Asthma
Last updated 18th June 2020 - Tom Heaton
Asthma is a chronic inflammatory condition of the airways.
It is characterised by paroxysmal and reversible airway obstruction.
These notes will focus primarily on the acute disease form, rather than chronic disease management.
This is a nice introductory video from the Osmosis team: https://www.youtube.com/watch?v=gvxF_TJhHiA
This podcast is also useful: https://ibccpodcast.libsyn.com/ibcc-episode-58-asthma
It is characterised by paroxysmal and reversible airway obstruction.
These notes will focus primarily on the acute disease form, rather than chronic disease management.
This is a nice introductory video from the Osmosis team: https://www.youtube.com/watch?v=gvxF_TJhHiA
This podcast is also useful: https://ibccpodcast.libsyn.com/ibcc-episode-58-asthma
Pathophysiology
The key features are:
Patients with asthma generally have some predispositional state.
On exposure to a particular trigger inflammatory cells (e.g. mast cells, eosinophils) in the bronchiolar walls are stimulated to release their internal contents (e.g.histamine, leukotrienes).
This causes an inflammatory effect on the surrounding tissues i.e. the bronchioles.
There is:
This has some important physiological implications on the respiratory dynamics:
This reduces the expiratory time for the lungs to empty, potentially leading to a vicious circle of gas trapping, also referred to as auto-PEEP.
Here there is gas remaining in the lungs at the start of the next inspiratory breath.
This increases total lung volume, reduces the optimal location of the lungs on the compliance curve, making breathing harder.
There can also be an adverse CVS impact.
Increased intrathoracic pressures can impede venous return, reducing cardiac output.
There can be notable respiratory variation visible in patients with arterial lines.
As noted, there is usually a trigger.
Common triggers include:
- Small airway inflammation
- Mucous formation with airway plugging
- Bronchospasm from smooth muscle contraction
Patients with asthma generally have some predispositional state.
On exposure to a particular trigger inflammatory cells (e.g. mast cells, eosinophils) in the bronchiolar walls are stimulated to release their internal contents (e.g.histamine, leukotrienes).
This causes an inflammatory effect on the surrounding tissues i.e. the bronchioles.
There is:
- Increased mucus production by the goblet cells (which can cause plugging)
- Bronchiolar wall oedema
- Spasm/constriction of the smooth muscle layer
This has some important physiological implications on the respiratory dynamics:
- Increased work of breathing
- V/Q mismatch from impaired gas exchange
This reduces the expiratory time for the lungs to empty, potentially leading to a vicious circle of gas trapping, also referred to as auto-PEEP.
Here there is gas remaining in the lungs at the start of the next inspiratory breath.
This increases total lung volume, reduces the optimal location of the lungs on the compliance curve, making breathing harder.
There can also be an adverse CVS impact.
Increased intrathoracic pressures can impede venous return, reducing cardiac output.
There can be notable respiratory variation visible in patients with arterial lines.
As noted, there is usually a trigger.
Common triggers include:
- Infection
- Pollen
- Dustmite
- Drug
- NSAIDs
- Beta-blocker
- NSAIDs
- Cold air
- Exercise
- Animal dander
Presentation
Presenting features can include:
There may be a more subacute deterioration, with deterioration of chronic disease over a longer period (usually 48 hours).
There can be a slower response to treatment in these patients.
There is usually an escalation in self bronchodilator therapy, although without benefit,
Severe, sudden deterioration can also occur e.g. under 3 hours.
This phenotype commonly occurs overnight, usually in response to a significant allergen exposure, and can be more responsive to treatment.
This is a less common presentation.
Important features in the history include:
Most presenting cases are likely to have a diagnosis of asthma.
It may need to be a differential in new presentations of respiratory compromise in patients without a diagnosis.
Similarly, alternative diagnoses should still be borne in mind when patients with known asthma present e.g. anaphylaxis.
It is patients with chronic severe asthma that are more likely to be at risk of severe adverse outcomes (including death) and so the exploration of these risk factors from the history is important.
Chronic asthma severity can be roughly understood based on the level of treatment:
- SOB
- Cough (dry)
- Chest tightness
- Audible wheeze
There may be a more subacute deterioration, with deterioration of chronic disease over a longer period (usually 48 hours).
There can be a slower response to treatment in these patients.
There is usually an escalation in self bronchodilator therapy, although without benefit,
Severe, sudden deterioration can also occur e.g. under 3 hours.
