Asthma

Clinically asthma is diagnosed when a patient has reversible airway obstruction. This is manifested by:

Increasing evidence has shown that inflammation is present in virtually all asthmatics. The initiating event for an "attack" can be either IgE mediated (extrinsic=postinfectious, occupational, exercise-induced), or non-IgE mediated (intrinsic=allergic=pollens, molds, mites, animal dander, rarely foods/occupational agents or drugs).

Asthma can present as wheezing, cough (variant in upto 15%), dyspnea, tachypnea or excessive fatigue (especially in patients with upper respiratory allergy).

In creating a differential diagnosis, always remember that "not all that wheezes is asthma", nor, "not all asthma wheezes."

This patient presents with a severe asthma exacerbation. This is important to recognize. She is tachypneic, can not speak in a full sentence, she is diaphoretic and is having pleuritic chest pain (possibly due to respiratory muscle cramps). She needs aggressive treatment with bronchodilators. Albuterol, a beta agonist, is helpful in opening up the small airways of the lung. Ipratropium (=Atrovent), an anticholinergic agent, is more useful in COPD. However, this agent works on the larger airways, so theoretically the use of Ipratropium may open up the larger airways and allow more albuterol to get to the hyperreactive smaller airways. Subcutaneous Terbutaline (beta agonist) has been shown to help in infants and children with acute asthma attacks. Studies in adults have not been so conclusive but many people will use it as another adjunctive therapy.

Fortunately, most asthmatics are young and can tolerate the tachycardia and muscle jitters that accompany aggressive use of beta agonists. Another side effect of beta agonists is a hypokalemia and for many you can actually judge how effective and frequent an asthmatic used his albuterol treatments at home by the degree of temporary hypokalemia (the potassium is shifted into cells via a beta receptor on cells).

Cromyln is a mast cell stabilizer and is used as a PROPHYLACTIC agent in patients with IgE mediated exacerbations. This is particularly useful in athletes just before an event. Thus, this is not a useful agent in a patient undergoing an acute attack as the mast cells have already degranulated.

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Question 21:

The blood gas on room air is essentialy normal. HOWEVER, she is still tachypneic! If she did not have a reactive airway disease, with a respiratory rate of 35 she should have a respiratory alkalosis with a PCO2 in the teens to low 20's. This goes points to an old premise: "never treat the numbers, treat the patient". Despite the normal blood gas she is still quite ill with a respiratory rate of 35. You need to watch her closely and either observe her clinically for evidence of hypercarbia (headaches, somnolence, nausea) and/or repeat another blood gas to see how she is trending. The ABG phases of asthma are as follows:

So based on these distinctions you should continue to observe and treat her aggressively and hope that she continues to improve clinically or by objective evidence (decreased respiratory rate, normal ABG). You do not want to intubate her yet and you DEFINITELY do not want to take away her respiratory drive with a sedative like Ativan (benzodiazepene).

References:

  1. McFadden ER, Gilder IA. Asthma. N Engl J Med 327: 1927-1937, 1992.
  2. Busse WW, Reed CE. Asthma: Definitions and pathogenesis. IN Allergy: Principles and Practice, 4th Ed., Middleton E et. al CV Mosby, St. Louis, 1993, pp. 1173-1202.
  3. Berman BA. Asthma: managing the disease, not just the symptoms. Masters in Allergy 2:4-8, 1990.
  4. Barnes PJ. Inflammatory mechanisms and nocturnal asthma. Am J. Med. 85: 64-70, 1988.
  5. Siegel SC. Evaluating agents for moderate to severe asthma. J. Resp. Dis 12:S18-S24, 1991.
  6. Mathison DA. Asthma in adults. Diagnosis and treatment. IN Allergy: Principles and Practice, 4th Ed. Middleton E. et. al CV Mosby, St. Louis, 1993, pp. 1263-1300.

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