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Asthma ventilation strategies

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In spite of your best medical management, the 9-year-old boy with severe asthma that you have been medically managing continues to deteriorate.  People are starting to mention ventilation.  Is doesn’t seem like a great idea…

The post is based on podcasts by Andy Neill (Emergency Medicine Ireland), Scott Weingart (EMCrit) and Colin Parker (EMPEM) and is the follow-up to this post on the medical management of asthma.

Non-invasive ventilation

The aim of non-invasive ventilation is to increase the functional residual capacity and reduce the work of breathing. It’s not that we are simply placing a giant mask over someone’s face when they are already struggling. The aim is to help with their muscular fatigue. By this stage, the asthmatic is not moving much air due to fatigue.  Giving them some NIV pressure support helps relieve this – all they need to do is initiate the breath.

One of the issues with asthmatics is air trapping. You can demonstrate this yourself: take a breath in and then breath out but stop half-way. Then breathe in again and do the same thing. You will find that it becomes harder and harder to breathe. This is air trapping. Asthmatics are not getting the chance to completely empty their lungs before taking the next breath and this problem gets worse with every breath. This air-trapping (or stacking) gives them auto-PEEP (i.e., they have their own PEEP that they then need to overcome to breathe).

Patients on NIV need inspiratory pressure support to help with their inhaled volume, but they also benefit from PEEP.

For someone to take a breath, they need to be able to generate a negative intrathoracic pressure (-2 or -3cm H2O). They already have a higher intrathoracic pressure than normal and so have further to go to be able to generate the negative pressure required for a breath. By giving some PEEP we are reducing the effort required to take the breath. So, for example, if the asthmatic’s intrathoracic pressure is 10, they’d have to overcome the pressure difference of 12 to be able to get to -2 and take a breath. If we give them a PEEP of 8, they only need to overcome 2. Their work of breathing on inspiration is greatly offset by the PEEP.

However, there is not much evidence to support NIV.  A review in 2012 (206 patients across 5 studies) concluded that there was not enough data to support its use.

Ventilation

Essentially, ventilating the asthmatic should be avoided if at all possible. Intubating them means that the rest of your treatments have failed – putting a tube into an asthmatic’s throat could kill them. It certainly exposes them to further risks of pneumothorax and cardiac arrest. Don’t do it unless you have someone very experienced with you who thinks that it’s a good idea.

If you’re going to ventilate a patient, we often use ketamine for sedation. It does have some bronchodilator effects. Use in sub-dissociative doses, not like for procedural sedation. Sometimes ketamine can relieve agitation and that will allow people to continue on NIV for a bit longer.

Other potentials for induction are propofol and IV or inhaled lignocaine – this can reduce the bronchospasm response to the ETT.

You do not want to miss the tube, getting it first time is essential. Weingart says that patients should either be completely out cold or awake – having a semi-sedated state will not help with intubation.

The main principles of ventilation are: – low PEEP; adequate flow rates; and slow rates.

Ventilating a patient can lead to hypotension and giving some fluid prior to ventilation can help minimize this.

Low PEEP

Additional PEEP in asthmatics is controversial and there are many theories on how best to use this.

At its simplest, as patients are already generating auto-PEEP through air trapping (as discussed above), external PEEP can simply make this worse. So low PEEP is good.

However, giving some PEEP can offset the work needed to overcome the auto-PEEP and therefore can be useful in ventilated patients who are triggering their own breaths.  This doesn’t apply in a fully sedated and ventilated patient.

External PEEP can also splint the airways open and therefore prevent auto-PEEP – so can sometimes be useful in the sedated ventilated patient too.

If a ventilated asthmatic suddenly deteriorates – disconnect the ventilator. Often you will hear a rush of air (air trapping) and the blood pressure will improve.  See Chris Nickson on LITFL for some great teaching on this.

Adequate flow rates

Patients do need longer expiratory periods, and ensuring adequate inspiratory flow allows a higher I:E ratio. Note that a higher expiratory time does not mean short inspiratory times, just relatively short. Our aim is to adequately oxygenate them until they recover.

Slow rates

Asthmatics need slow rates to allow for emptying of the lungs and to prevent air trapping.  This can lead to a high CO2 and we allow this – permissive hypercapnia. In order to adequately oxygenate them we let them have a high CO2 and acidosis. This can be resolved after the bronchoconstriction has been reversed.

