When air is forced through severely narrowed airways they vibrate and produce a sound we recognize as wheezing1. This can occur during inspiration or expiration, or during both. Any process that significantly decreases the internal airway diameter can produce wheezing. Simply inhaling an irritating substance may produce airway constriction and wheezing; or catching a cold that causes airway swelling; or developing pulmonary edema with fluid partially obstructing the airway.
You can make a wheeze if you take a deep breath and forcefully exhale, or try shouting the word ‘wheeze’ in a high-pitched voice. The wheeze will be coarser than what you are used to hearing with a stethoscope, but a wheeze it is. And it is expiratory wheezing, hallmark of the disease we call asthma.
Asthma is an ancient Greek word meaning ‘noisy breathing’ and is a disease of the bronchi and bronchioles that can attack on three fronts: airway constriction, airway hyper-responsiveness and airway inflammation3.
Remember that venus fly trap you had as a kid that you overfed and over-stimulated during its short life? Or maybe that was just my childhood experience. It was great for decimating the fly population around the house but the overly frequent input from the insects or my finger to trigger the leaf closure was not so good for the plant’s health and longevity. Asthma triggers can similarly impact the health and longevity of asthma patients.
These triggers can initiate bronchial smooth muscle contraction thus inducing bronchoconstriction, trigger an inflammatory reaction that produces swelling (think ‘hives’ inside the bronchi and bronchioles), trigger increased mucous production and trigger bronchial smooth muscle to become over sensitive to stimulation that causes it to contract (hyper-responsiveness). Common asthma triggers include infection, dust mites, cockroach parts, smoke, exercise, and stress3. The patient is often familiar with their personal triggers and may be able to tell you which one set them off this time.
Asthma cases are on the upswing and you are more likely to develop asthma if your mother smoked during pregnancy and immediately after you were born; or if you grew up in a location exposing you to dust mites or cockroaches; or if you work in an occupation where you are exposed to irritant chemicals4.
Treatment
If you had asthma in the early part of the last century your treatment may have included a prescription for asthma cigarettes or an adrenalin vaporizer5. Current therapies available for the asthmatic patient include medications to reverse bronchoconstriction, decrease inflammation or block the action of inflammatory messengers or mediators.
The inhaled bronchodilator medications either stimulate the beta 2 sympathetic receptors or block the parasympathetic receptors on the bronchial smooth muscle and induce muscle relaxation that opens the airways. Beta 2 agonist medications are the most effective at bronchodilation and include the short acting albuterol and the long acting salmeterol.
Parasympathetic receptor antagonist medications include the short acting ipratropium and the long acting tiotropium. Albuterol and ipratropium can be combined as in a Combivent inhaler. Remember that asthma cigarette? The brands that worked best were laced with stramonium leaves which affect the bronchioles like ipratropium5. The result was that your asthma got better but you died from lung cancer.
Anti-inflammatory steroids for asthma are most commonly inhaled, like Azmacort or Flovent or may be combined with a long-acting bronchodilator such as Advair or Symbicort. Steroids may also be administered intravenously or intramuscularly using methylprednisolone (Solumedrol) or taken orally as prednisone.
Suppression of the inflammatory response decreases airway edema and the production of inflammatory mediators that can cause further bronchoconstriction and swelling. These mediators include histamine and leukotrienes and do the bidding of the inflammatory cells when released into the airways.
Specific medications have been developed to block some of these mediators. Omalizumab (Xolair) is used to block the antibody IgE which is responsible for releasing histamine and other substances that trigger allergic reactions and induce asthma exacerbations. Montelukast (Singulair) and zafirlukast (Accolade) block the actions of leukotrienes which cause bronchoconstriction, hyper-responsiveness and increased mucous production3.
Chronic asthma treatment is determined by the patient’s disease severity and triggers. Mild cases may simply require intermittent bronchodilators while the more severe asthmatic will need multiple medications to maintain a steady state. For acute exacerbation or aggravation of asthma the treatment focuses on opening the narrowed airways and fortunately we can begin that process in the field with inhaled albuterol.
