ABCDE breathing Flashcards
target oxygen saturation level in acute asthma
94-98
assessment ABCDE breathing
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
interventions and investigations ABCDE breathing
if o2 sats low
- oxygen 15L NRM
- ABG
- CXR
what are the different types of oxygen delivery and their corresponding FiO2 range limits (WARD BASED)
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
why are venturi masks useful?
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
what is PEEP
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.
what oxygen delivery methods have PEEP
High-flow nasal cannula
CPAP
Non-invasive ventilation (BiPAP)
Mechanical ventilation
what intervention may be needed for type 1 resp failure if normal O2 delivery methods not adequate
CPAP
what intervention may be needed for type 2 resp failure if normal O2 delivery methods not adequate
biPAP
how are NIV and BiPAP different?
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.
is CPAP a type of NIV?
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).
what is ECMO
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.
what is Cheyne-Stokes respiration
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.
what is Kussmaul’s respiration
deep, sighing respiration associated with metabolic acidosis (e.g. diabetic ketoacidosis).
tracheal deviation causes? which way would it go?
The trachea deviates away from tension pneumothorax and large pleural effusions.
The trachea deviates towards lobar collapse and pneumonectomy.
cause of symmetrical reduction in chest expansion
pulmonary fibrosis reduces lung elasticity, restricting overall chest expansion.
hyperinflation eg copd
causes of asymmetrical reduction in chest expansion
pneumothorax, pneumonia and pleural effusion can all cause ipsilateral reduced chest expansion.
cause stony dullness
typically caused by an underlying pleural effusion.
cause dullness to percussion
suggests increased tissue density (e.g. cardiac dullness, consolidation, tumour, lobar collapse).
Stony dullness: typically caused by an underlying pleural effusion.
what is bronchial breathing
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.
what is wheeze? causes?
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
what are coarse crackles?
discontinuous, brief, popping lung sounds typically associated with fluid/secretions
pneumonia, bronchiectasis and pulmonary oedema.
what are fine crackles? causes?
sounding similar to the noise generated when separating velcro. Fine end-inspiratory crackles are associated with pulmonary fibrosis.
what is type 1 resp failure? pathophysiology?
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
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
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
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.
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)
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.
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.
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.
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
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.
what are reduced breath sounds? causes?
diminished or absent breath sounds
- pleural effusion
- pneumothorax
classifications pneumothoraces
Spontaneous
–> primary sponteaneous
–> secondary spontaneous
Traumatic pneumothorax
Iatrogenic pneumothorax
any of above can cause Tension pneumothorax
what is the cuase of spontaenous pneumothroax in 3-6% of menstruating women?
endometriosis within the thorax
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
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)
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
Management of tension pneumothroax
- 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. - Next, insert chest drain into triangle of safety
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)
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
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
management persistent/recurrent pneumothorax
consider
video-assisted thoracoscopic surgery (VATS) to allow for mechanical/chemical pleurodesis +/- bullectomy.
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
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)
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
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
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
Define near-fatal asthma
Raised PaCO₂ (>6kPa) and/or need for mechanical ventilation.
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.
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.
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.
What are the sections of acute asthma management
- Oxygen
- inhaled bronchodilators
- steroids
- second line
- follow up
Management of acute asthma
- If O2 sats <94 or severe/LT features: Oxygen 15L non-rebreather, titrate down to achieve SpO2 94-98
- 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
- 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).
- Children IV salbutamol (single bolus dose 15 micrograms/kg over 10 minutes) in a severe asthma attack
- Children IV aminophylline - severe or life-threatening asthma unresponsive to maximal doses of bronchodilators and steroids.
- Anaesthetics and ICU
Oxygen acute asthma
If O2 sats <94 or severe/LT features: Oxygen 15L non-rebreather, titrate down to achieve SpO2 94-98
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
- 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 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
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).
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
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
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
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
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).
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.
Children IV salbutamol dose
single bolus dose 15 micrograms/kg over 10 minutes
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%.
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.
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.
triggers for acute exacerbation of COPD
respiratory tract infections (most commonly rhinovirus)
Smoking
Environmental pollutants.
most common infective causes of COPD exacerbations?
Viral
- rhinovirus
Bacterial
- Haemophilus influenzae (most common cause)
Streptococcus pneumoniae
Moraxella catarrhalis
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
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.
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)
Management acute exacerbation of COPD
- 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
what can be used if oral steroid not able to be takena cute exacerbation of
IV hydrocortisone
what can be used if a pt with acute exacerbation of COPD doesn’t respond to nebulised bronchodialtors
IV theophylline
what to do if acute exacerbation of COPD not responding and pt in type 2 resp failure and resp acidosis
NIV eg BiPAP
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)
what scoring systems can be useful to use to rule-out/in pulmoanry embolisma nd guide next steps
PERC
wells score for PE
when should you use PERC?
when you aren’t suspecting PE but want to rule it out for reassurance
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)
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
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
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
what may be missed in CTPA
peripheral emboli affecting subsegmental arteries may be missed
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
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.
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)
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
causes pleural tap low glucose
rheumatoid arthritis, tuberculosis
causes pleural tap raised amylase
pancreatitis, oesophageal perforation
causes pleural tap heavy blood staining
mesothelioma, pulmonary embolism, tuberculosis
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
management of transudate pleural effusion
treat cause
pleural tap if unsure of cause
don’t drain, just treat the underlying cause…
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.
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
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.
investigations ?pulmoanry oedema
Bedside
ECG
CXR
Bloods
Renal function, electrolytes
Glucose
Cardiac enzymes
LFTs
Clotting tests (INR)
ABG
BNP
Imaging
echo
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
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
causes high output heart failure
anaemia, thyrotoxicosis, pagets disease, arteriovenous malformations
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
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)
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)
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
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
Management of ARDS
need HDU/ITU
need PEEP
what is pneumonia
Infection of lung tissue → inflammation → sputum filling airways
what is community aquired pneumonia (CAP)?
develops outside hospital or within 48 hours of hospital admission
what is hospital aquired pneumonia (HAP)?
develops more than 48 hours after hospital admission
what is aspiration pneumonia
develops as a result of aspiration - inhaling foreign material such as food
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
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
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
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)
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
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
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.
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).
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
what organism may be causing pneumonia in immunocompromised or COPD patients
moxarella catarrhalis
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
management pneumocystitis jiroveci
co-trimoxazole (trimethoprim/sulfamethoxazole) known by the brand name “Septrin”
auscultation heart failure
third heart sound
causes transudate pleural effusion
CARDIOVASCUALR
- heart failure
- fluid overlaod
- constrictive pericarditis
HYPOALBUMINAEMIA
- liver fialure
- nephrotic syndrome
- chronic infection
- malabsorption
HYPOTHYROID
MEIG’s SYNDORME
causes exudate pleural effusion
Pulmonary embolism
MALIGNANCY
- bronchial carcinoma
- mets
INFECTION
- TB
- empyema
INFLAMAMTION
- SLE
- RA
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
First line anticoagulant therapy for PE
RIVAROXABAN or apixaban
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)
Management of PE if severe renal impairment eg egfr <15/min
LMWH, unfractionated heparin or LMWH followed by a VKA
Management of PE in antiphospholipid syndrome
LMWH followed by a VKA should be used
length of anticoagulation for PE
provoked = 3 months
active cancer = 3-6 months
unprovoked = 6 months
Management of PE with haemodynamic instability ie circulatory failure (e.g. hypotension)
thrombolysis
who should get an abg asthma acute
ABGs for patients with oxygen sats < 92%
