Acute Respiratory Problems / Respiratory Failure Flashcards
What is respiratory failure?
When the lungs aren’t working correctly, resulting in hypoxia
there may or may not be raised levels of carbon dioxide in the blood
What are the main differences between type 1 and type 2 respiratory failure?
Type 1:
- there is hypoxia only
- this is focal - only one lobe / part of the lung is malfunctioning
- there is V/Q mismatch
Type 2:
- there is hypoxia and hypercapnia
- this is global - affects large areas of the lungs
- there is no global gas exchange
What abnormalities are shown on ABG for type 2 respiratory failure?
- elevated PaCO2
- reduced PaO2
- elevated HCO3-
What condition is very frequently associated with type 2 respiratory failure?
COPD
look for a history of heavy smoking
What is represented by the boats and lorries in this diagram?
boats are ventilation (V) and lorries are perfusion (Q)
in order for adequate lung function, both ventilation and perfusion need to be functioning
ventilation involves getting air into the alveoli
perfusion involves getting the oxygen from the alveoli to the rest of the body
What is meant by ventilation (V)?
the volume of gas inhaled and exhaled from the lungs in a given time period, usually one minute
this involves air entering the alveoli
What is meant by perfusion?
perfusion is the total volume of blood reaching the pulmonary capillaries in a given time period
this involves getting oxygen from the alveoli to the rest of the body
What would the ideal V/Q ratio be?
How does V/Q ratio differ in different parts of the lung and what does this mean?
the ideal V/Q ratio would be 1 for maximally efficient pulmonary function
the ratio varies depending on the part of the lung concerned
when standing up straight, the ratio is roughly 3.3 in the apex of the lung and 0.63 in the base
ventilation exceeds perfusion towards the apex
perfusion exceeds ventilation towards the base
What is meant by V/Q mismatch?
a mismatch between the alveolar ventilation and the alveolar blood flow
this can arise due to either reduced ventilation of part of the lung or reduced perfusion
gas exchange in the affected alveoli is impaired, resulting in a fall in pO2 and a rise in pCO2
Why does pCO2 in the blood not usually rise despite V/Q mismatch?
What physiological mechanisms are in place to prevent this?
- hypoxic vasoconstriction causes blood to be diverted to better ventilated parts of the lung
- the haemoglobin in these well ventilated alveolar capillaries will already be saturated
- RBCs will be unable to bind additional oxygen to increase the pO2
- the pO2 of the blood remains low, which acts as a stimulus to cause hyperventilation, resulting in either normal or low CO2 levels
What is involved in the principles of type 1 respiratory failure relating to solubility of CO2 and O2 and compensation?
CO2 is much more soluble than O2
(this is why O2 needs Hb to carry it)
- a good lung cannot hyper-oxygenate (>100% saturation)
- a good lung can hyperventilate to remove CO2
What is shown in this image of Type 1 respiratory failure?
- there is reduced ventilation in a part of the lung
- oxygen is not getting into the alveoli, but perfusion is normal
- the rest of the lung has increased ventilation to compensate
- perfusion to the rest of the lung is still normal and not increased
- the rest of the lung is at 100% capacity as it is fully oxygenating the blood
- due to the blue region, despite compensation, there is still hypoxia as you cannot go above 100% saturation
How can pneumonia lead to type 1 respiratory failure?
in pneumonia the alveoli are filled with exudate
this impairs the delivery of air to the alveoli and lengthens the diffusion pathway for respiratory gases
When does type 2 respiratory failure result from V/Q mismatch?
- the result of reduced ventilation / perfusion intially is hypoxia
- the lung is still able to remove CO2, so hypercapnia does not occur unless ventilation is severely limited
- in T2RF there is a global problem leading to complete loss of gas exchange due to malfunctioning alveoli
What are common causes of Type 1 respiratory failure?
- acute asthma
- atelectasis
- pulmonary oedema
- pneumonia
- pneumothorax
- pulmonary embolism
- ARDS
What are common causes of type 2 respiratory failure?
- acute severe asthma
- COPD
- upper airway obstruction
- neuropathies (GBS, MND)
- drugs - opiates
What is involved in the management of type 1 respiratory failure?
CPAP - continunous positive airway pressure
- air (above atmospheric pressure) is pumped into the lungs continuously, which opens deep distal airways
- this increases ventilation (V) so helps when there is a reduced V to an area of the lungs
What is involved in the management of type 2 respiratory failure?
BIPAP - bilevel positive airway pressure
- there is increased airway recruitment, which increases ventilation (V)
- in BIPAP, you receive positive air pressure on inspiration and expiration, but the air pressure is higher on inspiration
- CPAP involves the same amount of pressure being delivered on inspiration and expiration
- air is pumped in on inspiration, but CO2 is also sucked out on expiration
What is normal intrapleural pressure?
