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Effects of sodium bicarbonate administration during cardiopulmonary resuscitation
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 i v e n in c a r d i o p u l m o n a r y r e s u s 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 l o o d w a s a n a l y s e d for b l o o d gas, alcohol, b l o o d u r e a nitrogen, e l e c t r o l y t e and o s m o l a l i t y . The b l o o d w a s d r a w n after r e s u s c i tation in s u c c e s s f u l c a s e s , a n d w h i l e e f f e c t i v e m a s s a g e and v e n t i l a t i o n were b e i n g a p p l i e d in u n s u c c e s s f u l r e s u s c i t a t i o n s . S e v e n o f t h e 17 resuscitations w e r e s u c c e s s f u 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 r a n g e d f r o m 135 to 154 w i t h o n e e x c e p t i o n a n d did n o t c o r r e l a t e w i t h the a m o u n t o f sodium b i c a r b o n a t e a d m i n i s t e r e d . Arterial pH r a n g e d f r o m 6.38 to 7.71; only o n e p a t i e n t h a d m e t a b o l i c a l k a l o s i s . S e r u m o s m o l a l i t y r a n g e d f r o m 301 to 407. The d a t a s u g g e s t s a net i n c r e a s e in o s m o l a l i t y of 6 m O s m / 5 0 mEq o f s o d i u m b i c a r b o n a t e .
White BC, Yintinalli JE: Effects of sodium bicarbonate administration during cardiopulmonary resuscitation. JACEP 6:187-190, May, 1977. sodium bicarbonate, resuscitation. INTRODUCTION The role of sodium b i c a r b o n a t e in cardiopulmonary resuscitation has recently been r e - e x a m i n e d by s e v e r a l authors. 1-3 One s t u d y 1 suggests t h a t as little as 90 m E q sodium bicarbonate given d u r i n g c a r d i o p u l m o n a r y resuscitation may produce lifethreatening 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 Emergency Department, Detroit General Hospital. 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, Detroit, Michigan 48226.
' ~ [ ~ P 6:5 (May) 1977
hypernatremia. F i l l m o r e e t al 2 suggests t h a t the acidosis of cardiac a r r e s t is best corrected by vigorous ventilation. M a t t a r et al 3 s t a t e s t h a t , in t h e a b s e n c e o f 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 s o d i u m b i c a r b o n a t e m a y produce s i g n i f i c a n t alkalemia. I n o u r e x p e r i e n c e , s e r i o u s alk a l e m i a or h y p e r n a t r e m i a were unusual occurrences after successful cardiopulmonary resuscitation. Therefore, ' t h i s s t u d y was u n d e r t a k e n to prospectively e v a l u a t e blood gas, electrolyte, glucose, and osmolality changes o c c u r r i ~ d u r i n g cardiopulm o n a r y r e s u s c i t a t i o n in which curr e n t l y accepted doses of sodium bic a r b o n a t e were administered.
MATERIALS AND METHODS We performed 17 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 s in the e m e r g e n c y dep a r t m e n t of Detroit G e n e r a l H o s p i t a l d u r i n g A p r i l a n d M a y of 1976. Victims of t r a u m a are not included in t h i s study. Cardiac a r r e s t occurred outside the hospital in all cases. The p a t i e n t s were b r o u g h t to t h e h o s p i t a l by t h e e m e r g e n c y m e d i c a l s e r v i c e p e r s o n n e l who a d m i n i s t e r e d b a s i c 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 n d o t r a c h e a l i n t u b a t i o n was p e r f o r m e d i m m e d i a t e l y by the emergency p h y s i c i a n when the p a t i e n t arr i v e d a t the hospital. In ac~dition to electrical defibrillation and conventional cardiac medications, treatm e n t consisted of a 100 m E q bolus of s o d i u m b i c a r b o n a t e followed by 50 m E q every five to ten m i n u t e s thereafter, t o t a l i n g 100 mEq to 250 mEq. E x t e r n a l m a s s a g e r a t e s of 60 to 80/ m i n u t e were used w i t h a v e n t i l a t i o n to-compression ratio of one to three. A t the conclusion of each resuscitation, s p e c i m e n s of a r t e r i a l blood were s e n t for blood gas a n a l y s i s a n d alcohol, glucose, blood u r e a n i t r o g e n (BUN), e l e c t r o l y t e a n d o s m o l a l i t y d e t e r m i n a t i o n s . In t h e cases of unsuccessful resuscitations, arterial specimens were d r a w n while effective m a s s a g e and v e n t i l a t i o n were b e i n g applied. 187/17