This phenotype commonly occurs overnight, usually in response to a significant allergen exposure, and can be more responsive to treatment.
This is a less common presentation.
Important features in the history include:
- Asthma history
- Normal symptoms when well
- Bronchodilator use
- Previous hospital admission inc. ICU
- Known triggers
- Normal symptoms when well
- Medication history
- Asthma therapy - level of treatment
- Pattern of use
- Asthma therapy - level of treatment
- Other PMH
Most presenting cases are likely to have a diagnosis of asthma.
It may need to be a differential in new presentations of respiratory compromise in patients without a diagnosis.
Similarly, alternative diagnoses should still be borne in mind when patients with known asthma present e.g. anaphylaxis.
It is patients with chronic severe asthma that are more likely to be at risk of severe adverse outcomes (including death) and so the exploration of these risk factors from the history is important.
Chronic asthma severity can be roughly understood based on the level of treatment:
- Intermittent short acting beta agonist
- Regular inhaled steroid
- Long acting beta agonist
- Fourth line agent (e.g. leukotriene antagonist) + inhaled steroid dose increase
- Oral steroids
Assessment
These patients can be severely unwell and an A to E approach can be warranted.
Features in the clinical examination constitute a significant part of the severity assessment.
Remember that asthma remains a disease that kills people, and this can potentially be avoided - treat it with caution in the first instance.
A/B
Chest examination will usually reveal a wheeze.
This is most commonly expiratory but can be biphasic.
It may be inaudible in severe disease when there is minimal air entry, thus should provoke concern.
Similarly, the failing asthmatic may progress back through ‘looking normal’ as the increased work of breathing fails, giving a ‘normal’ respiratory rate despite profound ventilatory failure.
Features in the clinical examination constitute a significant part of the severity assessment.
Remember that asthma remains a disease that kills people, and this can potentially be avoided - treat it with caution in the first instance.
A/B
- SpO2
- RR
- Auscultation
- Work of breathing
- Ability to speak
- Posture
- Ability to speak
- Peak Expiratory Flow Rate
- Compared to best or predicted
- Compared to best or predicted
- HR
- Pulsus paradoxus
- Pulsus paradoxus
- NIBP
- Neurological status
- Rash
- Sweating
Chest examination will usually reveal a wheeze.
This is most commonly expiratory but can be biphasic.
It may be inaudible in severe disease when there is minimal air entry, thus should provoke concern.
Similarly, the failing asthmatic may progress back through ‘looking normal’ as the increased work of breathing fails, giving a ‘normal’ respiratory rate despite profound ventilatory failure.
Severity
The BTS/SIGN guidance provides categorisation of severity based on initial and ongoing clinical assessment.
Moderate
Essentially absence of the more severe features.
There is an increase in symptoms of asthma from baseline.
PEFR 50-75% best or predicted/
Severe
Any one of:
Life-threatening
Can be remembered as organ system compromise/major disturbance.
Near fatal
Raised pCO2 and/or requiring mechanical ventilation with raised inflammatory pressures.
- Moderate
- Severe
- Life-threatening
- Near fatal
Moderate
Essentially absence of the more severe features.
There is an increase in symptoms of asthma from baseline.
PEFR 50-75% best or predicted/
Severe
Any one of:
- PEFR 33-50% best/predicted
- RR >25
- HR >110
- Inability to complete full sentences
Life-threatening
Can be remembered as organ system compromise/major disturbance.
- Respiratory
- Hypoxia - SpO2 <92
- Silent chest
- PEFR <33%
- ‘Normal’ pCO2 - indicating impending failure
- Exhaustion/poor respiratory effort
- CVS
- Arrhythmia
- Hypotension
- CNS
- Altered conscious level
- PEFR < 33%
Near fatal
Raised pCO2 and/or requiring mechanical ventilation with raised inflammatory pressures.
Investigations
Bloods
PEFR
CXR usually provides little information in patients presenting with asthma.
They should be used to look for specific pathology:
Lung ultrasound may be useful in these patients presenting with severe disease.
It can provide rapid assessment of alternative causes e.g. cardiac failure, as well as some of the potential associated problems e.g. pneumothorax.
There is some debate about the use of PEFR.
There are descriptions about the use of the values to guide severity.
However, it is well recognised how much this is dependent on technique, thus bringing the validity of any results into question.
