- Email: [email protected]
Use of peak expiratory flow rates to eliminate unnecessary arterial blood gases in acute asthma
ORIGINAL CONTRIBUTION arterial.blood gases; asthma, acute, ABG; asthma, acute, PEFR; peak expiratory flow rates
Use of Peak Expiratory Flow Rates to Eliminate Unnecessary Arterial Blood Gases in Acute Asthma Arterial blood gas (ABG) measurements are used frequently in acute asthma. Because ABGs are expensive and m a y have significant side effects, a method is needed to identify those patients at risk for a significantly abnormal ABG. We studied the use of peak expiratory flow rates (PEFR) to identify those patients at such risk. Data from 89 emergency visits by 51 asthmatic patients were analyzed. A small but significant correlation between ABG parameters and PEFR was observed (P < 0.05). No patient with a PEFR >1 25% predicted had a PaC02 > 45 m m Hg or pH < 7.35. This suggests that only those patients with a PEFR < 25% predicted are at risk for significant hypercarbia or acidosis. We concluded that PEFR may be used as a simple screening tool to safely eliminate ABGs in at least 40% of acute asthmatic patients. [Martin TG, Elenbaas RM, Pingleton SH: Use of peak expiratory flow rates to eliminate unnecessary arterial blood gases in acute asthma. Ann Emerg Med 11:70-73, February 1982.]
INTRODUCTION Acute asthma is potentially a life-threatening problem. It is unfortunate that information derived from the history and physical examination is often unreliable in assessIng gas exchange or airflow obstruction, for these parameters are the major factors dictating appropriate therapy. Direct measurement of arterial blood gases (ABGs) is the most reliable measure of gas exchange. Because the clinical examination is unreliable in predicting the magnitude of airflow obstruction, it has been recommended that ABGs be measured on every patient presenting to the emergency department with acute asthma.l~3 However, because the procedure is associated with moderate pain, substantial cost, and occasional complications, 4 a reliable method is needed to identify those patients likely to have abnormal ABGs. If alteration in gas exchange is related to the degree of airflow obstruction, then simple pulmonary function tests should predict the presence of abnormal ABGs. The peak expiratory flow rate (PEFR) is a simple pulmonary function test which can be used to measure the severity of airflow obstruction in asthma. 5,6 The purposes of our study were the following: 1) to assess the relationship between changes in pulmonary fimction as measured by PEFR and ABG measurements; and 2) to evaluate the capacity of PEFR to screen for severely abnormal ABG measurement in patients presenting with acute asthma.
Thomas G. Martin, MD* Robert M. Elenbaas, PharmD* Susan H. Pingleton, MDt Kansas City, Missouri
From the Departments of Emergency Health Services* and Pulmonary Medicine, t Truman Medical Center, University of Missouri - - Kansas City School of Medicine, Kansas City.
Address for reprints: Robert M. Elenbaas, Pharm D, Department of Emergency Medicine, Truman Medical Center, 2301 Holmes, Kansas City, Missouri 64108.
Presented at the University Association for Emergency Medicine Annual Meeting in San Antonio, Texas, April 1981.
MATERIALS A N D METHODS Patients of either sex between the ages of 15 and 39 years who met the American Thoracic Society criteria for asthma z and presented to the Emergency Department of Truman Medical Center in August and September 1979 with an acute episode of airway obstruction were included. Prior to therapy (including supplemental oxygen), an arterial blood specimen was obtained percutaneously from the radial artery and analyzed for pH, PaO2, and PaCO2. PEFR was measured using the Wright Peak Flow Meter [Armstrong Industries, Inc, Northbrook, IL) either immediately before or after obtaining the arterial specimen. The PEFR procedure was administered by either an emergency physician or a nurse, with the patient in the sitting 11:2 February 1982
Annals of Emergency Medicine
70/31
PEAK EXPIRATORY FLOW RATES Martin, Elenbaas & Pingleton
position. The best of three patient attempts was recorded and Utilized in subsequent data analysis. The Wright Peak Flow Meter used is incapable of quantitating a flow rate less than 60 L/rain; therefore, flow rates below quantification were recorded as 60 L/min and this value was used in subsequent statistical analysis. PEFR was normalized between patients for sex, age, and height from data 8 supplied with the instrument by its manufacturer and was expressed as percentage of predicted PEFR. Arterial pH, PaO2, and PaCO2 were individually compared with absolute and percentage of predicted PEFR using the Pearson correlation coefficient. Arterial specimens were analyzed using an Instrumentation Laboratory 813 Blood Gas Analyzer (Instrumentation Laboratory, Lexington, MA). Informed consent was obtained from each patient prior to inclusion in the study. The study protocol was approved by the Clinical Research Review Board of Truman Medical Center and the Institutional Review Board of the University of Missouri - - Kansas City.
