Pediatric Annals

Assessment of Respiratory Distress in the Asthmatic Child: When Should We Be Concerned?

Michael O Gayle, MD; Niranjan Kissoon, MD

Abstract

There has been a worldwide increase in hospitalization rates of children with asthma1 as well as an increase in childhood deaths from this disease.2 The increased fatality from asthma probably can be explained by several reasons.3"7 Some of these reasons include the reclassification of asthmatic bronchitis as asthma rather than bronchitis,8,9 actual increases in prevalence and severity of asthma,10,11 identification of sociologie and biological risk factors,12 possible effects of drug toxicity,1316 and geographic or environmental effects.17,18 A critical review of the events surrounding deaths from asthma, however, suggests that underestimation of the disease severity by both the patient and physician,19 and a lack of aggressive therapy for acute episodes are also significant contributors.20 It is therefore critical that the child with acute asthma be accurately assessed as to the severity of respiratory distress so that a rational and appropriate treatment plan can be formulated. This article addresses pertinent issues in assessment including historical factors as well as the physical examination and ancillary laboratory investigations.

MEDICAL HISTORY

Features of previous acute asthmatic attacks can be helpful in identifying children at risk for acute decompensation. For instance, it is likely that close observation and early aggressive therapy will be necessary if previous attacks exhibited similar symptoms and progression but required intensive care admission. Children who have had life-threatening asthma attacks usually have a history of monosyllabic speech, history of intubation and mechanical ventilation, nighttime wheezing, and rapid progression of attacks.21 The time frame over which attacks develop, particularly if they have occurred over a prolonged period, may indicate the development of significant airway inflammation. The intensity of the symptoms can be gauged from the effects they have on exercise, sleep, and other normal activities. Interruption of exercise may not be of major clinical significance; however, loss of sleep indicates clinically relevant airway compromise. Overuse of beta-agonists for symptomatic relief may indicate a severe attack (perceived or real) or an attack refractory to conventional therapy. Alternatively, it may be a clue to the presence of complications such as air leak syndromes or pneumonia. Information such as duration of attack and specific triggering factors also should be sought. In children, it is quite common for an upper respiratory tract infection to precipitate an attack. Prolonged use of oral steroids or high-dose inhaled steroids is also an indication of severe disease.22

Appropriate attention to the medical history, therefore, may assist the treating physician to judge the severity of symptoms and the likely clinical course in a particular child with asthma. Older children should be questioned as to their estimation of severity because patients often have a better appreciation of the degree of their airway obstruction than their physician.23 In younger patients, close attention to the history and parental impression is vital for the physician to determine severity.24

Although the presence of recurrent episodes of coughing and wheezing in childhood signifies asthma, other diseases with similar symptoms also should be considered. For example, causes of lower airway obstruction such as congenital malformations of the respiratory, cardiovascular, or gastrointestinal systems, foreign bodies in the airway or esophagus, bronchiolitis, cystic fibrosis, and immunologic deficiency diseases may involve the lung and mimick asthma. In children in whom the diagnosis is not yet established, the physician should consider other diagnostic possibilities as "All that wheezes is not asthma." In addition, a thorough history and physical examination according to age and clinical state will assist the physician in formulating an age-appropriate differential diagnosis.

PHYSICAL EXAMINATION

The appreciation of the variability of respiratory rate and heart rate in relationship to age and clinical state in children is important in the overall assessment…

There has been a worldwide increase in hospitalization rates of children with asthma1 as well as an increase in childhood deaths from this disease.2 The increased fatality from asthma probably can be explained by several reasons.3"7 Some of these reasons include the reclassification of asthmatic bronchitis as asthma rather than bronchitis,8,9 actual increases in prevalence and severity of asthma,10,11 identification of sociologie and biological risk factors,12 possible effects of drug toxicity,1316 and geographic or environmental effects.17,18 A critical review of the events surrounding deaths from asthma, however, suggests that underestimation of the disease severity by both the patient and physician,19 and a lack of aggressive therapy for acute episodes are also significant contributors.20 It is therefore critical that the child with acute asthma be accurately assessed as to the severity of respiratory distress so that a rational and appropriate treatment plan can be formulated. This article addresses pertinent issues in assessment including historical factors as well as the physical examination and ancillary laboratory investigations.

