ABCDE breathing Flashcards

1
Q

target oxygen saturation level in acute asthma

A

94-98

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2
Q

assessment ABCDE breathing

A

Vitals:
- RR
- SpO2

look:
- cyanosis
- increased work of breathing
- cough
- inability to speak in full sentences

feel:
- tracheal position
- chest expansion
- percussion

listen:
- breath sounds and added sounds

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3
Q

interventions and investigations ABCDE breathing

A

if o2 sats low
- oxygen 15L NRM

  • ABG
  • CXR
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4
Q

what are the different types of oxygen delivery and their corresponding FiO2 range limits (WARD BASED)

A

Nasal cannula: 24 – 44% oxygen
Simple face mask: 40 – 60% oxygen
Venturi masks: 24 – 60% oxygen
Face mask with reservoir (non-rebreather mask): 60 – 95% oxygen

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5
Q

why are venturi masks useful?

A

Venturi masks can be used to deliver exact concentrations of oxygen. The most common use for these is in patients with COPD who are at risk of retaining carbon dioxide if the FiO2 is too high

this means it is a ‘fixed performance device’ - the fraction of inspired oxygen (FiO2) remains constant regardless of inspiratory flow rates

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6
Q

what is PEEP

A

Positive end-expiratory pressure (PEEP)

End-expiratory pressure refers to the pressure that remains in the airways at the end of exhalation.
Additional pressure in the airways at the end of exhalation stops the airways from collapsing.

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7
Q

what oxygen delivery methods have PEEP

A

High-flow nasal cannula
CPAP
Non-invasive ventilation (BiPAP)
Mechanical ventilation

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8
Q

what intervention may be needed for type 1 resp failure if normal O2 delivery methods not adequate

A

CPAP

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9
Q

what intervention may be needed for type 2 resp failure if normal O2 delivery methods not adequate

A

biPAP

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10
Q

how are NIV and BiPAP different?

A

NIV is a form of breathing support delivering air, usually with added oxygen, via a facemask by positive pressure, used in respiratory failure.

The term NIV is often used interchangeably with the trade name BiPAP (Bi-level Positive Airway Pressure), which is the most commonly used machine in the UK.

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11
Q

is CPAP a type of NIV?

A

CPAP does not technically involve “ventilation”, as it provides constant pressure and the job of ventilation is still dependent on the respiratory muscles. Therefore, CPAP is not technically classed as non-invasive ventilation (NIV).

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12
Q

what is ECMO

A

Blood is removed from the body, passed through a machine where oxygen is added and carbon dioxide is removed, then pumped back into the body. The process is similar to haemodialysis but for respiratory support rather than renal support.
ECMO is only used short-term, where there is a potentially reversible cause of respiratory failure.

Extracorporeal membrane oxygenation (ECMO) is the most extreme form of respiratory support and is very rarely used. It is used where respiratory failure is not adequately managed by intubation and ventilation.

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13
Q

what is Cheyne-Stokes respiration

A

cyclical apnoeas, with varying depth of inspiration and rate of breathing. May be caused by stroke, raised intracranial pressure, pulmonary oedema, opioid toxicity, hyponatraemia or carbon monoxide poisoning.

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14
Q

what is Kussmaul’s respiration

A

deep, sighing respiration associated with metabolic acidosis (e.g. diabetic ketoacidosis).

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15
Q

tracheal deviation causes? which way would it go?

A

The trachea deviates away from tension pneumothorax and large pleural effusions.

The trachea deviates towards lobar collapse and pneumonectomy.

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16
Q

cause of symmetrical reduction in chest expansion

A

pulmonary fibrosis reduces lung elasticity, restricting overall chest expansion.

hyperinflation eg copd

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17
Q

causes of asymmetrical reduction in chest expansion

A

pneumothorax, pneumonia and pleural effusion can all cause ipsilateral reduced chest expansion.

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18
Q

cause stony dullness

A

typically caused by an underlying pleural effusion.

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19
Q

cause dullness to percussion

A

suggests increased tissue density (e.g. cardiac dullness, consolidation, tumour, lobar collapse).

Stony dullness: typically caused by an underlying pleural effusion.

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20
Q

what is bronchial breathing

A

harsh-sounding (similar to auscultating over the trachea), inspiration and expiration are equal and there is a pause between. This type of breath sound is associated with consolidation.

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21
Q

what is wheeze? causes?

A

a high-pitched, musical, adventitious lung sound produced by airflow through an abnormally narrowed or compressed airway(s)
Wheezing can be either expiratory, inspiratory, or both. Expiratory wheezing is more common and may mean that a person has a mild blockage causing the wheezing.

asthma, COPD and bronchiectasis. pulmonary oedema

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22
Q

what are coarse crackles?

A

discontinuous, brief, popping lung sounds typically associated with fluid/secretions

pneumonia, bronchiectasis and pulmonary oedema.

