by Robin R. Hemphill, MD


This is a 52 year old black male brought by EMS with an asthma exacerbation. Pt notes worsening shortness of breath for 2 days not responding to nebs. Not responding to MDI at home. No fever/chills. No cough. One albuterol neb given in field with little to no change.

Never intubated, several previous hospitalizations, but none in the last 6 months. No long term steroid use.

PMHx: Asthma

PSHx: Appy

Meds: MDIs

Cardiac Risks: None.

Thin male diaphoretic and pale sitting upright in obvious distress. Speaks in 2-3 word sentences.

Exam significant for: Decreased breath sounds with little air movement throughout. Positive accessory muscle use. Positive prolonged expiratory phase. Minimal wheezing heard.

Cardiac: Tachycardic but regular.

No JVD, tracheal deviation, or leg edema. No unilateral leg swelling.

The remainder of the exam is essentially normal.

ECG: Sinus tachycardia with no acute changes.

CXR: No infiltrate or pneumothorax.

ED Course:

The patient receives two nebulizations and steroids with no response to therapy. He remains tachycardic, diaphoretic, and severely short of breath. An ABG is drawn and shows the following results: Gas on 100%: 7.25/203/53/23.

Goals and Objectives for Medical Students and Interns:

1. Be aware of the historical features of an asthmatic patient that increases their risk of a complicated course.

2. Be able to discuss the differential diagnosis of asthma and the pathophysiology.

3. Be aware of the well proven pharmacologic therapies available for asthmatic patients and the indications for each.

4. Be aware of the need for laboratory testing and radiographs in the asthmatic patient.

5. Be able to discuss the implications of the above ABG.

6. Be able to discuss admission criteria for the asthmatic patient.

ED course continued:

The patient has received three albuterol nebulizations, steroids and has made no progress. His chest is quiet with little air movement and he can only speak single word sentences. He now appears slightly confused and will not respond to directed questions. His pulse oximeter is reading 94% on a 100% non-rebreather.

Goals and Objectives for Junior residents:

1. Be able to answer the goals and objectives for students and interns.

2. Be able to discuss the pharmacologic interventions that are less well proven for severe asthma exacerbations, but might be of benefit.

3. This patient is nearing respiratory failure. Be able to discuss the pros and cons of nasal vrs. Oral intubations.

4. Be able to discuss the different medications available for rapid sequence intubation, the potential risks of each type of medication.

5. Be able to manage the asthmatic patient on a ventilator.

ED course continued:

The patient has had a modified rapid sequence intubation done and is now on a ventilator. The patient is tachycardic, but suddenly develops a heart rate of 170-200. The blood pressure is stable at 130/85.

The ECG is shown.

Goals and Objectives for Senior residents:

1. Be able to answer the goals and objectives for interns, and junior level residents.

2. Be able to discuss the complications of an acute asthma exacerbation.

3. Be aware of the complications that occur in the intubated asthmatic.

4. Be able to treat dysrhythmias in the asthmatic patient.


Asthma is one of the most common respiratory diseases, with an incidence of more than 5% of the total population in industrialized countries. The prevalence and severity of asthma appear to be increasing in these countries, and there has been an increase in the death rate. This trend is disturbing since treatment modalities were thought to have been improving.


Asthma is defined as a condition of airway hyperreactivity and reversible airflow obstruction that results in intermittent symptoms of wheezing, dyspnea, and cough. However, asthma is more than simple reversible airflow obstruction. A working definition of asthma should include underlying airway inflammation with its physiologic correlate, bronchial hyperresponsiveness. While the vast majority of patients with this disease are easily managed in the outpatient setting, any patient with asthma has the potential to develop status asthmaticus. Status is defined as asthma that is severe at its onset or progresses rapidly despite standard therapy. Without successful management it may progress to ventilatory failure and death.


