The Sick Asthmatic
The sick asthmatic is one of the scariest calls you may run. You need to understand this is different from other respiratory distress. Your treatments can have a profoundly negative impact on the patient if you don’t understand the physiology. But if you do understand what is going on, you can make a real difference and save a life.
The 5 Principles of Asthma
- Asthma is an exhalation problem not on inhalation problem
- Understanding this is paramount
- Bronchodialators are the mainstay of treatment
- Albuterol, albuterol, and more albuterol
- Epi is a potent bronchodialator and should be considered in life threatening asthma
- Use the same dose as in anaphylaxis
- NIVPP ventilation can be used as an attempt to temporize and avoid intubation and to assist in delivering medications
- NIVPP can improve medication delivery, decrease work of breathing and avoid intubation. We really want to avoid intubation if we can.
- Intubation almost always makes things worse and should only be preformed if absolutely necessary.
- If you must intubate, make sure your allowing proper exhalation time. Pay attention to you I:E.
Thankfully, today, with better access to healthcare and increasing use of asthma controller medications the super sick asthmatic, patient is rare. So when we do see these patients most commonly it’s because they’ve run out of their meds or simply have been noncompliant with their meds.
Asthma is an exhalation problem not on inhalation problem
Understanding this is paramount
This very point is what helps us to understand why asthma can be so difficult to treat and why we can’t approach it like we do any other respiratory disease process.
COPD, CHF, and pneumonia are problems mainly of inhalation or gas exchange. What that means is, in these diseases, we can use positive pressure to drive air in and help improve oxygenation.
But in asthma it’s SOOOOOO important to understand, they don’t have a problem getting air in. They have a problem getting air out. So we can force more air into the lungs but then they still can’t get that air you forced in out and this leads to over inflation by a process referred to as air trapping.
Picture blowing up an air mattress by mouth. As it fills up, it becomes more difficult to blow more in past the air that’s already trapped in the mattress. At some point, so much air gets trapped in the mattress that you can’t force any more in. It just goes into the valve and comes right back out. In addition, you feel that trapped air pushing back against you as you try to get it passed the valve. This is what we call dead space ventilation. Dead space ventilation is the air exchange between just the trachea and the bronchi.
- This is referred to as the dead space because there’s no oxygen exchange in these areas.
In order for oxygen to be delivered to the blood it must make it to the alveoli. But the alveoli have become so over distended with trapped air that they can’t let any fresh air in.
This is what makes asthma so challenging to treat. Because sure, if we really want to, we can force more air into the alveoli by increasing the driving pressure of inspiration. This is what we do when we put someone on positive pressure ventilation like intubation or to a lesser degree CPAP. For diseases like CHF, COPD, and even Pneumonia this often works great. But in the case of asthma where the problem is that they still can’t get air out. We just worsened our problem by increasing the over distension and air trapping that’s occurred within the alveoli.
- At some point the overdistension in the alveoli may become so severe that a spontaneous pneumothorax can occur.
Bronchodilators are the mainstay of treatment
Once we understand the pathophysiology we can better understand why bronchodilators are so important.
- It is imperative to open up those bronchioles in order to let that trapped air out.
Beta-agonists, such as albuterol, work primarily on the beta-2 receptors in the lungs leading to bronchodilation.
- Albuterol can cause some transient tachycardia. But if you see an increase in heart rate make sure to reassess your patient and assure you are not missing something before you blame it on the albuterol.
Epi is a potent bronchodialator and should be considered in life threatening asthma
Albuterol, albuterol, and more albuterol is almost always the answer. But there are some advantages to epinephrine.
1st of all it’s rapid onset and high efficacy. This makes epinephrine an ideal medication for life threatening asthma.
- The patient you’re worried might die in front of you.
The other advantage to epinepherine is that it is given intramuscularly and thus does not rely on the delivery to the bronchioles.
- If the patient is not improving despite albuterol it may be that the patients bronchoconstriction and air trapping is so severe that your medications are not making it deep enough into the respiratory tract to have the desired effect.
The dosing for this is similar to your anaphylactic dosing. You’ll give it intramuscular at a dose of 0.3 – 0.5mg for an adult and 0.15mg for peds. And you can repeat after 5min as needed.
Epinephrine does have disadvantages though. Epi is a potent non-selective beta agonist. Meaning it non-selectively activates the beta – 2 receptors in your lungs as well as the beta-1 receptors in your heart.
