Relationship between arterial blood gases and spirometry in acute exacerbations of chronic obstructive pulmonary disease

ORIGINAL CONTRIBUTION arterial blood gase s , chronic obstructive pulmonary disease; spirometry, chronic obstructive pulmonary disease

Relationship Between Arterial Blood Gases and Spirometry in Acute Exacerbations of Chronic Obstructive Pulmonary Disease Previous studies have established spirometric criteria for arterial blood gas analysis during acute a s t h m a t i c attacks. However. only general guidelines have been available regarding the need for blood gas analysis during an 3cute exacerbation of chronic obstructive p u l m o n a r y disease (COPD). We c o n d u c t e d a s t u d y to d e t e r m i n e the relationship b e t w e e n arterial blood gases and splrometry m 70 emergency department patients during j c u t e exacerbations of COPD. Arterial blood gas analysis and spirometry were performed on arrival at the emergency department. A l l of the patients with a p C O 2 of more than 45 m m Hg had an FEV 1 of less than 35% of the predicted normal. We found patients with a p O 2 of less than 60 m m Hg who had an FEV 1 as high as 54% of the predicted normal. There was no correlation between the FEV~ and p O 2. Because spirometry was not reliable for identifying patients with significant hypoxemia, we conclude that arterial blood gas analysis is indicated for patients presenting to the ED w i t h acute exacerbations o r COPD. Spirometric criteria that have been used to eliminate the need for arterial blood gases in a s t h m a t i c patients cannot be applied safely to patients w i t h COPD. fEmerman CL. Connors AE Lukens T W Effron D. M a y ME: Relationship between arterial blood gases and spirometry m acute exacerbations of chronic obstructive pulmonary disease. A n n Emerg M e d M a y 1989;18:523-527.]

INTRODUCTION Chronic obstructive pulmonary disease (COPD) is characterized by emphysema, chronic bronchitis, and limited expiratory airflow - either alone or in combination. 1 Acute exacerbations of COPD with increased dyspnea lead to emergency department visits for many of these patients. The evaluation of the patient in acut e distress with COPD is focused on identifying the inciting factors and assessing the degree of severity of the acute exacerbation. This evaluation may include chest radiography, white blood cell counts, drug levels, sputum examination, and, frequently, spirometry as well as arterial blood gas analysis. These considerations are similar to those faced in the evaluatioff of the acute asthmatic patient. Th e frequency with which both asthmatic and COPD patients present to the ED mandates close scrutiny of the appropriateness and necessity of diagnostic testing. Since clinical signs can be misleading, z direct measurements of lung function with bedside spirometry and arterial blood gas sampling have been advocated to assess the severity of the physiologic impairment in acute exacerbations of both asthma 1,3,4 and COPD. 1,s Because of the correlation between the severity of airflow .limitation and derangement of gas exchange in patients with acute asthma,3, 4 several investigators have suggested that arterial blood gases are only necessary in the initial evaluation of patients who have severe reduction in expiratory airflow. 6-8 The relationship between airway obstruction and blood gases has not been studied extensively for patients with acute exacerbation of COPD. Further, only general guidelines have been developed for the indications for arterial blood gas analysis in these patients. I The purpose of our study, was to determine whether spirometric criteria could be established to limit the need for arterial blood gases in patients with acute exacerbation of COPD.

Charles L Emerman MD*¢ Alfred = Conn0rs MDI-§ Thomas W Lukens MD*:r David Effron MD*¢ Michael E May, MD*¢ Cleveland. Ohio From the Deoartments of Emergency Medicine* ana Medicine- Clevelana Metrooolitan General Hospital: ana the Departments of Surgery= and Medicine,§ Case Western Reserve University, Cleveland Ohio Received [or uubllcat~on May 9. 1988 Revision recewea November 21 1988. Acceoted for puo,cation January 18, 1989 Presented al tile Scientific Assemb y of the American College of Emergency Physicians, New Orleans, September 1988. Address for reprints: Charles L Emerman, MD, FACER Department of Emergency Medicine, $441, Cleveland Metropolitan General Hospital, 3395 Scranton Road, Cleveland, ©hie 44109.

METHODS This study was performed in the Cleveland Metropolitan General Hospi18:5 May 1989

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FIGURE 1. Scatterp/ot of p O e versus initial FEV 1 (r = .07, P > .05).

