Serum potassium concentration as a predictor of resuscitation outcome in hypothermic cardiac arrest

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1 Wilderness and Environmental Medicine, 6, (1995) ORIGINAL ARTICLE Serum potassium concentration as a predictor of resuscitation outcome in hypothermic cardiac arrest PAUL R. BENDER, MD, PhD, DANIEL J. DEBEHNKE, MD,* GARY L. SWART, MD, and KENT N. HALL, MD DepartmentofEmergency Medicine, Medical College of Wisconsin, 8700 West Wisconsin Avenue, DH-204, Milwaukee, Wisconsin, USA The purpose of this study was to determine whether serum potassium concentration (SK) can predict resuscitation outcome in a canine model of severe hypothermic cardiac arrest. Fifteen adult mongrel anesthetized dogs were immersed to the neck in a 4 C water bath and ventilated with room air, with ventilation halved at 45 min and stopped at 90 min. After cardiac arrest, 14 of the dogs were kept in the water bath for periods of 2-7 h, and another was held in arrest for 13 h. Following 10 min of closed chest cardiopulmonary resuscitation (CPR) (simulating a short transport time to a hospital), animals were placed on cardiopulmonary bypass and rapidly rewarmed. With appearance of ventricular fibrillation, animals were defibrillated up to three times. Standard advanced cardiac life support was initiated at a core temperature (Tc) of 30 e. Eight of the 15 dogs had return of spontaneous circulation (ROSC), at Tc ranging from 30.4 to 36.soe. The eight dogs with ROSC did not differ from the seven without ROSC in time to arrest (128 ± 48 versus 128 ± 23 min) (mean ± SD) or Tc at arrest (18.1 ± 2.2 versus 17.9 ± 3.1 C), but had higher Tc at the end of the arrest period (9.7 ± 3.0 versus 5.2 ± 2.0 C), reflecting a shorter arrest period in the dogs with ROSC (225 ± 95 versus 420 ± 193 min). SK (meg litec 1 ) did not differ between dogs with and without ROSC at baseline (3.5 ± 0.4 versus 3.7 ± 0.4) or at arrest (3.4 ± 0.7 versus 4.3 ± 2.2), but there was a trend toward higher SK at the end of arrest in the group without ROSC (4.6 ± 1.5 versus 9.4 ± 6.3; range versus ;p =.053). SK was similar after 10 min of CPR in the groups with and without ROSC (6.6 ± 2.9 versus 9.0 ± 2.4; range versus ;p =.107). SK after 10 min of CPR was higher in some animals with ROSC (9.6 and 11.1) than in others which did not have ROSC (4.5 and 7.9). We conclude that very high SK following prolonged hypothermic cardiac arrest may be suggestive of an inability to resuscitate. However, SK after both prolonged hypothermic cardiac arrest and a brief period of CPR is not a good predictor of resuscitation using cardiopulmonary bypass rewarming in an animal model. Key words: hypothermia, hyperkalemia, resuscitation, cardiac arrest, prognosis Introduction Prognostic indicators for recovery from profound hypothermic cardiac arrest are lacking. Persons with wide ranges of physical signs and laboratory values have been resuscitated from hypothermic cardiac arrest [1-8]. The only definite criterion of death in profound 'To whom all correspondence should be addressed Chapman & Hall

2 274 Bender et al. hypothermia is failure to respond to resuscitation and rewarming [5]. However, it has been suggested that "extreme hyperkalemia during acute hypothermia appears to be a reliable marker of death" [5]. The use of serum potassium (SK) as a predictor of resuscitative outcome in hypothermic cardiac arrest has not been studied prospectively. Prior retrospective studies have not separated out concomitant factors such as trauma, drowning, and medication or intoxicant ingestion. If SK is a reliable indicator of death in hypothermic patients, its use would provide a basis for not rewarming patients who are dead, thereby minimizing waste of limited financial and physical resources. Our purpose was to prospectively study whether SK is a reliable predictor of resuscitation outcome in hypothermic cardiac arrest. Our null hypothesis was that following cardiac arrest in a canine model of prolonged hypothermia, there would be no difference in SK between animals resuscitated with cardiopulmonary bypass rewarming and those animals not resuscitated. Materials and methods The study was approved by the Animal Care Committee at the Medical College of Wisconsin. Anesthesia and instrumentation Fifteen shaved adult mongrel dogs (14 male, 1 female) were anesthetized with thiamylal (13 mg kg-i), intubated, and mechanically ventilated with 100% O 2 (experiments 1-3) or room air (experiments 4-15). Tidal volume and respiratory rate