There is also concern about the potential to trigger bronchospasm in unwell patients.
- FBC
- U&E
- Blood gas
- In severe cases, primarily to assess pCO2
- A decent argument that clinical impression is more relevant
- CXR
- Lung US
PEFR
CXR usually provides little information in patients presenting with asthma.
They should be used to look for specific pathology:
- Pneumothorax
- Consolidation
Lung ultrasound may be useful in these patients presenting with severe disease.
It can provide rapid assessment of alternative causes e.g. cardiac failure, as well as some of the potential associated problems e.g. pneumothorax.
There is some debate about the use of PEFR.
There are descriptions about the use of the values to guide severity.
However, it is well recognised how much this is dependent on technique, thus bringing the validity of any results into question.
There is also concern about the potential to trigger bronchospasm in unwell patients.
Differential Diagnosis
Some key differentials to be mindful of include:
- Anaphylaxis
- Upper airway obstruction
- Foreign body
- Croup
- Vocal cord dysfunction
- Foreign body
- Respiratory tract infection
- Bronchiolitis
- Pneumonia
- Bronchiolitis
- Pneumothorax
- Heart failure
Management
Can be categorised as supportive and specific.
Supportive management primarily relates to supplementary oxygen therapy.
Advanced respiratory support is discussed below.
Normalisation of electrolytes, particularly potassium, may be needed.
Supportive management primarily relates to supplementary oxygen therapy.
Advanced respiratory support is discussed below.
Normalisation of electrolytes, particularly potassium, may be needed.
Specific
Key components of specific therapy include:
Steroids
Steroids are an essential part of the overall treatment.
They act to stop the inflammatory cascade that is a key part of the pathophysiology.
However, these effects are delayed so will not have much impact on the initial stages of management.
Early administration remains essential to reduce the duration of the exacerbation.
They should be given to all patients with an acute exacerbation.
There is minimal difference in route, so prednisolone (adult dose 40-50mg) via the oral route is generally preferred unless there are concerns about enteral absorption.
Hydrocortisone IV 100mg 6 hourly may be utilised in cases where the enteral route is not trusted.
Steroids should be continued until recovery (minimum 5 days).
Beta-agonists
The beta-agonists form the mainstay of acute management.
Salbutamol is given as needed to treat symptoms.
This can be given as an inhaler (especially via a spacer) in the prehospital/home setting, but nebulised therapy is generally used as soon as this is available.
The standard dose is 5mg neb, and the frequency is dependent on what is needed.
“Back to back” nebs are described in severe disease, and this is important to provide i.e continuous topping up of the neb chamber when empty.
IV beta-agonists are rarely used in adult care, but may have a role in the sickest patients, such as those ventilated or in extremis.
There is limited evidence for their use however.
There is no clear logical role for them above nebulised treatment where the pharmacological effect will be much more targeted.
The guidance in children tends more towards using IV therapy in severe cases, in addition to maximal nebulised therapy.
Again, the thoughts are that their role is when you are concerned that nebulised therapy in not adequately reaching the target site.
Caution is needed regarding pseudo-treatment failure with these agents in particular.
They can lead to notable CVS side effects, including tachycardia and lactate generation.
The metabolic demand of this may put additional strain on the ventilatory system
(as it tries to compensate) and thus appear to be a case of worsening clinical condition.
Ipratropium
The anticholinergic effect of ipratropium can be seen as having a clear synergistic effects alongside beta-agonists with regards to bronchodilation.
This physiology is backed up clinically.
The addition of 0.5mg ipratropium 4 hourly is recommended.
Some clinicians recommend a ‘loading’ with 1.5mg in the first hour.
Magnesium
Magnesium sulphate has been used for its bronchodilatory effects in asthma for a while.
The evidence about IV magnesium is a little better, although not completely compelling.
Importantly though is that it is a very benign intervention, and thus its use is recommended.
1.2-2g is given IV in severe asthma that doesn’t respond to initial therapy.
Nebulised magnesium has a much less strong evidence base, and is not recommended.
Aminophylline
The clinical evidence for aminophylline is similarly dubious.
In contrast to magnesium, however, there is a notably narrower therapeutic window and less benign side effect profile.
This means its use must be more of a deeply considered option.
The BTS/SIGN guidance states that whilst IV aminophylline is unlikely to provide any additional bronchodilation above standard therapy, patients with life threatening or near fatal asthma may gain some additional benefit.
