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Caring for a patient with an acute asthma exacerbation or status asthmaticus is quite common in critical care. In this article, I'll review the pathophysiology and management of a severe asthma exacerbation so you'll be prepared to monitor your patient's response to therapy and intervene appropriately should the patient's clinical status deteriorate rapidly.
Asthma is a chronic inflammatory disorder of the airway characterized by airway hyperresponsiveness, mucus hypersecretion, and reversible airflow limitation. Chronic inflammation associated with asthma thickens the airway walls or changes their structure, a process known as airway remodeling. In an acute episode, the patient also has airway edema and bronchoconstriction. Asthma is variable in terms of genotypes, clinical phenotypes, susceptibility to environmental factors, pathogenesis, expression, severity, and response to treatments.1-3
Asthma triggers include viral respiratory infection, exposure to an allergen or irritant, exercise, stress, smoking, cold air, gastroesophageal reflux, nonadherance to pharmacologic therapies or sudden withdrawal from corticosteroids, and consumption of certain foods or intake of certain drugs such as aspirin, beta-blockers, nonsteroidal anti-inflammatory drugs, cocaine, or heroin.1,2,4-6
Asthma exacerbations can be classified as mild, moderate, severe, or respiratory arrest imminent.1 (For more details, see Severity of asthma exacerbations.) A severe exacerbation, the focus of this article, is characterized by severe airflow limitation and dynamic hyperinflation (also called air trapping), in which end-expiratory lung volume increases because patients can't exhale fully, but are trying to maintain near-normal gas exchange.2,4-8 Bronchospasm, edema, excessive secretions, and mucus plugs lead to progressive airway narrowing, increased airway resistance, insufficient expiratory time, and respiratory muscle fatigue. As a result, dynamic hyperinflation and elevated intrinsic positive end-expiratory pressure (PEEPi) occur. (In a healthy patient, a small amount of air remains in the lungs at end-expiration, creating normal PEEP of 3 to 5 cm H2O. However, in a patient with dynamic hyperinflation secondary to an asthma exacerbation, more air is left in the lungs at end-expiration than the physiologic normal volume, resulting in increased PEEPi.)
Airflow obstruction diminishes ventilation, reduces oxygen intake, and increases ventilation/perfusion (V./Q.) mismatching. In addition, frequent coughing to clear sputum or airway secretions, using accessory muscles of respiration, and being agitated increase oxygen consumption and carbon dioxide (CO2) production. Without timely and appropriate treatment, a patient with an acute severe asthma exacerbation will develop hypoxemia and hypercapnia, leading to anaerobic metabolism, lactic acidosis, and acid-base imbalance.4,5,7
Clinical manifestations of an acute asthma exacerbation vary among patients and by the severity of asthma. The common signs and symptoms include cough, wheezing, shortness of breath, chest tightness, diaphoresis, tachypnea, and tachycardia. Remember that the absence of typical signs and symptoms doesn't mean that the patient's condition isn't getting worse-in a drowsy or confused patient, it can signal imminent respiratory arrest.1,2,4,6,9
Because of great variability in clinical manifestations, severity, and response to treatments, your patient may need to be admitted to the ICU for close monitoring and aggressive treatment.1,2 Here are the recommended interventions for an asthma exacerbation:
* Administer supplemental oxygen as soon as possible to achieve oxygen saturation of 90% or greater. A patient in an acute exacerbation inevitably suffers from hypoxia. Supplemental oxygen reduces V./Q. mismatching, promotes bronchodilation, and reduces pulmonary vasoconstriction.6,10
If your patient also has chronic obstructive pulmonary disease (COPD), administering a large amount of supplemental oxygen may blunt his respiratory drive.4,8,11 These patients also are at risk of oxygen toxicity if they receive a fraction of inspired oxygen concentration (FIo2) greater than 0.5 to 0.6 for a prolonged period.11-14 However, the benefit of administering a large amount of oxygen (relieving hypoxemia in an acute asthma exacerbation) may outweigh the risks. Monitor your patient closely and titrate the oxygen to minimize the risks.