were adjusted to maintain end-tidal CO 2 between 30 and 40 mm Hg. Anesthesia was initially maintained with inhaled halothane (0.5%). Surgical cutdowns were performed on the femoral vessels and both external jugular veins. For pressure monitoring, a micromanometer-tipped catheter was placed in the left femoral vein and advanced to the level of the right atrium, and a separate micromanometer-tipped catheter was advanced from the left femoral artery to the ascending thoracic aorta. Catheter positions were confirmed by the presence of appropriate waveforms. For cardiopulmonary bypass, a 12 French bypass cannula was placed in the right femoral artery and a 23 French bypass cannula placed in each external jugular vein. For drug administration and blood sampling, a fluid-filled catheter was placed in the right femoral vein and advanced to the proximal inferior vena cava. An esophageal temperature probe was placed to measure core temperature. Hypothermic cardiac arrest Baseline measurements were made of heart rate, blood pressure, and end-tidal COz, and blood samples drawn for SK and arterial blood gas. Pancuronium (0.1 mg kg- I LV.) was given to eliminate shivering. Animals were then immersed to the neck in a 4 C ice bath and ventilated with 100% O 2 (experiments 1-3) or air (experiments 4-15) and halothane (0.5%) (all experiments). We prevented sudden asphyxia by ventilating animals during the initial portion of the hypothermia exposure, decreasing ventilation at 45 min and stopping it (and halothane anesthesia) at 90 min after immersion in the ice bath; spontaneous ventilation would be expected to decline gradually and eventually cease with progressive severe hypothermia in the nontraumatized hypothermic human. To prevent iatrogenic induction of ventricular fibrillation, no handling of animals was done after immersion in the bath.

3 Serum potassium concentration and resuscitation outcome 275 Animals were kept in the ice bath until the occurrence of cardiac arrest (asystole, ventricular fibrillation, or slow pulseless electrical activity), then for a specified arrest period. At the end of a 2-7-h period of cardiac arrest, animals were removed from the ice bath and dried off. The exception was that one animal had an arrest period of 13 h. The 2-7-h period of cardiac arrest was determined by the investigators to correspond with an approximately 50% rate of return of spontaneous circulation (ROSe) for the total study group, in accordance with the overall aim of the study of resuscitation of half of the animals. Resuscitation Animals then received 10 min of closed chest cardiopulmonary resuscitation (CPR) (simulating a short transport time to a hospital) while being ventilated with 100% O 2, using a pneumatic chest compression device (Michigan Instruments Thumper ). The time from animal removal from the ice bath until the start of CPR was less than 4 min. The Thumper delivered 80 compressions per minute with a 50% duty cycle and a compression to ventilation ratio of5 : 1. Compression depth was 2 in. During this lo-min period ofcpr, ml of room-temperature normal saline was administered LV. to allow adequate preload to permit cardiopulmonary bypass rewarming. The goal was to infuse 1000 ml of saline, but thevolumevaried due to difficulty in infusion rate in some animals. After the 10 min of CPR, animals received 150 units kg- I heparin and cardiopulmonary bypass was begun at flow rates up to 100 m! kg- I min- I using an extracorporeal circulation/ oxygenation apparatus (Medtronic Biomedicus, Inc., Bioconsole Model 520, Biopump Model BP80, flow transducer model TX20, Maxima Membrane Oxygenator model 1380, Eden Prairie, MN). Rewarming was done using a cardiopulmonary bypass warming circuit (Medtronic Biomedicus, Inc., BioCal Model 370, Eden Prairie, MN). Additional normal saline was infused as necessary to maintain adequate bypass flow rates. As animals converted from asystole to ventricular fibrillation during rewarming, they were electrically cardioverted up to three times at 200, 300, and 360 J. At a core temperature (Tc) of 30 C, use of advanced cardiac life support (ACLS) medications was initiated. Animals received epinephrine (0.02 mg kg-i) through the inferior vena cava catheter at 3-5-min intervals, as well as atropine (0.02 mg kg-i) when appropriate for the monitored cardiac rhythm. Return of spontaneous circulation was defined as a spontaneous cardiac rhythm with a mean arterial pressure greater than 50 mm Hg for 1 min without bypass support. Once Tc reached 34 C, ACLS was continued for a maximumof20min, then terminated ifthere was no return of spontaneous circulation during this time. Postarrest Any animal with ROSC was maintained for 1 h on cardiopulmonary bypass. An epinephrine infusion was used to maintain spontaneous mean arterial pressure greater than 50 mm Hg. Ail animals were euthanized with standard euthanizing solution at the end of the experiment. Monitored variables Tc was monitored with an esophageal probe throughout the experiment. Aortic and right atrial pressures, end-tidal CO 2, and electrocardiogram were continuously monitored and recorded with a computer-based waveform recording system on an IBM compatible

