Arrest Asthma

Author: James Yates / Reviewer: Christopher McCoy / Codes: / Published: 16/10/2017 / Reviewed: 16/04/2024

Asthma kills.

In the UK, more than 1400 adults and children died from Asthma in 2018, an increase of 8% compared to the previous year. England and Wales recorded almost 13,000 deaths in the ten years 2008-2018 with a 33% increase in mortality across the decade.

Many of these patients will have their cardiac arrest in the pre-hospital environment, whilst others will present to the emergency department with a deteriorating acute attack.

It is, therefore, crucial that we get the treatment right for the 138 patients per day that visit our UK emergency departments with an acute exacerbation of asthma – regardless of the severity.

A peri-arrest asthma exacerbation can be a nightmare scenario to manage if you aren’t prepared. There is an, often young, otherwise healthy patient dying in front of you, so knowing the best approach to take is critical.

Initial Treatment

As a Specialist Paramedic, I think it is important to highlight that prehospital practice mirrors the BTS/SIGN guidelines almost exactly and the severity of the attack will have been classified using the same criteria. As such, a patient suffering from a life-threatening asthma attack will be receiving back-to-back nebulisers of salbutamol and a single dose of 500mcg ipratropium will have been added to one of these. An intravenous dose of 100mg hydrocortisone should also have been given. No surprises so far.

The IM Adrenaline & Nebuliser via T-Piece Controversy

However, the ambulance crew may have given the patient 0.5mg IM adrenaline, which does not feature in the BTS guidelines. This treatment is included in the ambulance guidelines, in part, due to the chance of misdiagnosing anaphylaxis and therefore the chance of inappropriately withholding adrenaline from this cohort. It also represents a relatively safe final treatment option for those patients with failing ventilation, in whom inhaled bronchodilators may be ineffective but who still urgently require bronchodilation. Interestingly, the UK Resuscitation Council suggest that IM adrenaline can be used as a first line drug in asthmatic cardiac arrest if IV access cannot be rapidly gained, stating that the benefit is uncertain but it is unlikely to be harmful.

Previous pre-hospital guidelines included utilising a T-piece to deliver nebulised bronchodilator therapy via an endotracheal tube and ventilation circuit however, this was removed due to risk of a tension pneumothorax. It is postulated that the 6-8L/min of oxygen driving the nebuliser may create a high degree of PEEP which would lead to increased gas trapping in the alveoli, worsening the efficacy of ventilation and reducing venous return through the increased intrathoracic pressure. Add this trapped volume to the positive pressure tidal volume from a BVM and this also increases the chance of barotrauma and subsequent tension pneumothorax. This is no longer current practice in the UK, nor part of the Resus Council Guidelines.

Resus Room Management

So, the patient is wheeled into your resus bay with a life-threatening asthma attack despite the best efforts of the prehospital team. Where do you go from here?

Firstly, it is useful to remind ourselves on how acute asthma presentations are graded and what we mean by Life-threatening Asthma. The BTS Guideline summarises characteristics of acute presentations in this table.

Having recognised features of life-threatening asthma the BTS guideline recommends the following treatments: Supplementary oxygen via face mask or nasal cannula should be given to hypoxaemic patients and adjusted to maintain SaO2 of 94-98%. In the case of lack of, or poor trace, pulse oximetry, do not delay oxygen administration.

B2 agonist therapy should be given via an oxygen driven nebuliser. The BTS guideline refers to terbutaline being as efficacious as salbutamol for the treatment of bronchospasm, however most departments will stock salbutamol nebules as standard. There is no significant benefit for the administration of nebulised adrenaline. Continuous rather than bolus nebulisation therapy may be of benefit to patients with acute asthma at the severe and life-threatening end of the spectrum.

What about intravenous B2 agonists? These should be reserved for patients in whom the nebulised version of the drug cannot be reliably administered. Intravenous bronchodilators such as salbutamol and aminophylline are not without risk and require senior medical input (which if you havent asked for yet you definitely should do now!).

Many pre-hospital teams are now administering hydrocortisone 100mg prior to patient arrival in the ED but it is vital to check and ensure a dose is given. Remember that patients may still self-present in extremis and may not have had any pre-hospital treatment.

Magnesium is pretty safe to give, with hypotension being the main side effect. You dont even need to know what the magnesium level is before giving the first dose! It is recommended for patients with acute severe asthma who have not had a good initial response to bronchodilator therapy. There is no role for nebulised magnesium therapy.

Often patients with life-threatening asthma are hypovolaemic and therefore intravenous fluid replacement and electrolyte correction (B2 agonists can cause hypokalaemia), should be considered.

Impending Doom

Some patients will respond well to these additional interventions, but for others a continued deterioration into cardiac arrest may be the unfortunate trajectory.

Cardiac arrest is ultimately the result of prolonged respiratory exhaustion, respiratory acidosis and impaired venous return due to the increased intrathoracic pressure.

As soon as cardiac arrest is identified Advanced Life Support should be initiated as normal but, as the resuscitation attempt gets established, there a few adaptions that may be required.