TABLE. S u m m a r y of patient data No. patients No. visits Males Females Black Non-black Age* (years) Absolute PEFR* % predicted PEFR* PaO2* PaCe2* pH*
51 89 20 (39%) 31 (61%) 43 (84%) 8 (16%) 22 -+ 5.9 135 -+ 81 L/min 26 _+ 15 68.9 _+ 11.6mm Hg 34.8 _+ 5 . 3 m m Hg 7.39 _+ 0.05
*Mean ± standard deviation.
7.50 745 •
i8 •• 811
•
l,.'~.o:'.:
7.40
• o• • o•
~. 7.55
• ----•o • •o
•
7.:50
RESULTS Fifty-five patients comprising 99 emergency visits were studied during August and September 1979. Ten patient visits were excluded because the protocol was not completely followed, leaving 89 visits by 51 patients. Data describing the patient sample are given (Table). Arterial pH, PaO2, and PaCO2 as a function of percentage of predicted PEFR are shown (Figures 1 to 3). Rather small Pearson coefficients of correlation were obtained for each of these parameters, even though a statistically significant relationship at the 5% level was achieved. As expected, an even smaller correlation was found between arterial pH, PaO2, and PaCO2 and absolute PEFR. Therefore, these data were not considered in
r =.:545
p< 01
725 I
i
Io
I
20 25 30
L
I
I
I
I
I
I
40
50
60
70
80
90
100
% Predicted Peek Expiretory Flow I00 90 80~ o •e
~ 7o~
. •e
ell ¸
: •o
II o o e
•lSJ • X" ".'"
60
• 0•
•
•0 •
•o
:
r = .375 p, 001
*co
Fig. 1. p H versus % predicted PEFR. Note no patient with a PEFR >~ 25% had a p H < 7.35. Fig. 2. Pa02 versus % predicted PEFR. Note three patients with Pa02 <- 60 and PEFR > 25% predicted. 32/71
50 I
0
I0
*l
I
•
20 25 30
I
I
1
L
I
l
I
40
50
60
70
80
90
I00
% Predicted Peek Expiratory Flow
2 Annals
of Emergency
Medicine
11:2
February 1982
Fig. 3. P a C 0 2 versus % predicted PEFR. Note no patient with a PEFR >1 25% predicted had a PaC02 > 45. 5O
'
~4o^I
3 U ~ -
'. ".'.'I v • ,'0
•
"
20
i
2
p< .05
101 0
I I0
I 20
I
I I I I L 40 50 60 70 0 % Predicted Peak Expiratory Flow 50
further analyses. As demonstrated previously by Murray, 9 the correlation is better for pH (0.359) and PaCO2 (-0.449) wh*:n only patients with marked airway obstruction (PEFRs < 40% predicted) were examined. These data were significant at the 1% level. The correlation between 02 and PEFR actually fell to 0.199 when only patients with a PEFR < 40% predicted were examined. No patient having percentage of predicted PEFR/> 25% was noted to have a PaCO2 greater than 45 mm Hg or an arterial pH less than 7.35. However, hypoxemia (PaO2 ~ 60 mm Hg) was noted in four individuals with percentage of predicted PEFR/> 25%. DISCUSSION Traditionally information obtained from the history and physical examination has been relied on to evaluate the severity of asthma. Recent reports, however, question the accuracy of the clinical examination. McFadden 1° compared the relationship between severity of asthma as judged by the FEV1 or ABGs and historical information, such as the patient's age, age at onset of asthma, and duration of the acute attack. No significant correlation between this historical information and pulmonary hmction was found. In a separate report, McFadden et al n compared the presence of wheezing, dyspnea, and stemocleidomastoid muscle retraction 11:2 February 1982
I 90
I00
3
with the degree of pulmonary function impairment in acute asthma. Only retraction was found to correlate with the degree of functional impairment; when present, FEV1 was usually less than one liter. However, Kelson 12 found sternocleidomastoid retraction to be present in less than 50% of patients with acute asthma, and FEV1 less than one liter. The presence or absence of subjective (patient reported) or objective (auscultated) wheezing is also a poor predictor of pulmonary function in acute asthma. For example, in the course of treatment for acute asthma, wheezing may resolve even though FEV1 has been restored to only 55% to 65% of predicted normal; 1 1 further, wheezing may actually be absent in patients with very severe airflow obs t r u c t i o n and m i n i m a l air movement. 13 The patient complaint of dyspnea is an even less sensitive indicator of pulmonary function impairment and may not be offered until FEV1 has been reduced to less than 40% to 50% of normal, n While pub sus paradoxus has been observed in 50% to 60% of patients with severe airflow obstruction documented by pulmonary function testing, 14-16 it is obviously not a very sensitive test, for it may be absent up to half the time and difficult to elicit accurately in tachypneic, tachycardic patients in a noisy emergency department. Attempts have been made to correA n n a l s of Emergency Medicine
