Central venous pH as a predictor of arterial pH in prolonged cardiac arrest

Central venous pH as a predictor of arterial pH in prolonged cardiac arrest

ORIGINAL CONTRIBUTION acidosis, in cardiac arrest; cardiac arrest, acidosis Central Venous pH as a Predictor of Arterial pH in Prolonged Cardiac Arre...

340KB Sizes 0 Downloads 43 Views

ORIGINAL CONTRIBUTION acidosis, in cardiac arrest; cardiac arrest, acidosis

Central Venous pH as a Predictor of Arterial pH in Prolonged Cardiac Arrest Sixty-five patients who arrived in the emergency department in cardiac arrest were studied prospectively to determine whether central venous p H could be used as an accurate predictor of arterial p H in prolonged cardiac arrest. Central venous and arterial access were obtained as soon as possible after arrival in the emergency department. Simultaneous arterial and venous samples were drawn and sent for blood gas analysis. Under normal conditions, central venous p H (pHcv) approximates arterial p H (pHa). In prolonged cardiac arrest, however, our data reveal a m e a n pHa of 7.31 +_ 0.25 and a m e a n pHcv of 7.08 +_ 0.19. There was moderate correlation between pHa and pHcv when all patients were considered (r = .69, P < .01). The correlation was excellent, however, in the subgroup of 15 patients who had a pulse at some point during resuscitation (r = .95, P < .01). In 13 of these 15 patients the acid base status would have been managed correctly based on the predicted pHa (pHcv + 0.12 correction factor). The pHcv was also valuable in identifying a second subgroup of patients who required no further bicarbonate therapy; all patients who had a p H c v >t 7.15 had a pHa > 7.30 (21 patients). The central venous p H was found to be a useful index of arterial p H when applied to a definable subset of patients, which in this study constituted 45% of all patients in prolonged cardiac arrest. [McGilI JW,, Ruiz E: Central venous p H as a predictor of arterial p H in prolonged cardiac arrest. A n n Emerg Med September 1984 (Part I);13:684-687.]

John W McGill, MD Ernest Ruiz, MD Minneapolis, Minnesota From the Department of Emergency Medicine, Hennepin County Medical Center, Minneapolis, Minnesota. Received for publication June 1, 1983. Accepted for publication August 15, 1983. Presented at the University Association for Emergency Medicine Annual Meeting in Boston, June 1983.

INTRODUCTION A primary goal in the management of cardiac arrest is the correction of metabolic acidosis. O p t i m u m acid base management requires frequent monitoring of arterial blood gases. In cardiac arrest, however, it is often difficult to obtain arterial blood reliably. Under normal conditions, central venous pH approximates arterial pH3 Recently this relationship has been investigated in settings of physiologic stress. In both postoperative cardiothoracic patients 2 and a canine hypovolemic shock model, 3 arterial pH (pHa) could be extrapolated reliably from central venous pH (pHcv). If a similar relationship were to exist in the setting of cardiac arrest, central venous gases would be useful in the management of this condition. The purpose of this study was to determine whether venous blood drawn from a central venous catheter could be used to estimate arterial pH reliably under conditions of prolonged cardiac arrest in human beings.

MATERIALS AND METHODS Sixty-five patients who presented to the emergency department in cardiac arrest were studied prospectively. There were 53 men and 12 women, and the mean age was 68 years. All were presumed by their history to have suffered nontraumatic cardiac arrest (one patient was found to have a ruptured spleen at autopsy). Initial prehospital treatment was given by emergency medical technicians (EMTs) and paramedic personnel, and included the use of an esophageal obturator airway (EOA), defibrillation, and intravenous epinephrine and sodium bicarbonate. Radio contact was made with the hospital and further treatment was directed by the emergency physician. On arrival in the emergency department, all patients were endotracheaIly

13:9September 1984 (Part 1)