4 276 Bender et a1. Table 1. Baseline measurements a Rose No-Rose Number of dogs Weight (kg) Heart rate (bpm) Blood pressure (mm Hg) Systolic Diastolic Mean End-tidal CO 2 (mm Hg) Arterial ph Arterial PC0 2 (mm Hg) Arterial P0 2 (mm Hg) Arterial HC0 3 (mm Hg) ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± ± 4* ± ± ± ± 1 avalues expressed as mean ± SD. *p 5:.05. personal computer. SK (Ciba-Corning 480 Flame Photometer) and arterial blood gases (ABL3, Medtron, Radiometer Copenhagen Acid-Base Laboratory) were measured before immersion, every 30 min after immersion in the ice bath until cardiac arrest, every hour during the hypothermic cardiac arrest period, after 10 min of CPR, at ROSC, and either 1 h after ROSe or at the end of the experiment in animals who did not have ROSC. Blood for potassium was centrifuged, the serum placed in a separate tube, and the samples frozen until measurements were made. Statistical analysis SK, T e, hemodynamic data, and arterial blood gases (not corrected for temperature) were compared among animals with and without ROSe using independent samples two-tailed t-tests;p <.05 was considered statistically significant. Results Return of spontaneous circulation occurred in 8 of the 15 animals, at Te ranging from 30.4 to 36,SOC. There were no differences between animals with and without Rose in baseline measurements ofweight, blood pressure, and arterial blood gas values (Table 1). End-tidal e0 2 at baseline was higher in the ROSe group than in the group without ROSe, but PaeOzwas not different (Table 1). During hypothermia before and after arrest and after 10 min of epr, there were no differences between groups with and without ROSe in blood pressure, end-tidal eoz, and arterial blood gas values (Table 2). Animals with and without ROSe did not differ in mean time to arrest, but arrest duration was greater in animals who did not have ROSe (Table 3). The two groups did not differ in Te at baseline or arrest, but Te was lower at the end of arrest in the group without ROSe, reflecting a longer total cooling time (Table 3). Individual animal data for time to arrest and arrest duration, T e at arrest and at the end of arrest, and whether animals had ROSe are shown in Table 3. The arrest rhythm was ventricular fibrillation in nine animals,

5 Semm potassium concentration and resuscitation outcome 277 Table 2. Heart rate, blood pressure, end-tidal COz, and arterial blood gas measurements at arrest, end-arrest, and after 10 min of CPR Rose No-Rose Arrest Heart rate (bpm) Blood pressure (mm Hg) Systolic Diastolic Mean End-tidal COz (mm Hg) Arterial ph Arterial PCOz (mm Hg) Arterial paz (mm Hg) Arterial HC0 3 (mm Hg) End-arrest Heart rate (bpm) Blood pressure (mm Hg) Systolic Diastolic Mean End-tidal COz (mm Hg) Arterial ph Arterial PCOz (mm Hg) Arterial POz (mm Hg) Arterial HC0 3 (mm Hg) CPR 10 min Heart rate (bpm) Blood pressure (mm Hg) Systolic Diastolic Mean End-tidal COz (mm Hg) Arterial ph Arterial PCOz (mm Hg) Arterial paz (mm Hg) Arterial HC0 3 (mm Hg) 12 ± 3 9±3 10 ± 3 1 ± ± ± ± ± 3 11 ± 4 10 ± 4 11 ± 3 O±O ± ± ± ± 4 83 ± ± ± 3 2± ± ± ± ± 2 12 ± 5 11 ± 5 12 ± 5 O±O ± ± ± ± 5 9±2 8±2 9±2 O±O ± ± ± ± 4 94 ± ± 5 58 ± 6 3± ± ± ± 137 8±3 asystole in five animals, and slow pulseless electrical activity (PEA) in one animal. The time from start of cardiopulmonary bypass to 30 0 e was lower in the ROSe group (14 ± 10 min, range 6-36 min) than in the no-rose group (33 ± 27 min, range 5-86 min). All animals had ventricular fibrillation as the initial rhythm on rewarming. AlI animals were defibrillated three times below 30 o e, with the exceptions ofone animal in the ROSe group which received no shocks [because of a fast rewarming time to 30 0 e (8 min) in one experiment where insufficient technical help was available] and one in the no-rose group which received only one shock (because of conversion to PEA).

