Asthma

Published on 10/03/2015 by admin

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Chapter 21 Asthma

Ali Al-Alwan, MD , Gilman B. Allen, MD , David A. Kaminsky, MD

1 What are important factors to address when taking the history of patients with acute severe asthma?

Box 21-1 summarizes the important historical points in a patient with acute severe asthma. If the clinician is able to obtain a history from the patient, it is important to first exclude other possible causes of the patient’s presentation. A history of heart failure may suggest wheezing and shortness of breath resulting from left ventricular failure and pulmonary edema. A history of allergies or prior anaphylactic reactions, along with a recent exposure to certain foods, new medications, or other known triggers, could be an important warning of potentially imminent upper airway inflammation and closure. A history of recent-onset cough, wheezing, and hemoptysis with unilateral inspiratory and expiratory wheezes could be clues to an intrabronchial tumor, such as a carcinoid or carcinoma. Pulmonary embolism can also mimic asthma and should especially be considered in the patient with dyspnea, anxiety, and hypoxemia but clear breath sounds. In a patient with dyspnea, anxiety, and inspiratory stridor, vocal cord dysfunction should be considered. Spirometry can be an especially useful tool in the emergency department (ED) when evaluating these patients, and flow-volume loops often show the characteristic truncated or flattened inspiratory loops.

Box 21-1 Important Historical Points in Acute Asthma

History of asthma (i.e., when diagnosed, type of treatment, common triggers)

Timing of onset of symptoms (i.e., gradual versus sudden)

Nature of symptoms (e.g., wheezing, chest pain, intermittent versus continuous, associated cough, sputum production, fever)

Exclusion of other causes of shortness of breath (e.g., heart failure, pulmonary embolus)

Exclusion of other causes of wheezing (e.g., bronchospasm from allergic reaction, endobronchial tumor)

Consideration of paradoxical vocal cord closure on inspiration (i.e., vocal cord dysfunction)

3 Which patients are at greatest risk for near-fatal or fatal asthma?

A survey of North American adult patients with asthma seen in the ED identified a number of factors associated with a high number of ED visits, including nonwhite race, Medicaid, other public or no insurance, and markers of chronic asthma severity, such as history of prior hospitalization, intubation, or recent use of inhaled corticosteroids. Also at increased risk for near-fatal asthma are patients with a high degree of bronchial reactivity, those with a history of poor compliance with therapy and follow-up, and those judged to be poor at perceiving the severity of their own attack, as demonstrated by a poor correlation between reported symptoms and peak expiratory flow (PEF) values. These are patients for whom home monitoring of PEF is strongly indicated.

Patients in whom sudden, severe attacks develop or those who have severe, slowly progressive disease are both typically at risk. A history of marked diurnal variation in forced expiratory volume in 1 second (FEV₁) is also believed to be a risk factor, but this could simply be related to its being a marker for increased bronchial responsiveness. Historical data indicate that female sex, endotracheal intubation, and prolonged neuromuscular blockade are associated with more prolonged hospital stay, whereas elevated arterial CO₂ level and lower arterial pH within 24 hours of admission are associated with increased mortality.

Although not widely identified as a true marker of increased risk, the use of inhaled heroin is also frequently associated with near-fatal or fatal attacks of asthma. It is not known whether this is due to a direct effect of the inhaled drug (or its diluents), the degree of airflow limitation, or simply the impaired judgment of the user that delays arrival to the ED and initiation of appropriate care. However, opioids have long been known to cause bronchoconstriction via mast cell degranulation and histamine release. Although most reports of severe asthma attacks after inhalation of narcotics are in patients with known asthma, they have also been reported in patients without any history of asthma.

4 How should one treat a severe asthma attack?

Oxygen therapy to achieve an arterial oxygen saturation of 90% or greater.

