OR~IGINAL CONTRIBUTION

Effects of Sodium Bicarbonate Administration

During Cardiopulmonary Resuscitation

Blaine C. White, MD Judith E. Tintinalli, MD

Detroit, Michigan

To study w h e t h e r s o d i u m b i c a r b o n a t e g iven in c a r d i o p u l m o n a r y resus- citation m a y p r o d u c e l i f e - t h r e a t e n i n g h y p e r o s m o l a l i t y or h y p e r n a - tremia, arterial b lood w a s a n a l y s e d for b l o o d gas, a lcohol , b lood urea nitrogen, e l ec tro ly te and osmola l i ty . The b l o o d w a s d r a w n after resusc i - tation in succes s fu l cases , and whi le e f fect ive m a s s a g e and vent i la t ion were be ing appl ied in u n s u c c e s s f u l resusc i ta t ions . S e v e n of the 17 re- suscitations w e r e success fu l . S e r u m s o d i u m c o n c e n t r a t i o n s ranged from 135 to 154 wi th one except ion and did not corre la te wi th the a m o u n t of sodium b icarbonate adminis tered . Arterial pH r a n g e d from 6.38 to 7.71; only one pat ient had metabo l i c a lkalos i s . S e r u m o s m o l a l i t y ranged from 301 to 407. The data sugges t s a net increase in o smola l i t y of 6 mOsm/50 mEq of s o d i u m bicarbonate .

White BC, Yintinalli JE: Effects of sodium bicarbonate administration during cardiopulmonary resuscitation. JACEP 6:187-190, May, 1977. sodium bicar- bonate, resuscitation.

INTRODUCTION

The role of sodium bicarbonate in c a r d i o p u l m o n a r y r e s u s c i t a t i o n has recently been re -examined by severa l authors. 1-3 One s tudy 1 suggests t ha t as l i t t le as 90 mEq sodium bicarbo- nate g iven dur ing ca rd iopu lmona ry r e s u s c i t a t i o n m a y p r o d u c e l i fe - t h r e a t e n i n g h y p e r o s m o l . a l i t y or

From the Section of Emergency Medicine, Wayne State University, and the Emer- gency Department, Detroit General Hos- pital.

Presented at the ACEP/EDNA Scientific Assembly in New Orleans, October 1976.

Address for reprints: Blaine C. White, MD, Emergency Department , Detroit General Hospital, 1326 St. Antoine, De- troit, Michigan 48226.

h y p e r n a t r e m i a . F i l l m o r e e t al 2 suggests t ha t the acidosis of cardiac a r res t is bes t corrected by vigorous vent i la t ion . M a t t a r et al 3 s ta tes tha t , in t h e a b s e n c e of p r e - e x i s t i n g acidosis , a d m i n i s t r a t i o n of sod ium bicarbonate m a y produce s igni f icant a lka l emia .

In o u r e x p e r i e n c e , s e r i o u s a l - k a l e m i a or h y p e r n a t r e m i a were un- u s u a l o c c u r r e n c e s a f te r success fu l cardiopulmonary resuscitation. There- fore, ' t h i s s tudy was u n d e r t a k e n to prospect ively eva lua te blood gas, elec- t r o l y t e , g l u c o s e , and o s m o l a l i t y changes o c c u r r i ~ d u r i n g cardiopul- monary r e susc i t a t ion in which cur- r en t ly accepted doses of sodium bi- carbonate were adminis tered .