It may therefore have a ‘kitchen sink’ role here.
The dosing is:
- Steroids
- Beta-agonist
- Ipratropium
- Magnesium
- Aminophylline
Steroids
Steroids are an essential part of the overall treatment.
They act to stop the inflammatory cascade that is a key part of the pathophysiology.
However, these effects are delayed so will not have much impact on the initial stages of management.
Early administration remains essential to reduce the duration of the exacerbation.
They should be given to all patients with an acute exacerbation.
There is minimal difference in route, so prednisolone (adult dose 40-50mg) via the oral route is generally preferred unless there are concerns about enteral absorption.
Hydrocortisone IV 100mg 6 hourly may be utilised in cases where the enteral route is not trusted.
Steroids should be continued until recovery (minimum 5 days).
Beta-agonists
The beta-agonists form the mainstay of acute management.
Salbutamol is given as needed to treat symptoms.
This can be given as an inhaler (especially via a spacer) in the prehospital/home setting, but nebulised therapy is generally used as soon as this is available.
The standard dose is 5mg neb, and the frequency is dependent on what is needed.
“Back to back” nebs are described in severe disease, and this is important to provide i.e continuous topping up of the neb chamber when empty.
IV beta-agonists are rarely used in adult care, but may have a role in the sickest patients, such as those ventilated or in extremis.
There is limited evidence for their use however.
There is no clear logical role for them above nebulised treatment where the pharmacological effect will be much more targeted.
The guidance in children tends more towards using IV therapy in severe cases, in addition to maximal nebulised therapy.
Again, the thoughts are that their role is when you are concerned that nebulised therapy in not adequately reaching the target site.
Caution is needed regarding pseudo-treatment failure with these agents in particular.
They can lead to notable CVS side effects, including tachycardia and lactate generation.
The metabolic demand of this may put additional strain on the ventilatory system
(as it tries to compensate) and thus appear to be a case of worsening clinical condition.
Ipratropium
The anticholinergic effect of ipratropium can be seen as having a clear synergistic effects alongside beta-agonists with regards to bronchodilation.
This physiology is backed up clinically.
The addition of 0.5mg ipratropium 4 hourly is recommended.
Some clinicians recommend a ‘loading’ with 1.5mg in the first hour.
Magnesium
Magnesium sulphate has been used for its bronchodilatory effects in asthma for a while.
The evidence about IV magnesium is a little better, although not completely compelling.
Importantly though is that it is a very benign intervention, and thus its use is recommended.
1.2-2g is given IV in severe asthma that doesn’t respond to initial therapy.
Nebulised magnesium has a much less strong evidence base, and is not recommended.
Aminophylline
The clinical evidence for aminophylline is similarly dubious.
In contrast to magnesium, however, there is a notably narrower therapeutic window and less benign side effect profile.
This means its use must be more of a deeply considered option.
The BTS/SIGN guidance states that whilst IV aminophylline is unlikely to provide any additional bronchodilation above standard therapy, patients with life threatening or near fatal asthma may gain some additional benefit.
It may therefore have a ‘kitchen sink’ role here.
The dosing is:
- 5mg/kg loading over 20 mins (unless already on oral therapy)
- 0.5-0.7mg/kg/hr infusion
Respiratory Support
Institution of invasive mechanical ventilation may be required in severe cases.
Simple provision of oxygen should be given to all patients that require it to keep SpO2 levels at 94-98%.
NIV
The use of NIV may be an option in some patients with severe asthma, in either CPAP or NIV formats.
The theory is that the use of positive pressure can offset the impact of intrinsic PEEP, whilst NIV can assist in the work of breathing in those patients who are struggling.
Some of these principles are similar to those in COPD exacerbations, where there is good evidence.
There is some evidence of its effective use in asthma in the literature.
However, this population is one that remains at a significant risk of deterioration, and thus this is something that should be undertaken in a critical care environment with the facilities and staff to progress to intubation if needed.
There is also the potential problem of the NIV being poorly tolerated.
The claustrophobic feel of the mask may worsen the anxiety that is already very prevalent in this group.
There is described use of sedation to help tolerate this, although this will again clearly require very close observation.
Induction
Induction of anaesthesia will almost always be through an RSI approach.
Ketamine is advocated as an induction agent of choice due to its bronchodilatory properties, as well as its CVS profile.