Smooth muscle lines the respiratory tract from the trachea to the alveolar ducts and is under autonomic control. The sympathetic fibers lead to bronchodilatation and the parasympathetic fibers cause bronchoconstriction. These sympathetic fibers have receptors that are further broken into alpha and beta receptors with the beta -2 receptors being involved in bronchodilatation. During an asthma attack there are three components that lead to the clinical manifestation of wheezing. (1) Smooth muscle spasms under the influence of the cholinergic system leading to bronchoconstriction. (2) Additionally, there is a considerable amount of inflammatory exudate in the airways. This leads to an intense inflammatory reaction that causes increased mucosal permeability further exposing the smooth muscle and irritant receptors to the noxious stimuli. (3) Finally, there is mucus plugging of the segmental and subsegmental bronchioles.

Early Asthmatic Response:

Extrinsic asthma is characterized by a well-defined sensitivity to specific inhaled allergens. Mast cells appear to play an important role in the early response of allergic asthma. When the IgE-sensitized respiratory mast cell is exposed to a specific antigen, it results in degranulation of the mast cell. Mast cell derived mediators include histamine, bradykinin, leukotrienes, prostoglandins, etc. Release of histamine from luminal mast cells contributes to opening of tight junctions in the airways allowing entrance to allergens, inhaled particles, and other inflammatory mediators into the submucosa and subsequent stimulation of other mast cells. This begins within 10 minutes of inhalation of offending particles, peaks in 30 minutes, and resolves in 3 hours.

Late Asthmatic Response:

In some subjects who develop an early asthmatic response, the airway narrowing persists and either does not return to baseline or recurs after 3-4 hours and reaches a maximum in the next few hours, sometimes lasting up to 24 hours. This is the late asthmatic response. The late response is thought to be mediated by an influx of neutrophils, eosinophils, and mononuclear cells into the bronchoalveolar tissues. The exact stimulus for their migration is not clear. The clinical implications of the early and late asthmatic phases are crucial because therapy may be directed toward each phase.

Differential Diagnosis:

Several etiologies should be considered in the wheezing patient since we all know the phrase "all that wheezes is not asthma". An important illness to exclude is upper airway obstruction, in which stridor is the prominent differentiating sign. In older patients congestive heart failure (cardiac asthma) must be considered and excluded by history, CXR, and ECG. Older patients that are experiencing a first episode of wheezing should be evaluated for pulmonary embolism. COPD can mimic asthma, although a long history of smoking in an older patient usually helps clarify this picture. Often, the patient will be well versed about their disease and can tell you exactly what they have. Why not use every available resource? Other diseases to consider include, tracheobronchitis, due to infection or irritants, aspiration, anaphylaxis, proximal bronchial obstruction by tumor or foreign body, and rare cases of sarcoidosis, TB, and extrinsic alveolitis.

Clinical Features:

The most common symptoms of asthma are cough, wheeze, and dyspnea. Thus, patients often present with a complaint related to one or all of these symptoms. There are several historical features that should elevate the level of concern about the severity of the patient's asthma. Those that have a history of prolonged steroid use, previous and frequent hospital admission, hospital admissions despite prolonged steroid use, pneumomediastinum or pneumothorax, and prior intubations, have severe asthma and are at high risk for decompensation. Patients are at higher risk for death if they have chronically worsening asthma as documented by pulmonary function testing. Also at risk are asthmatics that return to the department with continued symptoms over hours, days, or weeks with no improvement documented. This longer duration of symptoms increases the amount of mucus and inflammation that are present. These patients are less likely to improve with emergency department interventions. Patient's with comorbid diseases such as coronary artery disease are at greater risk for compromise from both the disease as well as the treatments. This was a concern with the patient presented in the above case.

Physical exam:

Findings during an acute exacerbation of asthma are those of hyperinflation and diffuse wheeze in all lung fields. However, in severe cases, as muscle fatigue sets in, there may be few audible wheezes and the chest may be ominously quiet. The two most reliable physical findings in judging the severity of the acute attack are sternocleidomastoid muscle use, and the presence of pulses paradoxes greater than 12-20 mmHg. Additional clinical features suggestive of a severe asthma attack include mental status change with obtundation, late presentation of the patient, severe fatigue on arrival, paradoxical respirations, cyanosis, diaphoresis, significantly elevated pulse rate. The asthmatic too dyspneic to speak and sitting bolt upright is having a severe attack. Other features that may have precipitated the event should be sought, such as crepitance in the neck or chest indicating the possibility of pneumothorax. The trachea should be evaluated for deviation. Objective measurements of the degree of outflow obstruction can be made using bedside determination of PEFR or FEV1. It is usually easier to get a measurement of the PEFR. As a general rule a PEFR or FEV1 of less than 30-50% of predicted indicates a severe asthma exacerbation. This usually corresponds to a PEFR of 120 L/min and FEV1 of less than 1 liter. If the patient knows their personal best, a value of 30-50% less than this is concerning. Attempts to measure this value should not be done in the patient with a very severe attack.

