In a Prolonged Asthma Attack, Start at the End

I was recently intrigued by an article published on Ems World titled “In a Prolonged Asthma Attack, Start at the End”

The articles authors Gene Gandy, Steven Grayson and Jason Kodat discuss how the acute severe asthma attack starts and progresses. The article goes on to suggest that the treatment given during a (prolonged) asthma attack is given in the wrong order.

Below is the article reproduced in full, I would like to thank Jonathan Bassett, Editorial Director at Ems World for allowing me to do so.

The link to the original article is:
I can also recommend paying their website a visit for a wide range of interesting articles.

I would love to hear other people’s thoughts on this article.

In a Prolonged Asthma Attack, Start at the End

 By William E. “Gene” Gandy, JD, LP May 31, 2017


Asthma is a deadly disease. Rarely are EMS practitioners presented with a case where time is truly of the essence in whether a patient dies, but the prolonged severe asthma attack is one of those situations. Often called status asthmaticus, these attacks do not respond to routine prophylaxis and treatment with inhaled bronchodilators 

There are many reasons for this, including the patient’s family history, the agent causing the attack, the patient’s sensitivity to the causative agent, the patient’s general health and many others.  

There are many pitfalls in treating the acute severe asthma attack. One of the most common is failure to appreciate the seriousness of the patient’s condition and why it has not responded to prescribed bronchodilator drugs. This leads to repeating treatments that haven’t worked and won’t, and delay in administering the treatment that will do the patient some good.  

In this article, authors Gene Gandy, Steven Grayson and Jason Kodat discuss how the acute severe asthma attack starts and progresses. 

Jason: It turns out that even though the two main types of asthma, atopic (triggered by environmental allergens) and nonatopic (most often triggered by infection), have different developmental pathways, the acute attack is remarkably similar—possibly because the infections in nonatopic asthma simply increase the bronchioles’ responsiveness to environmental allergens.

Mast cells lining the bronchioles—the culprit in anaphylaxis as well—release their inflammatory granules, causing localized bronchoconstriction, airway edema and mucus production. Parasympathetic stimulation enhances the effect. This is the early phase and typically responds well to bronchodilators. If severe bronchospasm isn’t relieved within an hour of aggressive treatment, you can call it status asthmaticus.

Then there is the late phase, which is again multifactorial. The mast cells in the acute phase also release dozens of inflammatory mediators besides histamine: leukotrienes, prostaglandins, cytokines. These will cause additional inflammation up to eight hours later, lasting for a day or more. Additionally, other cells in the bronchioles have been found to release similar markers—other inflammatory cells, the vascular endothelium and even the airway epithelial cells themselves.

In the very long term, the airway can actually remodel itself to have thicker, more responsive smooth muscle, fibrotic changes that make the lungs less pliable and inclusion of inflammatory cells—which makes things even worse. 

Kelly: Typically we treat asthma patients with inhaled beta-2 agonist bronchodilators like albuterol sulfate or levalbuterol, often with concomitant administration of ipratropium bromide to block the parasympathetic pathways that lead to increased inflammation and mucus production. But typically we look at interventions like noninvasive positive pressure ventilation (NIPPV), intramuscular epinephrine, intravenous corticosteroids and magnesium sulfate as interventions of last resort.  

The problem is, by the time we get involved in patient care, our patient is often in that second phase of an asthma attack Jason mentioned. The inflammation mediated by those humoral antibodies, cytokines and leukotrienes is less easily broken with inhaled bronchodilators. If the symptoms could be easily relieved with inhaled bronchodilators, the patient wouldn’t have called 9-1-1.

Repeated administration of nebulized bronchodilators to these patients fits the definition of insanity: doing the same thing over and over, expecting a different result. There are more effective treatments we can employ if we can recognize the signs of a severe asthma attack and overcome mental and organizational barriers to rendering the proper treatment. In the status asthmaticus patient, those interventions of last resort should actually be our primary interventions. 

