Arterial blood gases during cardiac arrest: markers of blood flow in a canine model

101

Resuscirution, 23 (1992) 101-l 11 Elsevier Scientific Publishers Ireland Ltd.

Arterial blood gases during cardiac arrest: markers of blood flow in a canine model Mark G. Angelos, Daniel J. DeBehnke and James E. Leasure Wright State University School of Medicine, Department

of Emergency Medicine, Dayton, 0~ 45401_0927

(USA)

(Received August 15th, 1991; revision received January 6th, 1992; accepted February 5th, 1992)

Measures of CO, have been shown to correlate with coronary perfusion pressure and cardiac output during cardiac arrest. We evaluated arterial pH (pH,) relative to blood flow during cardiac arrest in a canine electromechanical dissociation (EMD) model of cardiac arrest using different resuscitation techniques. Following 15 mitt of cardiac arrest, 24 mongrel dogs received epinephrine with continued CPR or closed-chest cardiopulmonary bypass. Central arterial blood gases, end-tidal carbon dioxide (Pelco2), coronary perfusion pressure and cardiac output were measured. During CPR, prior to epinephrine or bypass, there was no correlation of pH,, PAcoz and P&oz, with cardiac output or coronary perfusion pressure. Immediately after instituting the resuscitation techniques, both pH, and P,co2 showed a significant correlation with cardiac output (pH,; R = -0.78, P < 0.001 and P,coz; R = 0.87, P < 0.001) and with coronary perfusion pressure (pH,; R = -0.75, P < 0.001 and Paco2; R = 0.75, P < 0.001). Eventual survivors (n = 15) had an early significant decrease in pH,, base excess and a significant increase in P.&oz which was not present in non-survivors (n = 9). Neither pH, nor Paco2 correlate with blood flow under low flow conditions of CPR. However, with effective circulatory assistance, pH, and P.&o1 reflect systemic blood flow and reperfusion washout.

Key words: cardiopulmonary

resuscitation; blood gas analysis; pH; cardiopulmonary arrest

INTRODUCTION

Previous studies have noted end-tidal CO* (PetCOZ) to be a good indicator of blood flow during cardiac arrest. In both animal and human cardiac arrest studies, Petcoz has shown a strong correlation with coronary perfusion pressure [ 11, cardiac output [2,3] and survival [4]. With restoration of spontaneous circulation, the very low P&oz values observed during CPR immediately increase above pre-arrest levels. This sudden rise in Petcoz was noted to be a sensitive early predictor of successful resuscitation [5,6]. However, recent reports have suggested the correlation between P&o2 and indicators of perfusion such as coronary perfusion pressure may be altered after the administration of epinephrine in cardiac arrest [7,8]. ro: Mark G. Angelos, Department of Emergency Medicine, The Ohio State University, 108 Means Hall, 1654 Upham Drive, Columbus, OH 43210-1228, USA.

Correspondence

0 1992 Elsevier Scientific Publishers Ireland Ltd. Printed and Published in Ireland

0300-9572/92/$05.00

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In addition to Petco2,there is some evidence that certain arterial blood gas values may be predictive of blood flow during cardiac arrest. In an animal model of cardiac arrest, P&o2 was noted to correlate highly with Petco2.Both P&o2 and P&o2 correlated with coronary perfusion pressure and cardiac output during CPR [9]. In an earlier study we noted central arterial pH, as well as Paco2,to correlate with coronary perfusion during the early reperfusion period of cardiac arrest [lo]. To date the relationship between pH and cardiac output during cardiac arrest has not been investigated. We therefore investigated the changes in arterial blood gases relative to cardiac output before and after augmentation of flow with epinephrine and cardiopulmonary bypass in a post countershock electromechanical dissociation (EMD) cardiac arrest model. This model and the investigational therapies used are reported elsewhere [ 111. In the present study, we focused on the relationship of arterial pH, Pc02 and P&o~ to cardiac output before and after different therapies were instituted to achieve restoration of spontaneous circulation. We hypothesized that arterial pH and Pcoz reflect cardiac output once a threshold level of perfusion is reestablished during cardiac arrest. MATERIALSANDMETHODS