β-Agonists: These are the first-line therapy in an acute asthma attack. It is now widely accepted that the inhaled forms of these drugs are superior to the subcutaneous or intravenous (IV) route, with fewer adverse affects, and their administration can be repeated up to three times within the first hour after presentation while monitoring for adverse effects such as tachyarrhythmia and lactic acidosis, the latter of which can be underrecognized. The subcutaneous route is still reserved for patients who have such severe dyspnea that they are unable to take deep-enough breaths, but these are usually the patients who later undergo intubation. It is also accepted that metered dose inhalers are as effective as aerosolized delivery, provided good technique is used with a spacer device. Nebulized or aerosolized delivery is still used frequently in the ED, in part from convention and in part because less instruction and observation are needed to ensure good delivery. The use of salmeterol as an outpatient monotherapy was recently shown to increase the risk of hospitalization. However, this increased risk was not seen among patients receiving combined therapy with inhaled corticosteroids and salmeterol (Table 21-1).

Corticosteroids: These drugs also play a key role in treatment, and typical dosage is 60 mg of IV or PO methylprednisolone every 12 to 24 hours for the first 24 hours. This must be delivered as soon as possible because peak onset of action can take several hours. Therapy is typically administered every 6 hours until the attack appears to be subsiding and then gradually tapered over days to weeks. Comparisons between oral prednisone and IV corticosteroids have not shown differences in the rate of improvement of lung function or in the length of the hospital stay. Thus the oral route is preferred for patients with normal mental status and without conditions expected to interfere with gastrointestinal absorption.

Anticholinergics: Many studies have shown a marginal benefit from adding inhaled ipratropium to β-agonist therapy (versus β-agonists alone) in the treatment of acute asthma.

Aminophylline: Oral theophylline is a third-line agent in the outpatient management of asthma. This is in part due to the recognition of its intrinsic antiinflammatory properties, even at serum levels lower than those once thought necessary to achieve significant benefit. However, the use of IV aminophylline in the treatment of acute asthma remains controversial and is no longer recommended.

Inhaled epinephrine: A recent meta-analysis of using inhaled epinephrine in refractory asthma demonstrated a similar degree of bronchodilation and PEF improvement when compared with albuterol. The use of inhaled epinephrine is safer than IV epinephrine, which is associated with a higher risk of acute myocardial infarction and tachyarrhythmias.

Inhaled anesthetic agents: In patients receiving mechanical ventilation with ongoing severe bronchospasm despite aggressive conventional treatment, inhaled anesthetic agents can be used for their intrinsic properties of bronchodilation. Because their delivery requires a special apparatus and conventional therapy is usually more effective, their use is often considered as a rescue therapy only. Isoflurane or enflurane are the agents of choice.

Antibiotics: There is no benefit to the routine use of antibiotics in the management of an acute asthma episode unless findings are suspicious for pneumonia or other bacterial infections.

^{Table 21-1} Primary Pharmacologic Treatment of Acute Asthma *

Agent	Dose	Comments
β-Agonists	4-8 puffs (90 mcg/puff) MDI + spacer, every 20 min up to 4 hr, then every 1-4 hr as needed or 2.5-5 mg nebulized every 20 min for 3 doses, then every 1-4 hr as needed

Inhaled better than subcutaneous or IV

MDI + spacer works as well as nebulized

Elevated lactate levels seen after high doses

Corticosteroids

40-80 mg per day PO or IV in 1 or 2 divided doses until PEF = 70% of predicted or personal best

Continue for 3-10 days, tapering if dose continues for longer than 7 days

Single 160-mg intramuscular depot injection of methylprednisolone has been found to be as effective as an 8-day tapering course of the same dose of oral methylprednisolone once patients discharged

Anticholinergics

8 puffs (18 mcg/puff) MDI + spacer, every 20 min as needed up to 3 hrs or

0.5 mg (500 mcg) nebulized every 20 min for 3 doses, then as needed

Improves lung function and reduces rate of hospitalization when added to standard care

Combined use with inhaled β-agonists is beneficial

Oxygen

Titrate to SaO₂ > 92%

Avoid excessive oxygenation, which can result in CO₂ retention

Use humidified oxygen

Other agents (magnesium sulfate, heliox, leukotriene antagonists, inhaled anesthetics) discussed in text.

MDI, Metered dose inhaler, SaO₂, oxygen saturation.

^* Per EPR3 Guidelines for treatment of acute asthma in adult patients.