Gene: So how do we address the asthma patient who is extremely sick and on the verge of respiratory and cardiac arrest? Let’s look at a case that illustrates the dangers of failure to appreciate the serious condition of a patient having a prolonged asthma attack: 

It is 1700 on a crisp November afternoon. Our patient, Roger, is a 47-year-old male with a long history of reactive airway disease. He takes inhaled corticosteroids and long-acting beta agonists to control his chronic symptoms. He is not, however, 100% compliant with his steroid medications and beta drugs because he does not like the way they make him feel. He has an albuterol/ipratropium inhaler he uses when needed.  

Today he begins to suffer symptoms of an asthma attack when he inhales smoke from a neighbor’s burning leaf pile. This happens shortly before noon. His first sign is coughing, which soon progresses to dyspnea and wheezing respirations. He uses his inhaler but gets little relief. Shortly thereafter he finds his inhaler empty and sends his wife to town to get a fresh one. When she returns she finds him in distress, so she helps him use the inhaler, but he continues to cough up mucus, and his breathing becomes more difficult.   

Roger is obese and has a low energy level. As his breathing gets harder and harder, he begins to sweat, and his respiratory rate increases to the point where he’s breathing 30 times a minute. His heart rate increases to around 100 bpm. His wife wants to call 9-1-1, but Roger resists and insists the albuterol just needs time to work.   

By now he is wheezing, has coarse crackles during both inspiration and expiration, is breathing with very short breaths and coughing up tons of thick, gooey mucus. He has used his inhaler more than a dozen times without any relief. In fact, his condition continues to worsen.

Gene: Jason, why isn’t Roger’s inhaler giving him any relief?

Jason: First, this has been going on long enough that the symptoms are now largely driven by those late inflammatory mediators—none of which are responsive to the beta-2 agonism albuterol is going to provide. Since exhalation is a passive process, the airway swelling has trapped air in the alveoli, making a deep breath impossible, which in turn makes delivery of albuterol to the bronchioles nearly impossible—not that it matters, because the rapid breathing during the attack has dehydrated the patient, and the mucus now being produced is too thick for the cilia to actually move it; thus the bronchioles are coated to the point where hardly any receptors would be exposed to the albuterol. Additionally, the patient can’t depend on a boost from native catecholamines—norepinephrine levels have been shown to increase during an asthma attack, but not epinephrine levels, and epinephrine is much more potent at the important beta-2 receptors.

Roger’s wife decides to call 9-1-1 in spite of his wishes, and by now he agrees. She tells the call-taker what is happening to Roger and that he has been using his inhaler over and over without any relief.   

Medic 6 is dispatched for “a man having an asthma attack.” After a 14-minute response, the crew locates his house and enters to find Roger standing and leaning against a kitchen counter, gasping for breath. He has audible wheezes and little short breaths in between coughing and spitting out mucus. He can only speak one or two words at a time. He is sweating and pale and has a look of panic on his face. 

The medic directs the EMT to get vital signs while he prepares an albuterol/ipratropium nebulizer treatment. The EMT reports a heart rate of 106, respiratory rate of 30 and unobtainable blood pressure because the EMT can’t hear the sounds over the patient’s breathing. His temperature is 98.4ºF by tympanic thermometer. He cannot tolerate an oral thermometer. 

The crew places the nebulizer on the patient and assists him to a chair to sit down. This effort seems to cause him to struggle to breathe even more. After a few minutes of this, he suddenly leans backward and begins to seize. The crew places him on the floor and determines he is not breathing and does not have a pulse.   

Kelly: The crew of Medic 6 believes they’re responding to an asthma attack. Dispatch told them that’s what the complaint was, and they found a patient wheezing and in respiratory distress. What the crew of Medic 6 doesn’t realize is that they’re responding to the end of an asthma attack. That the patient has taken multiple doses of his inhaler without relief didn’t make it into the dispatch notes, and the patient and his spouse are too panicked to relay that information. The patient is in the periarrest phase. All the signs are there: two-word dyspnea, severely diminished tidal volume, and the cool, clammy skin, tachycardia and tachypnea of a sympathetic nervous system response, only without—as Jason pointed out—the all-important beta-2 effects of epinephrine.   