* Administer rapid-acting inhaled bronchodilatorsas prescribed. Beta2-agonists stimulate beta2 receptors on airway smooth muscles, relieving bronchoconstriction, reducing the work of breathing, and decreasing resistance to airflow. Short-acting beta2-agonists (SABAs), quick-relief medications, are used to relieve bronchoconstriction, and are indicated for acute episodes and exacerbations.1 The commonly prescribed SABAs are albuterol (also known as salbutamol), terbutaline, levalbuterol, and pirbuterol.1,4,5,7,15
Nebulized salbutamol can be given intermittently or continuously. However, salbutamol that is given via inhaled or aerosolized routes may be unable to reach lower airways and lung tissues due to severe airflow obstruction and decreased tidal volume. If the patient's initial response to SABA therapy is poor, consider I.V. beta2-agonists.1
In the ICU, continuous I.V. infusion of terbutaline (the I.V. beta-agonist of choice in the United States) or salbutamol may be used to treat refractory asthma exacerbations.4,5,10,15 Subcutaneous injections of epinephrine or terbutaline may be considered if the patient fails to improve with nebulized beta2-agonists.3-5,15 Nebulized or I.V. epinephrine also may be effective in treating a severe attack.7
Anticholinergics cause mild bronchodilation by inhibiting muscarinic cholinergic receptors and lowering intrinsic vagal tone of the airway. Administering inhaled ipratropium bromide in conjunction with a nebulized beta2-agonist produces profound bronchodilation and significantly improves a patient's pulmonary function, with minimal cardiovascular adverse reactions.1,3,5,6,10,16
* Administer systemic corticosteroids as prescribed. Corticosteroids play a vital role in the suppression of airway inflammation. By inhibiting inflammatory cell migration and activation, and blocking late-phase reaction to allergens, corticosteroids reduce airway hypersensitivity, secretions, and edema. Systemic corticosteroids are an integral part of the first-line medication for moderate-to-severe asthma attacks.1,3 Prednisone, methylprednisolone, prednisolone, hydrocortisone, and dexamethasone are commonly prescribed and should be administered for 3 to 10 days. The dose reduction and duration of corticosteroid therapy are determined by the severity and chronicity of asthma.1,3-5,10,15,17 To prevent a relapse, the patient should be discharged with a 5- to 10-day course of oral systemic corticosteroids.1
Although corticosteroids are safe for short-term use, they can cause hyperglycemia, hypertension, fluid retention, hypokalemia, Cushing's syndrome, acute psychosis, gastric ulcer, allergic reactions, and immune function suppression.1,4,10,15 Closely monitor patients on long-term corticosteroid therapy for adverse drug reactions.
* Administer noninvasive positive-pressure ventilation (NPPV)as indicated. NPPV enhances alveolar ventilation, improves gas exchange, and reduces the need for endotracheal intubation and mechanical ventilation. Applying extrinsic positive end-expiratory pressure (PEEPe) with NPPV overcomes the effect of PEEPi, reduces the work of breathing, and rests fatigued respiratory muscles.5-8,18,19
No universal guidelines exist for when to implement noninvasive or invasive ventilation for asthma attacks, or for which ventilation strategy to use. However, NPPV may be used when aggressive treatments with bronchodilators and corticosteroids don't reverse a patient's condition, and if the patient can tolerate the therapy, manage his own airway secretions, and doesn't need immediate intubation.6,7,17-19
NPPV can be administered via facial or nasal masks, using either continuous positive airway pressure or bilevel positive airway pressure. Be aware that inappropriately set PEEPe may worsen a patient's hyperinflation. Other complications associated with NPPV include gastric distension, vomiting, aspiration, eye irritation, and stress ulcer.7,18,20 Some patients with severe asthma attacks can't tolerate NPPV.5,7 More and larger studies may be needed to determine the role of NPPV in managing severe asthma exacerbations.9,21
* Assist with endotracheal intubation and mechanical ventilation if indicated. Your patient may need to be endotracheally intubated if he develops respiratory or cardiac arrest, severe hypoxia, progressive hypercapnia with profound acidosis, life-threatening dysrhythmias, hemodynamic instability, copious amount of sputum, exhaustion, or decreased level of consciousness.1,4,5,8,10,22
Ventilating a patient with a severe asthma exacerbation often is challenging. Although mechanical ventilation improves gas exchange and rests fatigued respiratory muscles, it may lead to ventilator-induced lung injuries (VILI) such as barotrauma and volutrauma, and other complications. The ventilation strategy should aim to improve oxygenation, reduce dynamic hyperinflation, and PEEPi. The primary settings are for a low respiratory rate (8 to 10 breaths/minute), prolonged expiratory time (inspiratory-expiratory ratio of 1:2 to 1:6), and low tidal volume (4 to 8 mL/kg).6,9,21 Either volume control or pressure control ventilation can be used, depending on the healthcare provider's preference and experience. The mode and settings should be adjusted in response to significant changes in a patient's condition.5-7,10,22