MEDICAL HISTORY

Features of previous acute asthmatic attacks can be helpful in identifying children at risk for acute decompensation. For instance, it is likely that close observation and early aggressive therapy will be necessary if previous attacks exhibited similar symptoms and progression but required intensive care admission. Children who have had life-threatening asthma attacks usually have a history of monosyllabic speech, history of intubation and mechanical ventilation, nighttime wheezing, and rapid progression of attacks.21 The time frame over which attacks develop, particularly if they have occurred over a prolonged period, may indicate the development of significant airway inflammation. The intensity of the symptoms can be gauged from the effects they have on exercise, sleep, and other normal activities. Interruption of exercise may not be of major clinical significance; however, loss of sleep indicates clinically relevant airway compromise. Overuse of beta-agonists for symptomatic relief may indicate a severe attack (perceived or real) or an attack refractory to conventional therapy. Alternatively, it may be a clue to the presence of complications such as air leak syndromes or pneumonia. Information such as duration of attack and specific triggering factors also should be sought. In children, it is quite common for an upper respiratory tract infection to precipitate an attack. Prolonged use of oral steroids or high-dose inhaled steroids is also an indication of severe disease.22

Appropriate attention to the medical history, therefore, may assist the treating physician to judge the severity of symptoms and the likely clinical course in a particular child with asthma. Older children should be questioned as to their estimation of severity because patients often have a better appreciation of the degree of their airway obstruction than their physician.23 In younger patients, close attention to the history and parental impression is vital for the physician to determine severity.24

Although the presence of recurrent episodes of coughing and wheezing in childhood signifies asthma, other diseases with similar symptoms also should be considered. For example, causes of lower airway obstruction such as congenital malformations of the respiratory, cardiovascular, or gastrointestinal systems, foreign bodies in the airway or esophagus, bronchiolitis, cystic fibrosis, and immunologic deficiency diseases may involve the lung and mimick asthma. In children in whom the diagnosis is not yet established, the physician should consider other diagnostic possibilities as "All that wheezes is not asthma." In addition, a thorough history and physical examination according to age and clinical state will assist the physician in formulating an age-appropriate differential diagnosis.

PHYSICAL EXAMINATION

The appreciation of the variability of respiratory rate and heart rate in relationship to age and clinical state in children is important in the overall assessment of the asthmatic child in respiratory distress (Table 1). The heart rate is initially rapid at birth but gradually decreases as the child approaches adolescence.25'28 Sinus tachycardia can result from anxiety, fever, pain, blood loss, and any other insult that results in increased sympathomimetic activity. Respiratory distress with or without hypoxia is one of the most common causes of tachycardia in children. The respiratory rate decreases with age and shows its greatest variability in newborns and young infants.28 Reasons for variability in the respiratory rate are numerous and include anxiety, fear, fever, and sepsis. Ideally, the rate should be determined over at least a 1 -minute period on a few occassions for the calculation of average values.

Table

TABLE 1Normal Respiratory Rates In Childhood

TABLE 1

Normal Respiratory Rates In Childhood

The assessment of the child in respiratory distress should be conducted in a calm, efficient manner with the assistance of parents and with minimal intrusion from others. Clinical assessment of the asthmatic child should initially address the adequacy of gas exchange and the degree of respiratory compromise. The presence of triggering factors such as pneumonia or complications such as pneumothoraces also should be sought. The major pathophysiological derangement in asthma is hypoxemia, which affects all major organ systems in the body. To prevent or limit the effects of hypoxemia, it is important for the physician to recognize the symptoms and signs of respiratory insufficiency and the need for aggressive immediate treatment. Acute exacerbations of asthma can be classified as mild, moderate, or severe based on both clinical and physiological assessment of target organs (Table 2).