This study was approved by the University’s Laboratory Animal Utilization Committee. All animals were maintained in accordance with the recommendations specified in USDHHS, NIH Publication No. 85-23. Twenty-four mongrel dogs of either sex weighing 24.5 f 5.0 kg were anesthetized with thiopental (20 mg/kg), shaved, prepped, intubated and placed on a ventilator (Harvard@ , Model 607, Millis, MA). Tidal volume was set at 15-20 ml/kg, fractional inspired oxygen was 0.21 and the respiratory rate was adjusted to maintain a P&o2 between 35 and 40 mmHg. Supplemental thiopental (2-3 mg/kg) was administered intravenously, as needed, throughout the experiment to maintain general anesthesia. Cutdowns were performed on the femoral and neck vessels for placement of catheters and cannulae. All animals were instrumented for right atria1 and thoracic aortic pressure measurements using external fluid filled transducers. A right ventricular pacing catheter was placed to induce fibrillation. A central venous catheter was placed for fluid and drug administration. A left ventricular catheter was placed for microsphere injection and a separate aortic arch catheter was placed for blood flow reference sampling. In the cardiopulmonary bypass (CPB) animals, 16-gauge and 1Zgauge cannulae were placed in the external jugular veins and a 1Zgauge French femoral artery cannula was inserted. Continuous P&o2 (Nellcor, Inc., N-1000, Hayward, CA) was monitored in line with the ventilator tubing and the endotracheal tube. The canine EMD cardiac arrest model used has been described in detail elsewhere [l l] and is briefly summarized here. Following baseline measurements, ventricular fibrillation was induced by applying alternating current to the pacer (Medtronic A/C Fibrillator, Model 2039, Minneapolis, MN). A defibrillatory shock was given to induce post-countershock EMD after 5 min of ventricular fibrillation. All animals then received 10 min of chest compressions with a mechanical chest compressor and ventilator (Thumper, Michigan Instruments, Grand Rapids, MI) set to deliver 100 lb

103

of pressure at 60 compressions/mm. Ventilation was maintained with 100% O2 in a 15 ratio with compression. Following 15 min of cardiac arrest, animals received one of three resuscitation therapies. A treatment randomization order was determined prior to beginning the study. Group I (n = 8) received closed-chest cardiopulmonary bypass (CPB) with standard dose epinephrine (0.02 mg/kg) and the cessation of chest compressions. Group II (n = 8) received continued chest compressions and highdose epinephrine (HDE) (0.2 mg/kg). Group III (n = 8) received closed-chest CPR with standard dose epinephrine (SDE) (0.02 mg/kg). Respective epinephrine doses were repeated every 5 min until the return of spontaneous circulation (ROSC) or a total cardiac arrest time of 42 min. ROSC was defined as a perfusing heart rhythm with a mean arterial pressure greater than 60 mmHg in the absence of chest compressions or cardiopulmonary bypass. Thoracic aortic blood gases were drawn at baseline, prearrest and at the following times during cardiac arrest: 4, 8, 15, 17, 20, 22, 25, 27, 30, 32, 36 and 39 min. Once ROSC was achieved aortic blood gases were drawn at ROSC times 1, 5 and 10 min. When ROSC occurred early in the resuscitation protocol, the later cardiac arrest gases were not drawn. P&o~, right atria1 and thoracic aortic pressures were recorded at each blood gas draw. Cardiac arrest and ROSC 1 min arterial blood gas samples were immediately placed in ice and analyzed (Instrumentation Laboratory, Model 1304, Pittsburgh, PA) after resuscitation. This precluded the use of blood gas information to influence cardiac arrest therapy or resuscitation. No NaHCOs or other buffer was administered during cardiac arrest. Cardiac cutput measurements were performed at (1) baseline prearrest, (2) 12 min cardiac arrest during CPR (just prior to treatment protocol) and (3) 17 min cardiac arrest; 2 min after randomization to the different resuscitation groups. Blood flow was determined using a non-radioactive microsphere technique [ 121. Ten million 15-pm (S.D. 0.45 pm) color-labelled polystyrene-divinylbenzene microspheres (E-Z Trac, Inc., West Los Angeles, CA) were injected at each of the three time points. Simultaneous with injection of the microspheres into the left ventricle, blood was withdrawn through the aortic arch catheter by a withdrawal pump (Harvard Apparatus Co., Inc., Model 906, Dover, MA). Pump withdrawal occurred over 90 s beginning 5 s before microsphere injection. Blood samples were subsequently centrifuged and the sediment treated with a series of reagents prescribed by the manufacturer to lyse red blood cells. The number of microspheres was counted using an improved Neubauer ruled hemocytometer examined under a light microscope at x 100 power. Cardiac output was calculated by the following equation:

cardiac output =

R x ST CR

where R is blood withdrawal rate (ml/min), ST the total number of microspheres injected, CR the total number of microspheres in blood sample. Coronary perfusion pressure was calculated as the aortic diastolic pressure minus the right atria1 diastolic pressure.

104

Statistical

methods

Blood gas values, cardiac output, perfusion pressures and Petco2 values were determined as mean f standard deviation for each group. Mean values f standard deviations were also determined for resuscitated animals surviving 2 h, as well as animals not resuscitated. Group comparisons were analysed using ANOVA with a Tukey post-hoc test and paired t-tests. Correlation was determined using Pearson correlation coefficient. Statistical significance was considered at P < 0.05 after Bonferroni correction for multiple comparisons. RESULTS

Prearrest blood gas and hemodynamic variables were similar between groups (Table I). Arterial pH (pH,), Pac02, PetC02 and base deficit were similar between groups during the 5 min of VF and the 10 min of mechanical CPR (Table II). At 15 min of cardiac arrest, just prior to receiving therapy, pH, in Group II was less than the other two groups (I (CPB), 7.39 f 0.14; II (HDE), 7.26 + 0.05; and III @DE), 7.40 f 0.10; P < 0.05). Coronary perfusion pressure was similar in all groups during the first 15 min of cardiac arrest. At 15 min the respective therapies were instituted. Two minutes after onset of therapy there was a significant drop in pH and rise in P&o2 in the CPB Group (Table III). pH, and P&02 remained unchanged in the SDE and HDE Groups (Table III). The changes in pH, and PaCO2 in the CPB Group corresponded temporarily to the rise in coronary perfusion pressure. Coronary perfusion pressure increased from 3 f 8 mmHg to 76 f 44 mmHg in the CPB Group compared with 7 f 9 mmHg to 24 f 13 mmHg in the HDE Group and 15 f 49 mmHg to 3 f 14 mmHg in the SDE Group (P < 0.01). Cardiac output increased significantly in the CPB Group only (P < 0.01). Petcoz fell significantly in the HDE group and tended to decrease in the other two groups after receiving therapy (Table III). Cardiac output was low during CPR (cardiac arrest time 5-15 min) in all groups (Table III) and there was no correlation between either Paco2 or pHa and cardiac output. However, with the improvement of flow and coronary perfusion pressure 2 min after the onset of therapy, a good correlation was noted in all animals between

Table I.

Pre-arrest arterial blood gas values

Group

pH, units

P.&o2 mmHg (kPa)

Paoz mmHg (kPa)

BD, mequiv./l

I (CPB) (n = 8) II (HDE) (n = 8) III (SDE) (n = 8)

7.36 f 0.04

35 (4.7 33 (4.4 34 (4.5

90 (12.0 99 (13.2 106 (14.1

4*1

7.38 * 0.04 7.36 f 0.07

CPB, cardiopulmonary arterial base deficit.

f 3 ?? 0.4) f 3 ztz 0.4) ?? 5 f 0.7)

?? 9

f f f + f

1.2) 7 0.9) 14 1.9)

3*1 4*2

bypass; HDE, high dose epinephrine; SDE, standard dose epinephrine; BD,,

TabIe II.

Arterial

blood

gas values during

CPR.

Group

I (CPB) .