Historical and Physical Features Indicating Severe Asthma:

History: Physical:
  • Previous intubation
  • Patient sitting upright or leaning forward
  • Frequent hospitalizations
  • Diaphoresis
  • Hospitalizations despite chronic steroids
  • Pulses paradoxes greater than 12 mmHg
  • Chronic steroid use
  • Tachycardia greater than 120 beats/min
  • Pneumothorax/pneumomediastinum
  • Sternocleidomastoid muscle use
  • Prolonged attack
  • Cyanosis

  • Unable to speak more than 1-2 words

  • Silent chest on examination

  • Altered mental status

  • PEFR less than 30-50% predicted
  • Laboratory Testing:

    As the use of a pulse-ox has become standard in most emergency departments there is much less need for arterial blood gases (ABG) in those patients with mild to moderate asthma attacks. The oxygen level can easily be followed in these cases. However, in those patients with status asthmaticus and little improvement with treatment the ABG still has a role. As an asthma attack worsens the patient develops hypoxia, an increased PaCO2, and occasionally a metabolic acidosis. Patients with a concerning ABG not only require hospitalization, but may need admission to a monitored setting. Arterial blood gas values consistent with severe asthma include hypoxia (PaO2 < 60mmHq), acidosis (pH<7.35), and hypercarbia (PACO2 >40mmHg).

    Chest radiographs, like ABG's, have little use in the mild asthmatic patient. Several studies have noted a low occurrence of significant pathology in mild asthmatics. Chest radiograph should be considered if the history or physical exam suggest that an abnormality will be found (pneumonia, pneumothorax). Patients with severe asthma attacks who are going to be admitted should usually have a chest radiograph as it may show an unsuspected pneumothorax, infiltrate, or severe atelectasis.


    Asthmatic patients presenting to the department should be brought back for treatment immediately and should have supplemental oxygen initiated. A brief history should be taken to determine the severity of the patient's asthma and the degree of the present attack. Intravenous access should be obtained if the patient appears to be in severe distress.

    Acute Pharmacologic Interventions:


    Oxygen should be given to most asthmatics. The degree of hypoxia is often not reflective of the PEFR. Thus, patients who appear to have good PEFR may still be hypoxic. If pulse oximetry is not available, oxygen should be given to all asthmatic patients. Usually, patients are placed on 2-3 liters of oxygen by nasal cannula. Another good reason to place most asthmatics on oxygen is that their oxygen saturation may vary over time. It is not uncommon for the oxygen saturation to drop during the course of treatment.


    The beta2 -agonists are the fastest and most efficacious medication to help alleviate bronchospasm in the acute asthmatic and are clearly the treatment of choice. Epinephrine was the prototype of these medications and can still be used in extreme circumstances, but in most cases it does not appear to give added benefit. Beta2-agonists are catecholamine derivatives that act via an accumulation of cAMP in the cells thus causing relaxation. They should be considered the main therapeutic intervention for the asthmatic patient. While the beta2 -agonists relax bronchial smooth muscle, they also help decrease bronchospasm and constriction, and help inhibit the release of inflammatory mediators. Additionally, they appear to increase ciliary movement. Invariably there is some beta1 cross reactivity that causes the tachycardia frequently seen with these agents. The long acting beta-agonists such as salmeterol, have no place in the acute management of asthmatic patients in the emergency department because the onset of action is markedly delayed.