late changes in arterial blood gases with the perceived clinical severity of asthma. These data suggest that marked disturbances in gas exchange may occur in patients whose obstruction does not appear to be clinically severe. 17'1s Tai and Read TM have described 64 patients judged clinically not to have severe airway obstruction; 14 had a PaO2 < 60 mm Hg and 9 had a PaCO2 > 45 m m Hg. Conversely, Rebuck 16 observed central cyanosis in 25 of 58 patients with acute asthma, only three of whom had a PaO2 < 50 mm Hg. Thus no single clinical parameter is a reliable predictor of severe airflow obstruction or markedly impaired gas exchange in acute asthma. Our study describes the correlation between arterial pH, PaO2, and PaCO2 and PEFR in acute asthma. Other investigators have examined this relationship with results similar to ours. 9,10,12,16,18 As in our report, only a weak correlation between these parameters has previously been observed. 12 This association is obviously too weak to allow one to predict accurately one parameter with knowledge of the other. None of our patients with an initial percentage of predicted PEFR 1> 25% had a PaCO2 > 45 m m Hg or an arterial pH < 7.35. A few patients with percentage of PEFR >~ 25% had a PaO2 60 m m Hg and were considered hypoxemic. McFadden 1° has suggested that alveolar ventilation does not begin to fall in acute asthma until the FEV1 drops below 25% of normal, while hypercarbia does not occur until FEV1 is below 20% of normal. Our data are in agreement with this suggestion. Arterial CO~ tensions in excess of 45 mm Hg have been noted in individuals with FEV1 greater than 25% of normal; 16 however, that report included patients up to 69 years of age in whom chronic obstructive lung disease could not be ruled out. Our data suggest that measurement of arterial blood gases is unnecessary in acute asthmatic patients with percentage of predicted PEFR ~> 25%, for 72/33
PEAK EXPIRATORY FLOW RATES Martin, Elenbaas & Pingleton
hypercarbia or acidosis was not observed in any of these individuals. If ABGs had been performed only on patients w i t h percentage of predicted PEFR < 25%, 40% of our subjects w o u l d have been spared the procedure. Examination of data from previous reports suggests that measurement of ABGs m a y be withheld safely in as m a n y as 50% to 77% of patients ff they are performed only on i n d i v i d u a l s w i t h percentage of predicted PEFR or FEV1 < 25%. 9'12 Our data and those from previous studies indicate that hypoxia (PaO2 < 60 m m Hg) m a y o c c u r in a s m a l l number of patients w h e n either PEFR or FEV1 is >I 25% p r e d i c t e d . 9'1°'12 Many think that ventilation perfusion m i s m a t c h i n g rather than airflow obstruction is the major cause of hypoxia in acute asthma. West 19 has cited evidence suggesting that bronchospasm plays only a small role in producing hypoxia in asthmatics, and our data s u p p o r t this h y p o t h e s i s . T h u s while it m a y be acceptable to withhold ABG determination in these patients, unrecognized hypoxemia could still exist. Supplemental oxygen could be given without fear of producing respiratory arrest because none of these i n d i v i d u a l s h a d h y p e r c a r b i a . Even though our patients had a marked degree of airflow obstruction on present a t i o n (mean % p r e d i c t e d PEFR = 26%, Table), they comprised a select s a m p l e of y o u n g p e o p l e w h o m e t s t r i c t c r i t e r i a for t h e d e f i n i t i o n of asthma, and none had pneumonia or other complications which might adversely influence pulmonary gas exchange. Our results should not be extrapolated to older individuals having chronic o b s t r u c t i v e p u l m o n a r y disease, nor to patients w i t h pneumonia, p n e u m o t h o r a x , or o t h e r a c u t e or chronic lung disease.