I

II (HDE)

III @DE)

P.&o2

P&O2

B”a

P&02

PeP2

CorPP”

;k,

(mJ%)

&Pa)

(mequiv./l)

(mmHg)

(kPa)

(mmHg)

4min 8min

7.34 f 0.04 7.44 f 0.15

35* 22 f

5 10

4.7 f 0.7 2.9 + 1.3

10 * 5

1.3 * 0.7

6 zt 12

15 min 4min 8min 15 min

7.39 ?? 0.14 7.37 ?? 0.04 7.43 zt 0.06 7.26 f 0.05;

19* 33* 21 f 23~

7 3 5 9

2.5 f 0.9 4.4 ?? 0.4 2.8 zt 0.7 3.1 % 1.2

1.1 f

0.4

3*

8

1.5 f 1.5 f

0.4 0.5

-1 f 7*

13 9

4min 8min 15 min

7.32 f 0.07 7.50 f 0.16 7.40 * 0.10

31 f 17* 17*

9 5 7

4.1 f 1.2 2.3 f 0.7 2.3 + 0.9

1.1 f 1.1 f

0.4 0.7

-3 f 15 f

12 49

5*2 7*3 10 f 4+2

3

8zt3

I+2 14 * 2” 8 + 3* 6*6 11 f

11 f 3 11 * 4 8*4 8zt5

3

VorPP, coronary perfusion pressure. *P < 0.05 compared with other groups. **P < 0.05 compared

Table III.

Changes

with group

in perfusion

I.

and arterial

Group

blood

P&o2

(-His)

P&o2 (kPa) pH, (units) P&q

(mH&

P&o2 (kPa) BD, (mequiv./I) *P < 0.005 compared **P < 0.01 compared tP

< 0.05 compared

with therapy. Group

I (CPB)

CPR (15 min) CorPP (mmHg) C.O. (Vmin)

gas values

Therapy (17 min)

8zt3 1.1 f 0.4 7.39 ?? 0.14 19 f 7 2.5 zt 0.9 10 f 3 with CPR (15 mm). with group II and group with CPR (15 min).

6zt2 0.8 zt 7.02 f 49 f 6.5 f 18 zt

III.

0.3 0.04*~** 5*,** 0.7 2

7*9 1.1 ?? 1.2 11 1.5 7.26 23 3.1 14

?? 4

* f zt f *

Group Therapy (17 min)

CPR (15 min)

76 f 44+**+ 3.3 * 1.2*,**

3~8 0.6 zt 0.3

II (HDE)

0.5 0.05 9 1.2 2

CPR (15 min)

24 zt 13t 0.5 zt 0.6 6 0.8 7.27 22

zt zt zt *

2.9 f 14 f

III (SDE)

15 f 49 0.7 zt 0.8

It 0.1 0.07 5

8*5 1.1 ?? 0.7 7.40 ?? 0.10 17 f 7

0.7 2

2.3 zt 0.9 11 f 3

Therapy (17 min) 3 f 0.8 * 6+1 0.8 zt 7.40 f 14 f

14 1.6 0.1 0.10 3

1.9 ?? 0.4 12 f 3

106

7.44

7.20 Ia 7.12

I

6.80' -30

4

I 38

I 72

I

1

106

140

CORPP (mmHQ)

Fig. 1. Overall correlation of pH and coronary perfusion pressure between 17 and 30 min of cardiac arrest in all animals while still in cardiac arrest. Pearson correlation coefficient R = -0.675, (P < O.OOl), for 97 paired observations.

cardiac output and pH, (R = -0.78, P c 0.001) and P&o2 (R = 0.87, P < 0.001) as well as coronary perfusion pressure with pH, (R = -0.75, P < 0.001) and P&O2 (R = 0.75, P < 0.001). During the first 15 min of cardiac arrest, when coronary perfusion pressures were low, there was no significant correlation between coronary perfusion pressure and P&o2 or pH,. However, beginning at 17 min and continuing 60

r

I

-30

4

I

I

38

72

CCWP

(mmHQ)

I

106

I

1.40

Overall correlation of P&oz and coronary perfusion pressure between 17 and 30 min of cardiac arrest in all animals during cardiac arrest. Pearson correlation coefficient R = 0.706, (P < 0.001). for 97 paired observations.

Fig. 2.