RESULTS
Seven of the 17 r e s u s c i t a t i o n s were successful. W i t h the exception of pat i e n t (OL) who h a d a s e r u m sodium level of 170, all s e r u m sodium conc e n t r a t i o n s r a n g e d between 135 and 154 (Table 1), a n d the s e r u m sodium level did not increase with i n c r e a s e d a m o u n t s of s o d i u m b i c a r b o n a t e adm i n i s t r a t i o n (Figure 1). A r t e r i a l pH r a n g e d from 6,83 to 7.71. O n l y one patient had significant metabolic acidosis (Table 2). S e r u m o s m o l a l i t y r a n g e d from 301 to 407 and c o r r e l a t e s b e t t e r w i t h t h e s e r u m glucose t h a n w i t h the a m o u n t of sodium bicarbonate a d m i n i s t e r e d ( F i g u r e 2). I f t h e o s m o l a l i t i e s a r e calculated w i t h the s e r u m glucose c o n s t a n t l y corrected to 100 rag/100 ml and the alcohol corrected to 0, the r a n g e is 286 to 349 m O s m (Table 3). Our d a t a suggests a n e t increase in osmolality of about 6 mOsm/50 m E q of sodium bicarbonate ( F i g u r e 3).
150 ¢.-
140 ~ .£ z
tj'} C
oo
120 I I T 100 150 200 m E q NaHCO3 a d m i n i s t e r e d
} 250
1. Serum sodium level versus increasing sodium bicarbonate administerec
Fig.
Table 1 SUCCESSFUL C A R D I O P U L M O N A R Y RESUSCITATIONS Patient
mEq NaHCO3
Glucose
Na
K
100 100 200 150 250 200 150
214 614 630 663 1149 411 285
139 154 135 137 143 137 143
3,4 5.4 3.5 4.2 4.5 2.9
CS MD CL CW EB JD#86 WW
UNSUCCESSFUL C A R D I O P U L M O N A R Y RESUSCITATIONS Patient
mEq NaHCO3
Glucose
Na
K
150 200 150 250 250 200 200 150 200 150
212 330 403 822 380 1005 704 458 231 199
144 143 152 144 144 170 146 145 147 150
7.2 4.7 4.4 2.9 5.4 6.8 5.6 3.4 4.3 2.5
HF GM LF WK EH OL ES JF CL DW
Blood glucose r a n g e d from 199 to 1149 mg/100 ml. None of the p a t i e n t s were k n o w n diabetics. Three p a t i e n t s (CW, CL, a n d E B ) w e r e g i v e n a bolus of 25 gm of glucose d u r i n g resuscitation. All p a t i e n t s received int r a v e n o u s i n f u s i o n s of 5% d e x t r o s e a n d .3 n o r m a l s a l i n e (D5/.3NS).
410
-
400
DISCUSSION
18/188
13o
I 50
While aggressive efforts were m a d e to m a i n t a i n a d e q u a t e ventilation, our d a t a shows t h a t v e n t i l a t i o n alone was insufficient to correct the acidosis. W h i l e t e n p a t i e n t s h a d a p H of 7.4 or lower, only two of these (OL and HF) had severe respiratory acidosis (Table 3), and these p a t i e n t s had massive aspiration.
P a t i e n t s in c a r d i o p u l m o n a r y a r r e s t have severe respiratory and metabolic acidosis.4, 5 M e t a b o l i c acidosis depresses myocardial contractility, ~ is d e l e t e r i o u s to p u l m o n a r y function, ~ a n d lowers t h e m y o c a r d i a l t h r e s h old for v e n t r i c u l a r fibrillation, s The acidosis is corrected by e s t a b l i s h i n g a d e q u a t e v e n t i l a t i o n , m a i n t a i n i n g adequate circulation, and a d m i n i s t e r i n g sodium b i c a r b o n a t e . In view of the h a r m f u l effects of metabolic acidosis, it would be t h e r a p e u t i c a l l y d i s a s t r o u s to d i s r e g a r d the beneficial effects of sodium bicarbonate implying that even in judicious doses, it m a y produce let h a l h y p e r n a t r e m ~ a and hyperosmo-
E
390 380 370 -5 E
360
O
350
69
E E P 03
co
[]
® s s ~*
O ss S
340
O J
330 320 310 300 290
•
o.i.