    There are several ways that these agents can be administered including PO, SQ, via MDI's, and via nebulizers. The PO route is less useful in the acute situation and the most common route in the emergency department is via inhalation. There is good evidence that the MDI is as effective as the nebulized form if proper coaching can be done in the emergency department (especially if a spacer is available). However, in the young child, or those in severe distress the nebulized form may be the more effective route. This is clearly a debatable point and if time allows close coaching, supervision, and if a spacer is available, it is reasonable to attempt therapy with an MDI as it is fast and inexpensive. Previous treatments given at home should not limit the use of beta-agonists in the department unless the patient is having intolerable side effects (tachycardia, vomiting, arrythmia). When a nebulizer is used the dose is generally 2.5 mg (0.5cc in 2.5 cc of normal saline) of albuterol every 20 minutes for three doses. The patient should be reevaluated between doses, and if marked improvement is noted additional doses can be withheld. After three doses the patient should be assessed for improvement. If there is minimal progress at this point, additional therapy can still be given, but the clinician should begin to consider admitting the patient. Children appear to tolerate higher doses of albuterol than do adults and a "double dose (1.0 cc)" is generally considered safe in this population. Studies in children and adults also show that continuous nebs may be equally as beneficial as intermittent therapy with no greater increase in side effects. This may be particularly true for the more ill asthmatic. At our institution we do not routinely use continuous nebs for adults but do use it for pediatric patients. It is delivered via a Maxi-air device which at 8 liters of O2 flow delivers 20 cc of fluid an our. To this device is added 2 cc of albuterol (10 mg) solution mixed with 18 cc of normal saline. This will deliver 10 mg of albuterol per hour. The potassium level needs to be followed if continuous nebulization is to be used to insure hypokalemia does not develop.

    In severe cases of asthma a SQ form of beta-adrenergic therapy may be appropriate. Generally, the SQ routes do not offer any advantages over the inhaled route unless the patient is unable to take a nebulizer or has not responded to inhaled medication. Thus, patients with altered mental status, or those in extremis, may be given SQ doses of epinephrine or terbutaline. Obviously, in an older population the risks of giving these medications must be weighed with the possibility of inducing dysrhythmias or myocardial ischemia. If a pregnant patient is being treated in this manner, terbutaline is a better choice as epinephrine has been associated with birth defects. The dose of terbutaline is 0.25mg in adults. In extreme conditions intravenous beta-agonists can be considered if all other measures have failed (Epinephrine 1mg of 1:10,000).


    As discussed previously, the airway smooth muscle is controlled predominantly by vagal innervation. Anticholinergic drugs are used to antagonize this pathway. While the use of anticholinergics have been shown to be beneficial in COPD, the role in asthma is less clear. There are three preparations available in the United States. Atropine was used in the past but had significant side effects; thus, synthetic analogs of atropine are now used in place of atropine. Ipratropium bromide and glycopyrrolate have less systemic absorption and are better tolerated than atropine. Unlike the beta-agonists, the effects of these agents may not be not seen for 1.5-2.0 hours.

    Previously, the only nebulized form available was glycopyrrolate. Recently Atrovent (Ipratropium) has become available for use in a nebulized form. The exact role of these agents has yet to be defined but there does appear to be some benefit. At this point, it is difficult to make exact recommendations for use as some studies show no greater benefit to the use of anticholinergics than simply giving another dose of a beta-agonist. Other studies show benefit if the anticholinergic is mixed with a beta-agonist, still other studies show no benefit to this method of administration. Overall, since there does appear to be synergism between these two types of medications, and there is little evidence that administration of anticholinergics will cause severe side effects, it is reasonable to use these agents. However, the anticholinergic agents should probably be reserved for those patients with moderate to severe asthma exacerbations (500 mcg unit dose added to beta-agonist treatment). Care should be taken when giving anticholinergics to patients with a history of glaucoma as it is possible to precipitate acute angle closure.