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23
Q

what are fine crackles? causes?

A

sounding similar to the noise generated when separating velcro. Fine end-inspiratory crackles are associated with pulmonary fibrosis.

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24
Q

what is type 1 resp failure? pathophysiology?

A

low PaO2, normal PaCO2 (1 thing wrong)
pH likely normal

ventilation/perfusion (V/Q) mismatch

As a result of the VQ mismatch, PaO2 falls and PaCO2 rises. The rise in PaCO2 rapidly triggers an increase in a patient’s overall alveolar ventilation, which corrects the PaCO2 but not the PaO2 due to the different shape of the CO2 and O2 dissociation curves. The end result is hypoxaemia (PaO2 < 8 kPa /60mmHg) with normocapnia (PaCO2 < 6.0 kPa / 45mmHg).¹

Reduced ventialtion and normal perfusion:
- pulmonary oedema
- bronchoconstriction
- pneumonia

Reduced perfusion with normal ventilation:
- pulmonary embolism

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25
what is type 2 resp failure? pathophysiology?
low PaO2, high PaCO2 (2 things wrong) alveolar hypoventilation eg: - Pulmonary disease (COPD, asthma, pulmonary fibrosis, obstructive sleep apnoea) - Reduced respiratory drive – can be a result of sedentary drugs, trauma or CNS tumour - Neuromuscular disease – e.g. cervical cord lesion, diaphragmatic paralysis, polio, myasthaenia gravis - Thoracic wall disease - e.g. Flail chest, kyphoscoliosis, hyperinflation, large pleural effusions, obesity, and thoracoplasty
26
When to suspect resp acidosis? causes?
low pH raised PaCO2 things that cause type 2 resp failure - Pulmonary disease (COPD, asthma, pulmonary fibrosis, obstructive sleep apnoea) - Reduced respiratory drive – can be a result of sedentary drugs, trauma or CNS tumour - Neuromuscular disease – e.g. cervical cord lesion, diaphragmatic paralysis, polio, myasthaenia gravis - Thoracic wall disease - e.g. Flail chest, kyphoscoliosis, hyperinflation, large pleural effusions, obesity, and thoracoplasty
27
resp acidosis with metabolic compensation makes you think?
During an acute episode of respiratory acidosis, bicarbonate cannot be produced fast enough to compensate for the rising carbon dioxide. Raised bicarbonate indicates that the patient chronically retains CO2. Their kidneys have responded by producing additional bicarbonate to balance the acidic CO2 and maintain a normal pH. This is seen in patients with chronic obstructive pulmonary disease (COPD). In an acute exacerbation of COPD, the kidneys cannot keep up with the rising level of CO2, so the patient becomes acidotic despite having higher bicarbonate than someone without COPD.
28
when to suspect respiratory alkalosis? causes?
high pH low PaCO2 This is due to hyperventilation Respiratory alkalosis occurs when a patient has a raised respiratory rate and “blows off” too much CO2. They are breathing too fast and getting rid of too much CO2. There will be a high pH (alkalosis) and a low PaCO2. Anxiety (i.e. panic attack) - will have high PaO2 Pain: causing an increased respiratory rate. Hypoxia: resulting in increased alveolar ventilation in an attempt to compensate. Pulmonary embolism - will have low PaO2 Pneumothorax Iatrogenic (e.g. excessive mechanical ventilation)
29
how to tell the difference between resp alkalosis caused by hyperventilation syndrome vs PE
Patients with a PE will have a low PaO2, whereas patients with hyperventilation syndrome will have a high PaO2.
30
What would an ABG show acute asthma
The more severe the obstruction, the lower the PaO2 will be Low CO2 and resulting respiratory alkalosis suggests that the patient is breathing hard and blowing of CO2 Normal CO2 suggests the patient may be tiring and is a sign of life-threatening asthma High CO2 is a sign of near-fatal acute asthma as the patient is no longer breathing well. if the patient becomes hypercapnic they are likely to become acidotic. In very severe cases this can result in metabolic acidosis.
31
signs of co2 retention
Confusion – as a result of peripheral vasodilation Asterixis (renal failure, type 2 resp failure, liver failure) Warm extremeties Bounding pulse Morning headache – CO2 particularly high at these times.
32
if someone with copd and co2 retention needs treatment for type 2 resp failure
in an acute setting, if unknown or very unwell give 15L 100% O2 NRM if known retentive: Give controlled oxygen therapy, starting at 24% O2 Recheck the ABG after 20 minutes – if the PaCO2 is steady or lower, then you can increase the O2 to 28%. If the PaCO2 has risen >1.5kPa– then consider giving a respiratory stimulant such as doxapram (1.5-4mg/min IV) or assisted ventilation. You can also see CO2 retention as physical signs – the patient will become drowsy and confused If this fails consider intubation / ventilation
33
pathophysiology respiratory failure in copd
Significant ventilation/perfusion mismatching with a relative increase in the physiological dead space leads to hypercapnia and hence acidosis. This is largely the result of a shift to a rapid shallow breathing pattern and a rise in the dead space/tidal volume ratio of each breath. This breathing pattern results from adaptive physiological responses which lessen the risk of respiratory muscle fatigue and minimise breathlessness.