MATERIALS AND METHODS

We performed 17 ca rd iopu lmonary resusc i t a t ions in the emergency de- p a r t m e n t of Detroi t Genera l Hospi ta l d u r i n g A p r i l and M a y of 1976. Vict ims of t r a u m a are not included in th is s tudy. Cardiac a r r e s t occurred outs ide the hospi ta l in all cases. The pa t i en t s were brought to the hospi ta l by the e m e r g e n c y m e d i c a l se rv ice p e r s o n n e l who a d m i n i s t e r e d bas ic c a r d i o p u l m o n a r y r e s u s c i t a t i o n en route. E ndo t r a c he a l i n tuba t ion was per formed immedia t e ly by the emer- gency phys ic ian when the pa t i en t ar- r ived a t the hospital . In ac~dition to e lec t r ica l def ibr i l la t ion and conven- t i o n a l c a r d i a c m e d i c a t i o n s , t r e a t - men t consis ted of a 100 mEq bolus of sod ium b ica rbona te followed by 50 mEq every five to ten minu tes there- after , t o t a l ing 100 mEq to 250 mEq. E x t e r n a l massage ra tes of 60 to 80/ minu te were used wi th a vent i la t ion- to-compression rat io of one to three. At the conclusion of each resusci ta- t ion, spec imens of a r t e r i a l blood were sent for blood gas ana lys i s and al- cohol, glucose, blood u rea n i t rogen (BUN), e l e c t r o l y t e and o s m o l a l i t y de t e rmina t ions . In the cases of un- suc c e s s fu l r e s u s c i t a t i o n s , a r t e r i a l specimens were drawn while effective massage and vent i la t ion were be ing applied.

'~ [~P 6:5 (May) 1977 187/17

RESULTS

Seven of the 17 resusc i ta t ions were successful. Wi th the exception of pa- t i en t (OL) who had a serum sodium level of 170, a l l se rum sodium con- cen t ra t ions r anged between 135 and 154 (Table 1), and the serum sodium level did not increase with increased amoun t s of sodium bicarbonate ad- m in i s t r a t i on (Figure 1). Ar te r i a l pH ranged from 6,83 to 7.71. Only one p a t i e n t had s i g n i f i c a n t m e t a b o l i c acidosis (Table 2). Serum osmola l i ty ranged from 301 to 407 and cor re la tes be t t e r w i th the se rum glucose t han wi th the a m o u n t of sodium bicarbon- a te a d m i n i s t e r e d (F igure 2). I f the osmola l i t i es a re ca lcula ted wi th the se rum glucose cons tan t ly corrected to 100 rag/100 ml and the alcohol cor- rec ted to 0, the range is 286 to 349 mOsm (Table 3). Our da ta suggests a ne t increase in osmolal i ty of about 6 mOsm/50 mEq of sodium bicarbon- a te (F igure 3).

W h i l e a g g r e s s i v e e f fo r t s w e r e made to m a i n t a i n adequa te vent i la- tion, our da t a shows t ha t ven t i l a t ion alone was insuff ic ient to correct the acidosis. Whi le t en pa t ien ts had a pH of 7.4 or lower, only two of these (OL a n d H F ) h a d s e v e r e r e s p i r a t o r y acidosis (Table 3), and these pa t ien t s had mass ive aspi ra t ion .

Blood glucose ranged from 199 to 1149 mg/100 ml. None of the pa t i en t s were known diabetics . Three pa t i en t s (CW, CL, a n d EB) we re g i v e n a bolus of 25 gm of glucose dur ing re- susci ta t ion. All pa t i en t s received in- t r avenous infus ions of 5% dext rose and .3 no rma l sa l ine (D5/.3NS).

DISCUSSION

Pa t i en t s in ca rd iopu lmonary a r r e s t have severe r e s p i r a t o r y and meta - bolic acidosis.4, 5 Metabol ic acidosis depresses myoca rd i a l cont rac t i l i ty , ~ is de le te r ious to pu lmonary function, ~ and lowers the myoca rd i a l t h r e sh - old for ven t r i cu la r f ibr i l la t ion, s The acidosis is corrected by es tab l i sh ing adequate vent i la t ion , m a i n t a i n i n g ad- equate c i rcula t ion, and admin i s t e r ing sodium b ica rbona te . In view of the harmful effects of metabol ic acidosis, it would be t he r apeu t i c a l l y d isas t rous to d i s regard the beneficial effects of sodium bicarbonate implying that even in judic ious doses, it may produce le- tha l hyperna t rem~a and hyperosmo-

18/188

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140

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I I I T } 50 100 150 200 250

mEq NaHCO3 a d m i n i s t e r e d

F i g . 1. Serum sodium level versus increasing sodium bicarbonate administerec

Table 1 SUCCESSFUL CARDIOPULMONARY RESUSCITATIONS

Patient mEq NaHCO3 Glucose Na K

CS 100 214 139 3,4 MD 100 614 154 5.4 CL 200 630 135 3.5 CW 150 663 137 4 . 2 EB 250 1149 143 4.5 JD#86 200 411 137 2.9 WW 150 285 143

