Dr Seb Gray | Dr Katie Knight | Dr Kim Sykes

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If you have ever been involved in a case of asthma so severe the child ended up intubated, apologies for any unpleasant flashbacks as you read this..! Despite advances in the understanding and treatment of asthma, it is still a massive public health burden. Between 2 – 12% of the population have asthma and every year 12-27 children under the age of 14 die during an acute asthma exacerbation. Critically unwell asthmatics, not responding to a boat-load of bronchodilators and getting worse before your eyes, are one of the most pant wettingly scary scenarios we see in acute paediatrics. Ventilation (the last resort in status asthmaticus) is never taken lightly – it can be extremely challenging and comes with major risks (4).

To really understand ventilation strategies, you need to appreciate some pathophysiology.

In severe asthma, the bronchioles are narrower thanks to the combined nasties of bronchoconstriction and mucosal thickening. Top this off with mucus plugging, and you end up with areas of lung which are perfused normally but no gas exchange is going on – aka V/Q mismatch (4). Hypoxia and rising CO2 make you hyperventilate in an attempt to blow off CO2, which sets off a respiratory alkalosis. But even with a prolonged expiratory phase, airway obstruction prevents the alveoli from emptying – that CO2 is stuck in the alveoli, gets absorbed into the bloodstream and the pH falls.

Here’s a graph which looks like a fish

Figure 1: ‘Fish’ diagram showing how pH, PaO2 and PaCO2 change with increasing airway obstruction. PaCO2 initially falls with rise in pH. As decompensation occurs, the PaCO2 continues rising and pH continues to fall. PaO2 gradually falls with increasing obstruction.

When there is more resistance to expiration, the end-expiratory pressure in the alveoli shoots up – this is known as auto-PEEP. Air can only flow inwards when this high PEEP is overcome. In normal circumstances (i.e. not in the acute asthmatic), the respiratory muscles would just work harder to compensate. But after huffing and puffing for hours, an asthmatic child just doesn’t have the energy to keep the respiratory muscles working so hard.

Another issue in severe asthma is dynamic hyperinflation – this is when each expired breath is so prolonged (because of airway resistance) that the next breath ‘interrupts’ the previous one, and so the tidal volume can never be fully expired. This leads to air trapping or ‘breath stacking’. A hyperexpanded chest is not an efficient one, and respiratory muscles soon get tired. At this point you are heading towards a doomed spiral around the black hole of respiratory failure.

Obviously, we want to prevent asthmatics ever getting to the point of intubation. But when it comes to the crunch, we need to know the best strategy for safely ventilating this group of patients.

We did a literature review based on these searches:

  1. Asthma* AND
  2. P?ediatric* OR child* AND
  3. Ventilat*


Indications for intubation

Deciding to mechanically ventilate an asthmatic is a really big deal. Obviously it’s important to prevent severe hypoxia, but the actual process of intubation itself can cause more bronchoconstriction, worsening airway obstruction and increasing CO2. Unsurprisingly, asthmatics who are intubated have better outcomes if the intubation is done semi-electively, before there is complete collapse or arrest (19).

Exactly when to intubate is a clinical judgement based on various factors (see below) (13,14) and a bit of witchcraft, but the most important thing you are going to do is rapidly escalate management as soon as it is clear that things are going downhill (…in other words, don’t wait for the arrest to make the decision for you).

Indicators for mechanically ventilating children with acute severe asthma
Very severe respiratory distress & inability to speak* (despite maximal treatment)
Altered mental state/ falling Glasgow Coma Score (GCS)
Hypoxaemia* (despite delivering high concentration of O2)
Increasing hypercapnia* (despite maximal treatment)
Cardio-respiratory arrest

Table 1: *Hypoxia, hypercapnia and respiratory distress by themselves are not indicators for ventilation. However, unrecognised hypoxia with an agitated child +/- saturation probes ‘not picking up’ are the cases that die; you need to recognise clinically significant hypoxia and react rapidly. If you see hypoxia on the monitor, take it seriously!


Good sedation is totally essential once the decision is made to intubate. Sedation improves comfort, lowers O2 consumption, decreases production of CO2 and protects against barotrauma (14,20,25). Without good muscle relaxant there is the risk of laryngospasm at intubation, and even if the intubation is successful, a partially sedated patient is going to be really difficult to synchronise with the ventilator. Make sure your friendly anaesthetist is generous with short acting muscle relaxants at induction, and intubation shoukd go much more smoothly.

Rapid sequence induction (RSI) involves the use of an anaesthetic agent alongside a muscle relaxant. Ketamine is a popular anaesthetic in asthma as it has analgesic, sedating and bronchodilator effects (25); it can be used as an induction agent and as an infusion. With ketamine,  lung compliance improves, as do PaCO2 and peak inspiratory pressures (37). Just remember to consider the side effects of ketamine – annoyingly it can increase laryngeal secretions and can also cause dysphoria, hallucinations, and slightly abnormal heart rate and blood pressure (4,39). Then again, these cardiovascular effects might actually be viewed as a bonus if patients are dehydrated or haemodynamically unstable.

Fentanyl is another anaesthetic option – it’s an opiate agonist, does less nasty things to the blood pressure than morphine, and doesn’t cause histamine release (which could make respiratory distress worse) (20). It works well in when used with ketamine in a haemodynamically stable child, and is a pretty good choice for a post-induction sedation agent instead of morphine.