    It is important to remember that asthma is, at least in part, an inflammatory disease. Thus, the ability of steroids to treat inflammation, makes them useful agents. These agents can be administered in several ways, and there is clear benefit to their use either orally, IV, or IM. Recent studies have shown that oral dosing is as effective as IV forms if equivalent doses are given. They should be given routinely for all but the mildest asthma attack as they have clearly proven to decrease the rate of relapse and mortality. The use of inhaled steroids in the acute phase of the asthma attack is less clear. Some sources recommend against the use of a steroid MDI as the agents used in the MDI can actually be irritating. However, a recent study used nebulized steroids during an acute asthmatic attack and had good results. This area should probably be further studied. The clinical benefit is in part related to enhanced responsiveness of the beta 2- receptors to catecholamines after steroids are given. Corticosteroids also suppress synthesis of inflammatory mediators in the bronchial tree and inhibit migration and activation of inflammatory cells. If the patient is discharged home they can be put on a short 4-5 day burst of oral steroids (40-50 mg a day). If there is a concern of compliance with this regimen, a single IM dose of Depo-Medrol (methylprednisolone 2mg/kg up to 60-125 mg) can be used. There is no need for a steroid taper with this treatment. The need for steroid taper should be considered with those patients on chronic steroids, or with those who have had several recent treatments with steroid bursts. While the main benefit of steroids will not be seen for 4-6 hours, there is good evidence that they help decrease the rate of relapse.


    This agent is a methylxanthine that has been widely used in the prophylaxis and treatment of asthma. It is thought to work via several methods : 1) bronchodilator 2) increasing diaphragm strength and decreasing fatigue, 3) CNS respiratory stimulant, 4) and as a diuretic. The exact mechanism of how these effects occur is not clear. The role for theophylline in the setting of the acute asthma exacerbation is open to some debate. There are numerous studies that document the lack of effect of theophylline, and others that show an increased number of adverse effects when this drug is used. It appears that theophylline given as a single agent is not very effective. However, this agent is not typically used alone. Combined with other asthma medications there are some studies that show a decreased rate of hospitalization and improvement of asthma symptoms when theophylline is added. These types of studies would hint that some of the other mechanisms mentioned above might be beneficial to the asthmatic patient. Theophylline may also have a role in infants, children, or those who will be more compliant with an oral medication, than an inhaled one. Currently, the National Heart, Lung, and Blood Institute's panel recommends that methylxanthines not be used in the Emergency Department setting for the acute asthma exacerbation. This recommendation can be tempered in the patient who has life-threatening asthma as long as the patient is closely monitored as the medication is given. The usual loading dose of aminophylline is 6 mg/kg over 30 minutes followed by a 0.5 mg/kg/hr drip. This regimen needs to be altered in patients with liver disease or congestive heart failure because the clearance rate of aminophylline is decreased.


    Bolus infusions of magnesium (1.2-2.5 gm IV over 20 min) have recently been suggested as having use in severe asthma exacerbation. It is thought that magnesium infusion reverses bronchospasm by counteracting calcium-mediated smooth-muscle constriction. This mechanism has not been clearly proven. Benefit has only been shown in a few small studies or case reports, and larger controlled studies have not reproduced these results. It is possible that the rates of infusion were too slow or that magnesium is only useful in severely ill asthmatics, but these theories have yet to be proven. If given with care, magnesium is a safe medication and most studies have not documented any severe adverse reactions to the magnesium. No specific recommendations can be given about the use of magnesium at this point, but many centers do treat their severe asthmatics who are unresponsive to other medications, with a bolus of magnesium.


    Ketamine is an IV anesthetic that has sedative, analgesic, and bronchodilatory effects. It generally gives adequate sedation while leaving the airway reflexes intact and causing only minimal respiratory depression. Many sources have suggested the use of ketamine as an induction agent for asthmatic patients requiring mechanical ventilation. There have been multiple reports of intubation being avoided after ketamine was infused or a dramatic improvement in the respiratory status of the intubated asthmatic patient after ketamine was administered. There are few studies looking at whether low dose ketamine could be useful in the management of mild to moderate asthma exacerbations. One recent article found no difference in outcome in patients receiving low dose ketamine (0.1 mg/kg) compared with those receiving placebo. As one might imagine the patients receiving ketamine were more satisfied with their care. At this time, ketamine can be recommended as an induction agent as well as a sedating agent for a young otherwise healthy population of intubated asthmatic patients. In this setting it may provide both desired sedation as well as well as bronchodilatory effects. The dose is 1-2 mg/kg IV at a rate of 0.5mg/kg/min.