What happens if this is changed?
normal intrapleural pressure is from -5 to -8 cm H2O
this is a negative pressure that holds open the lungs
if it is changed (i.e. through pneumothorax) then ventilation cannot occur as effectively
What is a pneumothorax?
air within the pleural space
this air pushes on the outside of lung and makes it collapse
this could involve the collapse of entire lung or only a portion of the lung
What is the difference between a primary and a secondary pneumothorax?
Primary pneumothorax:
- this occurs spontaneously without an apparent cause and in the absence of significant lung disease
Secondary pneumothorax:
- this occurs in the presence of existing lung disease
What type of person is more likely to get a primary spontaneous pneumothorax?
How does it develop?
this is more likely to occur in a young, healthy person who does not have any significant lung disease
a bleb (lump in the pleura) bursts open, leading to air entering the pleural space
this is random and spontaneous
What are the risk factors that increase the likelihood of primary pneumothorax?
- men are more likely to get pneumothoraces than women
- smoking
-
Marfanoid habitus
- really tall individuals with elongated limbs & hypermobility of joints
Who is more likely to get a secondary pneumothorax?
- patients with a smoking history
- patients are usually over 50 with lung disease already diagnosed
- this would include younger patients with cystic fibrosis
How does secondary pneumothorax occur in someone with emphysema?
the alveolar bullae in emphysema can burst, allowing air to rush into the pleural space
What happens in a tension pneumothorax?
a one-way valve is formed
- with each inspiration, some air is pumped into the pleural space
- upon expiration, the air cannot leave the pleural space
- with every breath, more air enters the pleural space and the pneumothorax gets bigger
What are the signs and symptoms of tension pneumothorax?
Due to lung compression:
- severe dyspnoea
- tracheal deviation (away from the lesion)
- silent chest with hyperresonance and reduced expansion on lesioned side
Due to mediastinal shift:
- hypotension
- tachycardia
How does someone die from a tension pneumothorax?
death from tension pneumothorax is cardiac, rather than respiratory
- the pneumothorax becomes so large that it presses against the vena cava in the mediastinum
- this leads to a loss of venous return and circulatory collapse
- tachycardia is present to try and compensate for the hypotension
Which direction does the trachea deviate in tension pneumothorax?
as the tension pneumothorax balloons, it will push the trachea away from itself
the trachea deviates AWAY from the side of the pneumothorax
What does the chest sound like in a tension pneumothorax?
the chest sounds silent
it is hyperresonant due it just being air present in this region and no lung tissue
What is the management for tension pneumothorax?
large bore cannula in the 2nd intercostal space midclavicular line
this is an orange or grey cannula
this needs to be inserted just above the 3rd rib to avoid the neurovascular bundle resting underneath the ribs
How are other pneumothoraces (not tension pneumothoraces) managed?
chest drain or needle aspiration
this needs to be inserted in the safe triangle
this is in the 2nd intercostal space, midclavicular line using a sterile technique
What are the stages involved in the pneumothorax treatment algorithm?
if the patient is symptomatic (breathless) or the pneumothorax is >2cm then management is different
large or symptomatic secondary pneumothorax - go straight for the chest drain
regardless of the size of the pneumothorax, if the patient is symptomatic then different management needs to be taken
D - needle aspiration and give O2
the pneumothorax is primary and less than 2cm
however, the patient is symptomatic (breathless) so needle aspiration is performed
if this is not successful, then a chest drain would be performed
What is a pulmonary embolism?
Where does it originate from?
PE tends to come from a VTE - a clot that forms elsewhere in the body
these tend to be DVTs that occur in the deep veins of the calves
this is because the compliance is massive and the pressure is low here
What are the stages involved in a PE developing from a thrombus?
a small part of the thrombus breaks off and drains into the inferior vena cava
this enters the right side of the heart and into the pulmonary artery, to become lodged in the lungs
What are the 3 different types of PE?
- acute massive PE
- acute submassive & small PE
- chronic PE
What is an acute massive PE and what are the typical symptoms?
this involves sudden complete occlusion of the pulmonary artery
this results in:
- collapse
- central crushing chest pain
- severe dyspnoea
What is an acute submassive & small PE?
What are the typical symptoms?
sudden incomplete occlusion of pulmonary artery or distal artery
this results in:
- pleuritic chest pain
- haemoptysis
- dyspnoea
What is a chronic PE?
What symptoms does this present with?
this involves chronic occlusion of pulmonary microvasculature
this results in exertional dyspnoea
What might be seen on CXR for someone with PE?
- classical S1Q3T3 pattern
- right axis deviation
- right bundle branch block
- sinus tachycardia
What is meant by S1Q3T3 pattern on ECG?
- big S wave in lead 1
- pathological Q wave in lead 3
- inverted T wave in lead 3
- this is a sign of right heart strain
- right side strain is increased to try and overcome the obstruction in the pulmonary vasculature
What sign might be seen on CXR for pulmonary embolism?