Low tidal volume or controlled hypoventilation elevates partial pressure of arterial carbon dioxide (PaCO2). In patients with a severe asthma exacerbation, hypercapnia and respiratory acidosis are allowed to occur gradually in an effort to keep plateau pressure below 30 cm H2O and reduce VILI.6,10,23,24
However, excessive hypercapnia causes intracellular acidosis and related cytotoxicity and induces pulmonary vasoconstriction that exacerbates preexisting pulmonary hypertension. Hypercapnia also causes cerebral vasodilation that increases intracranial pressure and leads to cerebral edema.24-26 No consensus exists on the upper limit of hypercapnia or the safe level of acidosis. The prevailing views are to keep PaCO2 below 90 mm Hg and to maintain pH greater than 7.1.10,15,22,24,26
The use of PEEPe is controversial, because it reduces venous return and cardiac output, induces hypotension, and intensifies hyperinflation. Some healthcare providers advocate no PEEPe; others recommend applying a low PEEPe to reduce the work of breathing, improve patient-ventilator synchrony, and promote recovery of fatigued respiratory muscles.6,8-10,24,27 The current prevailing recommendation is to apply PEEPe at a level of about 80% of a patient's PEEPi for spontaneously breathing patients.8,22,28 (The various methods used to detect and measure a patient's PEEPi are beyond the scope of this article.)
* Assist with sedation and neuromuscular blockade if indicated. Patient-ventilator dyssychrony is common in patients with a severe asthma exacerbation, because of extreme anxiety, agitation, and PEEPi. Sedation and paralysis rest fatigued respiratory muscles, reduce oxygen consumption and CO2 production, ameliorate patient-ventilator dyssynchrony, improve patient comfort, and enhance the effectiveness of mechanical ventilation.8,29
Ketamine, midazolam, and propofol are commonly used for intubation and mechanical ventilation. Rocuronium or suxamethonium (neuromuscular blocking agents) often are prescribed to induce paralysis.7,10 Sedatives may lead to respiratory depression and delay weaning from mechanical ventilation. Neuromuscular blocking agents may cause myopathy or muscle weakness, so they should be used sparingly and only for a short time.5-9,24 Because corticosteroids may potentiate myopathy, they shouldn't be administered concomitantly with neuromuscular blockers.30
* Administer adjunctive medications as prescribed. Magnesium sulfate causes smooth muscle relaxation. The Global Initiative for Asthma (GINA) guidelines recommend administering I.V. magnesium sulfate in certain cases, including adults who fail to respond to initial treatment.1 In combination with beta-agonists and systemic corticosteroids, this drug may be beneficial to patients in a severe asthma exacerbation.4,6,31 However, clinical evidence is inadequate to prove that magnesium improves a patient's condition, and its therapeutic effect remains controversial.4,6,9,10,15,31,32
Methylxanthines such as aminophylline and theophylline were part of the standard treatment for severe asthma exacerbations in the past. But they can cause severe adverse reactions such as cardiac dysrhythmias, headache, nausea, tremor, seizures, and encephalopathy. Also, these drugs have a very narrow therapeutic range. As a result, aminophylline and theophylline are seldom prescribed, but may be used as second-line therapy for refractory asthma.2,4,10,17 Short-acting theophylline may benefit respiratory drive, although it doesn't appear to provide additional bronchodilation over other SABAs.1
The GINA guidelines also recommend administering nebulized heliox as an adjunct treatment for severe exacerbations unresponsive to intensive treatments with SABAs, anticholinergics, and systemic corticosteroids.1 Using adjunct treatments may avoid the need for intubation. However, administering aminophylline or theophylline in the ED isn't recommended.3
Other second-line options include inhaled anesthetic agents, mucolytics, and nitric oxide. Large studies are needed to evaluate the efficacy and safety of these agents and to determine their roles in treating severe acute asthma exacerbations.4,5,7,17
Closely monitor and regularly assess your patient to determine when therapy needs to be adjusted to improve patient response and minimize adverse reactions.1,2 Assess and support the patient's airway, breathing, and circulation and monitor his clinical status and vital signs. Help him assume a comfortable position (high Fowler's or sitting, unless contraindicated by his hemodynamic status) and encourage him to relax. Maintain a calm environment and reassure the patient that you're there to ensure his safety. Explain to him that agitation will worsen his breathlessness, and that relaxing will help reduce oxygen consumption and improve his condition.