Annals of Emergency Medicine

684/63

CENTRAL VENOUS pH McGill & Ruiz

Fig. 1. Distribution of pHa-cv differences in all patients intubated. As soon as possible after arrival, central venous and arterial access were established (mean time, 10.5 rain). Central venous access was obtained p r e d o m i n a n t l y through the right subclavian vein using the supraclavicular (in 30 patients) and the infraclavicular (in 14 patients) approaches. Three patients had right internal jugular cannulations; the site of placement in the remaining 17 patients was not recorded. Radiographic confirmation of catheter tip placement in either the superior vena cava or the right atrium was available in only six patients. A r t e r i a l a c c e s s was o b t a i n e d through a right radial cutdown and p l a c e m e n t of a 36-inch-long a r m catheter. Simultaneous arterial and central venous samples were then drawn and immediately underwent blood gas analysis in the emergency department. The interval between initiation of advanced cardiac life support (ACLS) treatment and the drawing of blood s a m p l e s averaged 37 minutes. All patients received at least one ampule of bicarbonate prior to the drawing of samples (mean, 2.1 ampules). With the exception of three patients, all received bicarbonate more than ten minutes prior to the drawing of samples. The shortest t i m e between bicarbonate administration and blood drawing was six minutes. The data were subjected to linear regression analysis, and correlation coefficients were derived. The significance of the correlation coefficients was determined using the Student t test. RESULTS Statistical analysis of the data is presented (Table 1). The distribution of the pHa-cv differences (pHa-cvA) is shown {Figure 1). There was a moderate correlation between pHcv and pHa (r = .69, P < .01}. The linear regression equation that predicts the pHa (pHaP) for any m e a s u r e d p H c v is shown (Figure 2). The actual pHa values are also shown for comparison. The pHa was always >/ pHcv, and in the 21 patients with a pHcv ~> 7.15, the pHa was always > 7.30. Retrospectively a subgroup of patients was identified in which the correlation between pHcv and pHa was high (r = .95, P < .01}. This subgroup 64/685

12

10 O9

4

0

S

0.0

011

012

013

1

014

~

0.5

016

~

0.'7

0.'8

pHa-cv A

TABLE. Summary of statistical analysis of central venous pH (pHcv) and

arterial pH (pHa) data

All Patients (N = 65)

Patients Who Had a Pulse at One Time in the ED (n = 15)

Mean pHa (SD)

7.31 + 0.25

7.30 + 0.19

Mean pHcv (SD)

7.08 +_ 0.19

7.18 _+ 0.20

Mean pHa-cv (SD)

0.24 _+ 0.18

0.12 + 0.07

.69

.95

Data

Correlation coefficient pHcv to pHa Range of pHa

6.80 -

8.12

7.03 -

7.74

Range of pHcv

6.70 -

7.70

6.94 -

7.70

Regression equation

pHa = 0.94 + 0.90 pHcv

had a pulse at some time during resuscitation (15 patients). The data are presented (Table 1). The pHa-cvA distribution noted in this group is shown (Figure 3). The predicted pHa values, as defined by the.regression equation, and the actual pHa values were plotted (Figure 4). A correction factor of 0.12 unit, the m e a n difference between pHcv and pHa, when added to pHcv was found to be comparable to the linear regression equation in predicting pHa. Using the correction factor, the mean absolute difference between the actual and the predicted pHa was 0.05 and ranged from -0.08 Annals of Emergency Medicine

pHa = 0.84 + 0.90 pHcv

to +0.17. If an acceptable end point for pHa management is considered to be between 7.30 and 7.40, then 13 of the 15 patients (87%) would have been managed appropriately using the predicted pHa (pHcv + 0.12 correction factor). One of the two patients who would have b e e n managed suboptimally using the pHcv plus the correction factor had a predicted pHa of 7.21 and an actual pHa of 7.38; the arterial PCO z (PCOza) was 20. The second patient had a predicted pHa equal to the actual pHa (7.06), but the acidosis was predominantly respiratory with a PCOza of 68. 13:9 September 1984 (Part 1)

Fig. 2. A comparison of predicted pHa

to actual p H a m all patients.

8,4-

Fig. 3. Distribution of pHa-cv dif-

ferences in patients who had a pulse in the emergency department.