Overall Assessment

An initial assessment of the child should include a search for evidence of diaphoresis, pupillary dilatation, and fear, which are all features of "the fight or flight" adrenergic response to hypoxia. Posture provides a clue as to the degree of comfort of the child and hence infers the degree of respiratory difficulty. The child who is alert and lying comfortably is in minimal difficulty. However, the child who prefers the sitting or tripod position is in moderate to severe difficulty and is attempting to derive maximal diaphragmatic excursion since the diaphragm is approximately 4 cm higher in the supine position.29

Table

TABLE 2Assessment of the Severity of Acute Asthma*

TABLE 2

Assessment of the Severity of Acute Asthma*

Central Nervous System

Of all vital organ systems, the central nervous system is the least tolerant to hypoxia; therefore, evaluation of the central nervous system will provide early signs of impending respiratory failure. Central nervous system assessment in the asthmatic child does not entail a full neurological examination initially, but is limited to assessment of global central nervous system function such as alertness, cooperation, and motor activity. The child who is alert, cooperative, and active is not compromised to any great degree. However, the child who is restless and irritable, or manifests any signs of confusion, such as inability to recognize parents and has decreased level of consciousness, should be considered to be in respiratory failure. While seizure is an uncommon presenting sign, generalized seizures in an acutely ill asthmatic patient indicate significant central nervous system oxygen deficiency and require aggressive treatment.30,31

Respiratory System

The pattern of breathing, which includes the respiratory rate, rhythm, and effort, provides a useful practical tool for assessing the respiratory system. Tachypnea, is commonly seen with asthma but also can be seen with metabolic acidosis, fever, agitation, or psychological factors. Tachypnea is the expected compensatory response in acute asthma. However, the finding of bradypnea in acute asthma is an ominous sign. Grunting due to decreased lung compliance is common in acute asthma but may be absent in the child who is becoming fatigued. The presence of dyscoordinated breathing (lack of coordination between thoracic and diaphragmatic muscles of respiration) is also a poor sign.32 In its extreme form, there is failure of synchronization and the chest moves inward during inspiration.

Increased respiratory effort and work of breathing may be evaluated by assessment of accessory muscle use, subcostal and intercostal retractions, nasal flaring, and the rate and depth of respiratory effort. Children in moderate to severe respiratory distress will present in the initial stages with marked accessory muscle activity as well as subcostal and intercostal retractions. Nasal flaring may indicate mild asthma, but use of sternocleidomastoid and other accessory muscles signifies increasing respiratory effort. The older child may be able to communicate the subjective experience of breathing difficulty or dyspnea. The child with moderate asthma may be able to speak in phrases or partial sentences whereas the severely affected asthmatic often can speak only in single words or short phrases. Decreased work of breathing in the child with moderate to severe asthma may indicate extreme fatigue and signals decompensation.

Examination of the respiratory system of the asthmatic child includes a complete chest examination to rule out other diagnostic possibilities and inciting or triggering factors and to exclude complications. Performance of percussion will detect hypersonance in asthma but not if pneumonia or severe atelectasis is present. Palpation of the chest wall will detect the presence of crepitations from surgical emphysema or tracheal deviation due to a pneumothorax. Finally, auscultation may reveal minimal or no breath sounds (silent chest) indicative of severe airflow obstruction.

Color

The color of the skin and mucous membranes of the acutely ill asthmatic may be normal, pale, or cyanotic depending on severity and other factors. Central cyanosis suggests severe desaturation of hemoglobin but may not be recognized in the presence of anemia, poor perfusion, hypocapnia, or poor lighting in the examination room.33 In addition, the evaluation of cyanosis is subjective.34 If present, therefore, cyanosis is a useful sign of compromised oxygenation but if absent should not be construed as indicating adequate oxygenation. Fortunately, an objective measure of oxygenation, pulse oximetry, is now widely available.35

Cardiovascular Status

In the acutely ill asthmatic child, tachycardia is the usual physiologic response. However, a normal heart rate or bradycardia in the presence of hypoxemia signifies severe myocardial oxygen deprivation. Pulsus paradoxus is a valuable clinical tool in assessing the severity of airway obstruction in status asthmaticus.36 The presence of a pulsus paradoxus >20 mm Hg is associated with moderate to severe airway obstruction. However, its utility is limited to older children and adults because it is difficult to elicit in the young child. This is usually due to the use of inappropriate sized (too large) blood pressure cuffs or difficulty in auscultation of heart sounds due to noisy breathing in the child. However, in conjunction with the overall clinical status of the patient, frequent pulse oximetry, and blood gas determination, pulsus paradoxus may allow for better evaluation of the older child with status asthmaticus.

The physician should be able to have an overall impression of the severity of the child's attack based on the assessment outlined in Table 2. In many cases, and especially in acute severe asthma, treatment and evaluation may occur concurrently. In addition, therapy for severe acute asthma should not be withheld pending laboratory evaluation.

