COPD; cystic fibrosis; lung fibrosis; sarcoidosis
• Infection: TB; pneumonia; lung abscess
• Traumatic: including iatrogenic (CVP line insertion, pleural aspiration or biopsy,
percutaneous liver biopsy, positive pressure ventilation).
• Carcinoma
• Connective tissue disorders: Marfan’s syndrome, Ehlers–Danlos syndrome

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31
Q

Symptoms of pneumothorax

A
  • Can be asymptomatic (especially in fit young people with small pneumothoraces)
  • sudden onset of dyspnoea and/or pleuritic chest pain.
  • Patients with asthma or COPD may present with a sudden deterioration.
  • Mechanically ventilated patients can suddenly develop hypoxia or an increase in ventilation pressures.
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32
Q

Signs of pneumothorax

A
  • Reduced expansion,
  • Hyper-resonance to percussion
  • Diminished breath sounds on the affected side.
  • With a tension pneumothorax, the trachea will be deviated away from the affected side and the patient will be very unwell.
33
Q

What is tension pneumothorax?

A

Air drawn into the pleural space with each inspiration has no route of escape during expiration. The mediastinum is pushed over into the contralateral hemithorax, kinking and compressing the great veins. Unless the air is rapidly re- moved, cardiorespiratory arrest will occur.

34
Q

Signs of tension pneumothorax

A

Respiratory distress, tachycardia, hypotension, distended neck veins, trachea deviated away from side of pneumothorax. Increased percussion note, reduced air entry/breath sounds on the affected side.

35
Q

Treatment of tension pneumothorax

A

To remove the air, insert a large-bore (14–16G) needle with a syringe, partially filled with 0.9% saline, into the 2nd intercostal interspace in the midclavicular line on the side of the suspected pneumothorax. Remove plunger to allow the trapped air to bubble through the syringe (with saline as a water seal) until a chest tube can be placed. Alternatively, insert a large-bore Venflon in the same location.
 Do this before requesting a CXR.
 Then insert a chest drain.

36
Q

Name some organsims that cause pneumonia

A

• Community-acquired pneumonia (CAP) may be primary or secondary to underlying disease:
Streptococcus pneumoniae
• Haemophilus influenzae.
• Mycoplasma pneumoniae.
• Staphylococcus aureus found more commonly in ICU patients.
• Legionella species and Chlamydia psittaci.
• Viruses including influenza account for up to 15%

Hospital-acquired (nosocomial; >48h after hospital admission). Most commonly Gram negative enterobacteria or Staph. aureus. Also Pseudomonas (esp in COPD), Klebsiella, Bacteroides, and Clostridia..

37
Q

Symptoms of pneumonia

A
  • Fever
  • rigors,
  • malaise
  • cough
  • purulent sputum (classically ‘rusty’ with pneumococcus)
  • haemoptysis
  • pleuritic chest pain.
  • dyspnoea
  • anorexia
38
Q

Sx of pneumonia

A

Pyrexia, cyanosis, confusion (can be the only sign in the elderly—may also be hypothermic), tachypnoea, tachycardia, hypotension, signs of consolidation (diminished expansion, dull percussion note, increase tactile vocal fremitus/vocal resonance, bronchial breathing), and a pleural rub

39
Q

Pneumonia Ix

A

•Assess oxygenation: oxygen saturation, (ABGs if SaO2 <92% or severe pneumonia) and BP
•Blood tests: FBC, U&E, LFT, CRP, blood cultures.
•Sputum for microscopy and culture.
In severe cases:
•check for Legionella (sputum culture, urine antigen)
• atypical organism/viral serology (PCR sputum/BAL, complement fixation tests acutely, paired serology)
•and check for pneumococcal antigen in urine.
•Pleural fluid may be aspirated for culture.
•Consider bronchoscopy and bronchoalveolar lavage if patient is immunocompromised or on ITU.