8.287.8A

7]6-

~

A

ZX

A

ZX

A

Ga

T

o_ 7.4

a ~, ~ - , ~a~a a A a

7.2

~

",

Linear Regression_ Equation:

~aaA/4~A =a4~a~

pHa -- 0,94 + 0.90 pHcv

A

x/~

7

,,

/,.

~

Predicted pH = x

&

a ~

6.8 6.6 6.6

Actual pH = z~

618

7

712 7.'4 pHcv

716

718

14 12 10 O9

g8

2_ :76

X

0

)< 0.0

0.1

0.2

0.3

In an attempt to increase the ability to predict the pHa on the basis of central venous blood gases, linear regression analysis was p e r f o r m e d using two variables, central venous PCO 2 {PCO2cv) and pHcv. The correlation between PCO2cv and PCO2a was only fair (r = .48), however, and the resultant regression equation was not substantially more accurate in predicting pHa than was the e q u a t i o n using pHcv alone. The mean central venous PCO 2 of 13:9 September 1984 (Part 1)

0.4 pHa-cv A

0.5

0.6

0.7

0.8

3

the study population was 85 _+ 38 torr, and the mean arterial PCO 2 was 35 -+ 19 torr. In the subgroup of patients noted to have a pulse in the e m e r g e n c y d e p a r t m e n t , the m e a n PCO2cv was 54 + 13 tort, and the mean PCO2a was 34 _+ 13 tort.

DISCUSSION The validity of using central venous pH as an approximation of arterial pH in critical care patients has been well established.2,4, s In patients dying from Annals of Emergency Medicine

traumatic shock, however, a substantial difference between pHcv and pHa was noted (mean pHa-cvA, 0.10 pH unit). 6 A greater disparity b e t w e e n these two values was reported in a canine model of prolonged hypovolemic s h o c k ( c o r r e c t i o n factor, 0.15 pH unit). 3 It should not be surprising, in this study of prolonged cardiac arrest, that an even greater difference between pHcv and pHa was found (mean pHa-cvA, 0.24). In the previous studies z5 that evaluated the relationship between pHcv and pHa, a correction factor was identified which, w h e n added to pHcv, resulted in a clinically acceptable estimate of the pHa. In our study population, with its wide range of pHa-cv differences (Figure 1), no such correction factor was found that could be applied to all patients. Nevertheless two groups of patients, constituting 45% of all p a t i e n t s , were i d e n t i f i e d in w h i c h the p H c v w o u l d have been helpful as a guide to bicarbonate therapy. The central venous pH was found to have its widest application in patients who had a pHcv /> 7.15 (32% of the study population). All these patients had a pHa > 7.30. Given this relationship, pHcv could be used as a reliable substitute for pHa in determining the need for further bicarbonate therapy. T h e s e c o n d group of p a t i e n t s in whom pHcv might have reliably guided bicarbonate therapy was the subset of patients noted to have a pulse at one time in the emergency department. Assuming that a pHa in the range of 7.30 to 7.40 is an acceptable goal in cardiac arrest, 13 of the 15 p a t i e n t s in this group w o u l d have been managed appropriately if bicarbonate had been given on the basis of the predicted pHa (pHcv + 0.12 correction factor). The two patients who w o u l d have been m a n a g e d suboptimally using the predicted pHa had extremes in PCO2a relative to the rest of the patients in the group. One patient had a predicted pHa of 7.21 and an actual pHa of 7.38. Although he had a mild metabolic acidosis, it was being compensated by hyperventilation (PCO2, 20 torr) and thus did not 686/65

CENTRAL VENOUS pH McGill & Ruiz

Fig. 4. A comparison of predicted pHa to actual pHa in patients who had a pulse in the emergency department.