LABORATORY EVALUATION

Pulmonary Function Testing

Rapid assessment of respiratory compromise may be obtained by assessment of pulmonary function (forced expiratory volume in 1 second [FEV.]) and peak expiratory flow rate (PEFR) in children. Peak expiratory flow rate is the greatest flow that can be obtained during a forced expiration starting from full inflation of the lung (ie, total lung capacity). Peak expiratory flow rate assessment is an excellent tool for monitoring the severity of respiratory insufficiency as well as for following the progress of children with lower airways obstruction. The procedure is simple to perform using a hand-held spirometer37,38 and is endorsed by the National Asthma Education program.39 Peak expiratory flow rate assessment can be done by the cooperative and trained patient, pediatrician, emergency physician, or nurse. As this test is effort-dependent, the usefulness, accuracy, and reliability of the results (especially in the pediatric age group) relies heavily on close supervision of performance. A peak expiratory flow meter or a mini FEV1 meter can be used to measure PEFR and FEV. in children capable of utilizing these devices (usually older than 5 years of age).

The interpretation of PEFR or FEV1, which measures airway obstruction, should be made after correcting for age and sex.23 In the mild asthmatic child, PEFR is 70% to 90% of baseline or predicted normal, moderate is 50% to 70% of baseline or predicted normal, and severe is <50% of baseline or redicted normal. Peak expiratory flow rate assessment should be attempted in the cooperative asmathic child older than 5 years. However, it should not delay therapy in the moderately or severely ill child. Attempts at PEFR testing also should be discontinued if the child undergoes obvious deterioration during testing.

Pulse Oximetry

Pulse oximetry is a noninvasive method of measuring circulating oxygen (ie, arterial oxygen saturation) and can be used either on an intermittent basis or continuously.34,35 This monitor has the advantage of noninvasiveness and does not require calibration before use. It also provides continuous readings and no frequent changes of sites are required. However, the disadvantage of pulse oximetry is that it does not reflect decreasing PaO2 until the PaO2 is approximately <80 mm Hg (Figure). For patients with TS8O2 <75% to 80%, oxygenation values often are not an accurate reflection of arterial blood gases. In addition, the accuracy of oximetry can be affected by patient movement, compression of the sensor on the oximeter, low perfusion states, abnormal hemoglobin, (methemoglobinemia), nail polish, and infrared heat lamps.35

For patients at sea level, a mild asthmatic patient should have a TS3O2 >95%, a moderate asthmatic 90% to 95%, and a severe asthmatic <90%. The clinical usefulness of the pulse oximeter in children with acute asthma recently was demonstrated by Geelhoed et al.40 They conducted a study on 280 children with a history of asthma who presented to an urban emergency department with wheezing. The aim of the study was to evaluate the initial measurement of arterial saturation (using a pulse oximeter) as a predictor of outcome in acute childhood asthma compared with other factors of past and present asthma history. They concluded that the initial level of arterial saturation reflects severity as it predicts the likelihood of "poor outcome." Poor outcome was defined as hospital admission or a second visit to the emergency department with ongoing symptoms for those discharged from the emergency department. While there was no absolute cutoff value, a TS8O2 <91% was likely to result in admission or a second emergency visit.40 Pulse oximetry is widely available and should be used in all cases to judge oxygenation during acute asthma therapy.

Arterial Blood Gases

The arterial blood gas is useful and provides objective evidence of pulmonary gas exchange impairment, ie, oxygen saturation and carbon dioxide (PaCO2). However, its utility in the young asthmatic is limited since sampling may be difficult. In addition, the pain and anxiety associated with attempts at obtaining arterial gases may cause further deterioration in clinical status. A typical aterial gas during an acute uncomplicated asthma attack reveals normal PaO2 low PaOO2, and respiratory alkalosis. Hypoxemia in a PaO2 range of 60 to 80 mm Hg frequently is found even in moderately severe asthma.41 However, a PaO2 <60 mm Hg may indicate severe disease.

Figure. Oxygen hemoglobin dissociation curve demonstrating its sigmoid nature. Partial pressures >65 torr are associated with >95 % saturation.

