Vol. 12 •Issue 5 • Page 12
Allergy & Asthma
Recognizing Life-threatening Asthma
Asthma treatment never should be taken for granted. The disease may be a common occurrence, and most patients with asthma experiencing an acute attack may very well respond to rescue beta-agonist therapy, but respiratory therapists shouldn’t be lulled into a sense of routine.
Unfortunately, inadequate assessment and misdiagnosis have contributed to the increased incidence of severe attacks. Even patients with a mild form of asthma are at risk for a life-threatening attack, due to lack of recognition and intervention.
Patients suffering a life-threatening asthma attack can be classified into three groups:
• the typical case, which is a patient who presents with a gradual deterioration over time and experiences a severe attack
• the patient with relatively mild, symptomatic chronic asthma who suffers an acute episode in a relatively short time frame
• the patient who’s a combination of the previous two classes.1
The severity of asthma, as defined by the National Institutes of Health, is classified into four steps.2 The higher the patient is on the staircase, the greater he or she is at risk for the development of a life-threatening attack. (See Table)
Therapists should be aware of the potential for a life-threatening attack when a patient with asthma doesn’t respond to first- or second-line therapeutic interventions. A sign of a severe attack is increased work of breathing, which is characterized by the use of accessory muscles, noted by flexing of the neck and shoulder muscles. Use of these muscles is strongly correlated with the severity of an acute asthma exacerbation.
Other signs include a decrease in mental status despite multiple clinical interventions and a continual deterioration in respiratory function. Often the therapist can be fooled by what appears to be an improvement in respiratory status but is in reality an increase in carbon dioxide induced relaxation.
Asthma assessment should begin with obtaining a brief medical history focusing on the duration of the current attack and what medications have been administered so far. Discovering what causative factor triggered the current attack also is beneficial information.
However, if a severe asthma attack is already under way, treatment interventions shouldn’t be delayed while obtaining this medical information. A more extensive medical history and physical can be obtained when the patient is stabilized.
Diagnostic evaluation should include the following: peak flow measurements, pulse oximetry and/or arterial blood gas, chest X-ray, vital signs, and breath sounds.
Peak flow can be used on a daily basis to monitor the severity of the disease. When peak flow is less than 100 liters/minute, the patient is at risk for a life-threatening attack. Normally, pulse oximetry is above 97 percent. A saturation less than 90 percent is indicative of a severe attack. If an arterial blood gas is obtained, often the PaCO2 will be elevated, an ominous sign indicating respiratory decompensation. The PaO2 will be low as a result of ventilation/perfusion mismatching. A PaO2 less than 55 torr is a precursor to respiratory failure. On chest X-ray, hyperinflation noted by widened rib margins, a flattened diaphragm and a reduced heart size can indicate severe air trapping.
Hemodynamic stress noted by an increase in heart rate and blood pressure often is seen in the air-hungry asthmatic. In the initial assessment of breath sounds, often profound inspiratory and expiratory wheezing is noted during auscultation. As the attack worsens, breath sounds can diminish secondary to a decrease or lack of gas flow.
ANATOMY OF AN ATTACK
During acute asthma, airways narrow because of bronchospasm, mucosal edema and mucus plugging, which trap air. As the functional residual capacity increases, the patient with asthma breathes close to total lung capacity, a state recognized by a hyperinflated, barrel-looking chest. As the work of breathing increases, the accessory muscles of breathing are employed. Additionally, hypoxemia is always present during severe asthma secondary to the mismatching of ventilation and perfusion.3
During the initial stages of an asthma exacerbation, alveolar ventilation is maintained and carbon dioxide levels are decreased. As the forced expiratory volume drops below 25 percent of predicted value, alveolar hypoventilation occurs. During a severe attack, hypoxemia and pulmonary hyperinflation may lead to an increase in pulmonary vascular resistance.
When the negative pleural pressures become more negative with increased hyperinflation, left ventricular failure can occur. These changes in pleural pressure and lung volumes are manifested in a pulsus paradoxus.4 Pulsus paradoxus is recognized by a decrease in amplitude of the arterial blood pressure and pulse oximetry waveform during the patient’s inspiratory phase. This drop in amplitude is a result of an increase in thoracic pressure from air trapping.
Patients who improve with standard asthma therapy should be observed for six hours to determine the likelihood of a relapse. Those who maintain a peak flow greater than 70 percent of predicted are generally safe to send home, while patients who have an incomplete response to therapy exemplified by a peak flow less than 70 percent should be admitted to either the emergency room or general medical ward for frequent monitoring. Those patients who either have decreased sensorium, hypercapnea or peak flow less than 50 percent should be admitted to a critical care unit for possible ventilatory assistance.5
Patients experiencing a refractory attack will exhibit an upright position and be diaphoretic, tachypnic and tachycardic. They’ll use accessory muscles with sternal retractions and will demonstrate a pulsus paradoxus if being monitored via pulse oximeter or arterial line.