- This means it will cause an increase in heart rate and blood pressure.
This will lead to an increase in myocardial oxygen demand which can be detrimental in certain circumstances. So we won’t reach for it in the mild-moderate asthma exacerbation. But in the life threatening super sick asthmatic we should absolutely reach for this as it can be life saving.
Terbutaline is very similar to epi in that it is an intramuscular beta-agonist. But it has the advantage of being more beta-2 selective with less effects on beta-1 and so doesn’t have as much of the undesirable effects on heart rate and blood pressure.
- That being said, the rarity of the sick asthmatic patient and the limited uses for terbutaline make it less practical to keep stocked on an ambulance.
NIVPP ventilation can be used as an attempt to temporize and avoid intubation as well as to assist in delivering medications
If your medications aren’t working, of course consider alternative diagnosis, but if you’re still sure this is asthma, one of three things are likely true.
- You need more albuterol and then more albuterol.
- You may need a different route of delivery that doesn’t rely on the respiratory system, i-e. intramuscular epi.
- You need to buy more time for the medications to start working.
I touched on the dangers of positive pressure in asthma above, and it’s for that reason that historically CPAP and BiPAP have been considered ineffective for asthma. But principal 5, which we’ll get to, says that intubation almost always makes things worse and should be avoided unless absolutely necessary. So, if we’re trying to avoid intubation CPAP and BiPAP make a lot of sense. They can decrease the patients work of breathing and help prevent them from tiring out.
- This will hopefully buy more time for the medications to start working.
In addition, the non-invasive positive pressure may help facilitate delivery of our albuterol deeper into the lower airways.
Intubation almost always makes things worse and should only be preformed if absolutely necessary.
But as we all know, sometimes we don’t get the choice to avoid the things we don’t want to do.
The reasons that push you to have to intubate in asthma most commonly include:
- Inadequate respirations secondary to respiratory muscle fatigue
- Failure to oxygenate despite the measures we discussed before.
If one of these occurs you may be forced to intubate.
- If you must intubate, use the method you are most comfortable and facile with.
Goal here is to be as fast as possible. But, remember, slow is smooth and smooth is fast. If you have RSI capabilities, Matt recommends 1.5 mg/kg of Ketamine and Rocuronium each. Ketamine has bronchodilation properties and so may be the ideal sedative to use in this situation.
- Once intubated make sure you’re allowing proper exhalation time. Pay attention to your I:E. Ideally for every 1 second of inhalation you would allow at least 5 seconds of exhalation time.
Magnesium- We purposefully did not discuss magnesium in this episode. Some may use this medication in a “kitchen sink” approach in the severe asthmatic. Magnesium causes smooth muscle relaxation. The goal here is to relax the smooth muscles within the lungs and allow for more bronchodilation.
That being said, its use is somewhat controversial and recent studies have called into question its theoretical utility. Regardless, it is not the medication that is going to save the patient’s life. Your primary focus should be on beta-agonists and more beta-agonists. If there’s time after that, you can consider whether magnesium may be helpful.
Pneumothorax- As discussed earlier, because of all that air trapped in the alveoli, the inspiratory pressure needed to get air in rises sharply. If the peak pressures become too high, the patient can develop a spontaneous pneumothorax. The majority of the time, this is because of us adding positive pressure to the system with intubation. But, it can rarely occur in the spontaneously breathing patient too.
Signs that this may have just occurred are:
- A sudden increase in work of breathing
- A sudden decrease in oxygen saturations
- Tracheal deviation
- Crepitus to the chest wall or neck from subcutaneous air.
You can diagnose this by recognizing the signs and symptoms just mentioned combined with absent or decreased breath sounds unilaterally.
- This is treated just like any other tension pneumothorax, with needle decompression.
Word of caution: I will say these are very complicated patients who have multiple reasons to have an increased work of breathing and decreased oxygen saturations outside of a pneumothorax; if you think this may have happened and are considering needle decompression, it may be worth a phone call to your medical control to discuss what you are seeing and get a fresh mind and ear on the case.
- This can be a good check to make sure you’re not missing something.
Cardiac Arrest- In the setting of cardiac arrest secondary to asthma exacerbation, consider pneumothorax as a possible etiology. But use the same principles as above to diagnose and determine if needle decompression is warranted. I do not recommend empirically decompressing.