•
.=.-'6 ~sS •
60
---Predicted osmolality change with increasing glucose.
•
®Alcohol = 297 mg/100 ml [gAIcohol = 167 mg/100 ml /*Alcohol = 51 mg/100 ml
J I r J I t 200 400 600 800 1000 1200 S e r u m G l u c o s e m g / 1 0 0 ml
F i g . 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 common. previous s t u d i e s of o s m o l a l i t y changes during cardiopulmonary arrest have failed to consider the effects of blood glucose or alcohol. Our finding of hyperglycemia and related hyperosmolality is not surprising. Claude Bernard was the first to note that h : ~ p e r g l y c e m i a o f t e n a c c o m panies shock2 In hypovolemic shock, the blood glucose often rises in relation to the severity of shock, l° but the e t i o l o g y 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 v e n o u s i n s u l i n levels increased. This was t h o u g h t to be due to decreased peripheral use or clearance of insulin. T h i r t e e n of t h e 17 p a t i e n t s received single or multiple injections of epinephrine, a potent stimulator of hyperglycemia and supressor of pancreatic islet eell function. 12 In humans in t r a u m a t i c shock, the blood glucose remains high but begins declining after about five hours. It has been suggested t h a 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-resuscitation survived. ~3 The routine administration of 25 gm of glucose intravenously during r e s u s c i t a t i o n does not s e e m w a r ranted in view of the significant incidence of hyperglycemia in our series. In a d d i t i o n , u s i n g .5 n o r m a l saline as t h e r o u t i n e i n t r a v e n o u s fluid in cardiopulmonary resuscitation a p p e a r s m o r e p h y s i o l o g i c . Further studies will be carried out to e v a l u a t e t h e e f f i c a c y of s u c h solutions. R o b i n s o n and L o e b 4 reviewed the m a r k e d changes in serum osmolality resulting from ethanol injestion. 14 Three of our ~patients (MD, HF, and GM) had elevated serum alcohol levels with concommitant elevations in osmolality. Consideration of such variables in the analysis of osmotic changes is essential. REFERENCES 1. Bishop RL, Weisfeldt ML: Sodium bicarbonate administration during cardiac arrest. JAMA 235:506-509, 1976. 2. Fillmore SJ, Shapiro M, Killip T: Serial blood gas studies during cardiopulmoJ ~
6.5 (May) 1977
Table 2 ARTERIAL BLOOD GAS STUDIES SUCCESSFUL CARDIOPULMONARY RESUSCITATIONS Patient
PO2
PCO2
pH
HCO3
cs MD CL CW EB JD WW
98 57 224 280 42 176 248
46 47 32 27 33 24 16
702 7.24 7.39 7.4 7.48 7.54 7.54
11 17 14 16 25 21 19
Aspiration
NaHCO3 (given) 100 100 mEq 200 150 250 200 150
bl ood ... gastric ... •..
UNSUCCESSFUL CARDIOPULMONARY RESUSCITATIONS NaHCOz Patient PO2 PCO2 pH HCOs Aspiration (given) HF GM LF WK EH OL ES JF CL DW
8
90
6.85
23
59 123 99 80 38 173 64 176 144
40 42 31 34 106 46 31 24 18
7.14 4.18 7.21 7.28 7.29 7.45 7.45 7.54 7.71
18 16 7 16 49 31 21 21 36
blood, massive ... . •. • •. gastric gastric ... •• ... ...
150 200 150 250 250 200 200 150 200 150
33ot 320"-~ 310-~-
.D
0
3ool29o 28o
E
270~
o E U) .m
50
100
150
200
250
mEq NaHC03 given
Fig 3. Osmolality corrected for hyperglycemia and alcohol (means and one standard deviation). Table 3 SUCCESSFUL CARDIOPULMONARY RESUSCITATIONS Patient
Glucose
Ethanol
CS MD CL CW EB JD#86 WW
214 614 630 663 1149 411 285
0 297 0 0 0 0 0
Measured Osmolality 301 371 326 316 369 303 307
Corrected* Osmolality 294 277 297 286 311 286 297
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.
189/19
n a r y r e s u s c i t a t i o n . A n n Intern 72:465-469, 1970.