Your service may also have a protocol for administering steroids, but don’t expect any immediate help as it takes steroids a few hours to kick in, however when given in the field it may decrease the potential for subsequent hospital admission6. Fortunately bronchodilators and oxygen improve the majority of asthma patients with an acute exacerbation, but on occasion the patient just won’t cooperate. Near-fatal asthma patients often end up in an intensive care unit and may need intubation and mechanical ventilation to survive7.
Near-fatal asthma patients come in two varieties, those that present with the sudden onset of a life-threatening asthma exacerbation but respond quickly to treatment and those that develop their near-fatal event over several days or weeks and require a longer course of treatment. The most common and most likely to cause death is the slow onset/slow response patient with a typical history of severe asthma and medication non-compliance. Less common is the fast onset/fast response patient often with a history of recent allergen exposure or an emotional crisis7.
Either way, when your patient spirals down that near-fatal asthma path with continued hypoxia, increasing carbon dioxide levels, respiratory fatigue and altered mental status despite your best efforts and you’re thinking that tracheal intubation will soon be necessary, is there anything else you can offer this patient?
Got epi? Epinephrine or adrenalin for asthma has been around for a long time, inhaled and injected. Recall that epinephrine is a beta and alpha agonist, it is a potent bronchodilator (beta 2) but will also increase the heart rate and contractility (beta 1) and induce vasoconstriction (alpha). Fortunately the unwanted effects are generally well tolerated in the patient with life-threatening asthma even if small doses are administered intravenously8,9. However, if the patient has an adequate blood pressure, epinephrine is well absorbed from a subcutaneous or intramuscular injection. The goal is to evade all the problems that accompany positive pressure ventilation of the asthma patient.
Summary
The number of asthma patients is growing and many are plagued with other chronic diseases or practice bad habits like smoking or drug use. Anytime we complicate one chronic disease like asthma with other chronic diseases or with unhealthy habits, we increase the chance of unwanted asthma exacerbations or episodes of near-fatal and fatal asthma. And since the incidence of chronic disease in general continues to increase and there appears to be no decrease in our bad habits, you can expect increasing opportunities to care for the patient with asthma.
References
1. Forgacs P. The Functional Basis of Pulmonary Sounds. Chest 1978;73;399-405
2. Saunders KB. Origin of the Word Asthma. Thorax. 1993; 48(6):647
3. U.S. Department of Health and Human Services, National Institutes of Health, National Heart, Lund, and Blood Institute. (2007). The Expert Panel Report 3 (EPR-3) Full Report 2007: Guidelines for the Diagnosis and Management of Asthma (NIH Publication No. 07-4051). Retrieved from http://www.nhlbi.nih.gov/guidelines/asthma/asthsumm.pdf
4. King CS, Moores LK. Clinical Asthma Syndromes and Important Asthma Mimics. Respiratory Care. 2008;53(5):568-582
5. Chu EK, Drazen JM. Asthma One Hundred Years of Treatment and Onward. Am J Respir Crit Care Med. 2005;171:1202-1208
6. Kanpp B, Wood C. The Prehospital Administration of Intravenous Methylprednisolone Lowers Hospital Admission Ratres for Moderate or Severe Asthma. Prehospital Emergency Care. 2003;7:423–426
7.Restrepo RD, Peters J. Near-fatal Asthma: Recognition and Management. Current Opinions in Pulmonary Medicine. 2008;14:3-23
8. Putland M, Kerr D, Kelly AM. Adverse Events Associated With the Use of Intravenous Epinephrine in Emergency Department Patients Presenting With Severe Asthma. Ann Emerg Med. 2006;47:559-563
9. Delbridge T, Domeier R, Key CB. Prehospital Asthma Management. Prehospital Emergency Care. 2003;7:42-47
