Diffuse Wheezing: asthma, COPD, cystic fibrosis, bronchiolitis obliterans, cardiac asthma
Focal Wheezing: endobronchial tumors/foreign bodies
Stridor: laryngospasm, epiglottitis, upper airway tumors
Normal value < 10 mm Hg. Elevated values imply the combination of airways obstruction AND continued patient effort.
Normal peak flow varies with age and size but is typically greater than 400.
Accessory Muscles: trapezius, sternocleidomastoids, strap muscles.
Intercostal Retractions imply the generation of significant negative intrapleural pressure in an attempt to overcome the increased airways resistance.
When using a nebulizer, medication is placed within a holding chamber through which air is continuously bubbled creating a mist of medication which is then inhaled by the patient through a mask placed over the nose and mouth, for ten to twenty minutes until the chamber is empty.
MDI’s are small, hand-held devices which emit a spray containing a specific dose of medication when activated, typically by squeezing the MDI between the thumb and third finger. MDI’s are often used in conjunction with a “spacer” which reduces the need for coordinating the timing of MDI triggering with inhalation and also reduces the amount of large particles which are more likely to impact upon the back of the pharynx (as opposed to the smaller particles which are inhaled into the airways).
There is no data that nebulizers are more effective than MDI’s. Furthermore, nebulizers involve greater resource utilization since a therapist and/or nurse must monitor the nebulization which may take up to twenty minutes. Many patients however, especially those who are acutely bronchospastic and tachypneic, find MDI’s difficult to use effectively and thus nebulizers are more commonly used in emergency room environments.
Asthma is a disease of the airways characterized by hyperactivity manifested clinically by episodic dyspnea, wheezing, cough, and chest tightness.
Yes, this patient fits the clinical definition of asthma.
Smooth muscle hyperplasia, mucous hypersecretion, inflammatory cell infiltration, mucosal edema.
Environmental, allergens, medications (such as aspirin), pollution, occupational exposures, infections, exercise, emotional stress.
a. Cough-Variant Asthma
Cough-Variant Asthma: In a substantial number of patients the only symptom is cough.
b. Exercise-Induced Asthma
Exercise-Induced Asthma: Bronchoconstriction occurs several minutes after completion of exercise, is caused by airway drying related to the increased minute ventilation, and can be prevented by the use of pre-exercise beta-agonist inhalation. EIA may also be reduced by wearing a mask over the mouth (which traps humidity during exhalation) or by exercising in a more humid environment, i.e., swimming.
c. GERD-Associated Asthma
GERD-Associated Asthma: asthma which is triggered or exacerbated by esophageal reflux of acid. The exact mechanism is unclear. However, treatment of GERD is often associated with improvement in asthma symptoms.
d. Cardiac Asthma
Cardiac Asthma: During periods of worsening CHF, many patients develop bronchospasm. Acute relief with bronchodilators may be helpful. However, treatment of the underlying CHF is paramount.
e. Sampter’s Triad
Sampter’s Triad: the association of asthma + nasal polyps + aspirin sensitivity.
ABPA: the syndrome of bronchial hyper-reactivity to airway colonization with aspergillosis. Associated with migratory pulmonary infiltrates on CXR, expectoration of mustard colored plugs of sputum, skin test hypersensitivity to aspergillus antigen, and elevated antibodies to aspergillus. Treatment focuses primarily on long-term low dose prednisone although more recent trials suggest some potential role for oral anti-aspergillus therapy as well.
a. family history
b. associated allergic conditions
Both of these is increased in patients with asthma.
c. chronic sinus congestion / post-nasal drip
Many asthmatics have exacerbations which are triggered by chronic sinus congestion and treatment is necessary before their asthma can be controlled.
The generation of both wheezing and increased pulsus paradox requires patient respiratory muscle effort. As the patient's obstruction worsens, he/she may fatigue. At that point, wheezing may dissipate and pulsus paradox normalize.