34
what are reduced breath sounds? causes?
diminished or absent breath sounds - pleural effusion - pneumothorax
35
classifications pneumothoraces
Spontaneous --> primary sponteaneous --> secondary spontaneous Traumatic pneumothorax Iatrogenic pneumothorax any of above can cause Tension pneumothorax
36
what is the cuase of spontaenous pneumothroax in 3-6% of menstruating women?
endometriosis within the thorax
37
presentation pneumothorax
Symptoms tend to come on suddenly: dyspnoea chest pain: often pleuritic Signs hyper-resonant lung percussion reduced breath sounds reduced lung expansion tachypnoea tachycardia
38
features of tension pneumothorax
respiratory distress tracheal deviation away from the side of the pneumothorax Tachycardia Tension pneumothorax → obstructive shock jugular venous distension haemodynamic instability (hypotension)
39
causes of secondary spontaneous pneumothroax
pre-existing lung disease, such as COPD, asthma, cystic fibrosis, lung cancer, Pneumocystis pneumonia. Certain connective tissue diseases such as Marfan's syndrome are also a risk factor
40
Management of tension pneumothroax
1. Insert large bore cannula in 2nd intercostal space in the midclavicular line (above rib to avoid vascular/neuro bundle) In patients with tension pneumothorax, perform chest decompression before imaging only if they have either haemodynamic instability or severe respiratory compromise. 2. Next, insert chest drain into triangle of safety
41
what makes up the triangle of safety
5th intercostal space (or the inferior nipple line) Midaxillary line (or the lateral edge of the latissimus dorsi) Anterior axillary line (or the lateral edge of the pectoralis major)
42
Management spontaneous pneumothorax
1) is the pt symptomatic/physiologically compromised - no --> conservative management - yes --> assess for high risk features 2) high risk features: haemodynamic compromise (suggesting a tension pneumothorax) significant hypoxia bilateral pneumothorax underlying lung disease ≥ 50 years of age with significant smoking history haemothorax - no HRF --> choice of conservative, ambulatory device (pleural vent) or needle aspiration - yes HRF --> chest drain if safe 3) is it safe to drain? - 2cm laterally or apically on chest x-ray, or - any size on CT scan which can be safely accessed with radiological support
43
management iatrogenic pneumothorax
less likelihood of recurrence than spontaneous pneumothorax majority will resolve with observation, if treatment is required then aspiration should be used ventilated patients need chest drains, as may some patients with COPD
44
management persistent/recurrent pneumothorax
consider video-assisted thoracoscopic surgery (VATS) to allow for mechanical/chemical pleurodesis +/- bullectomy.
45
discharge advice pneumothorax
- no smoking - might not be able to fly The British Thoracic Society used to recommend not travelling by air for a period of 6 weeks but this has now been changed to 1 week post check x-ray - permenantly avoid scuba dibing
46
History and examination acute asthma
Airway: can they talk in complete sentences? Cyanosis? Breathing: RR, SpO2, silent chest? Feeble respiratory effort? Circulation: HR? BP? Disability: GCS? Confusion? Everything else: PEFR, ECG Arterial blood gas (ABG) is indicated if the patient's SpO₂ is <92% or PEFR is ≤30% of best or predicted. (life threatening signs)
47
Define moderate acute asthma
PEFR 50-75% best or predicted Oxygen saturations >92 Speech normal RR adults < 25 RR >5 years < 30 RR 1-5 years <40 Pulse adults < 110 bpm Pulse >5 years <125 bpm Pulse 1-5 years <140 bpm
48
Define acute severe asthma
PEFR 33 - 50% best or predicted Oxygen saturations >92 Can't complete sentences RR adults > 25 RR >5 years > 30 RR 1-5 years >40 Pulse adults > 110 bpm Pulse >5 years > 125 bpm Pulse 1-5 years > 140 bpm
49
Define life threatening asthma
PEFR < 33% best or predicted Oxygen sats < 92% 'Normal' pC02 (4.6-6.0 kPa) Silent chest Cyanosis Poor respiratory effort Bradycardia Dysrhythmia Hypotension Exhaustion Confusion Coma
50
Define near-fatal asthma
Raised PaCO₂ (>6kPa) and/or need for mechanical ventilation.
51
Criteria for admission/discharge at start of presentation
Admit patients with any feature of a life-threatening or near-fatal asthma attack. Admit patients with any feature of a severe asthma attack persisting after initial treatment. Patients whose peak flow is greater than 75% best or predicted one hour after initial treatment may be discharged from ED, unless there are other reasons why admission may be appropriate.
52
Who needs referring to ICU
requiring ventilatory support with acute severe or life-threatening asthma, who is failing to respond to therapy, as evidenced by: - deteriorating PEF - persisting or worsening hypoxia - hypercapnia - ABG analysis showing pH or H+ - exhaustion, feeble respiration - drowsiness, confusion, altered conscious state - respiratory arrest.
53
What would an ABG show acute asthma