5 Does magnesium sulfate offer any benefit in the treatment of status asthmaticus?

Although a small number of controlled trials have yielded mixed results, one controlled study suggests that patients with severe asthma (FEV₁ < 25% predicted) treated with IV magnesium sulfate in the ED had significantly reduced admission rates compared with those treated with placebo. A more recent meta-analysis did not support these findings. Proposed mechanisms of possible benefit are as follows:

Blockage of calcium channels and reduced calcium entry into smooth muscle cells, leading to bronchodilation

Possible inhibition of mast cell degranulation

Improving respiratory muscle function by correction of lower baseline serum levels

Because the only reported adverse side effects from a single dose of magnesium are flushing, mild fatigue, or burning at the IV site, its use in the treatment of persons with severe asthma may be warranted by its potential for lowering admission rates, but this remains a controversial topic. Magnesium sulfate is generally delivered as 2 gm in 50 mL of normal saline solution given IV over a 20-minute period. Interestingly, inhaled magnesium sulfate administered with inhaled β- agonist has also been shown to improve lung function and may reduce the rate of hospital admission.

6 How can one best decide when to admit a patient and when to discharge a patient from the ED?

Patients who have a poor response to treatment are defined by persistent wheezing, dyspnea, and accessory muscle use at rest despite 3 hours of treatment in the ED. Such patients should be admitted to the hospital. One study suggests that in persons with severe asthma (peak expiratory flow rate [PEFR] and FEV₁ < 35% of predicted), improvement in PEFR measured 30 minutes after initiation of therapy may be an early predictor of response to treatment after 3 hours. Any patient with worsening PEFR, rising PaCO₂, or advancing fatigue should, at the very least, be monitored in the intensive care unit and possibly undergo intubation. A recent study developed a classification tree for use in risk stratification for hospital admission for acute asthma. This validated scheme involved three key variables, history of hospitalization, peak flow, and oxygenation, and was entitled the CHOP classification:

Change in PEF severity category

History of prior hospitalization for asthma

Oxygen saturation with room air

Initial peak expiratory flow

Signs of good response to therapy in the ED that would allow a patient to be discharged include a sustained response of at least 1 hour after the last treatment with FEV₁ or PEF ≥ 70% predicted, no distress, and improvement in physical examination results. The Expert Panel Report 3 (EPR3) guidelines emphasize that such patients be instructed to continue their therapy at home with inhaled short-acting β-agonists; be given a 3- to 10-day course of oral corticosteroids; consider initiation of inhaled corticosteroids; receive education on medications, inhaler technique, and use of a written action plan and possibly a PEF meter; and arrange for medical follow-up within the next 1 to 4 weeks.

7 Which patients need to have an endotracheal tube (ETT) placed?

Any patient with apnea, near apnea, or cardiopulmonary arrest should have an ETT placed. Any patient with progressive lethargy, somnolence, near exhaustion, or unresponsiveness should have an ETT placed. An elevated PaCO₂ level on admission, although shown to be associated with increased mortality, may not necessarily warrant immediate endotracheal intubation. Any patient with a progressive rise in PaCO₂ despite therapy and increasing fatigue most likely will require intubation. Other signs would include a silent chest, an inability to maintain oxygenation by mask (oxygen saturation < 90%), and visible cyanosis. Other relative indications are coexistent medical conditions that can increase minute ventilation requirements or compromise oxygen delivery, such as sepsis, myocardial infarction, metabolic acidosis, or life-threatening arrhythmias.

8 Is normocapnia or hypercapnia an absolute indication for intubation in a person with asthma?

Most persons with severe asthma are initially seen with hypocapnia because of the hyperventilation associated with dyspnea and hypoxemia. A normal or elevated PaCO₂ is usually a sign of fatigue but can also be due to a high dead space–to–tidal volume ratio resulting from air trapping and ineffective ventilation of noncommunicating segments of lung. In either case, it should be taken seriously and can be a sign of impending respiratory failure. Studies indicate, however, that most patients with normal or elevated PaCO₂ on blood gas analysis at initial evaluation improve with time in response to conventional therapy and do not require intubation. Because mechanical ventilation in severe asthma can be complicated by increased air trapping and barotrauma, it is advisable not to perform intubation and mechanical ventilation in a patient with acute asthma merely on the basis of an elevated PaCO₂, unless concomitant somnolence, progressive fatigue, or worsening acidosis exists.