CXR can show Westermark’s sign, which has a high positive predictive value
it is a finding of oligaemia (increased translucency) distal to a large vessel that is occluded by a PE
What mnemonic is used to remember the risk factors for PE?
CT, s’il vous plait
WHY - because you will be asking the radiologist for a CTPA
What does C stand for in the mnemonic CT s’il vous plait?
- cancer
- chemotherapy
- cardiac failure
- COPD
- Factor C deficiency
What does T stand for in the mnemonic CT s’il vous plait?
- trauma
- time (age)
- thrombocytosis
What does S stand for in the mnemonic CT s’il vous plait?
- stasis
- surgery
- Factor S deficiency
What does V stand for in the mnemonic CT s’il vous plait?
- varicose veins
-
virchow’s triad (3 factors important in development of venous thrombosis)
- stasis of blood flow
- endothelial injury
- hypercoagulability
- Factor V Leiden
What does P stand for in the mnemonic CT s’il vous plait?
- pill (OCP)
- pregnancy
- puerperium (period of 6 weeks after childbirth)
- previous VTE
- polycythaemia
- paraprotein deposition
What are the NICE guidelines for preventing VTE?
How can the mechanisms for preventing VTE be remembered?
- everyone must be VTE risk assessed within 24 hours of hospital admission
- mechanical prevention involves anti-embolic stockings (TED stockings)
- pharmacological prevention involves low-molecular-weight-heparin (tinzaparin)
- this can be remembered as “TEDs & Tinz”
What score is used to stratify PEs?
the Well’s score
- a score <4 is a low-risk PE and a D-dimer test is done
- a score of 4 or more is a high-risk PE and CTPA is done
What factors are scored in the Well’s score?
What mnemonic is used to remember this?
can be remembered using “PE SCORE”
- P - previous DVT / PE
- E - evidence of DVT
- S - stasis
- C - cancer
- O - opinion is PE
- R - rate raised (>100)
- E - exsanguination (haemoptysis)
What question must be asked before deciding how to manage a patient with PE?
are they haemodynamically stable?
i. e. systolic blood pressure < 90
* if YES then this is a submassive/small PE
* if NO then this is a massive PE
What is the treatment for submassive/small PE?
- respiratory support
- anticoagulation
- the aim of the treatment is not to eradicate the PE that is already present, but to prevent further PEs
What type of anticoagulation is used to treat a submassive / small PE?
-
Fondaparinux / Heparin is given for 5 days
- this is “bridging warfarin”
- warfarin takes a few days to take effect clinically and is a procoagulant in the acute phase, so heparin needs to be given to bridge this effect
- Warfarin is then given for 3 months
- a DOAC (e.g. dobigatran) is also started
What are the treatments for someone presenting with a massive PE (not haemodynamically stable)?
- respiratory support
- 1st line treatment is thrombolysis with a clot-busting drug
- 2nd line treatment is embolectomy
What type of drugs are used for thrombolysis?
Why are they not used to treat a submassive/small PE?
IV thrombolytics (fibrinolytics)
such as alteplase and streptokinase
these have risks associated with them, and the risks outweight the benefits for small/submassive PE
What is the definition of ARDS?
ARDS is a form of hypoxaemic acute lung injury
it is a non-cardiogenic pulmonary oedema (i.e. pulmonary oedema occurring due to an immune reaction)
it is a type of respiratory failure characterised by rapid onset of widespread inflammation in the lungs
What are the common causes of ARDS?
In what type of patient is it particularly common?
- drugs
- ventilation
- nearly drowning
- severe burns
- sepsis
- pneumonia
- transfusion reactions
it is particularly common in critically ill (ITU) patients
How does ARDS lead to alveolar collapse and shunt?
- the body responds to the cause with a profound inflammatory response
- this increases vascular permeability and allows fluid into the lungs, resulting in pulmonary oedema
- fluid in the alveoli weighs on the alveoli and ruins their structure and integrity
- this leads to alveolar collapse and diffuse alveolar damage
- fluid leaks into the space between the capillary and the alveolus, increasing this space
- this leads to a shunt in 50% of the alveoli
What criteria is used to define ARDS?
the Berlin criteria, which can be simplified to:
- A - alternative cause (i.e. not cardiogenic pulmonary oedema)
- R - rapid onset (< 1 week)
- D - dyspnoea
- S - similar on CXR
What are the 3 main symptoms of ARDS?
- dyspnoea (shortness of breath)
- bluish discolouration of the skin (cyanosis)
- tachypnoea (rapid breathing)
What are the investigations performed for ARDS?
- arterial blood gas (ABG)
- CXR / CT
- Echocardiogram
- Covid swab - COVID-19 has been seen to cause ARDS
it is important to treat the underlying cause and be aware that it exists
A - apixaban
- the patient is haemodynamically stable as SBP > 90
- alteplase should not be given as thrombolysis is not in the patient’s best interest at this stage
- a DOAC, such as apixaban, should be given