Med
3. M a t t a r JA, Well MS, Shubin H, et al: Cardiac a r r e s t in the critically ill. A m J Medicine 56:162-168, 1974. 4. S t e w a r t JSS, Stewart WK, Gillies HG: C a r d i a c a r r e s t a n d acidosis. L a n c e t 2:964-967, 1962. 5. G i l s t o n A, Leeds MB: C l i n i c a l a n d biochemical aspects of cardiac resuscitation. Lancet 2:1039-1043, 1965. 6. Marsiglia JC, Cingolani HE, Gonzalez NC: Relevance of beta receptor blockade to the negative inotropic effect induced by m e t a b o l i c acidosis. Cardiouasc Res 7:336-343, 1973. 7. S i n h a R, T i n k e r MA, Hizon R, et al:
20/190
Metabolic acidosis and lung mechanics in dogs. A m Rev Respir Dis 106:881-891, 1972. 8. Gerst PH, Fleming WH, Malm JR: A q u a n t i t a t i v e evaluation of the effects of acidosis and alkalosis upon the ventricul a r f i b r i l l a t i o n t h r e s h o l d . Surgery 59: 1050-1060, 1966. 9. B e r n a r d 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. Philadelphia, W B Saunders, 1973, pp 10-11. 11. Heibert JM, McCormick JM, Egdahl RH: Direct m e a s u r e m e n t of insulin secr e t o r y rate. A n n Surgery 172:296-304, 1972.
12. The rive vest
Porte D, Graber AL, Kuzuya T et~ effect of epinephrine on immu~0rJ insulin levels in man. J Clinical 45:228-236, 1966.
13. Carey L, Lowrey BD, Cloutier £~ Blood s u g a r a n d insulin response in h~: r o a n s in shock. A n n Surgery 172.3~' 1972. "~ 14. Robinson AG, Loeb JN; Ethanol jestion - - commonest cause of elevat~ p l a s m a o s m o l a l i t y ? N E n g l J Ig~ 284:1253-1255, 1971. 15. McCurdy DK: Mixed metabolic aN respiratory acid-base disturbances, dia~ nosls a n d t r e a t m e n t . Chest 62 {suppll: 355-445, 1972.
6:5 (May)1977J ~ P
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 i v e n in c a r d i o p u l m o n a r y r e s u s 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 l o o d w a s a n a l y s e d for b l o o d gas, alcohol, b l o o d u r e a nitrogen, e l e c t r o l y t e and o s m o l a l i t y . The b l o o d w a s d r a w n after r e s u s c i tation in s u c c e s s f u l c a s e s , a n d w h i l e e f f e c t i v e m a s s a g e and v e n t i l a t i o n were b e i n g a p p l i e d in u n s u c c e s s f u l r e s u s c i t a t i o n s . S e v e n o f t h e 17 resuscitations w e r e s u c c e s s f u 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 r a n g e d f r o m 135 to 154 w i t h o n e e x c e p t i o n a n d did n o t c o r r e l a t e w i t h the a m o u n t o f sodium b i c a r b o n a t e a d m i n i s t e r e d . Arterial pH r a n g e d f r o m 6.38 to 7.71; only o n e p a t i e n t h a d m e t a b o l i c a l k a l o s i s . S e r u m o s m o l a l i t y r a n g e d f r o m 301 to 407. The d a t a s u g g e s t s a net i n c r e a s e in o s m o l a l i t y of 6 m O s m / 5 0 mEq o f s o d i u m b i c a r b o n a t e .
White BC, Yintinalli JE: Effects of sodium bicarbonate administration during cardiopulmonary resuscitation. JACEP 6:187-190, May, 1977. sodium bicarbonate, resuscitation. INTRODUCTION The role of sodium b i c a r b o n a t e in cardiopulmonary resuscitation has recently been r e - e x a m i n e d by s e v e r a l authors. 1-3 One s t u d y 1 suggests t h a t as little as 90 m E q sodium bicarbonate given d u r i n g c a r d i o p u l m o n a r y resuscitation may produce lifethreatening 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 Emergency Department, Detroit General Hospital. 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, Detroit, Michigan 48226.