Either way, CVS stability of agent needs consideration due to the high risk for disturbance with induction, so may warrant adjunctive vasoactive agent.
Rocuronium is also commonly used as a muscle relaxant.
Agents that promote histamine release are generally avoided e.g. morphine, atracurium.
CVS instability is a notable risk with these cases due to a combination of (SH!T):
Ventilation
Careful ventilation management is essential in these patients.
Hazards include:
The approach to avoid this therefore includes:
Aiming to reduce the duration of neuromuscular blockade is another important part of reducing the complications.
PEEP
The role of PEEP in asthma is a topic of discussion.
As described, the intrinsic PEEP/auto-PEEP is a key feature of the pathophysiology.
This video explains the issue well: https://www.youtube.com/watch?v=jmtuRsV9iu4
This is another good explanation: https://www.youtube.com/watch?v=D1qioSm1Obk
There is a variation in how much you can get into adjusting the set extrinsic PEEP.
There is some argument that any small amount (e.g. 5cmH2O) is probably reasonable.
This is especially the case in spontaneously breathing patients where measuring the intrinsic PEEP is not really feasible.
When it is possible, the 60-80% of intrinsic PEEP seems a good target.
In essence, the main point is to assess the response to treatment.
An appropriate extrinsic PEEP should improve work of breathing and expiratory flow, whilst not worsening the gas trapping process.
The effect of any adjustments on ventilatory parameters should therefore be closely monitored.
The application of external PEEP has benefits for both inspiration and expiration.
During inspiration, the presence of ePEEP means that there is less of a difference between the iPEEP and ePEEP, and therefore the lungs have to create less of a gradient for the ventilator to be triggered.
This reduces the work of breathing in a spontaneously ventilating patient.
During expiration, the application of ePEEP may help to resist the collapse of small airways that may be a risk, and would worsen expiratory flow.
As long as the ePEEP is below the iPEEP, this will not notably worsen the pressures within the respiratory system as may be feared.
Simple provision of oxygen should be given to all patients that require it to keep SpO2 levels at 94-98%.
NIV
The use of NIV may be an option in some patients with severe asthma, in either CPAP or NIV formats.
The theory is that the use of positive pressure can offset the impact of intrinsic PEEP, whilst NIV can assist in the work of breathing in those patients who are struggling.
Some of these principles are similar to those in COPD exacerbations, where there is good evidence.
There is some evidence of its effective use in asthma in the literature.
However, this population is one that remains at a significant risk of deterioration, and thus this is something that should be undertaken in a critical care environment with the facilities and staff to progress to intubation if needed.
There is also the potential problem of the NIV being poorly tolerated.
The claustrophobic feel of the mask may worsen the anxiety that is already very prevalent in this group.
There is described use of sedation to help tolerate this, although this will again clearly require very close observation.
Induction
Induction of anaesthesia will almost always be through an RSI approach.
Ketamine is advocated as an induction agent of choice due to its bronchodilatory properties, as well as its CVS profile.
Either way, CVS stability of agent needs consideration due to the high risk for disturbance with induction, so may warrant adjunctive vasoactive agent.
Rocuronium is also commonly used as a muscle relaxant.
Agents that promote histamine release are generally avoided e.g. morphine, atracurium.
CVS instability is a notable risk with these cases due to a combination of (SH!T):
- Stacking
- Hypovolaemia
- Induction drugs
- Tension pneumothorax
Ventilation
Careful ventilation management is essential in these patients.
Hazards include:
- Breath stacking (dynamic hyperinflation)
- Barotrauma
- Inadequate ventilation
The approach to avoid this therefore includes:
- Adequate ventilation
- Ideal TV 6ml/kg (lung protective)
- May need TV 7-8ml/kg for CO2/pH (but generally accept high CO2)
- Supplemental FiO2 as needed - titrate down once stable
- Allow adequate expiration
- Extensive expiratory phase
- High I:E ratios (e.g. 1:4)
- Low resp rate e.g start 10 in adult
- Extrinsic PEEP
- Target 60-80% of intrinsic PEEP
- Extensive expiratory phase
- Limit barotrauma
- Aim for plateau pressures <30cmH2O
- PC waveform may improve distribution
- Accept hypercapnia to facilitate (pH 7.2 threshold)
- An argument that not to really worry about pH
Aiming to reduce the duration of neuromuscular blockade is another important part of reducing the complications.
PEEP
The role of PEEP in asthma is a topic of discussion.