Clinical studies suggest that the patient population that doesn’t respond to standard therapy often has an increase in neutrophic inflammation rather than eosinophilic inflammation, which is associated with stable chronic asthma.6 Also, there’s increasing production of mucin-like glycoprotein, which results in mucus plugging of the distal airways and an increase of air trapping. Stagnant mucus can act as a reservoir for bacteria proliferation leading to the development of pneumonia.
For these patients, treatment needs to be aimed not only at the elimination of bronchospasm, but directed at enhancement of secretion removal and the decreasing of inflammation. Techniques for mobilization of secretions can include chest physiotherapy, vibration modalities, such as positive expiratory pressure, and intrapulmonary percussion.
In patients who develop an acute asthma attack, the first line of therapy is repeated aerosolized beta-agonist treatments or continuous large-volume aerosol beta-agonist treatments. Additional aerosolized therapy with an anticholingeric drug may be helpful if larger airways are obstructed.
Subcutaneous epinephrine can be considered, but it should be used with caution in patients with suspected cardiac disease. For airway edema, systemic corticosteroids infusion should be added to the treatment regimen. In unresponsive asthma, the presence of hypomagnesemia can cause an increase in smooth muscle responsiveness. To promote bronchodilation, magnesium sulfate can be administered via intravenous infusion.
Because of an increased work of breathing and airway turbulence, heliox via mask can be given. Helium is less dense than air and crosses narrowed airways with reduced resistance. This decreases work of breathing and promotes better gas exchange with less effort.
Noninvasive mechanical ventilation also is an option. Administered via airway pressure of 8 cmH2O to 10 cmH2O, noninvasive mechanical ventilation can maintain airway dilation and improve carbon dioxide elimination.7
All interventions should be exhausted prior to the institution of mechanical ventilation. In patients who deteriorate to the point of carbon dioxide retention and fatigue, however, intubation is needed to gain airway control and provide ventilatory support.
The goal of mechanical ventilation is to minimize hyperinflation and slowly correct hypercapnia and provide adequate oxygenation. Often heavy sedation or neuro-muscular blockade is required to maximize ventilatory control.
Avoidance of high airway pressures is mandatory to prevent ventilator-induced trauma. The peak inspiratory pressure should be kept below 50 cmH2O and the plateau pressure maintained below 35 cmH2O. The setting of a long expiratory time helps facilitate CO2 removal and prevent intrinsic air trapping.
In the case of unresponsive refractory asthma, anesthesia drugs can be used.3 Halothane, enflurane and isoflurane are inhaled anesthetics that have bronchodilator effects. However, they also can have hemodynamic effects including myocardial depression and hypotension. They should be limited to short-term use and as a last resort.8
Having the evaluation and diagnostic tools, as well as the constant vigilance, to recognize and treat asthma patients is crucial. A complete assessment coupled with a predetermined treatment regimen can limit a severe attack.
1. Weiss KB, Wagoner DK. Changing patterns of asthma mortality: identifying target populations at high risk. JAMA. 1990;264:97-103.
2. Second Expert Panel on the Management of Asthma. Guidelines for the diagnosis and management of asthma. National Institutes of Health. 1998. p. 1-20.
3. Rodriguez-Rosin R, Ballester E, Roca J, et al. Mechanism of hypoxemia in patients with status asthmaticus requiring mechanical ventilation. Am Rev Respir Dis. 1989;139:732-39.
4. Hallstrand T, Fahy J. Practical management of acute asthma. Respiratory Care. 2002;47:171-82.
5. Fuhrman B, Zimmerman J. Pediatric critical care. 1st Ed. St. Louis: Mosby; 1992. p. 419-22.
6. Sur S, Cotty TB, Kephart GM, et al. Sudden onset fatal asthma: a distinct entity with few eosinophils and relatively more neutrophils in the airway submucosa. Am Rev Respir Dis. 1993;148:713-19.
7. Medure G, Cook T, Turner R. Noninvasive positive pressure ventilation in status asthmaticus. Chest. 1996;110:767-74.
8. Saulnier FF, Durocher AV, Deturck RA, et al. Respiratory and hemodynamic effects of halothane in status asthmaticus. Intensive Care Med. 1990;.16(2):104-7.
Miller and Cornman are clinical educators in respiratory care services at Lehigh Valley Hospital, Allentown, Pa.
THE RISK OF DEATH
Fortunately, while life-threatening asthma is a real risk in asthma care, the incidence of death isn’t skyrocketing. Asthma’s prevalence is rapidly increasing, and the number of severe attacks has been on the rise, but its mortality rate has actually remained stable over the last decade.3
That’s not to say death isn’t a danger. Mortality is most prominent in people under the age of 35 and in blacks, who have death rates that are five times higher than those of whites.2 Patients who have frequent hospital admissions or previous instances of life-threatening asthma are most susceptible to asthma mortality. In the United States, approximately 5,000 individuals die of asthma every year.2