Monitor your patient's fluid balance. He may be dehydrated because of decreased oral intake and increased insensible fluid loss caused by agitation, increased work of breathing, and tachypnea. Administer fluid replacement as needed. Mechanically ventilated patients are at high risk of developing hypotension, so maintaining adequate intravascular volume is essential. However, be careful not to overhydrate your patient because of the risk of fluid volume overload and pulmonary edema.4,7
If your patient needs NPPV, apply the facial or nasal mask properly and explain the therapy to your patient. Provide reassurance and emotional support to help him tolerate the therapy. Assess him regularly for the need for endotracheal intubation and mechanical ventilation. If he needs mechanical ventilation, monitor him for complications and take steps to identify and minimize VILI.
Teach the patient and his family about asthma control and prevention. (See Keeping asthma under control, every day.) Review potential triggers and how the patient can control risk factors for acute attacks. Help him understand the importance of taking his medications and taking an active part in managing his disease.
Assess his ability to use his inhalers and to manage his asthma at home. Teach him to use a peak flowmeter and how to recognize trends that indicate an increasing risk of an acute attack. He should know the signs and symptoms of asthma exacerbations and when to seek medical attention. Arrange a follow-up appointment and refer him to an asthma self-management education program or asthma specialist as appropriate.
By understanding the management of an asthma exacerbation and how to empower patients to prevent future attacks, you can help your patient breathe easier.
The goal of asthma therapy is to keep asthma under control. Therapy is based on asthma severity and adjusted according to periodic monitoring of asthma control.1 Here are steps you can help your patient take.
* Identifying potential asthma triggers and avoiding exposure to them.
* Establishing an individual asthma management plan and adhering to it.
* Maintaining a healthful lifestyle.
Long-acting beta2-agonists such as salmeterol and formoterol, in combination with inhaled corticosteroids, are recommended for long-term control, and to prevent exacerbations or relapses. Inhaled corticosteroids such as beclomethasone, budesonide, flunisolide, and fluticasone are the most effective long-term control medications for persistent asthma.1
Leukotriene modifiers such as montelukast, zafirlukast, and zileuton, can be used as additional therapy in patients with persistent asthma or aspirin-sensitive asthma. These adjuncts may help reduce the dosage of corticosteroids needed, and the adverse effects of corticosteroids.1
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2. Balkissoon R. Asthma overview. Primary Care-Clin Office Pract. 2008;35(1):41-60. [Context Link]
3. National Heart, Lung, and Blood Institute. National Asthma Education and Prevention Program. Expert Panel Report 3: Guidelines for the diagnosis and management of asthma. Full report, 2007. http://www.nhlbi.nih.gov/guidelines/asthma. [Context Link]
4. Mannix R, Bachur R. Status asthmaticus in children. Curr Opin Pediatr. 2007;19(3):281-287. [Context Link]
5. Restrepo RD, Peters J. Near-fatal asthma: recognition and management. Curr Opin Pulm Med. 2008;14(1):13-23. [Context Link]
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10. Marcoux KK. Current management of status asthmaticus in the pediatric ICU. Crit Care Nurs Clin North Am. 2005;17(4):463-479. [Context Link]