The more severe the obstruction, the lower the PaO2 will be High CO2 and resulting respiratory alkalosis suggests that the patient is breathing hard and blowing of CO2 Normal CO2 suggests the patient may be tiring and is a sign of life-threatening asthma High CO2 is a sign of near-fatal acute asthma as the patient is no longer breathing well. if the patient becomes hypercapnic they are likely to become acidotic. In very severe cases this can result in metabolic acidosis.
54
What are the sections of acute asthma management
- Oxygen - inhaled bronchodilators - steroids - second line - follow up
55
Management of acute asthma
1. If O2 sats <94 or severe/LT features: Oxygen 15L non-rebreather, titrate down to achieve SpO2 94-98 2. Inhaled B2 agonist (salbutamol) - Adult and children 2-10 puffs repeat every 10-20 minutes - give via large volume spacer - each puff is equivalent to 100 micrograms. If not controlled or LT → hospital - OR inhalation of nebulised solution. Adult 5mg, repeat every 20-30 mins or when required - give via oxygen-driven nebuliser. Child 1 month - 4 years 2.5mg, repeat every 20-30 mins or when required - give via oxygen-driven nebuliser. In between ages 2.5-5 mg 3. Add nebulised ipratropium bromide to β₂ agonist treatment for patients with acute severe or life-threatening asthma or those with a poor initial response to β₂ agonist therapy. - Adult (0.5 mg 4–6 hourly) - Aged > 1 year 250 micrograms/dose mixed with nebulised B2 agonist solution Steroids - Oral prednisolone. (10 mg of prednisolone If < 2 years of age, 20 mg if aged 2–5 years and 40 mg for children >5 years ) 40-50mg in adults - IV hydrocortisone (4 mg/kg repeated six hourly - max per dose 100mg - adults give 100mg) if can’t take oral. Give until oral pred can be given Second line 4. Magnesium sulphate - Children - Nebulised magnesium sulphate (150 mg magnesium sulphate to each nebulised salbutamol and ipratropium in the first hour in children with a short duration of acute severe asthma symptoms presenting with an SpO2 <92%) - Adults - Consider giving a single dose of IV magnesium sulphate to patients with acute severe asthma (PEF <50% best or predicted) who have not had a good initial response to inhaled bronchodilator therapy. Magnesium sulphate (1.2–2 g IV infusion over 20 minutes) should only be used following consultation with senior medical staff. - In children who respond poorly to first-line treatments, consider the addition of intravenous magnesium sulphate as first-line intravenous treatment (40 mg/kg/day). 5. Children IV salbutamol (single bolus dose 15 micrograms/kg over 10 minutes) in a severe asthma attack 6. Children IV aminophylline - severe or life-threatening asthma unresponsive to maximal doses of bronchodilators and steroids. 7. Anaesthetics and ICU
56
Oxygen acute asthma
If O2 sats <94 or severe/LT features: Oxygen 15L non-rebreather, titrate down to achieve SpO2 94-98
57
inhaled bronchodialtors acute asthma
Inhaled B2 agonist (salbutamol) - Adult and children 2-10 puffs repeat every 10-20 minutes - give via large volume spacer - each puff is equivalent to 100 micrograms. If not controlled or LT → hospital - OR inhalation of nebulised solution. Adult 5mg, repeat every 20-30 mins or when required - give via oxygen-driven nebuliser. Child 1 month - 4 years 2.5mg, repeat every 20-30 mins or when required - give via oxygen-driven nebuliser. In between ages 2.5-5 mg 3. Add nebulised ipratropium bromide to β₂ agonist treatment for patients with acute severe or life-threatening asthma or those with a poor initial response to β₂ agonist therapy. - Adult (0.5 mg 4–6 hourly) - Aged > 1 year 250 micrograms/dose mixed with nebulised B2 agonist solution
58
steroids acute asthma
- Oral prednisolone. (10 mg of prednisolone If < 2 years of age, 20 mg if aged 2–5 years and 40 mg for children >5 years ) 40-50mg in adults - IV hydrocortisone (4 mg/kg repeated six hourly - max per dose 100mg - adults give 100mg) if can’t take oral. Give until oral pred can be given
59
Magnesium sulphate acute asthma
Magnesium sulphate - Children - Nebulised magnesium sulphate (150 mg magnesium sulphate to each nebulised salbutamol and ipratropium in the first hour in children with a short duration of acute severe asthma symptoms presenting with an SpO2 <92%) - Adults - Consider giving a single dose of IV magnesium sulphate to patients with acute severe asthma (PEF <50% best or predicted) who have not had a good initial response to inhaled bronchodilator therapy. Magnesium sulphate (1.2–2 g IV infusion over 20 minutes) should only be used following consultation with senior medical staff. - In children who respond poorly to first-line treatments, consider the addition of intravenous magnesium sulphate as first-line intravenous treatment (40 mg/kg/day).
60
dose salbutamol acute asthma
pMDI and spacer Adult and children 2-10 puffs repeat every 10-20 minutes - give via large volume spacer - each puff is equivalent to 100 micrograms. If not controlled or LT → hospital Nebulised inhalation of nebulised solution- 2.5mg, repeat every 20-30 mins or when required - give via oxygen-driven nebuliser
61
dose ipatropium bromide acute atshma