CONCLUSION A c c u r a t e a s s e s s m e n t of gas ex-
34/73
change or airflow obstruction in acute asthma is not possible with information derived solely from the history and physical examination. Arterial b l o o d gases are f r e q u e n t l y u s e d to assess severity in acute a s t h m a and to guide therapy. The pain, cost, and risk of side effects, however, preclude their use in every patient presenting with an acute exacerbation of asthma. Our data, supported by those of previous reports, suggest that s i m p l e pulmonary function testing can be used to screen for patients at high risk of having significant hypercarbia or acidosis. I n i t i a l a r t e r i a l b l o o d gas s a m p l i n g should be reserved for those patients presenting w i t h a percentage of predicted PEFR < 25% and those with s u s p e c t e d c o m p l i c a t i o n s , s u c h as pneumothorax or pneumonia. Because hypoxia is unpredictable both on pres e n t a t i o n 1,17 a n d f o l l o w i n g t r e a t ment, 2° supplemental oxygen should be c o n s i d e r e d in all a s t h m a t i c patients.
The authors thank Barbara Hollendorf and Niki Sims for their clerical assistance.
REFERENCES 1. McKenzie SA, Edmunds AT, Godfrey S: Status asthmaticus in children - - A one year study. Arch Dis Child 54:581-586, 1979. 2. Dworetzky M: Immediate assessment of acute respiratory distress in asthma, in The Asthmatic Patient in Trouble. Greenwich, CT, CPC Communications, Inc, 1976. 3. Berte JB: Pulmonary Emergencies. Philadelphia, JB Lippincott, 1977, p 105. 4. Felkner D: A protocol for teaching and maintaining arterial puncture skills among respiratory therapists. Respiratory Care 18{6):700-705, 1973. 5. Wright BM, McKerrow CB: Maximum expiratory flow rate as a measure of ventilatory capacity. Br Med J 7:1041-1047, 1959.
Annals of Emergency Medicine
6. Saunders KB, Rudolf M: The interpretation of different measurements of airway obstruction in the presence of lung volume changes in bronchial asthma. Ch'n Sci Mol Med 54:313-321, 1978. 7. American Thoracic Society: Chronic bronchitis, asthma, and pulmonary emphysema. A m Rev Respir Dis 85:762-768, 1962. 8. Gregg I, Nunn AJ: Peak expiratory flow in normal subjects. Br Med J 3:282, 1973. 9. Murray AB: Assessing severity of asthma with Wright peak flow meter. Lancet 1:708, 1977. 10. McFadden ER, Lyons HA: A controlled study of the effects of single doses of hydrocortisone on the resolution of acute attacks of asthma. A m J Med 60:52-59, 1976. 11. McFadden ER, Kaiser R, DeGroot WJ: Acute bronchial asthma - - Relations between clinical and physiological manifestations. N Engl ] Med 288:221-225, 1973. 12. Kelsen SG, Kelsen DP, Fleegler BF, et al: Emergency room assessment and treatment of patients with acute asthma - Adequacy of the conventional approach. A m J Med 64:622-628, 1978. 13. Crofton J, Douglas A: Respiratory Disease. London, Blackwell Scientific Publications, 1975, p 439. 14. Gluck JC, Busto R, Marks MB: Pulsus paradoxus in childhood asthma - - Its prognostic value. Arm Allergy 38:405-407, 1977. 15. Knowles GK, Clark TJH: Pulsus paradoxus as a valuable sign indicating severity of asthma. Lancet 2:1356-1359, 1973. 16. Rebuck AS, Read J: Assessment and management of severe asthma. A m ] Med 51:788-798, 1971. 17. Rees HA, Millan JS, Donald KW: A study on the clinical course and arterial blood gas tensions of patients in status asthmaticus. Q J Med 148:541:561, 1968. 18. Tai E, Read J: Blood gas tensions in bronchial asthma. Lancet 1:644-646, 1967. 19. West JB: Pulmonary gas exchange, in Ventilation Blood Flow and Diffusion, vol 1. New York, Academic Press, 1980. 20. Tai E, Read J: Response of blood gas tensions to aminophylline and isoprenaline in patients with asthma. Thorax 22:543549, 1967.