They’re busily fogging albuterol and ipratropium around his upper airways—the only ones left open—because their decision-making in this patient started at the beginning of their asthma protocol. The patient was beyond that point before his spouse ever called 9-1-1. They need to start at the end of their asthma protocol, with that series of interventions that often follow the words by physician order only.   

Jason: At this point everything we’ve talked about has come to a head: inability of the drugs to reach the target receptors, lack of protection from the body’s own catecholamines, a sludge of mucus further narrowing already-bronchospastic airways. Inhaled drugs of any sort aren’t going to cut it at this point. Now you need the big guns: mag sulfate, epi or terbutaline, ketamine if you’re going to intubate. CPAP or BiPAP might help you avoid intubation, although the literature on it isn’t as strong as the literature on positive pressure in CHF. Steroids are also essential (125 mg of methylprednisolone IV or 10 mg of dexamethasone IV), although they’re going to take longer to work.

Magnesium is a great smooth muscle relaxer and can help open the bronchioles—and its effect has shown to be greatest in the sickest patients. Intramuscular epi or terbutaline can give a catecholamine boost, which nicely reverses all the bad effects of the mast cells and parasympathetic nerves. (Our friends in countries outside the States can actually use IV albuterol.)

Ketamine is the induction agent of choice in these folks (we’ve been looking at it since 1986 or before),2 although you really need to do everything possible to not intubate these patients. It may be less effective later in the attack, because part of its mechanism of action seems to include triggering native catecholamine release, but it’s also been shown to have direct effect on the smooth muscle. A couple of studies have shown no improvement in pulmonary function with ketamine, but they were using subanesthetic doses.3 Propofol also has some bronchodilatory properties, but given its effect on hemodynamics, it’s not used as often or studied as well as ketamine.

If you do intubate these patients, make sure to give them a nice, slow respiratory rate—8, maybe 10. They need time to exhale. Make sure their SpO2 is at least 90%, but don’t start ventilating faster, even if their EtCO2 is 70 mmHg. (This is called permissive hypercapnia.) If they start to stack breaths, disconnect them from the BVM or vent, and apply gentle pressure to the chest to help exhale. 

Gene: Now let’s run back the clock and start over with the crew being dispatched and arriving. 

The call-taker enters a note for the controller advising that the patient is having a prolonged asthma attack that has lasted over four hours and has not responded to over a dozen doses of the albuterol/ipratropium inhaler. Upon hearing this the medic grabs the drug box and begins preparing drugs to be given on arrival: epinephrine 1:1,000 0.5 mg and a vial of ketamine for use if needed. The crew discusses plans for arrival. After initial size-up, if Roger is in the shape they expect, the medic will give the epinephrine IM immediately and the EMT will get him on CPAP at 5 mmHg. Time will not be wasted obtaining initial vital signs. You can tell by looking that he’s in trouble. Knowing his blood pressure and temperature will do nothing to help you right now.

Immediate epinephrine 1:1000 IM (adult dose: 0.3–0.5 mg IM; pedi dose: 0.01 mg/kg up to 0.3 mg IM) would reactivate beta-2 receptor cells in the airway and cause bronchodilation. It will also counteract the histamine secretion from mast cells by reducing histamine release. If available, IM terbutaline would be an acceptable substitute.

CPAP will help push oxygen into the hyperinflated alveoli, and you can administer albuterol/ipratropium via CPAP by using a T connector as well. However, take care not to apply too much pressure, since the air sacs are hyperinflated and it is possible to cause a pneumothorax. 

Ketamine is a drug with powerful bronchodilation powers. While there is not a lot of evidence from trials on its use in acute asthma, there is empiric support for its use.4 An adult subsedation dose of 0.75–1 mg/kg (pedi: 1.5 mg/kg) can be given IM immediately to help with bronchodilation.