Neuromuscular blockade

Paralysis! Vecuronium, rocuronium or cis-atracurium – these drugs make controlled hypoventilation possible, reduce airway pressures, oxygen consumption and CO2 production. Atracurium should be avoided as it increases histamine release. Neuromuscular blockers are mostly needed in the first stages of ventilation. Once the patient is more stable, synchronised ventilation modes can be introduced.

These drugs don’t come without risk. Acute myopathy has been seen severly asthmatic patients needing muscle relaxants (14,19,20,23,25,42,43). Also, animal studies suggest there might be a link between neuromuscular blockade and corticosteroids causing severe myopathy (14,20). Given how essential steroids are in asthma treatment, neuromuscular blockers should be given at the lowest possible effective dose and stopped as soon as possible.

Ventilation strategy

The whole point of ventilation is to prevent dynamic hyperinflation, limit barotrauma and reduce haemodynamic compromise. So: ventilation should aim to limit pressures, with low tidal volumes, low respiratory rate and prolonged expiratory time. For a basic introduction to ventilation, click here.

Mode of ventilation

By the point of needing ventilation, these kids have been working hard for hours, and their respiratory muscles are knackered. Initially, controlled modes of ventilation are preferred. This lets muscles rest – later, a more patient-synchronised ‘assist’ mode can be considered.

Tidal volumes are chosen to keep inspiratory pressures under 40cmH2O. Respiratory rates are typically set below the physiological rate. This allows a long expiration time, which avoids dynamic hyperinflation.

Permissive hypercapnia

Most asthmatic ventilation strategies are based on controlled hypoventilation, and the CO2 is allowed to run a little high. Hypoventilating limits barotrauma and lets the hyperinflation gradually resolve itself (20). In normal lungs, hypoventilation generally leads to higher CO2 – but in asthmatics (because there is trapped gas in the alveoli) reducing down the ventilation by reducing the minute volume lets the trapped gas escape, reducing CO2.

Letting the CO2 run ‘high’ with a mild acidosis (above pH 7.25) is generally well tolerated (24) – the body’s buffer systems can compensate at this level (23, 24-27). However, high CO2 and acidosis can cause cerebral vasodilation, cerebral oedema, pulmonary vasoconstriction and decreased myocardial contractility (26,27) – so must be avoided if there is suspicion of raised ICP or myocardial dysfunction. In other words, if an asthmatic patient has been ventilated after a cardio-respiratory arrest, do not let that CO2 creep up. (25-27,29)

PEEP (positive end-expiratory pressure)

In asthmatics, PEEP dilates airways, reduces airway resistance and decreases the work of breathing. Dilating collapsed airways is helpful, because this lets the over-inflated alveoli get rid of their trapped gas without increasing lung hyperinflation (30).

There is always some PEEP generated by the patient (‘intrinsic’ PEEP) but with a ventilator, external PEEP can be added – adding PEEP means there is less pressure difference between alveolar pressure and central airway pressure, which makes inspiration easier. To trigger an assisted breath on the ventilator, the central airway pressure has to drop below the set level of PEEP before a mechanical breath is given.

If PEEP is too high, the end-expiratory volume goes up – this causes hyperinflation (exactly what you are trying to avoid). Hyperinflation interferes with inspiratory muscle activity, and can cause barotrauma and haemodynamic compromise (23,32-34).

Intrinsic PEEP and ‘Peak to Pause’ difference can be measured on most ventilators if a cuffed ETT is in place and the patient is well muscle relaxed; these should be used to guide ventilation settings.

Complications of intubation

Mechanical ventilation itself can have serious complications. These include hypotension, lobar collapse, pneumothorax and ventilator-associated pneumonia (17,23,44).

Hypotension can happen suddenly post-intubation in asthma for several reasons:

  • Sedation interferes with sympathetic drive and can cause a loss of vascular tone
  • There may have been reduced fluid intake during the acute illness (along with high insensible losses from tachypnoea), so the child could be hypovolaemic
  • Positive pressure ventilation increases the intrathoracic pressure which reduces venous return to the heart

Immediately after intubation, when the patient is being ventilated by hand, there’s also the risk that what we could politely call ‘over enthusiastic’ bagging could cause hyperinflation, leading to hypotension. If this happens, disconnecting the endotracheal tube from the bagging circuit (an ‘apnoea trial’) will let excessive air escape. Manual decompression should be carried out at the same time, as prolonged disconnection alone might just lead to hypoxia and arrest (not ideal). However – if this apnoea trial doesn’t rapidly improve haemodynamic instability in this sort of situation, you should have an extremely high clinical suspicion for tension pneumothorax (7,44). Sudden deterioration and arrest might also be due to excessive mucus plugging. The use of DNase for mucus plugging doesn’t have much of an evidence-base as yet, but can be life-saving and is in widespread use by intensivists across the UK. In the absence of DNase, physiotherapy with saline can also be attempted to alleviate mucous plugging; if you don’t have DNase – don’t just sit and do nothing!

At the simplest level the asthma mechanical ventilation strategy involves:
  • good sedation and paralysis
  • permissive hypercapnia;
  • …with pressure limits to avoid barotrauma;
  • …with a low respiratory rate for a prolonged expiratory phase.

While all this is important for the sickest patients, most of the asthma workload will always take place outside of PICU and the focus has to be on prevention. Follow up, education, appropriate use of preventers, check ups on compliance and inhaler technique – these are the real interventions which will ultimately stop asthmatic children dying.

Dr Seb Gray and Dr Katie Knight, paediatric registrars, with consultant input from Dr Kim Sykes, Consultant Paediatric Intensivist

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