107 Table

IV. Perfusion and arterial blood gas values in non-resuscitated group and survivor group.

CorPP (mmHg) CO. (I/min) Petcoz (mmHg) P&Z (kPa) pH, (units) Paco2

(~W

P&o2 (kPa) BD, (mequiv./l)

Non-resuscitated

(n = 9)

Eventual survivors (n = 15)

CPR (15 min)

Therapy (17 min)

CPR (15 min)

Therapy (17 min)

0*4 0.7 f 1.2 7&4 0.9 f 0.5 7.36 ?? 0.10 16 zt 6 2.1 + 0.8 13 * 3

6 f 16 0.2 f 0.8 5&l 0.7 f 0.04 7.37 ?? 0.08 16 zt 4 2.1 * 0.5 13 f 2

13 0.8 10 1.3 7.34 23 3.1 II

57 2.2 6 0.8 7.14 37 4.9 16

+ zt f f f + f f

36 0.6 4 0.5 0.13 8 1.1 3

f f & zt f f

43*-t 1.7*,t 2** 0.3 0.16**t 15**+ ?? 2.0 f 5**$

*P < 0.01 compared with CPR (15 min). **P < 0.05 compared with CPR (15 min). tP < 0.01 compared with not resuscitated group at same time. $P < 0.05 compared with not resuscitated group at same time.

30 min of cardiac arrest, a significant correlation between pH, and coronary perfusion pressure was noted in all animals still in cardiac arrest (R = -0.68, P c 0.001) (Fig. 1). Similarly, a significant correlation was noted between P.&o2 and coronary perfusion pressure from 17 to 30 min of cardiac arrest (R = 0.71, P c 0.001) (Fig. 2). During mechanical CPR, (cardiac arrest time 5-15 min) P&o2 failed to show a significant correlation with cardiac output (R = 0.24) or coronary perfusion pressure (R = 0.24). Within the HDE and SDE groups prior to epinephrine therapy, P&o2 exhibited a strong correlation with cardiac output (R = 0.81, P < 0.001). However, following epinephrine, between 17 and 30 min of cardiac arrest, the overall correlation between P&O2 and coronary perfusion remained low (R = 0.36). P.&o2 showed a strong correlation with P,coz (R = 0.86, P < 0.001) during mechanical CPR prior to therapy, but poor correlation with P&o2 after institution of therapy. In comparing those animals eventually resuscitated (n = 15; CPB = 8, HDE = 4, SDE = 3) with those animals which could not be resuscitated (n = 9), both pH, and P&o2 were significantly lower and higher, respectively in survivors than nonsurvivors at 17 min (Table IV). Simultaneously there was a significant rise in coronary perfusion pressure and cardiac output 2 min after therapy in eventual survivors (Table IV). Between 17 and 30 min of cardiac arrest both pH, and P&o2 remained significantly lower and higher respectively in eventual survivors than in non-survivors. After therapy, Petcoz fell significantly in the survivor group despite a significant improvement in coronary perfusion pressure and cardiac output (Table IV). through

DISCUSSION

Arterial blood gas interpretation during cardiac arrest has been confusing. Values reported, generally do not reflect the severe acid base abnormalities which exist in

