Not a common problem in most ICU’s, but you do get the occasional severe case of asthma. When you do, it can get a little hairy. Mostly because these are generally young people and there’s only so much you can do. Sort of like Covid when it gets bad, there’s not much to offer. You provide the medicine, the supportive devices and wait for their bodies to heal themselves. Same with asthma, you order the standard treatment and then pray it doesn’t get to a point where you have to intubate them. In large part, our primary goal in ICU asthma is to not make them worse with counter-intuitive ventilator strategies. Let’s talk asthma.

First order of business for asthma is pretty straight forward. Get them on the good meds:

1. Treat the bronchospasm: Nebulizers. Lots of nebs. Albuterol/Atrovent. Consistently. Consider continuous nebs over an hour or more.

2. Treat the airway edema: Steroids

3. Other bronchodilators: Epinephrine. Could be racemic, could be IM (aka epi-pen in the field), or Epi drip. Epinephrine is a Beta 2 agonist so it will open up those airways. The trade off is the Beta 1 effect - your HR and BP are lik

4. More bronchodilators: Magnesium, bolus 2g. Can repeat.

5. Treat any contributing issues: PNA - abx, mucous secretions/plugs - suction, bronchoscopy.

6. Sedation to reduce fatigue, ventilator asynchrony, and anxiety with high work of breathing. Ketamine has direct bronchodilator effects and Propofol does as well,.

Your main goal here is to try like heck to avoid having to ventilate them. And the main reasons are twofold.

1. Peri-intubation risk.

   These folks already have a certain degree of respiratory acidosis right? They have an obstructive disease and cannot blow off carbon dioxide. The heart does not tolerate severe acidosis very well. Acidosis is a common cause for PEA/asystolic arrest. The most effecient and rapid way the body has to compensate for acidosis is through the pulmonary system by increasing ventilation efforts. But these folks are already struggling with this. So you don’t have much you can offer them compensation wise if the ventilation efforts get worse (i.e. you sedate and or paralyze them and suddenly they are no longer breathing or breathing well enough). If you take away the ventilation efforts they did have and are not able to ventilate soon enough or effectively enough the acidosis rapidly deteriorates and they code. These are the people you do not want apneic or bradypneic so you NEED first pass success with intubation. You need to quickly take over the work of breathing for them.

   Secondly, they have significant air - trapping because they cannot exhale. More and more air volumes/pressures develop in the chest and this decreases venous return. This reduces your preload, and reduces your cardiac output and blood pressure - essentially places them at high risk for developing shock. When you apply positive pressure ventilation you are increasing this volume/pressure so now the air- trapping can get much worse.

   Thirdly, like any other pt in a state of fight or flight catecholamine induced sympathetic release, giving anesthesia and applying PPV takes away the catecholamine surge and the parasympathetic crash is at high risk of ensuing. This is why so many people drop their BP when you intubate.

   Plan: To mitigate this risk you have the most skilled person intubate, provide pristine BVM efforts until they are on the vent and then apply settings as discussed below. To mitigate shock risk start fluids pre-intubation, pre-mix an epinephrine drip and or have push dose epi at the bedside. I prefer epi over levophed because of the Beta 2 effects of bronchodilation. See the previous post here regarding epinephrine doses.

2. Don’t make them worse by trying to correct the acidosis.

   I stopped short of putting that sentence in shouty capitals. If you take away nothing else from this article, please, please, please have a deep understanding that this is often the biggest risk for our intubated asthmatics. Think about the patho-physiology of asthma. Narrowed and swollen airways with a decent amount of increased mucous production. Bronchospasm and bronchoconstriction are the hallmarks of asthma. The problem is not respiratory acidosis. They develop respiratory acidosis as a complication of the asthma because of the inability to blow off air with carbon dioxide. As a result air volumes/pressures rise and retained CO2 rises. (Thus you get the picture above - high ETCO2, high peak pressure). A common ABG will look something like 7.25/74/298. Once we intubate the knee jerk reaction is for people to try to correct the acidosis by increasing minute ventilation via increased respiratory rate or increased tidal volumes. Let me show you a picture of how this effects the ventilator graphics.

So what’s the solution? In this specific case just drop the itime and RR back down. Your goal should allow permissive hypercapnia to prevent this exact problem. A good ventilator strategy for severe asthma would be as follows:

• Set a low norm respiratory rate 6-8 is reasonable.

• Set a low norm TV 4-6ml/kg IBW is reasonable.

• Set a lower norm iTime to allow for long Etime. 1:4 or higher even. Should see a looooong exhalation phase of your waveform like in the initial vent photo.

• Set a fairly fast insp flow rate, around 100l/m or higher (increasing flow rate delivers breath faster and therefore reduces itime).

• Fio2 minimal to keep SPO2 >90. Typically hypoxia is not the problem.

• PEEP gets weird. At first you want a lower ePEEP setting to minimize mean airway pressure (because that is their inherent patho-physiological problem before we even put them on PPV). But some patients may need extrinsic PEEP added to help the pt overcome the autopeep. Why? For some, the higher intrinsic or auto peep means they need a higher pressure trigger to stimulate breathing. So you add PEEP to these patients. Bear in mind this can be tricky. Unless you are very adept at managing ventilators and interpreting the pt/vent interactions you should be doing this in conjunction with your supervising physician and a respiratory therapist.

• Allow for respiratory acidosis. Keep pH >7.2 but don’t shoot for normalization until the pt lets you know they are ready (the PIPs and ETCO2 will start to come down naturally with time and medications).