100

FIGURE 2. Scatterplot of p O 2 versus percent predicted n o r m a l FEV~ (r = .06, P > .05). tal ED. Patients more than 50 years old with a clinical history consistent with COPD presenting with acute respiratory distress were considered for entry into the study. All patients had initial spirometry demonstrating an FEV1 of less than 70% of the predicted normal value or an FEV1/FVC ratio of less than 60%. Patients were excluded from the study if they had a history of asthma with onset of episodes of respiratory distress before age 35. Patients were also excluded from the study if they had pneumonia, acute congestive heart failure, or pneumothorax. All patients gave informedwritten consent to a protocol a p p r o v e d by t h e h o s p i t a l ' s Human Investigation Committee. The diagnosis of COPD was verified by spirometry performed in our pulmonary function laboratory at a time of clinical stability either before or at least one month after entry into the study. For the purposes of our study, we accepted as verification of COPD a postbronchodilator FEV1 of less than 75% of the predicted normal value or an FEVJFVC ratio of less than 70%. To exclude patients with asthma, we limited the study to those patients with an increase in FEV 1 in response to inhaled isoproterenol of less than 30%. On arrival in the ED, spirometry was obtained with a computerized, portable, Fleisch pneumotach-type spirometer (Spiroscan 1000% Brentwood Instruments, Portland, Oregon}. Spirometry was obtained with the patient seated and wearing nose clips. A t least two and usually three acceptable 9 forced expiratory maneuvers were obtained from each patient. For this analysis, we used the curve with the greatest forced vital capacity and FEV 1. The spirometer was calibrated at least three times a week with a 3-L syringe and was always within 1% of the calibrating volume. All patients had a portable AP chest radiograph. A room air blood gas was obtained from the radial artery before the initiation of any therapy. The arterial blood was collected in a heparinized glass syringe that was placed on ice and immediately transported 76/524

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to our clinical blood gas laboratory for analysis. We tested for correlations between the results of the arterial blood gas analysis and the spirometric measurements using Pearson correlation coefficients. Comparisons between groups were made using X2 testing with Yates' correction for continuity. A P value of less than .05 indicated statistical significance. Results are reported as mean ± SD. RESULTS

Seventy patients met our criteria Annals

of Emergency

Medicine

for the diagnosis of COPD and had complete data available for arterial blood gas results and spirometry. The average age of the patients was 64.0 -+ 8.5 years, and there were 34 men and 36 women. Ninety-six percent of the patients were current or previous cigarette smokers and had a history of 60.2 ± 31.4 pack years of cigarette use. Ninety-seven percent of the patients gave a history of chronic bronchitis. 1 Eighty-eight percent of the p a t i e n t s were u s i n g t h e o p h y l l i n e products, while 20% of the patients were using a beta-agonist inhaler. 18:5 May 1989

F I G U R E 3. S c a t t e r p l o t o f p C O 2 versus FEV l (r = - . 4 6 , P < .00i).

70

F I G U R E 4. S c a t t e r p l o t o f p C O ~ versus percent o f predicted n o r m a l FEV 1 (r = - . 4 7 , P < .001). o

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FEV 1 (Figure 2}, the FVC, or the percentage of the predicted n o r m a l FVC. There was a moderate correlation between arterial pCO2 and the FEV~ as well as w i t h the percent of the predicted n o r m a l FEV 1 (Figures 3 and 4). Similarly, there was a w e a k correlation b e t w e e n p H and the FEV 1 (r = .33, P < .01} as w e l l as w i t h the percent of predicted FEV 1 lr = .36, P < .01}. We c o m p a r e d the changes in the blood gases from baseline testing w i t h the changes in t h e s p i r o m e t r y from the baseline results. There was no c o r r e l a t i o n b e t w e e n the p e r c e n t age change in pO2 and the percentage change in FEV 1 (r = .23, P = NS). T h e r e w a s a w e a k c o r r e l a t i o n bet w e e n the percentage change in FEV~ and the p e r c e n t a g e change in p C O 2 (r = - . 3 0 , P < .05}. All patients w i t h p H of less than 7.36 h a d an FEV 1 less t h a n 15% of predicted normal. All of the patients w i t h a p C O 2 of more t h a n 45 m m Hg had an FEV 1 of less t h a n 35% of pred i c t e d n o r m a l . Some p a t i e n t s w i t h pOa of less than 60 m m Hg had a percent of the predicted n o r m a l FEV 1 as h i g h as 54%. T h i r t y - s i x p e r c e n t of p a t i e n t s w i t h an FEV~ of less t h a n 35% of the p r e d i c t e d n o r m a l had a pO a of less t h a n 60 m m Hg as compared w i t h 39% of patients with an FEV~ equal to or m o r e than 35% of t h e p r e d i c t e d n o r m a l v a l u e s (P =