nebulised ipratropium bromide to β₂ agonist treatment for patients with acute severe or life-threatening asthma or those with a poor initial response to β₂ agonist therapy. Adult (0.5 mg 4–6 hourly) Aged > 1 year 250 micrograms/dose mixed with nebulised B2 agonist solution
62
prednisolone dose acute asthma
Oral prednisolone. (10 mg of prednisolone If < 2 years of age, 20 mg if aged 2–5 years and 40 mg for children >5 years ) 40-50mg in adults
63
IV hydrocortisone acute asthma dose
IV hydrocortisone (4 mg/kg repeated six hourly - max per dose 100mg - adults give 100mg) if can’t take oral. Give until oral pred can be given
64
children magnesium sulphate dose acute asthma
Nebulised magnesium sulphate (150 mg magnesium sulphate to each nebulised salbutamol and ipratropium in the first hour in children with a short duration of acute severe asthma symptoms presenting with an SpO2 <92%) In children who respond poorly to first-line treatments, consider the addition of intravenous magnesium sulphate as first-line intravenous treatment (40 mg/kg/day).
65
adults magnesium sulphate dose acute asthma
Consider giving a single dose of IV magnesium sulphate to patients with acute severe asthma (PEF <50% best or predicted) who have not had a good initial response to inhaled bronchodilator therapy. Magnesium sulphate (1.2–2 g IV infusion over 20 minutes) should only be used following consultation with senior medical staff.
66
Children IV salbutamol dose
single bolus dose 15 micrograms/kg over 10 minutes
67
when can children be discharged following an asthma attack?
Children can be discharged when stable on 3-4 hourly inhaled bronchodilators that can be continued at home. PEF and/or FEV1 should be >75% of best or predicted and SpO2 >94%.
68
Follow up after acute asthma adults
adults - the patient’s primary care practice is informed within 24 hours of discharge from the emergency department or hospital following an asthma attack - Keep patients who have had a near-fatal asthma attack under specialist supervision indefinitely - A respiratory specialist should follow up patients admitted with a severe asthma attack for at least one year after the admission.
69
follow up after acute asthma children
* Arrange follow up by primary care services within two working days * Arrange follow up in a paediatric asthma clinic at about one month after admission * Arrange referral to a paediatric respiratory specialist if there have been life-threatening features.
70
triggers for acute exacerbation of COPD
respiratory tract infections (most commonly rhinovirus) Smoking Environmental pollutants.
71
most common infective causes of COPD exacerbations?
Viral - rhinovirus Bacterial - Haemophilus influenzae (most common cause) Streptococcus pneumoniae Moraxella catarrhalis
72
presentation acute exacerbation of COPD
increase in dyspnoea, cough, wheeze there may be an increase in sputum suggestive of an infective cause patients may be hypoxic and in some cases have acute confusion
73
features of a SEVERE acute exacerbation of COPD
Marked breathlessness and tachypnoea. Pursed-lip breathing and/or use of accessory muscles at rest. New-onset cyanosis or peripheral oedema. Acute confusion or drowsiness. Marked reduction in activities of daily living.
74
admission criteria acute exacerbation of COPD
severe breathlessness acute confusion or impaired consciousness cyanosis oxygen saturation less than 90% on pulse oximetry. social reasons e.g. inability to cope at home (or living alone) significant comorbidity (such as cardiac disease or insulin-dependent diabetes)
75
Management acute exacerbation of COPD
1. increase frequency of bronchodialtor use and consider giving a nebuliser (salbuatmol/ipatropium) + prednisolone 30 mg daily for 5 days + abx if sputum is purulent or there are clinical signs of pneumonia - amoxicillin or clarithromycin or doxycycline O2 therapy: - if acutely unwell : start O2 therapy at 15L/min NRM. then get ABG to check hypercapnia and high HCO3- = if retentive picture = titrate down - if well enough use a 28% Venturi mask at 4 l/min and aim for an oxygen saturation of 88-92% for patients with risk factors for hypercapnia but no prior history of respiratory acidosis. then get ABG and adjust target range to 94-98% if the pCO2 is normal NIV should be considered in all patients with an acute exacerbation of COPD in whom a respiratory acidosis persists despite immediate maximum standard medical treatment
76
what can be used if oral steroid not able to be takena cute exacerbation of
IV hydrocortisone
77
what can be used if a pt with acute exacerbation of COPD doesn't respond to nebulised bronchodialtors
IV theophylline
78
what to do if acute exacerbation of COPD not responding and pt in type 2 resp failure and resp acidosis
NIV eg BiPAP
79
presentation of pulmonary embolism
chest pain- typically pleuritic dyspnoea Haemoptysis tachycardia tachypnoea respiratory examination classically the chest will be clear however, in real-world clinical practice crackles are often heard (PE triggered by underlying infection)
80
what scoring systems can be useful to use to rule-out/in pulmoanry embolisma nd guide next steps
PERC wells score for PE
81
when should you use PERC?
when you aren't suspecting PE but want to rule it out for reassurance