9 Can noninvasive mechanical ventilation be used safely to avoid intubation in a person with asthma?

Noninvasive positive-pressure ventilation (NIPPV) via face mask has been shown to be safe and effective when applied to a patient with severe asthma and hypercapnia whose condition fails to improve with conventional therapy. It can be effective in unloading respiratory muscles, improving dyspnea, lowering respiratory rate, and improving gas exchange. NIPPV has been shown to be an effective potential means of avoiding endotracheal intubation and may also help avoid the need for reintubation after extubation. However, it is also critical to determine early in a patient’s course whether he or she is responding appropriately to NIPPV, because delays in endotracheal intubation may be associated with worse outcomes. NIPPV should not be used in persons with asthma who have life-threatening hypoxemia, somnolence, or hemodynamic instability, and it should be aborted in patients whose conditions fail to improve or who cannot tolerate the mask.

10 Are helium admixtures of any proved benefit in treating severe asthma?

When helium (He) is blended with oxygen (in a 20% O₂, 80% He or 30% O₂, 70% He mixture), the gas density becomes approximately one-third that of room air, but viscosity is increased, leading to increased laminar flow and a reduction in airway resistance in areas of greatest turbulent flow. This can result in a reduction in the work of breathing required to meet the same minute ventilation requirement when breathing room air. Because work of breathing is reduced, it would seem likely that respiratory fatigue might be delayed until conventional therapy has had time to take effect. Despite numerous trials and two recent meta-analyses, no evidence yet exists that helium-oxygen (heliox) admixtures can prevent the need for endotracheal intubation. However, heliox has been shown to improve PEFR and reduce the degree of pulsus paradoxus in acute asthma attacks. This is presumably due to the decrease in airway resistance and lower generated negative pleural pressures but also possibly caused by improved expiratory flow and less dynamic hyperinflation (DHI). The improved laminar flow afforded by heliox may also allow deeper lung deposition of inhaled aerosols. Because heliox mixtures typically include only 20% to 30% oxygen, hypoxemia is a barrier to use of heliox. However, when the patient does not have hypoxemia, it is safe and worthwhile to use, particularly in patients with fatigue and hypercapnia who are at risk for progressing to the point of requiring mechanical ventilation.

11 Once a patient requires intubation, what is the best management strategy?

Intubation: Blind nasoendotracheal intubation is often better tolerated by an awake patient, but oral endotracheal intubation is the preferred method of intubation because it permits the use of an ETT with a larger internal diameter. This will lead to lower resistance within the respiratory circuit and allow easier deep suctioning of secretions and mucous plugs. It is important to remember that the resistance of a tube is indirectly proportional to its internal radius (to the fourth power), and the resistance of an 8-mm ETT is roughly one-half that of a 7-mm ETT. Oral intubation is indicated for patients with apnea and cyanosis. Because intubation in a person with asthma is often difficult and may induce laryngospasm or lead to increased bronchospasm, it should be performed by the most experienced person available, and rapid-sequence technique should be used. Because of its intrinsic sympathomimetic and bronchodilating properties, ketamine has been advocated by many as the induction agent of choice to avoid the possible loss of sympathetic tone and drug-induced vasodilation, thus helping to prevent cardiovascular collapse. The usual dose of ketamine for intubation is 1 to 2 mg/kg, given IV over a 2-minute period. Sedation is usually necessary, and, although sometimes warranted, paralysis should be avoided if possible. Barbiturates such as thiopental should not be used because of their association with histamine release and potential worsening of bronchoconstriction. Although the narcotic fentanyl is often useful because it inhibits airway reflexes and causes less histamine release than morphine, one should be aware of its potential to trigger bronchoconstriction and laryngospasm.