UNSUCCESSFUL CARDIOPULMONARY RESUSCITATIONS

Patient mEq NaHCO3 Glucose Na K

HF 150 212 144 7 .2 GM 200 330 143 4.7 LF 150 403 152 4.4 WK 250 822 144 2.9 EH 250 380 144 5.4 OL 200 1005 170 6.8 ES 200 704 146 5.6 JF 150 458 145 3.4 CL 200 231 147 4.3 DW 150 199 150 2.5

-5 E 69 O

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410 -

400

390

380

370

360

350

340

330

320

310

300

290

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• o.i. 6 0

.=.-'6 ~s S • •

J I r J I t 200 400 600 800 1000 1200

Serum G lucose mg/100 ml

---Predicted osmolali ty change with increasing glucose.

®Alcohol = 297 mg/100 ml [gAIcohol = 167 mg/100 ml /*Alcohol = 51 mg/100 ml

Fig . 2. Glucose versus osmolaIity for all patients.

6:5 (May) 1977 J ~ P

t~litY ' Indeed, our data demonstrates that such adverse effects are not com-

mon. previous s tud ies of o s m o l a l i t y

changes during cardiopulmonary ar- rest have failed to consider the ef- fects of blood glucose or alcohol. Our finding of hyperglycemia and related hyperosmolality is not surpr is ing . Claude Bernard was the first to note that h :~perg lycemia o f ten accom- panies shock2 In hypovolemic shock, the blood glucose often rises in rela- tion to the severi ty of shock, l° but the e t io logy of h y p e r g l y c e m i a in shock remains unclear. In one study of hemorrhagic shock in monkeys, 11 the insulin secretory rate decreased while p e r i p h e r a l venous i n s u l i n levels increased. This was thought to be due to decreased peripheral use or clearance of insulin.

Thi r teen of the 17 p a t i e n t s re- ceived single or multiple injections of epinephrine, a potent s t imula tor of hyperglycemia and supressor of pan- creatic islet eell function. 12 In hu- mans in t raumat ic shock, the blood glucose remains high but begins de- clining after about five hours. It has been suggested tha t few patients with a blood glucose g r e a t e r t h a n 500 rag/100 ml for 24 hours post-resusci- tation survived. ~3

The routine adminis t ra t ion of 25 gm of glucose intravenously dur ing resusc i ta t ion does not seem war- ranted in view of the significant in- cidence of hyperglycemia in our seri- es. In add i t ion , u s i n g .5 n o r m a l saline as the rou t ine i n t r a v e n o u s fluid in cardiopulmonary resuscita- tion a p p e a r s more phys io log ic . Further studies will be carried out to eva lua te t he e f f icacy of such so- lutions. R o b i n s o n and Loeb 4 re- viewed the marked changes in serum osmolality resul t ing from ethanol in- jestion. 14 Three of our ~ patients (MD, HF, and GM) had elevated serum al- cohol levels with concommitant ele- vations in osmolality. Consideration of such variables in the analysis of osmotic changes is essential.

REFERENCES 1. Bishop RL, Weisfeldt ML: Sodium bicarbonate administration during car- diac arrest. JAMA 235:506-509, 1976. 2. Fillmore SJ, Shapiro M, Killip T: Se- rial blood gas studies during cardiopulmo-

Table 2 ARTERIAL BLOOD GAS STUDIES

SUCCESSFUL CARDIOPULMONARY RESUSCITATIONS

NaHCO3 Patient PO2 PCO2 pH HCO3 Aspiration (given) c s 98 46 702 11 100 MD 57 47 7.24 17 b lood 100 mEq CL 224 32 7.39 14 200 CW 280 27 7.4 16 . . . 150 EB 42 33 7.48 25 gastr ic 250 JD 176 24 7.54 21 . . . 200 WW 248 16 7.54 19 • . . 150