' ~ [ ~ P 6:5 (May) 1977
hypernatremia. F i l l m o r e e t al 2 suggests t h a t the acidosis of cardiac a r r e s t is best corrected by vigorous ventilation. M a t t a r et al 3 s t a t e s t h a t , in t h e a b s e n c e o f 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 s o d i u m b i c a r b o n a t e m a y produce s i g n i f i c a n t alkalemia. I n o u r e x p e r i e n c e , s e r i o u s alk a l e m i a or h y p e r n a t r e m i a were unusual occurrences after successful cardiopulmonary resuscitation. Therefore, ' t h i s s t u d y was u n d e r t a k e n to prospectively e v a l u a t e blood gas, electrolyte, glucose, and osmolality changes o c c u r r i ~ d u r i n g cardiopulm o n a r y r e s u s c i t a t i o n in which curr e n t l y accepted doses of sodium bic a r b o n a t e were administered.
MATERIALS AND METHODS We performed 17 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 s in the e m e r g e n c y dep a r t m e n t of Detroit G e n e r a l H o s p i t a l d u r i n g A p r i l a n d M a y of 1976. Victims of t r a u m a are not included in t h i s study. Cardiac a r r e s t occurred outside the hospital in all cases. The p a t i e n t s were b r o u g h t to t h e h o s p i t a l by t h e e m e r g e n c y m e d i c a l s e r v i c e p e r s o n n e l who a d m i n i s t e r e d b a s i c 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 n d o t r a c h e a l i n t u b a t i o n was p e r f o r m e d i m m e d i a t e l y by the emergency p h y s i c i a n when the p a t i e n t arr i v e d a t the hospital. In ac~dition to electrical defibrillation and conventional cardiac medications, treatm e n t consisted of a 100 m E q bolus of s o d i u m b i c a r b o n a t e followed by 50 m E q every five to ten m i n u t e s thereafter, t o t a l i n g 100 mEq to 250 mEq. E x t e r n a l m a s s a g e r a t e s of 60 to 80/ m i n u t e were used w i t h a v e n t i l a t i o n to-compression ratio of one to three. A t the conclusion of each resuscitation, s p e c i m e n s of a r t e r i a l blood were s e n t for blood gas a n a l y s i s a n d alcohol, glucose, blood u r e a n i t r o g e n (BUN), e l e c t r o l y t e a n d o s m o l a l i t y d e t e r m i n a t i o n s . In t h e cases of unsuccessful resuscitations, arterial specimens were d r a w n while effective m a s s a g e and v e n t i l a t i o n were b e i n g applied. 187/17
RESULTS
Seven of the 17 r e s u s c i t a t i o n s were successful. W i t h the exception of pat i e n t (OL) who h a d a s e r u m sodium level of 170, all s e r u m sodium conc e n t r a t i o n s r a n g e d between 135 and 154 (Table 1), a n d the s e r u m sodium level did not increase with i n c r e a s e d a m o u n t s of s o d i u m b i c a r b o n a t e adm i n i s t r a t i o n (Figure 1). A r t e r i a l pH r a n g e d from 6,83 to 7.71. O n l y one patient had significant metabolic acidosis (Table 2). S e r u m o s m o l a l i t y r a n g e d from 301 to 407 and c o r r e l a t e s b e t t e r w i t h t h e s e r u m glucose t h a n w i t h the a m o u n t of sodium bicarbonate a d m i n i s t e r e d ( F i g u r e 2). I f t h e o s m o l a l i t i e s a r e calculated w i t h the s e r u m glucose c o n s t a n t l y corrected to 100 rag/100 ml and the alcohol corrected to 0, the r a n g e is 286 to 349 m O s m (Table 3). Our d a t a suggests a n e t increase in osmolality of about 6 mOsm/50 m E q of sodium bicarbonate ( F i g u r e 3).
150 ¢.-
140 ~ .£ z
tj'} C
oo
120 I I T 100 150 200 m E q NaHCO3 a d m i n i s t e r e d
} 250
1. Serum sodium level versus increasing sodium bicarbonate administerec
Fig.