Avoiding potential complications: Some authors advocate hand bag-ventilating patients with asthma immediately after intubation to assess the severity of bronchospasm and avoid dynamic hyperinflation by slowly delivering a rate of 4 to 5 breaths/min as a bridge to mechanical ventilation. Ensuring adequate humidification of inspired gas is particularly important to prevent thickening of secretions and drying of airway mucosa, which can promote mucous plugging and further bronchospasm.

DHI: When airflow limitation is severe, the next ventilated breath can be initiated before the lungs can fully empty to a normal functional residual capacity, resulting in progressive air trapping. This leads to DHI and elevated end-expiratory alveolar pressures, referred to as intrinsic positive end-expiratory pressure (PEEP_i). Measuring PEEP_i can be problematic, and it is often underestimated by the brief end-expiratory pause used to estimate it on the ventilator. This is due to the heterogeneous distribution of early airway closure that can prevent many hyperinflated segments from communicating their alveolar pressures to the transducer at the airway opening. Ideally, PEEP_i should be kept below 15 cm H₂O. The key determinants of DHI are minute ventilation, tidal volume, exhalation time, and severity of airflow limitation. DHI can often be predicted by elevated plateau pressures and failure to achieve zero expiratory flow before the next delivered breath. DHI can lead to less effective respiratory muscle contraction and added work because of less optimal curvature of the diaphragm, which in turn can lead to less effective triggering of the ventilator. DHI can also lead to decreased venous return and right ventricular preload, increased right ventricular afterload (via extrinsic compression of the pulmonary vasculature), and decreased left ventricular compliance, which can all lead to diminished cardiac output and hypotension. When strongly suspected, the best immediate solution (and test) is to briefly disconnect the ETT from the ventilator circuit to allow for more complete exhalation. The other concern with DHI is that the high degree of associated PEEP_i can ultimately lead to barotrauma.

Barotrauma: High airway pressures can potentially lead to pulmonary interstitial emphysema, subcutaneous emphysema, pneumomediastinum, pneumothorax, and even pneumoperitoneum. Barotrauma correlates directly with the degree of DHI. Plateau pressures are traditionally thought to be a good indicator of the degree of DHI, and a level below 35 cm H₂O is still a widely recommended target for minimizing barotrauma. However, one study has shown that elevated end-inspiratory lung volume (the exhaled volume measured from end inspiration to the relaxation volume during a period of apnea) may be a more reliable predictor of barotrauma than are airway pressures. The most feared consequence of barotrauma is tension pneumothorax, typically characterized by a precipitous rise in airway pressures (peak and plateau), a drop in oxygen saturation, hypotension, tachycardia, unilaterally absent breath sounds and chest excursions, and possibly tracheal deviation. Tension pneumothorax is a clinical diagnosis and, if strongly suspected in a patient in unstable condition, should be treated immediately with needle thoracotomy followed by chest tube placement. Fatal air embolism may also occur because of barotrauma.

Ventilator settings in asthma (Box 21-2): The best mode of ventilation is one that minimizes minute ventilation and allows for sufficient exhalation time to minimize DHI, while trying to maintain oxygen saturation > 92% (use 100% oxygen initially). This can generally be achieved with low tidal volumes of 6 to 8 mL/kg, a respiratory rate of 8 to 10 breaths/min, minimal added PEEP, and moderate inspiratory flow rates of 80 to 90 L/min. Decelerating flow waveforms may improve overall flow distribution and hence optimize gas exchange. Higher inspiratory flow rates with square waveforms allow for a shorter inspiratory time and hence, at the same respiratory rate, a longer expiratory time. It is the longer expiratory time, and not just the inspiratory-to-expiratory ratio, that is critical to limiting DHI. Lowering total minute ventilation is the most crucial goal, because a longer expiratory time and smaller burden of volume to be exhaled are what minimize DHI. Intentional hypoventilation with low minute volumes can significantly reduce the risk of DHI and barotrauma. Thus allowing for a maximum PaCO₂ of 80 mm Hg or a minimum pH of 7.20 is a safe and acceptable practice when performing ventilation in patients with severe airflow limitation. However, because an elevated PaCO₂ can increase cerebral perfusion, such use of “permissive hypercapnea” should be avoided in patients with intracranial bleeding, edema, or space-occupying brain lesions.