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Percent Predicted FEV1.0 T h e i n i t i a l r o o m a i r b l o o d gas showed average p H of 7.43 _+ .05; pCO 2, 39.7 ± 7.6 m m Hg; and pO~, 63.5 ± 11.8 m m Hg. O n initial presentation to the ED, 14 {20%} of the patients had a pCOa of m o r e than 45 m m Hg, w h i l e 24 [34%) of the patients had a pO 2 of less t h a n 60 m m Hg. O n l y three (5%) of the patients had p H less t h a n 7.36. C o m p a r e d w i t h t h e p a t i e n t s ' b a s e l i n e ,blood gases, the results of the ED blood gas analysis showed a decrease in pO2 of 4+2 ± 16.0 m m Hg, a d e c r e a s e in pCO 2 of 0.2 ± 7 3 m m Hg, and a de-

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NS1.

100 4

crease in p H of 0.02 --- 0.06. Before t r e a t m e n t , the i n i t i a l FVC was 1.34 +- 0.64 L (37.5 ± 15.7% of predicted normal} with an initial FEV 1 of 0.71 ± 0.36 L (25.7 +- 11.4% of p r e d i c t e d n o r m a l ) . T h e i n i t i a l FEV1/FVC r a t i o was 55.5 ± 14.7%. The s p i r o m e t r i c characteristics of the p a t i e n t s d u r i n g b a s e l i n e t e s t i n g is s h o w n (Table). T h e r e was no s i g n i f i c a n t correlation between pO 2 and the initial FEV 1 (Figure 1}. T h e r e also was no correlation b e t w e e n arterial pO 2 and the percent of the predicted n o r m a l A n n a l s of E m e r g e n c y

Medicine

DISCUSSION Only general guidelines have been available for the use of arterial blood gas analysis in p a t i e n t s w i t h acute exacerbations of COPD. A recent review on indications for arterial blood gas a n a l y s i s does n o t give specific r e c o m m e n d a t i o n s for the evaluation of COPD. s Daley discusses the interpretation of the arterial blood gases in COPD and its usefulness for staging t h e s e v e r i t y of C O P D b u t does not give instances in w h i c h the arterial blood gas is unnecessary,, lo The s t a n d a r d s for t h e c a r e of p a t i e n t s w i t h COPD published by the A m e r i can Thoracic Society r e c o m m e n d arterial blood gas a n a l y s i s in p a t i e n t s w i t h m o d e r a t e l y severe airflow lim-

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itation, which they define as an FEV l of less than 1.5 L, as well as in all patients hospitalized for respiratory insufficiency. 1 More specific r e c o m m e n d a t i o n s have been developed for the use of arterial blood gases in patients w i t h acute asthma. In asthmatic patients, the arterial blood gas has been advocated as a m e c h a n i s m to identify patients in danger of acute respiratory failure.11,12 Others have found that the use of spirometry or peak expiratory flow measurements could limit the number of patients who required arterial blood gas analysis. Murray et al found that a peak expiratory flow rate of less than 40% of the predicted normal value identified all the patients with pCO 2 of more than 45 m m Hg or pO 2 of less than 50 m m Hg. 13 Martin et al, on the other hand, advocated a peak expiratory flow rate of more than 25% of predicted normal to indicate patients who did not require arterial blood gas analysis. 7 Similarly, N o w a k et al found that an FEV 1 of less than 1.0 L or a peak expir a t o r y flow rate of less t h a n 200 L/min identified nearly all of the patients w i t h hypercarbia or hypoxemia. 6 However, T a i e t al found that an FEV 1 of less than 1 L did not identify all of the asthmatic patients with pO~ of less than 50 m m Hg or pCO 2 of more than 45 m m Hg. 3 In our study, we found hypoxemic patients with an FEV 1 of more than 50% of the predicted normal value. However, as has been demonstrated by others, low-to-relatively normal pCO2 was m a i n t a i n e d until severe airway obstruction was present.4,5,14,15 Other studies have found different relationships between spirometric values and blood gas values. Palmer and D i a m o n t found a correlation of .58 b e t w e e n FEV I and pO 2 w i t h a correlation of .60 between FEV 1 and p C O 2 in 45 p a t i e n t s w i t h s t a b l e COPD. 16 Similarly, M i y a m o t o et al found a correlation of .73 between pO 2 and percent predicted FEV 1 in a s t h m a t i c s . 14 O n the o t h e r hand, Gupta and Nehru found no correlation between pO2 and the FEV1/FVC ratio in asthmatics. ~7 We found poor although statistically significant correlations between pH, pCO2, and the percent predicted FEV2. However, we did not find a significant correlation between pO2 and FEV 1. Our findings imply that the severity of airway ob78/526