Figure. Oxygen hemoglobin dissociation curve demonstrating its sigmoid nature. Partial pressures >65 torr are associated with >95 % saturation.

Hypoxemia is due to ventilation perfusion mismatching, whereas low PaCO2 is a result of hyperventilation.42 A progressive increase in PaCO2 is an early warning sign of severe airway obstruction in a child with respiratory muscle fatigue. Arterial pH is an indicator of the overall balance between metabolic demand and respiratory compensation. Hypercapnia and metabolic acidosis despite aggressive medical treatment indicate severe illness and may support the provision of an artificial airway and mechanical ventilation. However, in assessing the acute asthmatic child, serial measurements of PaCO2, PaO2, and pH are more useful in following response to treatment rather than a single measurement. If multiple samples are contemplated, insertion of an indwelling arterial cannula would be preferable.

Clinical circumstances may arise in infants and small children when a blood gas estimation is desirable but arterial sampling is difficult or impractical. In a well-perfused infant, arterialized capillary blood will show a consistent correlation with arterial PcO2 and pH and will reflect a minimal arterial Po2 value. This technique is performed after warming a highly vascularized capillary bed (earlobe, heel, great toe, or finger) for 10 minutes and then making a deep puncture with a scalpel or specially designed lancet blade and then collecting free flowing blood in a heparinized capillary tube.43 The role of arterial blood gases in the emergency management of the acutely ill asthmatic would depend on several factors, of which the most important is the ease of sampling. The insertion of an indwelling arterial cannula greatly facilitates its utility.

Table

TABLE 3Common Pitfalls In Assessment of the Asthmatic Child

TABLE 3

Common Pitfalls In Assessment of the Asthmatic Child

RADIOLOGY

Chest radiographs are not routinely required in a child with mild and uncomplicated asthma. However, they should be obtained in every child with moderate to severe asthma to define the extent of any associated parenchymal disease or complications, and to differentiate other disease entities, eg, foreign bodies. A chest radiographic examination often is performed in the assessment of the acute asthmatic patient to examine for evidence of infection or the complications of hyperinflation (pneumothorax or pneumomediastinum) or in those not responding adequately or appropriately to therapy; however, there are no objective data to support this routinely.

Findley and Sahn44 reviewed radiographic films from 90 episodes of acute asthma in adults. The results of this prospective study were that 55 (59%) films were reported as normal, 33 (35%) showed hyperinflation, and 6 (6%) showed minimal interstitial tissue abnormalities that were unchanged from previous films. Although these data would support the policy of not routinely performing chest radiographic examinations in the assessment of acute asthma, this was an adult study and may not necessarily be applicable to children. However, radiographs always should be considered in suspected foreign body aspiration, pneumothorax, and pneumomediastinum, as well as in children with moderate to severe attacks requiring hospital admission or in patients not responding appropriately to therapy. The presence of pneumomediastinum, severe hyperinflation, pneumonia, or atelectasis is indicative of severity of disease.45

ELECTROCARDIOGRAM

An electrocardiogram is not routinely performed in patients with acute asthma unless cardiovascular symptoms or signs indicate myocardial compromise, insults, or abnormalities. Apart from sinus tachycardia, which is usually present in mild to moderate asthma, electrocardiographic findings in severe asthma episodes include P pulmonale, right ventricular strain, right bundle branch block, and right axis deviation.46 Electrocardiographic evaluation is more commonly done and is recommended in patients receiving a combination of high dose aerosolized or intravenous beta-adrenergic agents. Beta-adrenergic agonists, especially in combination, have been well documented to be associated with tachyarrhythmias, myocardial ischemia, and death.47'49

COMMON PITFALLS IN ASSESSMENT

The physician unfamiliar with the acutely distressed child ith asthma should be cognizant of some of the pitfalls in assessing these children (Table 3). Treatment of the child with asthma can only be given if the severity of the attack in the individual patient is appreciated. An accurate judgment of severity can only be done if the pitfalls outlined are avoided.