6 278 Bender et al. Table 3. Individual animal data for time to arrest and arrest duration (min), arrest temperature and temperature at the end of arrest (oq, and whether animals had ROSe Exp. Time to Arrest Arrest End of ROSe number arrest duration temp. arrest temp Yes Yes Yes Yes Yes Yes Yes Yes Mean ± SD 128 ± ± ± ± 3.0 Exp. Time to Arrest Arrest End of ROSe number arrest duration temp. arrest temp No No No No No No No Mean ± SD 128 ± ± 193* 17.9 ± ± 2.4* *p <.05. SK (meq liter-i) data are shown in Table 4. Mean SK was similar between animals with and without ROSe at baseline and at arrest, with little variation between animals. The exception was a value of 9.1 in one no-rosc animal at arrest, with prearrest values having ranged from 2.4 to 3.8. At the end of the arrest period there was a trend toward higher mean SK in the animals without ROSC (4.6 ± 1.5 versus 9.4 ± 6.3) (p =.053). At the end of the arrest period, SK in the animals without ROSC ranged from 3.5 to 21.4, whereas the highest value among animals with ROSC was 7.8. After 10 min of CPR, SK was similar in animals with and without ROSC (6.6 ± 2.9 versus 9.0 ± 2.4) (p =.107). The range in potassium concentrations after 10 min of CPR was wide in both groups ( in the ROSC group and in the no-rosc group). CPR had a variable effect on SK, lowering it in 2 animals from each group (range ) and raising it in the remaining 11 animals (range ). There was a correlation between arrest duration and SK at the end of the arrest period (r = 0.533, p =.033) but not between time to arrest and SK at arrest (p =.91) nor at the end of the arrest period (p =.97).

7 Serum potassium concentration and resuscitation outcome 279 Table 4. Serum potassium concentrations (meq liter-i) at various experimental time points in animals resuscitated and not resuscitated from hypothermic cardiac arrest ROSe No-Rose Mean ±SD 95%CI N Mean ±SD 95%CI N Baseline 3.5 ± 0.4 ( ) ± 0.4 ( ) 7 Hypothermia 30 min 2.5 ± 0.6 ( ) ± 0.6 ( ) 7 Hypothermia 60 min 2.5 ± 0.4 ( ) ± 0.8 ( ) 7 Hypothermia 90 min 2.9 ± 0.5 ( ) ± 0.5 ( ) 7 Arrest 3.4 ± 0.7 ( ) ± 2.2 ( ) 7 Arrest 1 h 3.8 ± 0.5 ( ) ± 1.9 ( ) 7 Arrest 2 h 4.1 ± 0.9 ( ) ± 1.2 ( ) 7 Arrest 3 h 3.4 ± 0.6 ( ) ± 1.5 ( ) 6 Arrest 4 h 4.4 ± 2.3 ( ) ± 1.9 ( ) 6 Arrest 5 h 3.6 ± ± 3.3 ( ) 5 Arrest 6 h 3.6 ± ± 5.7 ( ) 5 Arrest 7 h 10.5 ± 7.6 ( ) 4 End-arrest 4.6 ± 1.5 ( ) ± 6.3 ( ) 7 CPR 10 min 6.6 ± 2.9 ( ) ± 2.4 ( ) 7 ROSC 5.6 ± 1.2 ( ) 8 ROSC60min 5.1 ± 1.7 ( ) 8 End-experiment 7.1 ± 3.5 ( ) 7 Discussion We found a trend toward higher mean SK at the end of the arrest period in animals without ROSC than in those with ROSe. The range of SK in the no-rosc group was wide. The end of arrest values seem to support the statement by Schaller et al. [5] that "until more detailed data are available, a markedly elevated potassium level (perhaps greater than 10 meg liter-i) should be considered as an index of irreversibility." However, four of the seven animals without Rose had end of arrest values lower than the highest value among the animals with ROSC (7.8 meg liter-i). In addition, patients are likely to arrive at the hospital with CPR in progress, as specified by current American Heart Association [9] recommendations for hypothermic cardiac arrest victims in whom pulse and breathing are absent. We found the effect of 10 min of CPR on SK to be variable, lowering it in some animals and raising it in others, with the effect often being large. After 10 min of CPR, SK ranged from 10.3 to 11.0 meg liter-i in four of seven animals in the no-rosc group, yet two animals who did have ROSC had values of 9.6 and 11.1 meg liter-i. Return of spontaneous circulation in animals with such relatively high potassium values weakens support found in the end of arrest data that a markedly elevated potassium concentration reflects irreversibility. The mechanism of a variable effect of CPR on serum potassium concentration is unclear. In previous reports, nine hypothermic victims (rectal temperature range < C) of snow avalanches in cardiorespiratory arrest could not be resuscitated despite core rewarming with cardiopulmonary bypass or peritoneal lavage [5]. In contrast, 15 hypothermic patients (rectal temperature range C) following acute drug or alcohol intoxication

