ABCDE breathing Flashcards
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.
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 are reduced breath sounds? causes?
diminished or absent breath sounds
- pleural effusion
- pneumothorax
- copd
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 and anaphylaxis
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.
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 priamry pneumothorax
if the rim of air is < 2cm and the patient is not short of breath then discharge should be considered
otherwise, aspiration should be attempted
if this fails (defined as > 2 cm or still short of breath) then a chest drain should be inserted
management secondary pneumothorax
Admit for 24 hours….
<1cm = give O2 and monitor for 24 hours
1-2cm = aspiration, then drain if aspiration fails
> 50yo and >2cm or SOB = chest drain
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