SUMMARY

The physician caring for the acutely ill asthmatic child has a wide variety of signs and systems to assist in assessment. An assessment of the severity of the disease should be based on the medical history, and signs and symptoms due to hypoxia on various target organs. Laboratory evaluation, while helpful, has limited applicability in the young child but should be used as an adjunct to clinical assessment where necessary. Based on the history, physical examination, and laboratory assessment (when appropriate), acute asthma symptoms should be categorized as mild, moderate, or severe. Treatment then can be tailored to disease severity.50'51

REFERENCES

1. Mitchell EA. International trends in hospital admission rates for asthma. Ardi Dis Child. 1985;60:376-378.

2. Duggar DB, Lewis WF. Compatibility of diagnostic data collected by the 8th and 9th International Classification of Disease. Vital Health Stat [2]. 1987;104:1-31.

3. Lanier B. Who is dying of asthma and why? J Pediatr. 1989; 11 5:838-840.

4. Buist AS1 Vollmer WM. Reflections on die rise in asthma morbidity or mortality. JAMA. 1990;264:1719-1720.

5. Kravis LP1 Kolski GB- Unexpected death in childhood asthma. Am ) Dis Child. 1985;139:559-563.

6. Wilkins A1 Mao Y. Transient rates of admission to hospital on death from asthma among children and young adults in Canada during the 1980s. Con Med Assoc J. 1993;148:185-190.

7. Matsu 1, Baba M. Death from asrhma in children. Acta Paediatr Jpn. 1990;32:205-208.

8. Gergn P]1 Weiss BK. Changing partem of asthma hospitalization among children: 1979-1987. JAMA. 1990:264:1688-1692.

9. So Sy1 Ng MM1 Ip MS, et al. Rising asthma mortality among young males in Hong Kong 1976-85. Resptr Med. 1990;84:457-461.

10. Gergn PJ1 Mullally Dl1 Evans R. National survey of prevalence of asthma among children in the United States. 1976-1980. Pediatrics. 1988;81:1-7.

11. Miller BD1 Strunk RC Circumstances surrounding die deaths of children due to asthma. Am J Dis Child. 1989;143:1294-1299.

12. Birkhead G1 Attaway NJ1 Strunk RC1 et al. Investigation of a cluster of deaths of adolescents from asthma: evidence implicating inadequate treatment and poor patient adherence with medications. J Allergy CIm Immunol- 1989;84:484-491.

13. Crane J1 Pearce NE, Flatt A1 et al. Prescribed fenoterol and death from asthma in New Zealand 1981-1983: case control study. Lancet. 1989;1:918-922.

14. Pearce N1 Grainger J, Atkinson M1 et al. Case control study of prescribed fenoterol and death ftora asthma in New Zealand 1977-1981.ThOtOi- 1990;45:170-175.

15. Morely J1 Sanjar S1 Newth C. Viewpoint: untoward effects of beta-adrenoceptor agonists in asthma. Eur Respir J. 1990;3:228-233.

16. Pem ST, Suisse ML, Hemmel G, ce al. Is the association between inhaled beta agonist use and life threatening asthma because of confounding by severity.' Am Rev Rejpfr Dis. 1993;148:75-79.

17. Weiss KB, Wagener DK. Changing patterns of asthma mortality. JAMA. 1990;264:1683-1687.

18. Sly RM, O'Donnell R. Regional distribution of deaths from asthma. Ann Allergy. 1989;62:347-354.

19. Canny GJ, Levison H. Management of asthma: a Canadian perspective. Chest. 1986;90:46-52.

20. Jaimovich D, Kecslces SA. Management of reactive airway disease. Crit Care Clin. 1992;8:147-162.

21. FitrGerald JM, Hargreave FE. The assessment and management of acute life-threatening asthma. Chest. 1989;5:888-894.

22. Strunk RC. Identification of the fatality-prone subject with asthma. J Allergy CIm Immunol. 1989;83:477-485.

23. Lernen RJ. Pulmonary function testing in the office, clinic, and home. In: Chemick V, ed. Disorders of the Respiratory Track m Children. 5th ed. Philadelphia, Pa: WB Saunders Co-, 1990:147-174.

24. Ben-Noun L. Severity of asthma: parent's assessment versus the physicians. Practitioner. 1990:233:1052.

25. Furman RA, Halloran WR. Electrocardiograms in the first 2 months of life. J Pediatr. 1951;39:307-319.

26. Tudbury PB1 Atkinson DW. Electrocardiograms of 100 normal infants and young children. J Pediatr. 1950;36:466-481.

27. Alimurung MM, Joseph LG1 Nadas AS, et al. The Unipolar precordial and extremity electrocardiogram in normal infants and children. Circulation. 19S1;4:420 429.