8 280 Bender et al. and/or prolonged cold exposure were all resuscitated, including two in cardiorespiratory arrest. The avalanche victims had higher SK (mean 14.5 meq liter-i, range meq liter-i) than the nonavalanche group (mean 3.5 meq liter-i, range meq liter-i). In a nonhypothermic group of 13 patients dying in the hospital, SK progressively increased from 5.4 meq liter-i at the time of cardiac arrest to 7.2 meq liter- I after 1 h; the mean level 1 h after death was significantly higher than that measured in the resuscitated hypothermic patients after drug or alcohol intoxication and/or cold exposure [5]. In 22 hypothermic patients in cardiac arrest (age range 3-54 years, Tc range C) who were rewarmed by cardiopulmonary bypass, SK was higher in 12 patients without ROSe (8.7 meq liter-i) than in 10 patients with ROSe (5.0 meq liter- 1 ) [4]. Six (all avalanche victims) of the 12 patients without ROSe had SK above 9 meq liter-i. Two additional avalanche victims without ROSe and four with ROSe had SK ranging from 3.8 to 8.0 meq liter-i, whereas drowning or exposure victims with or without ROSe had SK ranging from 3.5 to 8.0 meq liter- 1 Only two patients survived to hospital discharge. In 10 severely hypothermic victims of a climbing disaster, the 2 survivors had SK less than 7 meq liter-i, whereas the nonsurvivors had SK greater than 10 meq liter- J [3]. A multicenter survey found that in patients with Tc ranging from 15.6 to 35 e and rewarmed by a variety of central and peripheral methods, SK was significantly higher in those who died (4.6 ± 1.6 meq liter-i) than in survivors (4.1 ± 0.8 meq liter-i) [2]. In this series, SK was lower than in the studies cited above, ranging from 1.5 to 9.3 meq liter-i. Wickstrom et al. [8] reported that two of three patients with Tc ranging from < 20 to 25 e were successfully resuscitated using cardiopulmonary bypass rewarming. Initial SK was 6.5 meq liter-i in the patient who could not be resuscitated and 5.6 meq liter-i in one of the successfully resuscitated patients. Three hypothermic victims of avalanche or cold immersion in cardiorespiratory arrest (rectal temperatures ranging from 19 to 24 e) were resuscitated using central.core rewarming and had no residual disabilities despite periods of circulatory arrest having lasted h [1]. Serum potassium concentrations were not reported. Southwick and Dalglish [6] reported the case of an asystolic alcohol-intoxicated patient with a Tc less than 27.8 e after prolonged exposure to cold ambient air who was successfully resuscitatedwith peritonealdialysis rewarming. His initial SK was 3.6 meq liter-i. Zell and Kurtz [10] have stated that cardiopulmonary bypass is the best rewarming method in arrested hypothermia, because "this technique rapidly raises core temperature and supports circulation in the face of nonperfusing cardiac rhythms." Rewarming with cardiopulmonary bypass avoids "rewarming shock" seen when profoundly hypothermic patients are treated with active external rewarming [1,10]. We were able to rewarm animals with ROSe faster than animals without ROSe, reflecting the lower Tc in the latter group at the end of the arrest period. Gradual-onset hypothermia has commonly been reported to lower SK [11-14]. In our study, SK declined in 13 of 15 animals during the first 30 min of hypothermia. The exact mechanism of hypothermic hypokalemia is unclear, but it is likely not related to acidosis, which develops with profound hypothermia but which would be expected to raise SK [14]. Schaller et al. [5] reported no correlation between arterial ph and SK in nine hypothermic victims of snow avalanches in cardiorespiratory arrest who could not be resuscitated despite core rewarming methods. There was also no correlation in 15 hypothermic patients following acute drug or alcohol intoxication and/or prolonged cold exposure who were all resuscitated, including two in cardiorespiratory arrest. In our study, mean arterial ph did not differ between the ROSe and no-rose groups during the hypothermia period or