11:2 February 1982
Use of Peak Expiratory Flow Rates to Eliminate Unnecessary Arterial Blood Gases in Acute Asthma Arterial blood gas (ABG) measurements are used frequently in acute asthma. Because ABGs are expensive and m a y have significant side effects, a method is needed to identify those patients at risk for a significantly abnormal ABG. We studied the use of peak expiratory flow rates (PEFR) to identify those patients at such risk. Data from 89 emergency visits by 51 asthmatic patients were analyzed. A small but significant correlation between ABG parameters and PEFR was observed (P < 0.05). No patient with a PEFR >1 25% predicted had a PaC02 > 45 m m Hg or pH < 7.35. This suggests that only those patients with a PEFR < 25% predicted are at risk for significant hypercarbia or acidosis. We concluded that PEFR may be used as a simple screening tool to safely eliminate ABGs in at least 40% of acute asthmatic patients. [Martin TG, Elenbaas RM, Pingleton SH: Use of peak expiratory flow rates to eliminate unnecessary arterial blood gases in acute asthma. Ann Emerg Med 11:70-73, February 1982.]
INTRODUCTION Acute asthma is potentially a life-threatening problem. It is unfortunate that information derived from the history and physical examination is often unreliable in assessIng gas exchange or airflow obstruction, for these parameters are the major factors dictating appropriate therapy. Direct measurement of arterial blood gases (ABGs) is the most reliable measure of gas exchange. Because the clinical examination is unreliable in predicting the magnitude of airflow obstruction, it has been recommended that ABGs be measured on every patient presenting to the emergency department with acute asthma.l~3 However, because the procedure is associated with moderate pain, substantial cost, and occasional complications, 4 a reliable method is needed to identify those patients likely to have abnormal ABGs. If alteration in gas exchange is related to the degree of airflow obstruction, then simple pulmonary function tests should predict the presence of abnormal ABGs. The peak expiratory flow rate (PEFR) is a simple pulmonary function test which can be used to measure the severity of airflow obstruction in asthma. 5,6 The purposes of our study were the following: 1) to assess the relationship between changes in pulmonary fimction as measured by PEFR and ABG measurements; and 2) to evaluate the capacity of PEFR to screen for severely abnormal ABG measurement in patients presenting with acute asthma.
Thomas G. Martin, MD* Robert M. Elenbaas, PharmD* Susan H. Pingleton, MDt Kansas City, Missouri
From the Departments of Emergency Health Services* and Pulmonary Medicine, t Truman Medical Center, University of Missouri - - Kansas City School of Medicine, Kansas City.
Address for reprints: Robert M. Elenbaas, Pharm D, Department of Emergency Medicine, Truman Medical Center, 2301 Holmes, Kansas City, Missouri 64108.
Presented at the University Association for Emergency Medicine Annual Meeting in San Antonio, Texas, April 1981.
MATERIALS A N D METHODS Patients of either sex between the ages of 15 and 39 years who met the American Thoracic Society criteria for asthma z and presented to the Emergency Department of Truman Medical Center in August and September 1979 with an acute episode of airway obstruction were included. Prior to therapy (including supplemental oxygen), an arterial blood specimen was obtained percutaneously from the radial artery and analyzed for pH, PaO2, and PaCO2. PEFR was measured using the Wright Peak Flow Meter [Armstrong Industries, Inc, Northbrook, IL) either immediately before or after obtaining the arterial specimen. The PEFR procedure was administered by either an emergency physician or a nurse, with the patient in the sitting 11:2 February 1982
Annals of Emergency Medicine
70/31
PEAK EXPIRATORY FLOW RATES Martin, Elenbaas & Pingleton
position. The best of three patient attempts was recorded and Utilized in subsequent data analysis. The Wright Peak Flow Meter used is incapable of quantitating a flow rate less than 60 L/rain; therefore, flow rates below quantification were recorded as 60 L/min and this value was used in subsequent statistical analysis. PEFR was normalized between patients for sex, age, and height from data 8 supplied with the instrument by its manufacturer and was expressed as percentage of predicted PEFR. Arterial pH, PaO2, and PaCO2 were individually compared with absolute and percentage of predicted PEFR using the Pearson correlation coefficient. Arterial specimens were analyzed using an Instrumentation Laboratory 813 Blood Gas Analyzer (Instrumentation Laboratory, Lexington, MA). Informed consent was obtained from each patient prior to inclusion in the study. The study protocol was approved by the Clinical Research Review Board of Truman Medical Center and the Institutional Review Board of the University of Missouri - - Kansas City.