82
questions to ask about MHx and DHx to answer some of PERC and wells score questions
rMHx: recent surgery in past 4 weeks, or immobilisation MHx: previous DVT/PE malignancy (on tratement, treated in past 6 mo, palliative) DHx: - oestrogen use (COCP, HRT)
83
interpretation of wells score for PE
PE likely - more than 4 points 1. arranage immediate CTPA + if delay in CTPA, interim therapeutic anticoagulation = direct oral anticoagulant (DOAC) such as apixaban or rivaroxaban if the CTPA is positive then a PE is diagnosed if the CTPA is negative then consider a proximal leg vein ultrasound scan if DVT is suspected PE unlikely - 4 points or less 1. d-dimer 2. if +ve --> CTPA and interim therapeutic anticoagualtion if delay
84
ECG changes PE
most common = sinus tachycardia classical = 'S1Q3T3' a large S wave in lead I, a large Q wave in lead III and an inverted T wave in lead III
85
what other invetsigation shoult pts with ?PE get?
a chest x-ray is recommended for all patients to exclude other pathology however, it is typically normal in PE possible findings include a wedge-shaped opacification
86
what may be missed in CTPA
peripheral emboli affecting subsegmental arteries may be missed
87
Causes pleural effusion
Transudate <30 (pushed out/cant come back in) CARDIOVASCUALR - heart failure - fluid overlaod - constrictive pericarditis HYPOALBUMINAEMIA - liver fialure - nephrotic syndrome - chronic infection - malabsorption HYPOTHYROID MEIG's SYNDORME Exudate >30 Pulmonary embolism MALIGNANCY - bronchial carcinoma - mets INFECTION - TB - empyema INFLAMAMTION - SLE - RA
88
presentation pleural effusion
symptoms - pleurtic chest pain - SOB signs- stony dull percussion note, diminished or absent breath sounds, decreased tactile vocal fremitus/vocal resonance bronchial breathing just above the effusion If the pleural effusion is large, the trachea may deviate away from the effusion. There may be signs of the underlying condition.
89
Investigation pleural effusion
PA CXR ultrasound guided pleural aspiration - Fluid should be sent for pH, protein, lactate dehydrogenase (LDH), cytology and microbiology bloods - LFTs (check for hypoalbuminaemia) - U&Es (to check for renal failure) - glucose (to compare to the pleural fluid sample)
90
pleural aspiration protein interpretation in pleural effusion
Exudate >30g/L Transudate <30 g/L If the protein level is between 25-35 g/L, Light's criteria should be applied. An exudate is likely if at least one of the following criteria are met: Pleural fluid protein divided by serum protein >0.5 Pleural fluid LDH divided by serum LDH >0.6 Pleural fluid LDH more than two-thirds the upper limits of normal serum LDH
91
causes pleural tap low glucose
rheumatoid arthritis, tuberculosis
92
causes pleural tap raised amylase
pancreatitis, oesophageal perforation
93
causes pleural tap heavy blood staining
mesothelioma, pulmonary embolism, tuberculosis
94
when should a chest drain be inserted for pleural effusion in association with sepsis or a pneumonic illness
If fluid is purulent or turbid/cloudy or pH is less than 7.2
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management of transudate pleural effusion
treat cause pleural tap if unsure of cause don't drain, just treat the underlying cause...
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management of exudate pleural effusion
treat cause + drain the effusion as neccessary Fluid should be removed slowly – 2L every 24hr max. Large, fast fluid cahnges can cause pulmonary oedema. In Malignancy – most cases will reccurr within a month, and so pleurodesis or long-term in-dwelling chest drains may be considered. Pleurectomy may be used in certain instances.
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Causes pulmonary oedema
CARDIOGENIC (increased pulmonary capillary pressure) - any acute or chronic heart problem - renal failure (excess ECF accumulation) - iatrogenic fluid overlaod NON-CARDIOGENIC (increased capillary membrane permeability) - ARDS - fat embolism - liver failure
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presentation pulmoanry oedema
SOB Dry or productive cough (sometimes pink, frothy sputum) Paroxysmal nocturnal dyspnoea or orthopnoea Signs Coarse crackles Respiratory distress, pale, sweaty, tachypnoeic and tachycardic. They may be cyanosed, have evidence of congested neck veins and a raised JVP.
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investigations ?pulmoanry oedema
Bedside ECG CXR Bloods Renal function, electrolytes Glucose Cardiac enzymes LFTs Clotting tests (INR) ABG BNP Imaging echo
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management pulmonary oedema?
Give high flow O2 Monitor with ABGs to avoid hypercapnia - insert IV cannula - mainstay of treatment: IV furosemide 20-40mg slowly may want a catheter to measure urine output treat underlying problem
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CXR pulmonary oedema
Compare vessels in lower and upper lobes (upper lobe should be thinner if normal) Pulmonary oedema - similar in size and crowded Kerley B lines (vessels in lung peripheries - interlobular septal thickening) - interstitial Whiter bits = alveolar oedema