108 the various tissue beds during cardiac arrest. This study demonstrates the flow dependency arterial blood gas values exhibit during cardiac arrest therapy. In this canine cardiac arrest model, neither P&O* nor pH, correlated with coronary perfusion pressure or cardiac output during CPR alone. The low flow state of CPR results in relatively normal appearing arterial acid base values (Table II). With improvement in flow, regardless of type of therapy, a drop in pH, and a rise in P&o2 occurred. These changes correlate with the improvement of coronary perfusion pressure and cardiac output. This correlation was strongest immediately after institution of therapy. However, a significant correlation could be shown during the 15min period following therapy in all animals still in cardiac arrest (Figs 1 and 2). During the 5 min of untreated VF and the subsequent 10 min of CPR, P&o2 and pH, were slow to change from normal values. The perfusion pressures and cardiac output during CPR were low and represent a low flow state. These values are similar to other canine CPR studies in which arterial pH and P&o2 values were reported [13,14]. In order to achieve successful resuscitation, it appears a certain threshold of blood flow must be achieved. Coronary perfusion pressure, as an indicator of blood flow during cardiac arrest, appears to correlate with resuscitation success. Niemann et al. noted a minimum coronary perfusion pressure of 18 mmHg to achieve successful resuscitation after 20 min of VF in their canine model [15]. Similarly, a recent clinical study noted a significant difference in coronary perfusion pressures between resuscitated and non-resuscitated patients. Mean coronary perfusion pressures ranged from 8.4 f 10.0 mmHg in those patients not attaining ROSC to 25.6 f 7.7 mmHg in those patients with ROSC [16]. Assessment of adequate blood flow or coronary perfusion pressure during CPR is difficult and invasive. Petcoz has been described as a reliable non-invasive marker of pulmonary blood flow during CPR [ 1,2]. However, two recent reports have noted epinephrine administration, currently a mainstay of cardiac arrest therapy, given during CPR may disrupt the relationship of Petcoz and coronary perfusion pressure. In a canine cardiac arrest model, a significant decrease in P&o2 was noted simultaneously with a significant increase in coronary perfusion pressure after epinephrine administration [7]. A report of six cardiac arrest patients who received varying doses of epinephrine noted an increase in arterial pressure and a decrease in P&o2 after each epinephrine dose [8]. These reports suggest P&02 may decrease after epinephrine despite an improvement in perfusion pressure. We noted a similar trend. Petcoz tended to decrease in all groups after institution of therapy. Whereas prior to epinephrine, there was a good correlation between P&O* and coronary perfusion pressure, after epinephrine this correlation no longer existed. Repeat doses of epinephrine were administered to those animals still in cardiac arrest between 17 and 30 min. P&o2 failed to reflect coronary perfusion pressure during this time. This lack of correlation did not change when only the HDE and SDE groups were analysed. In contrast to Petco2, pH, and P.&oz did reflect coronary perfusion pressure after the institution of the respective therapies. During CPR, pH, was noted to remain relatively unchanged or even increase during CPR due to the decrease in P&q. This early respiratory alkalosis during cardiac arrest is similar to blood gas results

109

reported in both animal [ 13,17,18] and clinical cardiac arrest studies [ 19,201. Ralston et al. noted a similar acid base pattern in a canine model. However, once restoration of spontaneous circulation was achieved arterial pH was noted to rapidly decrease to approximately 7.1 [2 11. This represented a sudden mean arterial drop of 0.24 pH units. Simultaneously, P&o2 was noted to increase an average of 25 mmHg. We noted a similar response of pH, and P&o2 not at the time of ROSC as in the study of Ralston et al., but at the time perfusion or blood flow was augmented by the different therapies. During the low flow conditions of CPR, neither pH, nor P&o2 reflected cardiac output. Only after a certain threshold of cardiac output was achieved, could a significant correlation between arterial blood gas values and cardiac output be demonstrated. In a previous study, we noted a similar correlation between pH, and coronary perfusion pressure only after coronary perfusion pressure increased from the low levels of standard external CPR [lo]. The dramatic changes in pH, and P,co~ once flow increased above the low flow levels of CPR, seem to be due to the circulation of acidotic blood from the tissue beds. Acidosis develops very rapidly in the venous blood as evidenced by mixed venous blood [21,24] sampling during cardiac arrest. Similarly, intramyocardial pH measured during ventricular fibrillation in a porcine model was noted to decrease from 7.24 f 0.04 to 6.88 f 0.2, while arterial pH did not drop below 7.30 [23]. Once resuscitation occurred, arterial pH fell and intramyocardial pH increased with restoration to normal levels within 60 min. Similar results were also seen in a canine model [ 131. The slow change in pH, during CPR reflects very low or no flow as well as the low metabolism rate occurring in the large arteries which are being sampled. These pH, and P&o2 changes with improved perfusion, assume that constant ventilation is occurring. Neither this pattern of pH, and P&O*, change nor the arteriovenous gradients of pH and PCO~ which occur during cardiac arrest and CPR, were seen with a respiratory arrest in which no ventilation was occurring [24]. The level of flow required to observe this marked drop in pH, is not known. A sudden drop in pH, may signal ROSC or as we noted, in this study, it may be a marker for sudden improvement in flow. The concept of a required threshold level above which blood gas values reflect flow has recently been noted in reference to P&o2 as a marker of perfusion [25]. In comparing cardiac arrest patients with perfusing rhythms with those patients having non-perfusing rhythms, they noted a good correlation between P&o2 and P&o2 in patients with a perfusing rhythm but not in those with a non-perfusing rhythm. They concluded that only when cardiac output exceeds a threshold level are P&O2 and P&O;! reflective of pulmonary blood flow. In another study, a good correlation between P&OZ and coronary perfusion pressure was noted in a porcine model of 5 min of ventricular fibrillation followed by 8 min of CPR [9]. In contrast to our study, this study noted a strong correlation between Paco2,P&OZ and coronary perfusion pressure during mechanical CPR [9]. We speculate this lack of correlation during CPR in our study was due to lower CPR generated blood flow. The failure of arterial blood gases to reflect tissue acid base changes during CPR is thought to limit their usefulness during cardiac arrest. However, arterial pH and P&o2 may be very useful as markers of CPR blood flow under conditions of constant ventilation. If ventilation is held constant during CPR, a normal arterial pH