    Ketamine increases laryngeal secretions and if it is being used for an induction agent the clinician should be prepared to handle this. Other risks of ketamine use result from the ability of this agent to increase heart rate and arterial blood pressure secondary to its sympathomimetic effects. Therefore, it should be used with care, if at all, in patients with high blood pressure, coronary artery disease, or increased intracranial pressure. It also may lower the seizure threshold and cause mood alteration and delirium in up to one-third of patients above the age of 16.


    Heliox is a mixture of helium and oxygen that has a density less than oxygen alone. The combination may be used as an 80:20, 70:30, or 60:40 helium:oxygen. These mixtures improve ventilation by decreasing resistance to flow and by increasing CO2 diffusion. It may be given through a tight fitting mask in non-intubated patients, or through the inspiratory limb of the ventilator apparatus. The decrease in airway resistance may decrease the work of breathing and help alleviate muscle fatigue. At this time heliox might be considered in the mechanically ventilated patient who has high peak inspiratory pressures and has an unresolving respiratory acidosis. For the non-intubated patients with moderate to severe asthma exacerbations, further studies need to be done before recommendations can be made about the routine use of heliox.


    Although it is well known that infections may trigger asthma exacerbations, the majority of infections are of a viral etiology. If patients have evidence of acute bacterial, mycoplasma pneumonia, or sinusitis antibiotics should be given. Those patients with fever and evidence of polymorphonuclear cells in a good sputum sample should also receive antibiotics. The routine use of antibiotics for other asthmatics is not recommended.

    Disposition Recommendations:

    If a patient has a good response to the therapeutic interventions then it is appropriate to discharge these patients home. The pulse oximetry should be checked prior to patient discharge to insure adequate oxygenation. Some experts recommend that PEFR be 70% of predicted prior to discharge, but it is important to remember that PEFR is a dependent on patient effort and at times other criteria need to be considered in allowing dismissal. All but the mildest asthma exacerbation should be sent out on a brief burst of oral steroids, a regular schedule of beta-agonist use, and arranged follow-up when possible. Those patients who have an incomplete response to treatment as indicated by continued wheezing, dyspnea, hypoxia, or a PEFR of 40-70% predicted should have hospital admission considered. If the patient is stable they can be admitted to a ward bed with close monitoring. Those patients who have already failed an outpatient trial of therapy for their exacerbation should also be considered for admission even if they appear to be improving.

    Patients who present with an asthma exacerbation and have deterioration during treatment are candidates for admission to an intensive care setting unless they have complete reversal of this trend. Other patients that show evidence of severe airflow obstruction, who are clearly deteriorating, who show evidence of impending respiratory failure, or who continue to show little response to maximal intervention should be admitted to the intensive care unit.

    Management of Respiratory Failure:

    Patients who continue to worsen despite maximum treatment can have sudden respiratory arrest and death. It is not optimal to wait until the patient is nearly moribund from CO2 narcosis to take control of the airway. Rather, if active airway intervention is inevitable, it is preferable to make this decision early in the presentation. This should not be cause to take this procedure lightly in the asthmatic patient. Those asthmatics that require intubation have a significant rate of morbidity and mortality.

    While it is possible to intubate the patient via the nasotracheal route there are several significant disadvantages. Nasotracheal intubations often take longer, the tube used must be smaller, there may be nasal trauma which will worsen the respiratory status and cause bronchoconstriction, and it may increase the anxiety level of the asthmatic patient. Several sources suggest that modified rapid sequence oral intubation by the most experienced clinician is probably the safest method of airway control in the asthmatic. The endotracheal tube should be as large as possible to allow adequate suctioning of mucus plugs and to decrease airway resistance. For those patients who are likely to be difficult to orally intubate (you know the types!) then a nasal placement is acceptable and allows the patient to remain awake and in control of their own airway.