As described, the intrinsic PEEP/auto-PEEP is a key feature of the pathophysiology.
This video explains the issue well: https://www.youtube.com/watch?v=jmtuRsV9iu4
This is another good explanation: https://www.youtube.com/watch?v=D1qioSm1Obk
There is a variation in how much you can get into adjusting the set extrinsic PEEP.
There is some argument that any small amount (e.g. 5cmH2O) is probably reasonable.
This is especially the case in spontaneously breathing patients where measuring the intrinsic PEEP is not really feasible.
When it is possible, the 60-80% of intrinsic PEEP seems a good target.
In essence, the main point is to assess the response to treatment.
An appropriate extrinsic PEEP should improve work of breathing and expiratory flow, whilst not worsening the gas trapping process.
The effect of any adjustments on ventilatory parameters should therefore be closely monitored.
The application of external PEEP has benefits for both inspiration and expiration.
During inspiration, the presence of ePEEP means that there is less of a difference between the iPEEP and ePEEP, and therefore the lungs have to create less of a gradient for the ventilator to be triggered.
This reduces the work of breathing in a spontaneously ventilating patient.
During expiration, the application of ePEEP may help to resist the collapse of small airways that may be a risk, and would worsen expiratory flow.
As long as the ePEEP is below the iPEEP, this will not notably worsen the pressures within the respiratory system as may be feared.
Rescue
Volatile Anaesthesia
The volatile anaesthetic agents are recognised as having an effective bronchodilatory effect.
Isoflurane and sevoflurane have been utilised in this role in intubated patients, allowing this effect as well as doubling as a sedative agent.
The challenges relate to the administration and scavenging of such agents in the critical care setting.
This is particularly relevant given that these patients need optimal ventilation. An anaesthetic machine is generally not sophisticated enough to fulfil this role.
The AnaConDa system is a device specifically designed for this purpose in the circuits of ICU ventilators, and may be an option.
ECMO
VV ECMO has been described as an option in patients with refractory near fatal asthma.
A registry study of 272 patients showed a survival to discharge rate of 83.5% (which is not bad) although there is a notable complication rate, as expected with ECMO.
It may be an option as a rescue therapy in those severely ill patients that remain refractory to treatment.
The volatile anaesthetic agents are recognised as having an effective bronchodilatory effect.
Isoflurane and sevoflurane have been utilised in this role in intubated patients, allowing this effect as well as doubling as a sedative agent.
The challenges relate to the administration and scavenging of such agents in the critical care setting.
This is particularly relevant given that these patients need optimal ventilation. An anaesthetic machine is generally not sophisticated enough to fulfil this role.
The AnaConDa system is a device specifically designed for this purpose in the circuits of ICU ventilators, and may be an option.
ECMO
VV ECMO has been described as an option in patients with refractory near fatal asthma.
A registry study of 272 patients showed a survival to discharge rate of 83.5% (which is not bad) although there is a notable complication rate, as expected with ECMO.
It may be an option as a rescue therapy in those severely ill patients that remain refractory to treatment.
Links & References
- British Thoracic Society. https://brit-thoracic.org.uk/quality-improvement/guidelines/asthma/
- Nickson, C. Acute severe asthma. LITFL. 2019. https://litfl.com/acute-severe-asthma/
- Tidy, C. Asthma. Patient.info. 2016. https://patient.info/doctor/asthma-pro
- Osmosis. Asthma. Youtube. 2018. https://www.youtube.com/watch?v=gvxF_TJhHiA
- Hasudungan, A. Asthma pathophysiology. Youtube. 2014. https://www.youtube.com/watch?v=NNfx27io8-k
- Tidy, C. Acute severe asthma and status asthmaticus. Patient.info. 2016. https://patient.info/doctor/acute-severe-asthma-and-status-asthmaticus
- The Internet Book of Critical Care Podcast. Asthma. 2019. https://ibccpodcast.libsyn.com/ibcc-episode-58-asthma
- The Internet Book of Critical Care. Asthma. EMCRIT. https://emcrit.org/ibcc/asthma/
- Sagar, AE. Morning rounds: understanding auto PEEP. Youtube. 2018. https://www.youtube.com/watch?v=jmtuRsV9iu4
- ICU REACH. Adding extrinsic PEEP in dynamic hyperinflation syndrome. Youtube. 2018. https://www.youtube.com/watch?v=D1qioSm1Obk