Table 1 SUCCESSFUL C A R D I O P U L M O N A R Y RESUSCITATIONS Patient
mEq NaHCO3
Glucose
Na
K
100 100 200 150 250 200 150
214 614 630 663 1149 411 285
139 154 135 137 143 137 143
3,4 5.4 3.5 4.2 4.5 2.9
CS MD CL CW EB JD#86 WW
UNSUCCESSFUL C A R D I O P U L M O N A R Y RESUSCITATIONS Patient
mEq NaHCO3
Glucose
Na
K
150 200 150 250 250 200 200 150 200 150
212 330 403 822 380 1005 704 458 231 199
144 143 152 144 144 170 146 145 147 150
7.2 4.7 4.4 2.9 5.4 6.8 5.6 3.4 4.3 2.5
HF GM LF WK EH OL ES JF CL DW
Blood glucose r a n g e d from 199 to 1149 mg/100 ml. None of the p a t i e n t s were k n o w n diabetics. Three p a t i e n t s (CW, CL, a n d E B ) w e r e g i v e n a bolus of 25 gm of glucose d u r i n g resuscitation. All p a t i e n t s received int r a v e n o u s i n f u s i o n s of 5% d e x t r o s e a n d .3 n o r m a l s a l i n e (D5/.3NS).
410
-
400
DISCUSSION
18/188
13o
I 50
While aggressive efforts were m a d e to m a i n t a i n a d e q u a t e ventilation, our d a t a shows t h a t v e n t i l a t i o n alone was insufficient to correct the acidosis. W h i l e t e n p a t i e n t s h a d a p H of 7.4 or lower, only two of these (OL and HF) had severe respiratory acidosis (Table 3), and these p a t i e n t s had massive aspiration.
P a t i e n t s in c a r d i o p u l m o n a r y a r r e s t have severe respiratory and metabolic acidosis.4, 5 M e t a b o l i c acidosis depresses myocardial contractility, ~ is d e l e t e r i o u s to p u l m o n a r y function, ~ a n d lowers t h e m y o c a r d i a l t h r e s h old for v e n t r i c u l a r fibrillation, s The acidosis is corrected by e s t a b l i s h i n g a d e q u a t e v e n t i l a t i o n , m a i n t a i n i n g adequate circulation, and a d m i n i s t e r i n g sodium b i c a r b o n a t e . In view of the h a r m f u l effects of metabolic acidosis, it would be t h e r a p e u t i c a l l y d i s a s t r o u s to d i s r e g a r d the beneficial effects of sodium bicarbonate implying that even in judicious doses, it m a y produce let h a l h y p e r n a t r e m ~ a and hyperosmo-
E
390 380 370 -5 E
360
O
350
69
E E P 03
co
[]
® s s ~*
O ss S
340
O J
330 320 310 300 290
•
o.i.
•
.=.-'6 ~sS •
60
---Predicted osmolality change with increasing glucose.
•
®Alcohol = 297 mg/100 ml [gAIcohol = 167 mg/100 ml /*Alcohol = 51 mg/100 ml
J I r J I t 200 400 600 800 1000 1200 S e r u m G l u c o s e m g / 1 0 0 ml
F i g . 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 common. previous s t u d i e s of o s m o l a l i t y changes during cardiopulmonary arrest have failed to consider the effects of blood glucose or alcohol. Our finding of hyperglycemia and related hyperosmolality is not surprising. Claude Bernard was the first to note that h : ~ p e r g l y c e m i a o f t e n a c c o m panies shock2 In hypovolemic shock, the blood glucose often rises in relation to the severity of shock, l° but the e t i o l o g y 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 v e n o u s i n s u l i n levels increased. This was t h o u g h t to be due to decreased peripheral use or clearance of insulin. T h i r t e e n of t h e 17 p a t i e n t s received single or multiple injections of epinephrine, a potent stimulator of hyperglycemia and supressor of pancreatic islet eell function. 12 In humans in t r a u m a t i c shock, the blood glucose remains high but begins declining after about five hours. It has been suggested t h a 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-resuscitation survived. ~3 The routine administration of 25 gm of glucose intravenously during r e s u s c i t a t i o n does not s e e m w a r ranted in view of the significant incidence of hyperglycemia in our series. In a d d i t i o n , u s i n g .5 n o r m a l saline as t h e r o u t i n e i n t r a v e n o u s fluid in cardiopulmonary resuscitation a p p e a r s m o r e p h y s i o l o g i c . Further studies will be carried out to e v a l u a t e t h e e f f i c a c y of s u c h solutions. R o b i n s o n and L o e b 4 reviewed the m a r k e d changes in serum osmolality resulting from ethanol injestion. 14 Three of our ~patients (MD, HF, and GM) had elevated serum alcohol levels with concommitant elevations in osmolality. Consideration of such variables in the analysis of osmotic changes is essential. REFERENCES 1. Bishop RL, Weisfeldt ML: Sodium bicarbonate administration during cardiac arrest. JAMA 235:506-509, 1976. 2. Fillmore SJ, Shapiro M, Killip T: Serial blood gas studies during cardiopulmoJ ~
6.5 (May) 1977
Table 2 ARTERIAL BLOOD GAS STUDIES SUCCESSFUL CARDIOPULMONARY RESUSCITATIONS Patient
PO2
PCO2
pH
HCO3
cs MD CL CW EB JD WW
98 57 224 280 42 176 248
46 47 32 27 33 24 16
702 7.24 7.39 7.4 7.48 7.54 7.54
11 17 14 16 25 21 19
Aspiration
NaHCO3 (given) 100 100 mEq 200 150 250 200 150
bl ood ... gastric ... •..