    The best agents to facilitate intubation is controversial. Ketamine, as mentioned previously, is an anesthetic agent that some authors recommend because of its sedating properties, lack of respiratory depression, and bronchodilating effects. However, others have stated concern that this agent causes myocardial sensitization to catecholamines which can precipitate dysrhythmias. Others advocate the use of pentothal even though there is concern of histamine release and many would say that this agent is contraindicated in asthma exacerbations. Another reasonable choice is to use low doses of benzodiazepines, particularly in patients who may have complications from the use of ketamine. Other sources advocate the use of propofol or etomidate as an induction agent as well as for protracted sedation. Morphine should be avoided because it releases histamine. The patient should then have a modified rapid sequence intubation with the initial doses of paralyzing agent being avoided so as not to depress respirations. The patient must be pre-oxygenated as much as possible. Induction can be accomplished with succinylcholine followed immediately by intravenous ketamine or other preferred agent. After intubation 2cc of 2% xylocaine can be injected down the endotracheal tube to improve tolerance of the tube (although IV lidocaine may help do this as well). As was the case for sedating agents for intubation, there are several choices of paralyzing agents. Pavulon is an agent which may have some bronchodilator activity, however, it can cause tachydysrhythmias. Succinylcholine has the potential to release histamine and worsening the bronchoconstriction. There is question if this is of clinical significance. Vecuronium is a reasonable agent since it has almost no cardiovascular effects. It is up to the clinician to determine whether there is even a need for paralyzing the asthmatic patient beyond the induction period.

    Management of these patients on the ventilator can be difficult and the significant mortality rates are contributed to by the high airway pressures generated during mechanical ventilation. These elevated airway pressures can lead to poor ventilation, circulatory compromise, and severe barotrauma. The goals of therapy are to achieve adequate alveolar ventilation, minimal circulatory compromise, and low risk of barotrauma. Muscle relaxation should be continued as should sedation during the initial period of post-intubation stabilization. Even the fully sedated patient will often exhibit high alveolar pressures. Most data indicates that the best way to manage the asthmatic patient is with small tidal volumes and high inspiratory flow to minimize dynamic hyperinflation. The high inspiratory flow rate will allow for a longer period of exhalation which is helpful in the hyperinflated asthmatic patient. Tidal volumes should be in the order of 8-10cc/kg with a respiratory rate of 12 - 15 and inspiratory flow of 60-100 L/min. Avoid giving applied PEEP to these patients. The goals of ventilatory therapy are an acceptable peak airway pressure (<50 cmH2o), minimal intrinsic PEEP (<15) , eucapnea, and stable circulation. If eucapnia is difficult to achieve without high airway pressures, then controlled hypoventilation may be attempted. Most patients are able to tolerated some degree of hypercapnea without adverse effect. However, if a severe respiratory acidosis develops this can be offset with a bicarbonate infusion. This type of procedure is best done in conjunction with a pulmonary or intensivist. If the patient continues to have problems on the ventilator halothane or enflurane anesthetics may be considered for their bronchodilating effects. When these medications are used there is usually a decrease in airway pressures and in PCO2 levels, but this effect stops when the agents are withdrawn. Both of these agents have significant cardiac depressant effects and should be used by an anesthesiologist.

    Noninvasive Ventilation in the Asthmatic Patient:

    Recently, nasal CPAP has been introduced for use in a specific subset of severe asthmatic patients. It is an option that can be tried for a limited period of time in an attempt to avoid intubating the asthmatic patient. It is thought to be appropriate in patients with hypercapnic ventilatory failure who are not in need of immediate intubation or in those who have severe asthma and have not yet responded to the pharmacologic interventions being provided. It cannot be used in the obtunded patient or those with an altered mental status. There are several studies showing good outcomes when this modality was used in severe asthmatics who still had the ability to cooperate with the procedure. Potential risks of this method of airway intervention include: gastric aspiration, patient discomfort, facial pressure necrosis, and the potential for deterioration.

    Further studies need to be done before this modality can be recommended for all severe asthmatics who are nearing respiratory failure. Until these studies are completed this procedure should be used with caution and only by those familiar with the CPAP device.

    Other Complications of Acute Asthma Exacerbation:

    Supraventricular tachydysrhythmias are common during an asthma exacerbation for multiple reasons. The combination of adrenergic stimulating agents, anticholinergics, hypoxia, electrolyte imbalances, and acidosis all add up to make the patient a high risk for dysrhythmias. Sinus tachycardia is the most common rhythm and is usually well tolerated by the patient. Unfortunately, there are a variety of other rhythms that can be more dangerous and will not be tolerated by the already stressed individual. Patients who develop these dysrhythmias tend to be older. When these dysrhythmias develop is incumbent upon the emergency medicine physician to be able to treat them in a logical manner.