11. Pruitt WC, Jacobs M. Breathing lessons: basics of oxygen therapy. Nursing. 2003;33 (10):43-45. [Context Link]
12. Fenstermacher D, Hong D. Mechanical ventilation: what have we learned? Crit Care Nurs Q. 2004;27(3):258-294. [Context Link]
13. Spritzer CJ. Unraveling the mysteries of mechanical ventilation: a helpful step-by-step guide. J Emerg Nurs. 2003;29(1):29-36. [Context Link]
14. Woodruff DW. A quick guide to vent essentials. RN. 2005;68(9);acute care focus:32ac2-7,2p. [Context Link]
15. Werner HA. Status asthmaticus in children: a review. Chest. 2001;119(6):1913-1929. [Context Link]
16. Kanazawa H. Anticholinergic agents in asthma: chronic bronchodilator therapy, relief of acute severe asthma, reduction of chronic viral inflammation and prevention of airway remodeling. Curr Opin Pulm Med. 2006;12(1):60-67. [Context Link]
17. Higgins JC. The 'crashing asthmatic.' Am Fam Physician. 2003;67(5):997-1004. [Context Link]
18. Beers SL, Abramo TJ, Bracken A, Wiebe RA. Bilevel positive airway pressure in the treatment of status asthmaticus in pediatrics. Am J Emerg Med. 2007; 25(1):6-9. [Context Link]
19. Carroll CL, Schramm CM. Noninvasive positive pressure ventilation for the treatment of status asthmaticus in children. Ann Allergy Asthma Immunol. 2006;96(3):454-459. [Context Link]
20. Manno MS. Managing mechanical ventilation. Nursing. 2005;35(12):36-42. [Context Link]
21. Ram FSF, Wellington SR, Rowe B, Wedzicha JA. Non-invasive positive pressure ventilation for treatment of respiratory failure due to severe acute exacerbations of asthma. Cochrane Database Syst Rev. 2005;3:CD004360. [Context Link]
22. Pilbeam SP. Final considerations in ventilator setup. In: Pilbeam SP, Cairo JM, eds. Mechanical Ventilation: Physiological and Clinical Application. 4th ed. St Louis: Elsevier Mosby; 2006:127-149. [Context Link]
23. Hager DN, Krishnan JA, Hayden DL, Brower RG. Tidal volume reduction in patients with acute lung injury when plateau pressures are not high. Am J Respir Crit Care Med. 2005;172(10):1241-1245. [Context Link]
24. Evans N, Skowno J, Hodgson E. The anaesthesiologist in the intensive care unit. Curr Opin Anaesthesiol. 2003;16(4):401-407. [Context Link]
25. Chonghaile MN, Higgins B, Laffey JG. Permissive hypercapnia: role in protective lung ventilatory strategies. Curr Opin Crit Care. 2005;11(1):56-62. [Context Link]
26. Mutlu GM, Factor P, Schwartz DE, Sznajder JI. Severe status asthmaticus: management with permissive hypercapnia and inhalation anesthesia. Crit Care Med. 2002;30(2):477-480. [Context Link]
27. Pruitt WC. Ventilator graphics made easy. RT. 2002;15(1):23-24, 50. [Context Link]
28. Blanch L, Bernabe F, Lucangelo U. Measurement of air trapping, intrinsic positive end-expiratory pressure, and dynamic hyperinflation in mechanically ventilated patients. Respir Care. 2005;50(1):110-124. [Context Link]
29. Hess DR. Thompson BT. Patient-ventilator dyssynchrony during lung protective ventilation: what's a clinician to do? Crit Care Med. 2006;34(1):231-233. [Context Link]
30. Larsson L, Li X, Edstrom L, et al. Acute quadriplegia and loss of muscle myosin in patients treated with nondepolarizing neuromuscular blocking agents and corticosteroids: mechanisms at the cellular and molecular levels. Crit Care Med. 2000;28(1):34-45. [Context Link]
31. Rowe BH. Camargo CA Jr. The role of magnesium sulfate in the acute and chronic management of asthma. Curr Opin Pulm Med. 2008;14(1):70-76. [Context Link]
32. Beasley R. Aldington S. Magnesium in the treatment of asthma. Curr Opin Allergy Clin Immunol. 2007;7(1):107-110. [Context Link]
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