TABLE. Characteristics of patient population Age (yr) Cigarette use (pack yr)

64.0

+

8.5*

60.2

_+ 31.4

Baseline spirometryt FEV 1 postbronchodilator FEV 1 percent predicted (%) FEVJFVC ratio (%) Percent change in FEV~ after isoproterenol (%)

1.37 +- 0.56 57.4 _+ 19.3 48.4 -+ 15.0 8.0

_+ 10.0

Baseline arterial blood gases*t pO 2 (ram Hg) pCO 2 (mm Hg) pH

67.6 _+ 10.7 40.3 + 5.8 7.43 _+ 0.05

*Values are mean _+ SD. tPerformed at a time of clinical stability either before or one month after entry into the study.

struction is a poor predictor of arterial blood gases and that, conversely, the results of arterial blood gases are of limited use in estimating the severity of airflow limitation. In our study, we have evaluated the use of spirometry to estimate arterial blood gas values. Spirometric m e a s u r e m e n t s are l i m i t e d in that they require patient cooperation and education. In our experience, m o s t patients are able to cooperate adequately to provide a reliable, reproducible FEV1. While some investigators have used peak-expiratory flow rates in asthmatic patients, these are also effort-dependent and require special devices for measurement at low flow rates. H o w e v e r , w h i l e direct c o m p a r i s o n s h a v e n o t b e e n performed in patients with an acute exacerbation of COPD, N o w a k et al found a good correlation between the FEV 1 and peak-expiratory flow rates in patients with acute asthma. 18 We have chosen to use a spirometer for our measurements because it is easily calibrated, is an accepted standard for the m e a s u r e m e n t of lung function, and provides graphic records of the test. While m a n y studies have f o u n d criteria by which arterial blood gases can be safely eliminated in young patients with asthma, our study does not support the extension of these criteria to older patients with acute exacerbations of COPD. We f o u n d that changes in pCO 2 during acute exacerbations of COPD m i m i c those t h a t o c c u r in p a t i e n t s w i t h a c u t e asthma in that alveolar ventilation is Annals of Emergency Medicine

maintained until severe airway obstruction is present. Thus, increases in pCO 2 would not be expected until the FEV 1 falls b e l o w 35% of predicted normal. In b o t h patients w i t h a s t h m a or w i t h COPD, the p r i m a r y cause of h y p o x e m i a is a b n o r m a l i t i e s in ventilation-perfusion relationships. However, there appear to be differences in the relationship of arterial pO 2 to s p i r o m e t r y b e t w e e n C O P D and asthma. We have found that hypoxemia can occur in patients with COPD with only moderate degrees of airway obstruction. The criteria used in acute a s t h m a that limit arterial blood gas analysis to patients with an FEV 1 of less than 1 L or with expiratory flow rates of less than 40% of the predicted n o r m a l value would n o t i d e n t i f y h y p o x e m i a in all patients with COPD. The use of criteria that limit arterial blood gas analysis in C O P D to p a t i e n t s w i t h an FEV 1 of less than 1.5 L would identify m o s t patients w i t h hypoxemia but would not be useful in eliminating m a n y blood gases in patients suffering from an acute exacerbation of their disease. We conclude that patients presenting with acute exacerbation of COPD require arterial blood gas analysis. T h e arterial blood gas alone, however, is a p o o r indicator of the severity of airway obstruction and should be used with spirometry to assess the extent of respiratory impairment. CONCLUSION H y p o x e m i a and h y p e r c a r b i a are 18:5 May 1989