UNSUCCESSFUL CARDIOPULMONARY RESUSCITATIONS NaHCOz Patient PO2 PCO2 pH HCOs Aspiration (given) HF GM LF WK EH OL ES JF CL DW
8
90
6.85
23
59 123 99 80 38 173 64 176 144
40 42 31 34 106 46 31 24 18
7.14 4.18 7.21 7.28 7.29 7.45 7.45 7.54 7.71
18 16 7 16 49 31 21 21 36
blood, massive ... . •. • •. gastric gastric ... •• ... ...
150 200 150 250 250 200 200 150 200 150
33ot 320"-~ 310-~-
.D
0
3ool29o 28o
E
270~
o E U) .m
50
100
150
200
250
mEq NaHC03 given
Fig 3. Osmolality corrected for hyperglycemia and alcohol (means and one standard deviation). Table 3 SUCCESSFUL CARDIOPULMONARY RESUSCITATIONS Patient
Glucose
Ethanol
CS MD CL CW EB JD#86 WW
214 614 630 663 1149 411 285
0 297 0 0 0 0 0
Measured Osmolality 301 371 326 316 369 303 307
Corrected* Osmolality 294 277 297 286 311 286 297
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.
189/19
n a r y r e s u s c i t a t i o n . A n n Intern 72:465-469, 1970.
Med
3. M a t t a r JA, Well MS, Shubin H, et al: Cardiac a r r e s t in the critically ill. A m J Medicine 56:162-168, 1974. 4. S t e w a r t JSS, Stewart WK, Gillies HG: C a r d i a c a r r e s t a n d acidosis. L a n c e t 2:964-967, 1962. 5. G i l s t o n A, Leeds MB: C l i n i c a l a n d biochemical aspects of cardiac resuscitation. Lancet 2:1039-1043, 1965. 6. Marsiglia JC, Cingolani HE, Gonzalez NC: Relevance of beta receptor blockade to the negative inotropic effect induced by m e t a b o l i c acidosis. Cardiouasc Res 7:336-343, 1973. 7. S i n h a R, T i n k e r MA, Hizon R, et al:
20/190
Metabolic acidosis and lung mechanics in dogs. A m Rev Respir Dis 106:881-891, 1972. 8. Gerst PH, Fleming WH, Malm JR: A q u a n t i t a t i v e evaluation of the effects of acidosis and alkalosis upon the ventricul a r f i b r i l l a t i o n t h r e s h o l d . Surgery 59: 1050-1060, 1966. 9. B e r n a r d 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. Philadelphia, W B Saunders, 1973, pp 10-11. 11. Heibert JM, McCormick JM, Egdahl RH: Direct m e a s u r e m e n t of insulin secr e t o r y rate. A n n Surgery 172:296-304, 1972.
12. The rive vest
Porte D, Graber AL, Kuzuya T et~ effect of epinephrine on immu~0rJ insulin levels in man. J Clinical 45:228-236, 1966.
13. Carey L, Lowrey BD, Cloutier £~ Blood s u g a r a n d insulin response in h~: r o a n s in shock. A n n Surgery 172.3~' 1972. "~ 14. Robinson AG, Loeb JN; Ethanol jestion - - commonest cause of elevat~ p l a s m a o s m o l a l i t y ? N E n g l J Ig~ 284:1253-1255, 1971. 15. McCurdy DK: Mixed metabolic aN respiratory acid-base disturbances, dia~ nosls a n d t r e a t m e n t . Chest 62 {suppll: 355-445, 1972.
6:5 (May)1977J ~ P