40
Q

Complications of pneumonia

A
  • Respiratory failure
  • Hypotension
  • AF
  • Pleural effusion
  • empyema
  • Lung abscess
  • septicaemia, pericarditis, myocarditis,
  • cholestatic jaundice- may be due to sepsis or secondary to anti- biotic therapy (particularly flucloxacillin and co-amoxiclav)
  • acute kidney injury
41
Q

What is the mechanism of PE?

A

Venous thrombi, usually from DVT, pass into the pulmonary circulation and block blood flow to lungs. The source is often occult.

42
Q

Risk factors for PE

A
  • Malignancy.
  • Surgery—especially pelvic and lower limb (much lower if prophylaxis used).
  • Immobility.
  • Combined oral contraceptive pill (there is also a slight risk attached to HRT).
  • Previous thromboembolism and inherited thrombophilia
43
Q

Sx PE

A

Hypotension, tachycardia, gallop rhythm, raised JVP, loud P2, right ventricular heave,
pleural rub, tachypnoea, cyanosis, AF.

44
Q

Symptoms of PE

A

Acute dyspnoea, pleuritic chest pain, haemoptysis, and syncope.

45
Q

PE Ix

A
  • U&;E, FBC, baseline clotting.
  • ECG: commonly normal or sinus tachycardia; right ventricular strain pattern V1–3, right axis deviation, RBBB, AF, may be deep S waves in I, Q waves in III, inverted T waves in III (‘SI QIII TIII’).
  • CXR: often normal; decreased vascular markings, small pleural effusion. Wedge-shaped area of infarction. Atelectasis.
  • ABG: hyperventilation + poor gas exchange: Pa O2 reduced, Pa CO2 reduced, pH often raised
  • Serum D-dimer: high sensitivity but low specificity (high if thrombosis, inflammation, post-op, infection, malignancy) excludes PE if normal D-dimer.
  • CT pulmonary angiography (CTPA) is sensitive and specific in determining if emboli are in pulmonary arteries. If unavailable, a ventilation–perfusion (V/Q) scan can aid diagnosis. If V/Q scan is equivocal, pulmonary angiography or bilateral venograms may help (MRI venography or plethysmography are alternatives).
46
Q

Mx PE

A

• Try to prevent further thrombosis with compression stockings.
• Low molecular weight heparin (LMWH) concurrently with warfarin until INR >2.
• If obvious remedial cause, 6 weeks of warfarin (p345) may be enough; otherwise, continue for ≥3–6 months (long term if recurrent emboli, or underlying
malignancy).
• Is there an underlying cause, eg thrombophilic tendency, malignancy (especially prostate, breast, or pelvic cancer), SLE, or polycythaemia?
If good story and signs, make the diagnosis.
Start treatment before definitive investigations: most PE deaths occur within 1h.

47
Q

how to prevent PE

A

Early post-op mobilization is the simplest method; also consider:
• Antithromboembolic (TED) stockings.
• Low molecular weight heparin prophylaxis SC.
• Avoid contraceptive pill if at risk, eg major or orthopaedic surgery.
• Recurrent PEs may be prevented by anticoagulation.

48
Q

What is obstructive effect vs restrictive effect in spirometry?

A

Obstructive defect (eg asthma, COPD) FEV1 is reduced more than the FVC, and the FEV1/FVC ratio is <75%.

Restrictive defect (eg lung fibrosis) FVC is reduced and the FEV1/FVC ratio is same or increased. Other
causes: sarcoidosis; pneumoconiosis, interstitial pneumonias; connective tissue diseases; pleural effusion; obesity; kyphoscoliosis; neuromuscular problems.
49
Q

What do TLC and RV tell us in lung disease?

A

Total lung capacity (TLC) and residual volume (RV) are useful in distinguishing obstructive and restrictive diseases. TLC and RV are increased in obstructive airways disease and reduced in restrictive lung diseases and musculoskeletal abnormalities.

50
Q

gas transfer coefficient is affected in which conditions?