TABLE. S u m m a r y of patient data No. patients No. visits Males Females Black Non-black Age* (years) Absolute PEFR* % predicted PEFR* PaO2* PaCe2* pH*
51 89 20 (39%) 31 (61%) 43 (84%) 8 (16%) 22 -+ 5.9 135 -+ 81 L/min 26 _+ 15 68.9 _+ 11.6mm Hg 34.8 _+ 5 . 3 m m Hg 7.39 _+ 0.05
*Mean ± standard deviation.
7.50 745 •
i8 •• 811
•
l,.'~.o:'.:
7.40
• o• • o•
~. 7.55
• ----•o • •o
•
7.:50
RESULTS Fifty-five patients comprising 99 emergency visits were studied during August and September 1979. Ten patient visits were excluded because the protocol was not completely followed, leaving 89 visits by 51 patients. Data describing the patient sample are given (Table). Arterial pH, PaO2, and PaCO2 as a function of percentage of predicted PEFR are shown (Figures 1 to 3). Rather small Pearson coefficients of correlation were obtained for each of these parameters, even though a statistically significant relationship at the 5% level was achieved. As expected, an even smaller correlation was found between arterial pH, PaO2, and PaCO2 and absolute PEFR. Therefore, these data were not considered in
r =.:545
p< 01
725 I
i
Io
I
20 25 30
L
I
I
I
I
I
I
40
50
60
70
80
90
100
% Predicted Peek Expiretory Flow I00 90 80~ o •e
~ 7o~
. •e
ell ¸
: •o
II o o e
•lSJ • X" ".'"
60
• 0•
•
•0 •
•o
:
r = .375 p, 001
*co
Fig. 1. p H versus % predicted PEFR. Note no patient with a PEFR >~ 25% had a p H < 7.35. Fig. 2. Pa02 versus % predicted PEFR. Note three patients with Pa02 <- 60 and PEFR > 25% predicted. 32/71
50 I
0
I0
*l
I
•
20 25 30
I
I
1
L
I
l
I
40
50
60
70
80
90
I00
% Predicted Peek Expiratory Flow
2 Annals
of Emergency
Medicine
11:2
February 1982
Fig. 3. P a C 0 2 versus % predicted PEFR. Note no patient with a PEFR >1 25% predicted had a PaC02 > 45. 5O
'
~4o^I
3 U ~ -
'. ".'.'I v • ,'0
•
"
20
i
2
p< .05
101 0
I I0
I 20
I
I I I I L 40 50 60 70 0 % Predicted Peak Expiratory Flow 50
further analyses. As demonstrated previously by Murray, 9 the correlation is better for pH (0.359) and PaCO2 (-0.449) wh*:n only patients with marked airway obstruction (PEFRs < 40% predicted) were examined. These data were significant at the 1% level. The correlation between 02 and PEFR actually fell to 0.199 when only patients with a PEFR < 40% predicted were examined. No patient having percentage of predicted PEFR/> 25% was noted to have a PaCO2 greater than 45 mm Hg or an arterial pH less than 7.35. However, hypoxemia (PaO2 ~ 60 mm Hg) was noted in four individuals with percentage of predicted PEFR/> 25%. DISCUSSION Traditionally information obtained from the history and physical examination has been relied on to evaluate the severity of asthma. Recent reports, however, question the accuracy of the clinical examination. McFadden 1° compared the relationship between severity of asthma as judged by the FEV1 or ABGs and historical information, such as the patient's age, age at onset of asthma, and duration of the acute attack. No significant correlation between this historical information and pulmonary hmction was found. In a separate report, McFadden et al n compared the presence of wheezing, dyspnea, and stemocleidomastoid muscle retraction 11:2 February 1982
I 90
I00
3
with the degree of pulmonary function impairment in acute asthma. Only retraction was found to correlate with the degree of functional impairment; when present, FEV1 was usually less than one liter. However, Kelson 12 found sternocleidomastoid retraction to be present in less than 50% of patients with acute asthma, and FEV1 less than one liter. The presence or absence of subjective (patient reported) or objective (auscultated) wheezing is also a poor predictor of pulmonary function in acute asthma. For example, in the course of treatment for acute asthma, wheezing may resolve even though FEV1 has been restored to only 55% to 65% of predicted normal; 1 1 further, wheezing may actually be absent in patients with very severe airflow obs t r u c t i o n and m i n i m a l air movement. 13 The patient complaint of dyspnea is an even less sensitive indicator of pulmonary function impairment and may not be offered until FEV1 has been reduced to less than 40% to 50% of normal, n While pub sus paradoxus has been observed in 50% to 60% of patients with severe airflow obstruction documented by pulmonary function testing, 14-16 it is obviously not a very sensitive test, for it may be absent up to half the time and difficult to elicit accurately in tachypneic, tachycardic patients in a noisy emergency department. Attempts have been made to correA n n a l s of Emergency Medicine