1. Intubate Early

Firstly, due to the high inflation pressures, this is one group of patients that should definitely be managed with a tracheal tube. Depending on the supraglottic device used these begin to leak at pressures around 20-30cmH2O and in an asthmatic patient, pressures exceeding this are not uncommon. Using a supraglottic device may therefore result in hypoventilation of a patient who is already critically hypoxic and hypercapnic. These increased inflation pressures are also higher than that of the lower oesophageal sphincter, increasing the chance of gastric inflation, regurgitation and aspiration, unless the airway is secured with an ETT.

2. Ventilate with Caution

With the airway secured attention should turn to an appropriate ventilation strategy. The respiratory rate advocated by the European Resuscitation Council is only slightly lower than normal, at 8-10 breaths per minute, with a tidal volume just enough to cause normal chest rise.

The reason for this is due to the potential for dynamic hyperinflation. This occurs when the expiratory time is not sufficient to allow complete exhalation. This results in a gradual increase in the residual volume in the alveoli, to the point at which the inspiratory reserve volume becomes minimal and further ventilation almost impossible.

This auto-PEEP, as well as affecting ventilation, also causes a significant rise in intrathoracic pressure, impeding venous return and reducing the efficacy of chest compressions.

Dynamic hyperinflation may be identified through an increasing resistance to ventilation, poor excursions of the chest wall and potentially a hyper-inflated appearance to the chest.

3. Manual Chest Deflation

Correction of the condition can be achieved by disconnecting the ETT and applying manual pressure to the patients’ chest. Air being forced out of the lungs may well be heard escaping from the ETT. If dynamic hyperinflation was the cause of difficult ventilation, an immediate improvement will be felt on reconnecting the BVM. This manual deflation technique may have to be repeated throughout the resuscitation attempt if the condition redevelops.

4. Think about Tension

An alternative cause of difficult ventilation is tension pneumothorax. If manual deflation of the lungs does not result in a reduction in the airway pressures, then tension pneumothorax should immediately be considered. A tension pneumothorax can be very difficult to identify in cardiac arrest but in asthmatic patients a low index of suspicion should be maintained, particularly if signs such as subcutaneous emphysema are noted. Consider the use of Point of Care Ultrasound in those trained to scan for pneumothorax but do not delay intervention if there is clinical suspicion. Decompression should be completed with a thoracostomy rather than needle decompression as multiple studies have highlighted concerns that a standard 14G cannula will not have an adequate length to penetrate the thoracic wall, as well as having a number of other limitations.

It should be remembered that decompression may be required bilaterally, but a quick review of the patient should be carried out after the first thoracostomy to ensure a second invasive procedure is not carried out unnecessarily.

5. Rehydrate

Dehydration can often be a finding in these patients’ due to the increased insensible losses associated with prolonged tachypnoea and mouth breathing. In the cardiac arrest setting this dehydration can have a couple of detrimental effects. Firstly, any degree of dehydration and reduction in intravascular volume is going to compromise effective chest compressions, particularly when found in conjunction with dynamic hyperinflation. Second, it is hypothesised that the mucus being secreted into the airways becomes thicker and therefore more likely to plug the respiratory bronchioles and small airways. This can worsen the, already significant, V:Q mismatch as well as contributing to dynamic hyperinflation. As a result, IV fluid during an asthmatic arrest may provide some benefit to these patients.


Extracorporeal Cardiopulmonary Resuscitation may be available in certain centres or within local network referral pathways. We are not all lucky enough to have an ECPR or ECMO service within our local hospitals to support our cardiac arrest management, but it is something that our Critical Care colleagues may consider for patients who achieve ROSC but continue to have ventilatory difficulties.

7. IV Drug therapy in Cardiac Arrest

There are no specific guidelines or evidence base here for moving away from a standard resuscitation algorithm with regards to IV drug administration in an asthmatic arrest. However, there is unlikely to be any harm in earlier administration of adrenaline in the case of a shockable cardiac arrest, and a bolus dose of IV salbutamol. If drugs are being given as part of a rapid sequence induction prior to cardiac arrest then there are potential bronchodilation benefits from ketamine that should prompt consideration of its use as an induction agent.


So, in summary, take a breath! Secure the airway with an endotracheal tube and watch for changes in the compliance of the BVM. Manually deflate the chest if there is resistance to ventilation and if there’s no improvement after, then decompress the chest. Get the IV fluid running and push the adrenaline early and often.

James Yates is a Specialist Paramedic (Critical Care) with the Great Western Air Ambulance based in Bristol. In his prehospital career to date, James has worked nationally and internationally in a range of clinical and educational roles. He has an interest in education and simulation.

References and Further Reading

  1. BTS/SIGN British Guideline on the Management of Asthma. British Thoracic Society, 2019.
  2. The Resus Room: Roadside to Resus series: Asthma, 2017.
  3. Resuscitation Council UK: Special Circumstances Guidelines, 2021.
  4. Asthma+Lung UK

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