28. lliff A, Lee VA. Pulse rate, respiratory rate and body temperature in children between 2 months and 18 years of age. Child Dev. 1952;23:237-245.

29. Wade OL, Gilson JC. Effect of posture on diaphragmatic movement and vital capacity in normal subjects. Thorax. 1951;6:103-126.

30. Nellhouse G, Neuman I, Ellis E, et al. Asthma and seizures in children. Pediatr CIm North Am. 1975;22:89-100.

31. Newcomb RW, Akhter J. Respiratory failure from asthma: a marker for children with high morbidity and mortality. AmJ Dis ChM. 1988;142:1041-1044.

32. Pontoppidon H, Geffin B1 Lowenstein E. Acute respiratory failure in the adult. N EngiJMed. 1972;287:743-752.

33. Nowak RM, Tomlanovich MC, Sarkar DD, et al. Arterial blood gasses and pulmonary function testing in acute bronchial asthma predicting patient outcomes. JAMA. 1983;249:2043-2046.

34. Stephen CR, Slater HM, Johnson AL, Sekelj P. The oximeter - a technical aid for the anesthesiologist. Anesthesiology. 1951;12:541-555.

35. Tremper KK, Barker SJ. Pulse oximetry. Anesthesiology. 1989;70:98-108.

36. Galant SP, Groncy CE, Shaw KC. The value of pulsus paradoxus in assessing the child with status asthmaticus. Pediatrics, 1978;61:46-51.

37. Plant TF. Children With Asthma: A Manual for Parents. Amherst, Mass: Pedipress; 1988.

38. Weng TR, Langer HM, Featherby EA, Levison H. Arterial blood gas tensions and acid-base balance in symptomatic and asymptomatic asthma in childhood. Am Rev RespirDis. 1978;101:274-282.

39. National Asthma Education Program. Guidelines /or the Diagnosis and Management of Asthma. Bethesda, Md: US Dept of Health and Human Services; 1991. Publication 91-3042A.

40. Geelhoed GC, Landau LI, LeSouif PN. Evaluation of SaO2 as a predictor of outcome in 280 children presenting with acute asthma. Ann Emerg Med. 1994;23:1236-1241.

41. Hargreave FE, Dolovich J, Newhouse MT. The assessment and treatment of asthma: a conference report. ] Allergy CIm Immunol. I990;85(b):1098-1 1 11.

42. West JB. Ventilation-perfusion relationships. Am Rev Respfr Dis. 1977;1 16:919-923.

43. Shapiro BA, Harrison RA, Cane RD, et al. Guidelines for obtaining blood gas samples. In: Shapiro BA, ed. Clinical Application of Blood Gases. 4th ed. Chicago, III: Year Book Medical Publisher lnc; 1989:248-264.

44. Findley LJ1 Sahn S. The value of chest roentgenograms in acute asthma in adults. Chest. 1981;80:535-536

45. Ellis ES. Asthma in childhood. J Allergy CIm Immunol. 1983;72:539-544.

46. Siegler D. Reversible electrocardiographic changes in severe acute asthma. Thorax. 1977;32:328-332.

47. Spitzer WO, Suina S, Emit P, et al. The use of β-agonists and the risk of death and near death from asthma. N Engl J Med. 1992;326:501-506.

48. Sly RM. Adverse effects and complications of treatment with beta-adrenergic agonist drugs. J Allergy CIm Immunol. 1985;75:443-449.

49. Crane J, Burgess C, Beasley R. Cardiovascular and hypokalemic effects of inhaled salbutamol, fenoterol, and isoprenaline. Thorax. 1989;44:136-140.

50. Provisional Committee on Quality Improvement. Practice parameter: the office management of acute exacerbations of asthma in children. Pediatrics. 1994:95:1 19126.

51. DeNicola LK, Monem GF, Gayle MO, Kissoon N. Treatment of critical status asthmaticus in children. Pediatr CIm North Am. 1994;41:1293-1324.

TABLE 1

Normal Respiratory Rates In Childhood

TABLE 2

Assessment of the Severity of Acute Asthma*

TABLE 3

Common Pitfalls In Assessment of the Asthmatic Child

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