9 Serum potassium concentration and resuscitation outcome 281 after 10 min of CPR. Sprung et al. [15] suggested that hypothermic hyperkalemia may be the result of severe tissue injury by deep and prolonged hypothermia, with irreversible cell membrane damage leading to massive release of intracellular potassium. This would represent an irreversible stage of tissue destruction, in contrast to hypokalemia which indicates that cellular mechanisms for maintaining potassium hemostasis are still functioning [15]. Hyperkalemia may result from a variety of reasons, including metabolic acidosis, crush injury, rhabdomyolysis, and renal failure [16]. Uncontrolled variables in prior studies of hypothermia have included length and type of exposure, concomitant injury, asphyxia, immersion, medication or intoxicant ingestion, frostbite, nutritional status, infection, age, baseline state of health, and behavioral responses [2]. Auerbach [16] suggested that it would be difficult to change traditional recommendations about rewarming hypothermic patients until there is a study of serum potassium associated with hypothermia in the absence of immersion or sudden asphyxia. We prevented sudden asphyxia because our model was intended to reflect the influence of hypothermia per se on serum potassium, rather than reflecting the influence of other possible contributors such as trauma or aspiration during drowning. We ventilated animals during the initial portion of the hypothermia exposure, decreasing ventilation at 45 min and stopping it at 90 min. Mean Tc was 21.1 ± 2.2 C in the ROSC group and 22.8 ± 2.6 C in the no-rosc group after 90 min of hypothermia; spontaneous ventilation would be expected to be minimal in the nontraumatized hypothermic human at similar temperatures. Our model differed from nontraumatic hypothermia exposure in humans in several ways. Our animals were initially mechanically ventilated and given halothane anesthesia. Pancuronium was given to eliminate shivering. Behavioral responses were eliminated. Our lo-min CPR period represented a short prehospital transport time. CPR per se influenced serum potassium values, and it is unclear what effect longer periods of CPR would have had on our results. We used standardized I.V. hydration during the lo-min CPR period, because without it we could not achieve adequate preload for pump rewarming. Cardiopulmonary bypass was immediately available because of prearrest instrumentation. Because of time and logistic constraints, long-term survival and neurologic function were not evaluated. We did not regard this as a limitation because in resuscitation of humans, any person with return of a spontaneous pulse and blood pressure would have continuation of resuscitative efforts until weaned from bypass, and then would be monitored in the ICU setting until neurologic and overall prognosis were determined. Our goal was to resuscitate animals to the decision point in humans where further resuscitative efforts would be continued or abandoned. Conclusions We conclude that very high SK following prolonged hypothermic cardiac arrest may be suggestive of an inability to resuscitate. However, SK after both prolonged hypothermic cardiac arrest and a brief period of CPR is not a good predictor of resuscitation using cardiopulmonary bypass rewarming in an animal model. Acknowledgments The study was funded by a Resident Research Grant from the Wilderness Medical Society. We thank Erez Gordon of the Department of Physiology at the Medical College of

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