UNSUCCESSFUL CARDIOPULMONARY RESUSCITATIONS NaHCOz

Patient PO2 PCO2 pH HCOs Aspiration (given) HF 8 90 6.85 23 blood, 150

massive GM 59 40 7.14 18 . . . 200 LF 123 42 4.18 16 . •. 150 WK 99 31 7.21 7 • •. 250 EH 80 34 7.28 16 gastr ic 250 OL 38 106 7.29 49 gastr ic 200 ES 173 46 7.45 31 . . . 200 JF 64 31 7.45 21 • • 150 CL 176 24 7.54 21 . . . 200 DW 144 18 7.71 36 . . . 150

.D

o E U)

0 .m

E

33ot 320"-~ 310-~- 3ool- 29o 28o 2 7 0 ~ 50 100 150 200 250

mEq N a H C 0 3 g i v e n

Fig 3. Osmolality corrected for hyperglycemia and alcohol (means and one standard deviation).

Table 3 SUCCESSFUL CARDIOPULMONARY RESUSCITATIONS

Measured Corrected* Patient Glucose Ethanol Osmolal i ty Osmolality CS 214 0 301 294 MD 614 297 371 277 CL 630 0 326 297 CW 663 0 316 286 EB 1149 0 369 311 JD#86 411 0 303 286 WW 285 0 307 297

UNSUCCESSFUL CARDIOPULMONARY RESUSCITATIONS Measured Corrected*

Patient Glucose Ethanol OsmolaUty Osmolality HF 212 167 370 327 GM 330 51 324 300 LF 403 0 333 315 WK 822 0 344 304 EH 380 0 320 304 OL 1005 0 407 349 ES 704 0 339 306 JF 458 0 319 300 CL , ~ 231 0 327 321 DW 199 0 305 300

*Osmolality corrected by calculation of the osmotic contribution of glucose over 100 mg/lO0 ml and of alcohol over 0 mg/lO0 ml.

J ~ 6 .5 (May ) 1977 189/19

n a r y r e s u s c i t a t i o n . Ann Intern Med 72:465-469, 1970.

3. Ma t t a r JA, Well MS, Shubin H, et al: Cardiac a r res t in the critically ill. A m J Medicine 56:162-168, 1974.

4. S tewar t JSS, Stewart WK, Gillies HG: C a r d i a c a r r e s t and acidosis . Lancet 2:964-967, 1962.

5. Gi l s ton A, Leeds MB: Cl in ica l and biochemical aspects of cardiac resuscita- tion. Lancet 2:1039-1043, 1965.

6. Marsigl ia JC, Cingolani HE, Gonzalez NC: Relevance of beta receptor blockade to the negat ive inotropic effect induced by m e t a b o l i c ac idosis . Cardiouasc Res 7:336-343, 1973.

7. S inha R, T inker MA, Hizon R, et al:

Metabolic acidosis and lung mechanics in dogs. A m Rev Respir Dis 106:881-891, 1972.

8. Gerst PH, Fleming WH, Malm JR: A quant i t a t ive evaluat ion of the effects of acidosis and alkalosis upon the ventricu- l a r f i b r i l l a t i on th reshold . Surgery 59: 1050-1060, 1966.

9. Bernard C: Lecons sur le diabete et la glycogenese animale. Paris Baillere, 1877, p 210.

10. Shires GT, Carrice CJ, Canizare PC: Shock, in Major Probl Clin Surg. Phila- delphia, W B Saunders, 1973, pp 10-11.

11. Heibert JM, McCormick JM, Egdahl RH: Direct measu remen t of insul in sec- re tory ra te . A n n Surgery 172:296-304, 1972.

12. Porte D, Graber AL, Kuzuya T et~ The effect of epinephrine on immu~0r J rive insul in levels in man. J Clinical vest 45:228-236, 1966.

13. Carey L, Lowrey BD, Cloutier £~ Blood sugar and insulin response in h~: roans in shock. Ann Surgery 172.3~' 1972. " ~

14. Robinson AG, Loeb JN; Ethanol jes t ion - - commonest cause of elevat~ p l a s m a o smo la l i t y? N Engl J Ig~ 284:1253-1255, 1971.

15. McCurdy DK: Mixed metabolic aN respiratory acid-base disturbances, dia~ nosls and t r e a t m e n t . Chest 62 {suppll: 355-445, 1972.

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