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causes high output heart failure
anaemia, thyrotoxicosis, pagets disease, arteriovenous malformations
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x-ray findings congetsiveheart failure
A- Alveolar oedema (bat wing opacities) B - Kerley B lines C- Cardiomegaly (cardiothoracic ratio > 0.5 D - upper lobe blood diversion E- pleural Effusions (bilateral blunting of costophrenic angles) F- fluid in the horizontal fissure
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Management acute heart failure
haemodynamically unstable : hypotensive or other signs of cardiogenic shock 1. Vasoactive drug (inotrope/vasopressor) - only administered in cardiac care unit or HDU 00. resp support haemodynamically unstable: hypertensive 1. Vasodilator IV eg glyceryl trinitrate (GTN) 1b. loop diuretic IV haemodynamically stable 1. Loop diuretic IV eg Furosemide: 20-40 mg intravenously (slowly)
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Investigations ?acute heart failure
Bedside: ECG immediately if haemodynamically unstable/resp failure (monitor continuously to look for life-threatening cause such as ACS) Chest XR (look for: pulmonary congestion, pleural effusion, interstitial/alveolar oedema, cardiomegaly) Bloods: NT-proBNP >300 or BNP > 100 FBC (to look for anaemia) troponin- for MI U&Es and creatinine (for a baseline to inform drug treatment decisions and to exclude concurrent or causative renal failure) LFTs - often elevated due to reduced CO and increased venous congestion. abnormal liver tests are associated with worse prognosis Glucose and HbA1c to screen for diabetes Thyroid function tests order TSH for anyone with newly diagnosed acute HF as both hypo and hyper can cause CRP D-dimer if PE suspected Further: Echo (determines LVEF)
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Causes ARDS
Primary/Direct (direct damage to alveoli) usually loacalised microvascualr effects Aspiration Pulmonary contusion Pneumonia Drowning Toxic inhalation Secondary (mainly damage to capillary membrane eg systemic inflammation) Sepsis Hypovolemic shock Fat emboli Trauma TRALI DIC Acute pancreatitis
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what is ARDS
Acute respiratory distress syndrome occurs due to a severe inflammatory reaction in the lungs, often secondary to sepsis or trauma. There is an acute onset of: Collapse of the alveoli and lung tissue (atelectasis) Pulmonary oedema (not related to heart failure or fluid overload) Decreased lung compliance (how much the lungs inflate when ventilated with a given pressure) Fibrosis of the lung tissue (typically after 10 days or more) Clinically there is: Acute respiratory distress Hypoxia with an inadequate response to oxygen therapy Bilateral infiltrates on a chest x-ray
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Management of ARDS
need HDU/ITU need PEEP
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what is pneumonia
Infection of lung tissue → inflammation → sputum filling airways
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what is community aquired pneumonia (CAP)?
develops outside hospital or within 48 hours of hospital admission
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what is hospital aquired pneumonia (HAP)?
develops more than 48 hours after hospital admission
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what is aspiration pneumonia
develops as a result of aspiration - inhaling foreign material such as food
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typical history and examination pneumonia?
PC: SOB, cough productive of sputum, fever, haemoptysis, pleuritic chest pain, delirium, sepsis o/e: tachypnoea, tachycardia, hypoxia, hypotension, fever, confusion Bronchial breath sounds - harsh breath sounds equally loud on inspiration and expiration Focal coarse crackles - air passing through sputum Dullness to percussion - due to lung collapse and/or consolidation
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what scoring system is used in priamry care for pneumonia ? how do you interpret?
CRB65 criteria: Criterion Marker C Confusion (abbreviated mental test score <= 8/10) R Respiration rate >= 30/min B Blood pressure: systolic <= 90 mmHg and/or diastolic <= 60 mmHg 65 Aged >= 65 years Patients are stratified for risk of death as follows: 0: low risk (less than 1% mortality risk) NICE recommend that treatment at home should be considered (alongside clinical judgement) 1 or 2: intermediate risk (1-10% mortality risk) NICE recommend that ' hospital assessment should be considered (particularly for people with a score of 2)' 3 or 4: high risk (more than 10% mortality risk) NICE recommend urgent admission to hospital
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interpretation of point of care CRP test for penumonia
NICE also mentioned a point-of-care CRP test. This is currently not widely available but they make the following recommendation with reference to the use of antibiotic therapy: CRP < 20 mg/L - do not routinely offer antibiotic therapy CRP 20 - 100 mg/L - consider a delayed antibiotic prescription CRP > 100 mg/L - offer antibiotic therapy