late changes in arterial blood gases with the perceived clinical severity of asthma. These data suggest that marked disturbances in gas exchange may occur in patients whose obstruction does not appear to be clinically severe. 17'1s Tai and Read TM have described 64 patients judged clinically not to have severe airway obstruction; 14 had a PaO2 < 60 mm Hg and 9 had a PaCO2 > 45 m m Hg. Conversely, Rebuck 16 observed central cyanosis in 25 of 58 patients with acute asthma, only three of whom had a PaO2 < 50 mm Hg. Thus no single clinical parameter is a reliable predictor of severe airflow obstruction or markedly impaired gas exchange in acute asthma. Our study describes the correlation between arterial pH, PaO2, and PaCO2 and PEFR in acute asthma. Other investigators have examined this relationship with results similar to ours. 9,10,12,16,18 As in our report, only a weak correlation between these parameters has previously been observed. 12 This association is obviously too weak to allow one to predict accurately one parameter with knowledge of the other. None of our patients with an initial percentage of predicted PEFR 1> 25% had a PaCO2 > 45 m m Hg or an arterial pH < 7.35. A few patients with percentage of PEFR >~ 25% had a PaO2 60 m m Hg and were considered hypoxemic. McFadden 1° has suggested that alveolar ventilation does not begin to fall in acute asthma until the FEV1 drops below 25% of normal, while hypercarbia does not occur until FEV1 is below 20% of normal. Our data are in agreement with this suggestion. Arterial CO~ tensions in excess of 45 mm Hg have been noted in individuals with FEV1 greater than 25% of normal; 16 however, that report included patients up to 69 years of age in whom chronic obstructive lung disease could not be ruled out. Our data suggest that measurement of arterial blood gases is unnecessary in acute asthmatic patients with percentage of predicted PEFR ~> 25%, for 72/33
PEAK EXPIRATORY FLOW RATES Martin, Elenbaas & Pingleton
hypercarbia or acidosis was not observed in any of these individuals. If ABGs had been performed only on patients w i t h percentage of predicted PEFR < 25%, 40% of our subjects w o u l d have been spared the procedure. Examination of data from previous reports suggests that measurement of ABGs m a y be withheld safely in as m a n y as 50% to 77% of patients ff they are performed only on i n d i v i d u a l s w i t h percentage of predicted PEFR or FEV1 < 25%. 9'12 Our data and those from previous studies indicate that hypoxia (PaO2 < 60 m m Hg) m a y o c c u r in a s m a l l number of patients w h e n either PEFR or FEV1 is >I 25% p r e d i c t e d . 9'1°'12 Many think that ventilation perfusion m i s m a t c h i n g rather than airflow obstruction is the major cause of hypoxia in acute asthma. West 19 has cited evidence suggesting that bronchospasm plays only a small role in producing hypoxia in asthmatics, and our data s u p p o r t this h y p o t h e s i s . T h u s while it m a y be acceptable to withhold ABG determination in these patients, unrecognized hypoxemia could still exist. Supplemental oxygen could be given without fear of producing respiratory arrest because none of these i n d i v i d u a l s h a d h y p e r c a r b i a . Even though our patients had a marked degree of airflow obstruction on present a t i o n (mean % p r e d i c t e d PEFR = 26%, Table), they comprised a select s a m p l e of y o u n g p e o p l e w h o m e t s t r i c t c r i t e r i a for t h e d e f i n i t i o n of asthma, and none had pneumonia or other complications which might adversely influence pulmonary gas exchange. Our results should not be extrapolated to older individuals having chronic o b s t r u c t i v e p u l m o n a r y disease, nor to patients w i t h pneumonia, p n e u m o t h o r a x , or o t h e r a c u t e or chronic lung disease.