c o m m o n findings in p atients presenting to t h e ED w i t h a c u t e e x a c e r b a t i o n s of C O P D . H y p e r c a r b i a w a s n o t found to occur in p a t i e n t s w i t h an I~EV~ of m o r e t h a n 35% of p r e d i c t e d normal. We found that patients with only m o d e r a t e d e g r e e s of a i r w a y obs t r u c t i o n m a y h a v e h y p o x e m i a . Prev i o u s l y p u b l i s h e d c r i t e r i a for l i m i t ing t h e u s e of a r t e r i a l b l o o d gases i n p a t i e n t s w i t h a c u t e a s t h m a c a n n o t be e x t e n d e d to p a t i e n t s w i t h a c u t e exace r b a t i o n s of C O P D . S p i r o m e t r y cann o t be u s e d to e l i m i n a t e t h e n e e d for arterial b l o o d gases i n m o s t p a t i e n t s w i t h a c u t e e x a c e r b a t i o n of C O P D . I n a d d i t i o n , a r t e r i a l b l o o d g a s e s are a poor g u i d e to t h e s e v e r i t y of t h e airflow limitation and cannot substit u t e for s p i r o m e t r y i n t h e a s s e s s m e n t of a i r w a y o b s t r u c t i o n .

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18:5 May 1989

bronchial asthma: Relations between clinical and physiologic manifestations. N Engl J Med 1973;288:221-225. 3. Tai D, Sydney MB, Read J: Blood gas tensions in b r o n c h i a l a s t h m a . L a n c e t 1967;1: 644~646. 4. McFadden ER Jr, Lyons HA: Arterial blood gas tension in asthma. N Engl [ Med 1968; 278:1027-1032. 5. Lane DS, Howell JBL, Giblin B: Relation between airways obstruction and COx tension in chronic obstructive airway disease. Br Med J 1968;3:707-709. 6. Nowak RM, Tomlanovich MC, Sarkar DD, et ah Arterial blood gases and pulmonary function testing in acute bronchial asthma, lAMA 1983;249:2043-2046.

7. Martin TG, Elenbaas RM, Pingleton SH: Use of peak expiratory flow rates to eliminate unnecessary arterial blood gases in acute asthma. Ann Emerg Med 1982;11:70-73. 8. Raffin TA: Indications for arterial blood gas analysis. Ann Intern Med 1986;105:390-398. 9. American Thoracic Society: Snowbird Workshop on Standardization of Spirometry. Am Rev Respir Dis 1979;119:831-838. 10. Daley RH: Chronic Obstructive Pulmonary Diseases in Emergency Medicine; Concepts and Clinical Practice. St Louis, CV Mosby Corn-

Annals of Emergency Medicine

party, 1988. 11. Weiss EB, Faling LJ: Clinical significance of PACO2 during status asthmaticus: The crossover point. _Ann Allergy 1968;26:545-551. 12. Rebuck AS, Braude AC, Chapman KR: Evaluation of severity of the acute asthma attack. Chest 1982;82:28S-29S, 13. Murray AB, Hardwick DF, Pirie GE, et ah Assessing severity of asthma with Wright peak flow meter. Lancet 1974;1:708. 14. Miyamoto T, Mizuna K, Furuya K: Arterial blood gases in bronchial asthma. J Allergy 1970;45:248-254. 1.5. Weng TR, Langer HM, Featherbee EA, et al: Arterial blood gas tensions and acid base balance in symptomatic and asymptomatic asthma in childhood. A m Rev Respir Dis 1979;101: 274-282. 16. Palmer KN, Diament ML: Dynamic and static lung volumes, blood gas tensions, and transfer factor in chronic obstructive bronchitis. Lancet 1969;1:1073-1075. 17. Gupta S, Nehru R: Clinical assessment, spirometry, arterial blood gas tension in status asthmaticus. J Ind Med Assoc 1984;82:49-52. 18. Nowak RM, Pensler MI, Sarkar DO, et ah Comparison of peak expiratory flow and FEV~ admission criteria for acute bronchial asthma. Ann Emerg Med 1982;11:64-69.

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