Heavy sedation and pain control can help reduce the carbon dioxide generated.

Other things to think about – barotrauma

High peak inspiratory pressures (PIP) does not correlate with barotrauma.  It’s the alveolar pressure that correlates with barotrauma not the airway pressure.

Airway pressure = flow x resistance + alveolar pressure

So, if the resistance is high (as with bronchoconstriction) then a high PIP will be required, but the pressure being delivered to the alveoli can still be reasonable.

One way to determine alveolar pressure in a patient on volume control ventilation, is to look at the inspiratory pause pressure.  Essentially you temporarily stop the flow.  At this point, flow in the equation above is 0 and therefore ‘flow x resistance’ is 0.  So, at that time, airway pressure is equal to the alveolar pressure, and you can read that from your vent.  The theory is that if you keep the alveolar pressures below 30 then you will be ok.

Again, this is so well explained in another of Chris Nickson’s LITFL posts.

Other things to think about – bronchial casts

It’s rare but if your patient is not ventilating well, it could be bronchial casts.  There are very thick plugs that clog up the airways and impair adequate ventilation.  Not something you are likely to diagnose but it’s worth a thought.

And finally, all ventilation is doing is supporting the patient until they recover, it isn’t curing them.  In the meantime you need to reverse the bronchoconstriction using the meds we discussed in this post.

References

Mitra AAD, Bassler D, Watts K, Lasserson TJ, Ducharme FM. Intravenous aminophylline for acute severe asthma in children over two years receiving inhaled bronchodilators. Cochrane Review. 2009.

Rodrigo GJ, Castro-Rodriguez JA. Anticholinergics in the treatment of children and adults with acute asthma: a systematic review with meta-analysis. Thorax. 2005;60(9):740-6.

Munro A, Maconochie I. Best evidence topic reports. Beta-agonists with or without anti-cholinergics in the treatment of acute childhood asthma? Emerg Med J. 2006;23(6):470.

Rowe BH, Bretzlaff J, Bourdon C, Bota G, Blitz S, Camargo CA. Magnesium sulfate for treating exacerbations of acute asthma in the emergency department. Cochrane Review. 2009.

Lawford P, Milledge JS. Intravenous versus inhaled salbutamol. Lancet. 1978;1(8058):269.

Salmeron S, Brochard L, Mal H, Tenaillon A, Henry-Amar M, Renon D, Duroux P, Simonneau G. Nebulized versus intravenous albuterol in hypercapnic acute asthma. A multicenter, double-blind, randomized study. Am J Respir Crit Care Med. 1994 Jun;149(6):1466-70.

Browne GJ, Penna AS, Phung X, Soo M. Randomised trial of intravenous salbutamol in early management of acute severe asthma in children. Lancet. 1997 Feb 1;349(9048):301-5.

Browne GJ, Trieu L, Van Asperen P. Randomized, double-blind, placebo-controlled trial of intravenous salbutamol and nebulized ipratropium bromide in early management of severe acute asthma in children presenting to an emergency department. Crit Care Med. 2002 Feb;30(2):448-53.

Rowe BH, Camargo CA Jr. The role of magnesium sulfate in the acute and chronic management of asthma. Curr Opin Pulm Med. 2008 Jan;14(1):70-6.

Markovitz B. Does magnesium sulphate have a role in the management of paediatric status asthmaticus? BestBets. 2004.

Nair P, Milan SJ, Rowe BH. Does an aminophylline injection in addition to bronchodilators for an asthma attack improve lung function and other outcomes or cause harm? Cochrane Review. 2012.

Mitra AAD, Bassler D, Watts K, Lasserson TJ, Ducharme FM. Intravenous aminophylline for acute severe asthma in children over two years receiving inhaled bronchodilators. 2009.

Lim WJ, Mohammed Akram R, Carson KV, Mysore S, Labiszewski NA, Wedzicha JA, Rowe BH, Smith BJ. Non-invasive positive pressure ventilation for treatment of respiratory failure due to severe acute exacerbations of asthma. Cochrane Review. 2012.

Stather DR, Stewart TE. Clinical review: Mechanical ventilation in severe asthma. Critical Care 2005;9:581-587.

Author

  • Tessa Davis is a Consultant in Paediatric Emergency Medicine at the Royal London Hospital and a Senior Lecturer at Queen Mary University of London.

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