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what scoring system is used for pneumonia in secondary care? interpretation?
Criterion Marker C Confusion (abbreviated mental test score <= 8/10) U urea > 7 mmol/L R Respiration rate >= 30/min B Blood pressure: systolic <= 90 mmHg and/or diastolic <= 60 mmHg 65 Aged >= 65 years NICE recommend, in conjunction with clinical judgement: consider home-based care for patients with a CURB65 score of 0 or 1 - low risk (less than 3% mortality risk) consider hospital-based care for patients with a CURB65 score of 2 or more - intermediate risk (3-15% mortality risk) consider intensive care assessment for patients with a CURB65 score of 3 or more - high risk (more than 15% mortality risk)
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Investigations ?pneumonia
chest x-ray in intermediate or high-risk patients NICE recommend blood and sputum cultures, pneumococcal and legionella urinary antigen tests CRP monitoring is recommend for admitted patients to help determine response to treatment
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Management of CAP
Low-severity CAP: 5 days abx 1. amoxicillin is first-line 2. if penicillin allergic then use a macrolide or tetracycline Moderate and high-severity CAP 1. dual antibiotic therapy is recommended with amoxicillin and a macrolide, a 7-10 day course is recommended + Consider a beta-lactamase stable penicillin such as co-amoxiclav, ceftriaxone or piperacillin with tazobactam and a macrolide in high-severity community acquired pneumonia
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discharge criteria pneumonia
NICE recommend that patients are not routinely discharged if in the past 24 hours they have had 2 or more of the following findings: temperature higher than 37.5°C respiratory rate 24 breaths per minute or more heart rate over 100 beats per minute systolic blood pressure 90 mmHg or less oxygen saturation under 90% on room air abnormal mental status inability to eat without assistance.
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what should happen after 6 weeks following pneumonia
CXR All cases of pneumonia should have a repeat chest X-ray at 6 weeks after clinical resolution to ensure that the consolidation has resolved and there is no underlying secondary abnormalities (e.g. a lung tumour).
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most common causes pneumonia
Streptococcus pneumoniae (50%) Haemophilus influenzae (20%) Moraxella catarrhalis in immunocompromised patients or those with chronic pulmonary disease Pseudomonas aeruginosa in patients with cystic fibrosis or bronchiectasis Staphylococcus aureus in patients with cystic fibrosis
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what organism may be causing pneumonia in immunocompromised or COPD patients
moxarella catarrhalis
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what organisms may be causing pneumonia in CF/bronchiectasis
Pseudomonas aeruginosa in patients with cystic fibrosis or bronchiectasis Staphylococcus aureus in patients with cystic fibrosis
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management pneumocystitis jiroveci
co-trimoxazole (trimethoprim/sulfamethoxazole) known by the brand name “Septrin”
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auscultation heart failure
third heart sound
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causes transudate pleural effusion
CARDIOVASCUALR - heart failure - fluid overlaod - constrictive pericarditis HYPOALBUMINAEMIA - liver fialure - nephrotic syndrome - chronic infection - malabsorption HYPOTHYROID MEIG's SYNDORME
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causes exudate pleural effusion
Pulmonary embolism MALIGNANCY - bronchial carcinoma - mets INFECTION - TB - empyema INFLAMAMTION - SLE - RA
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How to decide on admission vs outpatient treatment for PE
Pulmonary Embolism Severity Index (PESI) score key requirements would clearly be haemodynamic stability, lack of comorbidities and support at home
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First line anticoagulant therapy for PE
RIVAROXABAN or apixaban
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Second line treatment for PE if DOAC CI
LMWH followed by dabigatran or edoxaban OR LMWH followed by a vitamin K antagonist (VKA, i.e. warfarin)
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Management of PE if severe renal impairment eg egfr <15/min
LMWH, unfractionated heparin or LMWH followed by a VKA
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Management of PE in antiphospholipid syndrome
LMWH followed by a VKA should be used
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length of anticoagulation for PE
provoked = 3 months active cancer = 3-6 months unprovoked = 6 months
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Management of PE with haemodynamic instability ie circulatory failure (e.g. hypotension)
thrombolysis
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who should get an abg asthma acute
ABGs for patients with oxygen sats < 92%