CXR typically reveals hyperinflation, flat diaphragms, and vertical heart.
Normal acid-base status.
Early on ABG's reveal a respiratory alkalosis. Later, there may be pseudonormalization as the patient begins to fatigue. Finally, gross respiratory acidosis may occur.
A-a gradient = (PB - PH2O)FiO2 - PaCO2/RQ - PaO2
A-a gradient in this patient would be about 30. Normal is equal to 4 + age/4 and in this patient should be about 10.
Eosinophilia is frequently seen in asthmatics, however its absence does not rule out asthma.
Yellow sputum implies inflammation, not necessarily infection. Asthmatics frequently have sputum loaded with eosinophils.
Cover pneumococcus with any cheap, well tolerated antibiotic.
“Controllers” are medications which are taken on a regular basis and are aimed at reducing inflammation, thereby minimizing airway hyperreactivity. The most commonly used controllers include inhaled corticosteroids, long-acting B-agonists, leukotriene antagonists, theophylline, cromolyn, and oral corticosteroids.
“Relievers” are quick acting bronchodilators used for the immediate relief of acute bronchoconstriction. The most commonly used relievers are inhaled short-acting B-agonists.
Peak Flow meters are used for the long-term day to day monitoring of asthmatics. Over time, patients establish their “best” peak flows. Any subsequent deterioration in peak flows may be used as an indication for increased use of “controllers” hopefully before the patient suffers a severe exacerbation.
a. A patient with very infrequent, non-life-threatening exacerbations, which have always responded well to inhaled B-agonists?
· For patients with VERY infrequent, VERY mild exacerbations, the use of a B-agonist MDI on a PRN basis is appropriate (i.e., albuterol MDI, 2 puffs, PRN).
b. A patient with exacerbations which occur once or twice a week?
· For ALMOST ALL patients, standard initial therapy should consist of an inhaled corticosteroid used on a regular basis (a controller) along with PRN B-agonists (a reliever). While not clearly established in the literature as of this time, certain subsets of patients may be candidates for alternative first-line therapy:
n children may be candidates for cromolyn (a non-steroidal anti-inflammatory medication)
n patients with exercise induced asthma and/or aspirin sensitivity may be candidates for leukotriene antagonists as first line therapy
n patients who cannot understand or appropriately manipulate a metered dose inhaler (and therefore cannot use inhaled corticosteroids) may be candidates for an oral medication as first line therapy
c. What options exist for a patient such as that described in “b” above who fails to respond adequately to your initial recommended therapy?
Second line therapeutic options include:
· increasing the dosage of inhaled corticosteroids
· the addition of a long-term B-agonist
· the addition of a leukotriene antagonist
· the addition of theophylline
There is evidence that each of these options may be effective however there is little head-to-head comparison data indicating which is best.
· Oral candidiasis and hoarseness are the most common side effects and may be minimized and/or prevented through the use of a spacer and by rinsing out one’s mouth after each use.
· Other potential side effects include cataracts, suppression of the hypothalamic-pituitary-adrenal axis, and reduced bone mineral density. All are more likely when high dose inhaled corticosteroids are used and their risk must be balanced against the known morbidity and mortality associated with sub-optimally treated asthma.
PFT’s are most useful when the diagnosis of asthma is in doubt and/or the patient fails to respond to standard therapy. PFT’s are not necessary in the majority of patients with asthma, since the diagnosis is primarily made on clinical grounds.
Yes. These PFT's reveal obstruction (low FEV1 and FEV1/FVC ratio) as well as a significant bronchodilator response (as evidenced by at least a 10 to 15% increase in FEV1 in response to bronchodilator).
No. With emphysema, one would also see evidence of obstruction (low FEV1 and FEV1/FVC ratio) as well as hyperinflation ('d TLC) and gas trapping ('d RV) but one would expect the DLCO to be reduced and there to be less acute response to bronchodilator.
No. One would then consider performing a bronchoprovocation test such as methacholine or dry air challenge.