A

Low in emphysema and interstitial lung disease, high in alveolar haemorrhage

51
Q

signs of consolidation

A

diminished expansion, dull percussion note, increase tactile vocal fremitus/vocal resonance, bronchial breathing

52
Q

Management of pneumonia

A
  • Antibiotics : orally if not severe and not vomiting; severe give by IV.
  • Oxygen: keep PaO2 >8.0 and/or saturation ≥94%.
  • IV fluids (anorexia, dehydration, shock) and VTE prophylaxis.
  • Analgesia if pleurisy—eg paracetamol 1g/6h.
  • Consider ITU if shock, hypercapnia, or uncorrected hypoxia.
  • If failure to improve, or CRP remains high, repeat CXR and look for progression/complications.
  • Follow-up: at 6 weeks (±CXR).
53
Q

clinical features of pneumococcal pneumonia

A

fever, pleurisy, herpes labialis

54
Q

In which patients is pneumococcal pneumonia more common?

A 
elderly, 
alcoholics, 
post-splenectomy, 
immuno-suppressed, and 
patients with chronic heart failure/pre-existing lung disease
55
Q

Abx pseudomonas pneumonia

A

anti- pseudomonal penicillin, ceftazidime, meropenem, or ciprofloxacin + aminoglycoside.
Consider dual therapy to minimize resistance.

56
Q

Causes of lung abcess

A
  • Inadequately treated pneumonia •Aspiration (eg alcoholism, oesophageal obstruction, bulbar palsy) •Bronchial obstruction (tumour, foreign body)
  • Pulmonary infarction •Septic emboli (septicaemia, right heart endocarditis, IV drug use) •Subphrenic or hepatic abscess.
57
Q

Clinical features of lung abcess

A

Swinging fever; cough; purulent, foul-smelling sputum; pleuritic chest pain; haemoptysis; malaise; weight loss. Look for: finger clubbing; anaemia; crepitations. Empyema develops in 20–30%.

58
Q

Lung abcess: Ix

A

Blood:
FBC (anaemia, neutrophilia), ESR, CRP, blood cultures.
Imaging
CXR: walled cavity, often with a fluid level. Consider CT scan to exclude obstruction, and bronchoscopy to obtain diagnostic specimens
Special:
Sputum microscopy, culture, and cytology.

59
Q

Treatment of lung abcess

A
  • Antibiotics as indicated by sensitivities; continue until healed (4–6 wks).
  • Postural drainage.
  • Repeated aspiration, antibiotic instillation, or surgical excision may be required
60
Q

Pathology of bronchioectasis

A

Chronic infection of the bronchi and bronchioles leading to permanent dilatation of these airways

61
Q

Organisms causing bronchioectasis

A
  • H. influenzae
  • Strep. pneumoniae;
  • Staph. aureus;
  • Pseudomonas aeruginosa.
62
Q

Causes of Bronchiectasis

A
  • Congenital: cystic fibrosis (CF); Young’s syndrome; primary ciliary dyskinesia; Kartagener’s syndrome
  • Post-infection: measles; pertussis; bronchiolitis; pneumonia; TB; HIV.
  • Other: bronchial obstruction (tumour, foreign body); allergic bronchopulmonary aspergillosis (ABPA) hypogammaglobulinaemia; rheumatoid arthritis; ulcerative colitis; idiopathic
63
Q

Symptoms of Bronchiectasis

A
  • persistent cough
  • copious purulent sputum
  • intermittent haemoptysis.
64
Q

Sx Bronchiectasis

A

finger clubbing; coarse inspiratory crepitations; wheeze (asthma, COPD, ABPA)

65
Q

Complications of Bronchiectasis

A

pneumonia, pleural effusion; pneumothorax; haemoptysis; cerebral abscess; amyloidosis.

66
Q

Bronchiectasis: Ix

A

Bedside
•Spirometry often shows an obstructive pattern; reversibility should be assessed.
Imaging
•CXR: cystic shadows, thickened bronchial walls (tramline and ring shadows).
•HRCT chest: to assess extent and distribution of disease.
•Bronchoscopy to locate site of haemoptysis, exclude obstruction and obtain samples for culture.
Microbiology
•Sputum culture.
Other tests: serum immunoglobulins; CF sweat test; Aspergillus precipitins or skin-prick test.