8.2"

8require bicarbonate at t h a t time. In the second patient the predicted pHa equaled the actual pHa (7.06), but the acidosis was p r e d o m i n a n t l y respirat o r y in o r i g i n (PCO2, 68 torr) a n d w o u l d have been m a n a g e d better by improving ventilation than by administering bicarbonate. T h e v e n o u s c a t h e t e r tip l o c a t i o n was d o c u m e n t e d i n f r e q u e n t l y in our study. A l t h o u g h radiographic confirm a t i o n w o u l d have b e e n ideal, t h e lack of d o c u m e n t a t i o n was not felt to be a problem because Ramachandran et al 4 were unable to d e m o n s t r a t e a significant difference between the pHa-cvAs in blood taken from the superior vena cava, inferior vena cava, subclavian, and i n n o m i n a t e veins. In addition the supraclavicular approach to the subclavian vein was used m o s t frequently in our study, m i n i m i z i n g the chance of extrathoracic placement of the catheter tip. An observation of theoretical interest and p o t e n t i a l clinical application was m a d e c o m p a r i n g t h e m e a n p H and PCO 2 values of patients noted to have a pulse at one t i m e in the emerg e n c y d e p a r t m e n t to t h o s e of t h e study population as a whole. Contrary to w h a t m i g h t have b e e n expected, the m e a n arterial pH and PCO 2 of the subgroup, p o t e n t i a l l y t h e m o r e salvageable of the two groups, were nearly identical to the m e a n arterial pH and PCO 2 of the entire study population. It was only w h e n comparing the central venous data that a clear dist i n c t i o n could be m a d e b e t w e e n the two groups. While there was a m o d e s t difference b e t w e e n t h e m e a n p H of the s u b g r o u p a n d t h a t of t h e t o t a l study population ( + 0.10 pH unit), the most striking difference was between the m e a n central venous PCO2 levels, 54 and 85 tort respectively. These data suggest t h a t in prolonged cardiac at-

66/687

7.8 7.6 ¢g

TO_

7.4

A

A

~

7.2

)~

~

7

' ssion Equation: pHa = 0.85 + 0.90 pHcv Predicted pH = x Actual pH = a

6.8 6.6 6.6

A

e

6.8

7.'2

7.'4

716

7:8

pHcv

4

rest, central venous blood gases m a y be a better reflection of the patients' overall pathophysiologic status t h a n are arterial blood gases, and m a y prove to be useful in monitoring the efficacy of resuscitation in this setting. CONCLUSION In a prospective study, central venous pH was found to be a reliable index of arterial p H in a p p r o x i m a t e l y 50% of p a t i e n t s w h o arrived in the emergency d e p a r t m e n t in cardiac arrest. This group consisted of two subsets, patients who were noted to have a pulse at one t i m e in the emergency department and all patients who had a central venous pH /> 7.15. In the first group the addition of a correction factor (0.12) to the central venous pH resulted in a clinically acceptable estimate of arterial pH. The second group c o n s i s t e n t l y h a d an a r t e r i a l p H > 7.30, and thus did not require urgent bicarbonate therapy. For those patients who never had a pulse in the emergency d e p a r t m e n t or w h o had a central venous pH < 715, arterial blood gases w o u l d have been required to ensure appropriate acid base management.

Annals of Emergency Medicine

The authors thank John Faulhaber for his assistance with the statistical analysis, and the nurses and p a r a m e d i c s who helped make this study possible.

REFERENCES 1. Adams AP, Hahn CEW: Principles and Practice of Blood-gas Ana]ysJs, ed 2. London, Churchill Livingstone, 1982, p 32-33. 2. Steinberg JJ, Harken AH: The central venous catheter in the assay of acid-base status. Surg Gynecol Obstet 1981;152:221222. 3. Moore EE, Good JT: Mixed venous and arterial pH: A comparison during hemorrhagic shock and h y p o t h e r m i a . Ann Emerg Med 1982;11:300-302. 4. Ramachandran PR, Fairley HB, Laws AK: Central venous blood as an index of acid-base and oxygenation status. Can Anaesth Soc ] 1968;15:332-346. 5. Zahn R, Weil M: Central venous blood for monitoring pH and pCO2 in the critically ill patient. ] Thorac Cardiovasc Surg 1966;52:105. 6. Kazarian KK, DelGuercio LRM: The use of mixed venous blood gas determinations in traumatic shock. Ann Emerg Med 1980;9:179-189.

13:9 September1984(Part1)