    Paroxysmal atrial tachycardia may be treated with an agent such as verapamil (the usual contraindications apply) as it acts at the AV node and also has weak bronchodilating properties. As always, a patient with an unstable tachdysrhythmia should be cardioverted. Adenosine, normally the drug of choice for supraventricular tachycardias, should be avoided if possible as it may worsen bronchoconstriction. Beta blockers should be avoided due to the risk of worsening bronchospasm.

    Multifocal tachycardia is best treated by dealing with the underlying pulmonary problem. Try to find metabolic abnormalities such as hypokalemia, hypomagnesemia, hypoxia, and theophylline toxicity and correct them. Beta- agonist therapy may have to be held temporarily while rate control with an agent such as verapamil is attempted. If the blood pressure is stable, magnesium can probably be given to these patients.

    Atrial Fibrillation with rapid ventricular response can be treated with synchronized cardioversion if unstable. Otherwise digoxin and calcium channel blockers may be effective. Finally, ventricular dysrhythmias can develop and should be treated as normal. The addition of rapid IV push of magnesium should be considered early as it appears to be beneficial in ventricular tachycardia associated with asthma.


    1. Barbee R: National Asthma Education Program Guidelines for the Management of Asthma. Resident and Staff Physician 1993; 39: 35-46.

    2. Belloma R, McLaughlin, Tai E, et al.: Asthma requiring mechanical ventilation. A low morbidity approach. Chest 1994; 105:891-96.

    3. Bloch H, Silverman R, Mancherje N, et al.: Intravenous magnesium sulfate as an adjunct in the treatment of acute asthma. Chest 1995; 107:1576-81.

    4. Bone RC, Burch SG: Management of status asthmaticus. Ann Allergy 1991; 67:461-468.

    5. Corbridge TC, Hall JB: The assessment and management of adults with status asthmaticus. Am J Respir Crit Care Med 1995; 151:1296-1316.

    6. Dorn M, Wrenn K, Slovis C: When asthma attacks turn deadly: Principles of aggressive, effective intervention. Emerg Med Report 1991; 12:21.

    7. George R, Owens M: Bronchial asthma. DM 1991:143-191.

    8. Hemming A, MacKenzie I, Finfer S: Response to ketamine in status asthmaticus resistant to maximal medical treatment. Thorax 1994; 49:90-91.

    9. Howton JC, Rose J, Duffy S, et al.: Randomized, double-blind, placebo-contolled trail of intravenous ketamine in acute asthma. Ann Emergen Med 1996; 27:170-175.

    10. Karras D: Asthma: Current Therapeutic Strategis and Comprehensive Patient Management. Emerg Med Report 1994; 15:18.

    11. Kino, R: Asthma controversies: A literature review. 1995 Scientific Assembly Lecture.

    12. Kornrich W, Fontanarosa P: Determining the proper role of glucocorticosteroids in the emergency department. Emerg Med Report 1991; 12:25.

    13. McDonald A: Asthma. Emerg Med Clinics 1989; 7: 219-235.

    14. National Asthma Education Program: Executive summary: Guidelines for the diagnosis and management of asthma. Department of Public Health 1994.

    15. NIH Conference: Asthma. Ann Int Med 1994; 9: 698-708.

    16. NIH. Acute exacerbations of asthma: Care in a hospital-based emergency department. National Asthma Education and Prevention Program. U.S. Department of Health and Human Resources 1994.

    17. Portnoy J, Nadel G, Amado M, et al: Continous nebulization for status asthmaticus. Ann Allergy 1992; 69: 71-79.

    18. Spector S: Asthma and chronic obstructive disease: A pharmacologic approach. DM 1991.

    19. Weinberger M, Hendeles L: Theophylline in asthma, NEJM 1996; 334:1380-1338.

    Return to the Clinical Review first page Return to EMBBS Home Page