67
Q

Management of bronchiectasis

A

Conservative
•Chest physiotherapy may aid sputum expectoration and mucous drainage.
Medical
•Antibiotics should be prescribed according to bacterial sensitivities. Patients known to culture Pseudomonas will require either oral ciprofloxacin or IV antibiotics. If ≥3 exacerbations a year consider long-term antibiotics.
•Bronchodilators (eg nebulized salbutamol) may be useful in patients with asthma, COPD, CF, ABPA
•Corticosteroids (eg prednisolone) for ABPA.
•Postural drainage should be performed twice daily.

•Surgery may be indicated in localized disease or to control severe haemoptysis.

68
Q

Signs of CF in neonates

A

Failure to thrive; meconium ileus; rectal prolapse.

69
Q

Respiratory features of CF in children/young adults

A

•Respiratory: cough; wheeze; recurrent infections; bronchiectasis; pneumothorax; haemoptysis; respiratory failure; cor pulmonale.

70
Q

GI features of CF in children/young adults

A

•Gastrointestinal: pancreatic insufficiency (diabetes mellitus, steatorrhoea); distal intestinal obstruction syndrome (meconium ileus equivalent); gallstones; cirrhosis.

71
Q

Other features of CF in children/young adults

A

•Other: male infertility; osteoporosis; arthritis; vasculitis; nasal polyps; sinusitis; and hypertrophic pulmonary osteoarthropathy (HPOA).

72
Q

How is the diagnosis of CF usually made?

A
  • Sweat test: sweat sodium and chloride >60mmol/L; chloride usually > sodium. •Genetics: screening for known common CF mutations should be considered.
  • Faecal elastase is a simple and useful screening test for exocrine pancreatic dysfunction.
73
Q

Tests for CF

A

Bedside
•Spirometry: obstructive defect.
•Blood: FBC, U&E, LFT; clotting; vitamin A, D, E levels; annual glucose tolerance test •Bacteriology: cough swab, sputum culture.
•Radiology:
CXR; hyperinflation; bronchiectasis.
Abdominal ultrasound: fatty liver; cirrhosis; chronic pancreatitis;
•Aspergillus serology/skin test (20% develop ABPA, p168).
•Biochemistry: faecal fat analysis.

74
Q

What members of an MDT team may be involved in the care of a patient with CF?

A

physician, GP, physiotherapist, specialist nurse, and dietician, with attention to psychosocial as well as physical wellbeing

75
Q

How are patients with CF managed?

A

Physiotherapy regularly (postural drainage, active cycle breathing techniques or forced expiratory techniques). Antibiotics are given for acute infective exacerbations and prophylactically (PO or nebulized).
Mucolytics may be useful (eg DNase, ie Dornase alfa, 2.5mg daily nebulized).
Bronchodilators.

76
Q

How will GI symptoms experienced by patients with CF be managed?

A

Pancreatic enzyme replacement; fat soluble vitamin supplements (A, D, E, K); ursodeoxycholic acid for impaired liver function; cirrhosis may require liver transplantation

77
Q

What other treatments may be available to patients with CF related to other symptoms experienced?

A

Treatment of CF-related diabetes; screening for and treatment of osteoporosis; treatment of arthritis, sinusitis, and vasculitis; fertility and genetic counselling.

78
Q

Type 1 resp failure

A
  • Pneumonia
  • Pulmonary oedema
  • PE
  • Asthma
  • Emphysema
  • Pulmonary fibrosis
  • ARDS
79
Q

Type 2 resp failure

A
  • Pulmonary disease: asthma, COPD, pneumonia, end-stage pulmonary fibrosis, obstructive sleep apnoea
  • Reduced respiratory drive: sedative drugs, CNS tumour or trauma.
  • Neuromuscular disease: cervical cord lesion, diaphragmatic paralysis, poliomyelitis, myasthenia gravis, Guillain–Barré syndrome.
  • Thoracic wall disease: flail chest, kyphoscoliosis.

Specialties (4 decks)

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