As soon as IV access is accomplished, run normal saline wide open. Asthma patients become dehydrated for several reasons: They lose more moisture from rapid breathing, and they use more energy while fighting to breathe. This causes the airway to dry out and mucus secretions to dry and thicken, occluding access to beta receptors in the lining of the airway. Airway dehydration triggers exercise-induced bronchoconstriction.

Give methylprednisolone 125 mg IV (pedi: 2 mg/kg IV), or dexamethasone 12–20 mg IV (pedi: 0.6 mg/kg IV), and start giving magnesium sulfate 2 grams IV over 10 minutes (pedi: 50 mg/kg IV over 10 minutes). Now reassess the airway and see if the patient is responding to the drugs or if he will need to be intubated. If possible, monitor his capnography waveforms, looking for the typical “shark fin” wave pattern and determining if it is resolving toward a normal plateau. Also monitor his EtCO2, which should be coming down. If CPAP is not working, the patient should be intubated. Ventilation with the BVM is difficult in asthma patients, and they need to be on a ventilator if intubated. If he needs to be intubated, do not delay further. Sedate him the rest of the way with more ketamine and intubate.

If he is improving, you can now start an albuterol/ipratropium nebulizer treatment.   

Monitor the patient’s blood sugar level, since the energy expended in fighting to breathe will use up glucose. This is particularly true in diabetics. Give glucose based upon blood glucose levels as required.   

During this time do not do anything to further stress your patient, such as asking him to stand up and walk, or place him in another position. If he is in the tripod position, he has already found the best position for himself. Do not change that. You can intubate just as easily with him sitting up as lying down. In fact, if you use a forward pull on the laryngoscope (the so-called “tomahawk maneuver”), you will get an excellent view of the airway most of the time.   

Kelly: I often practice the ABCs (ambulate before carry), but there are certain instances where I would never walk a patient to the stretcher, and this is one of them. Patients in extremis, like Roger, simply may not have the reserves to take even a few steps to your cot.  

We need to remember that status asthmaticus is a different critter entirely than simple reactive bronchospasm, in the same way that anaphylaxis is a different animal than an uncomplicated allergic reaction. It needs to be treated far more aggressively. 

If your asthma protocols limit interventions like epinephrine, mag sulfate and intravenous corticosteroids to physician order only, come up with a plan to streamline that interaction. Contact medical control en route to the scene and try to obtain “if/then” orders. Lobby your medical director for a codicil that allows you to proceed with lifesaving interventions if the delay in obtaining orders would harm the patient. 

But whatever you do, don’t start at the beginning of your protocol when your patient is already at the end.

Jason: Asthma is one of those situations where you can legitimately take someone from the brink of death to stable in the time you spend on a typical ambulance call. You just have to know how to make that happen.  

William E. “Gene” Gandy, JD, LP, has been a paramedic and EMS educator for over 30 years. He has implemented a two-year associate degree paramedic program for a community college, served as both a volunteer and paid paramedic, and practiced in both rural and urban settings and in the offshore oil industry. He lives in Tucson, AZ.

Steven “Kelly” Grayson, NRP, CCEMT-P, is a critical care paramedic for Acadian Ambulance in Louisiana. He has spent the past 22 years as a field paramedic, critical care transport paramedic, field supervisor and educator. He is a frequent EMS conference speaker and author of the book En Route: A Paramedic’s Stories of Life, Death, and Everything In Between and the popular blog A Day in the Life of an Ambulance Driver.

Jason Kodat, MD, EMT-P, has been in EMS for more than 15 years. He has reviewed EMS textbooks and the USFA’s EMS Handbook for EMS Medical Directors, and lectures at regional EMS conferences regularly. He currently works as an emergency physician and associate EMS medical director at hospitals near Pittsburgh, PA.

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  1. Daniel Straw 13/01/2018 Reply

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