CONCLUSION A c c u r a t e a s s e s s m e n t of gas ex-
34/73
change or airflow obstruction in acute asthma is not possible with information derived solely from the history and physical examination. Arterial b l o o d gases are f r e q u e n t l y u s e d to assess severity in acute a s t h m a and to guide therapy. The pain, cost, and risk of side effects, however, preclude their use in every patient presenting with an acute exacerbation of asthma. Our data, supported by those of previous reports, suggest that s i m p l e pulmonary function testing can be used to screen for patients at high risk of having significant hypercarbia or acidosis. I n i t i a l a r t e r i a l b l o o d gas s a m p l i n g should be reserved for those patients presenting w i t h a percentage of predicted PEFR < 25% and those with s u s p e c t e d c o m p l i c a t i o n s , s u c h as pneumothorax or pneumonia. Because hypoxia is unpredictable both on pres e n t a t i o n 1,17 a n d f o l l o w i n g t r e a t ment, 2° supplemental oxygen should be c o n s i d e r e d in all a s t h m a t i c patients.
The authors thank Barbara Hollendorf and Niki Sims for their clerical assistance.
REFERENCES 1. McKenzie SA, Edmunds AT, Godfrey S: Status asthmaticus in children - - A one year study. Arch Dis Child 54:581-586, 1979. 2. Dworetzky M: Immediate assessment of acute respiratory distress in asthma, in The Asthmatic Patient in Trouble. Greenwich, CT, CPC Communications, Inc, 1976. 3. Berte JB: Pulmonary Emergencies. Philadelphia, JB Lippincott, 1977, p 105. 4. Felkner D: A protocol for teaching and maintaining arterial puncture skills among respiratory therapists. Respiratory Care 18{6):700-705, 1973. 5. Wright BM, McKerrow CB: Maximum expiratory flow rate as a measure of ventilatory capacity. Br Med J 7:1041-1047, 1959.
Annals of Emergency Medicine
6. Saunders KB, Rudolf M: The interpretation of different measurements of airway obstruction in the presence of lung volume changes in bronchial asthma. Ch'n Sci Mol Med 54:313-321, 1978. 7. American Thoracic Society: Chronic bronchitis, asthma, and pulmonary emphysema. A m Rev Respir Dis 85:762-768, 1962. 8. Gregg I, Nunn AJ: Peak expiratory flow in normal subjects. Br Med J 3:282, 1973. 9. Murray AB: Assessing severity of asthma with Wright peak flow meter. Lancet 1:708, 1977. 10. McFadden ER, Lyons HA: A controlled study of the effects of single doses of hydrocortisone on the resolution of acute attacks of asthma. A m J Med 60:52-59, 1976. 11. McFadden ER, Kaiser R, DeGroot WJ: Acute bronchial asthma - - Relations between clinical and physiological manifestations. N Engl ] Med 288:221-225, 1973. 12. Kelsen SG, Kelsen DP, Fleegler BF, et al: Emergency room assessment and treatment of patients with acute asthma - Adequacy of the conventional approach. A m J Med 64:622-628, 1978. 13. Crofton J, Douglas A: Respiratory Disease. London, Blackwell Scientific Publications, 1975, p 439. 14. Gluck JC, Busto R, Marks MB: Pulsus paradoxus in childhood asthma - - Its prognostic value. Arm Allergy 38:405-407, 1977. 15. Knowles GK, Clark TJH: Pulsus paradoxus as a valuable sign indicating severity of asthma. Lancet 2:1356-1359, 1973. 16. Rebuck AS, Read J: Assessment and management of severe asthma. A m ] Med 51:788-798, 1971. 17. Rees HA, Millan JS, Donald KW: A study on the clinical course and arterial blood gas tensions of patients in status asthmaticus. Q J Med 148:541:561, 1968. 18. Tai E, Read J: Blood gas tensions in bronchial asthma. Lancet 1:644-646, 1967. 19. West JB: Pulmonary gas exchange, in Ventilation Blood Flow and Diffusion, vol 1. New York, Academic Press, 1980. 20. Tai E, Read J: Response of blood gas tensions to aminophylline and isoprenaline in patients with asthma. Thorax 22:543549, 1967.
11:2 February 1982