110

in conjunction with arterial hypocapnia suggests very low or no flow regardless of therapy. In contrast, a low pH, or a sudden drop in pH, may signal ROSC or at least an increase in flow above a not yet determined threshold. These characteristic changes are only seen in arterial blood and not in regional tissue beds or mixed venous blood. Understanding arterial blood gas changes and their significance during cardiac arrest has important clinical implications for the management of cardiac arrest. Arterial blood gases continue to be frequently obtained during resuscitation attempts. In general, they are more accessible than mixed venous or localized tissue bed samples. A better understanding of the changes in P&o2 and arterial blood gases after epinephrine administration is needed, as epinephrine remains a critical resuscitative tool. CONCLUSIONS

Using a canine model, we investigated the relationship of arterial pH and blood flow during cardiac arrest. Both arterial pH and P&o2 were noted to correlate with cardiac output and coronary perfusion pressure once flow increased above a threshold level. Arterial blood gases, while not reflective of the systemic acid base state, may serve as markers of perfusion during cardiac arrest, when ventilation is held constant. ACKNOWLEDGEMENTS

The authors gratefully acknowledge laboratory assistance from Eric Ramnath, laboratory assistance and manuscript preparation by Andrea Arnold, and equipment support by Medtronic Biomedicus, Eden Prairie, Minnesota and Nellcor, Inc., Hayward, California. REFERENCES A.B. Sanders, M. Atlas, G.A. Ewy and K.B. Kern, Expired pCOz as an index of coronary perfusion pressure, Am. J. Emerg. Med., 3 (1985) 147-149. M.H. Weil, J. Bisera, R.P. Trevino and E.C. Rackow, Cardiac output and end tidal carbon dioxide, Crit. Care Med., 13 (1985) 907-909. C.V. Gudipati, M.H. Weil, J. Bisera, H.G. Deshmukh and E.C. Rackow, Expired carbon dioxide: A noninvasive monitor of cardiopulmonary resuscitation, Circulation, 77 (1988) 234-239. A.B. Sanders, K.B. Kern, C.W. Otto, M.M. Milander and G.A. Ewy, End-tidal carbon dioxide monitoring during cardiopulmonary resuscitation. A prognostic indicator for survival, J. Am. Med. Assoc., 262 (1989) 1347-1351. J.L. Falk, E.C. Rackow and M.H. Weil, End-tidal carbon dioxide concentration during cardiopulmonary resuscitation, N. Engl. J. Med., 318 (1988) 607-611. A.R. Garnet& J.P. Ornato, E.R. Gonzalez and E.B. Johnson, End-tidal carbon dioxide monitoring during cardiopulmonary resuscitation, J. Am. Med. Assoc., 257 (1987) 512-515. G.B. Martin, N.T. Gentile, N.A. Paradis, T.J. Appleton and R.M. Nowak, Effect of epinephrine on end-tidal carbon dioxide monitoring during CPR, Ann. Emerg. Med., 19 (1990) 396-368. E.R. Gonzalez, J.P. Omato, A.R. Garnett, R.L. Levine, D.S. Young and E.M. Racht, Dose dependent vasopressor response to epinephrine during CPR in human beings, Ann. Emerg. Med., 18 (1989) 920-926.

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