RECOVER 2.0 Worksheet

QUESTION ID: MON-08

PICO Question:
In cats and dogs in CPA (P), does the identification and treatment of (arterial or venous) Na+ or K+ disorders during CPR (I) compared to not addressing Na+ and K+ disorders (C) improve ... (O)?

Outcomes:
Favorable neurologic outcome, Survival to Discharge, ROSC

Prioritized Outcomes (1= most critical; final number = least important):

1. Favorable neurologic outcome

2. Survival to discharge

3. ROSC

4.

5.

Domain chairs: Selena Lane, Ben Brainard, review MB

Evidence evaluators: Dominic Barfield, Sarah Robbins

Conflicts of interest:

Search strategy: See attached document

Evidence Review:

Study Design

Reduced Quality Factors 0 = no serious, - = serious, - - = very serious

Positive Quality Factors 0 = none, + = one, ++ = multiple

Dichotomous Outcome Summary

Non-Dichotomous Outcome Summary Brief description

Overall Quality High, moderate, low, very low, none

No of studies

Study Type

RoB

Indirectness

Imprecision

Inconsistency

Large Effect

Dose-Response

Confounder

# Intervention with Outcome

# Control with Outcome

RR (95% CI)

Outcome: favorable neurologic discharge

5

OB

-

--

0

0

0

0

0

Very low

Outcome: survival to discharge
4	OB	-	--	0	0	0	0	0					Very low
Outcome: ROSC
6	OB	-	--	0	0	0	0	0					Very low

PICO Question Summary

Introduction

Severe hyperkalemia (e.g., >6.5 mmol/L) or hypokalemia (eg, < 3 mmol/L) can cause life-threatening cardiotoxicity.1–3 Severe potassium abnormalities can be the cause of CPA or can occur as a consequence of hypoxic-ischemic processes that evolve during CPR. Martin (1986) reported in dogs with experimental VF arrest and 5 minutes down time, that serum potassium concentrations increased as CPR progressed (from 3.5±0.4 mmol/L to 4.6±0.5 mmol/L after 5 minutes of CPR; P<0.001), remained static until the end of CPR, resolving rapidly after ROSC.4 In addition, an experimental study in pigs documented a progressive increase in serum potassium concentration of nearly 10% per minute of CPR.5 Changes in sodium concentrations are of less immediate concern as a much wider variation in extracellular sodium concentrations can be tolerated without fatal consequences, but fluid shifts can occur with rapid fluctuations in sodium concentrations, possibly leading to neurologic injury.6 This question aims to explore whether routine assessment of potassium and sodium concentrations in dogs and cats undergoing CPR is warranted and if the potassium and sodium abnormalities should be addressed to improve outcome.

Consensus on science

We did not identify any studies that directly compared the effect of measurement of sodium and potassium concentrations during CPR on favorable neurologic outcome, survival to discharge or ROSC. However, we identified multiple observational studies that explored the association between potassium or sodium concentration and relevant outcomes, and that thus provide indirect evidence to support or oppose the measurement of these electrolytes. Outcome 1: Favorable neurologic outcome For the most critical outcome of survival with favorable neurologic outcome, we located 5 observational studies (very low quality of evidence, downgraded for serious risk of bias, and very serious indirectness). These studies examine the role of potassium concentration as a marker of severity of hypoxic-ischemic injury in populations of humans with OHCA. Shin et al (2017), evaluated registry data from 2229 OHCA patients analyzing the first electrolyte value examined at admission and found that none of the patients that had potassium concentrations > 8.5 mmol/L survived with good neurological function.7 Torres and colleagues (2020) prospectively studied functional outcomes in 1552 non-traumatic OHCA patients.8 Venous blood samples were obtained when initially establishing vascular access. Potassium concentrations were significantly lower in those patients with FNO (CPC 1-2; K+=3.95±0.79 mmol/l) compared to those with CPC 3-5 (K+=4.49±1.21 mmol/L; OR 1.725 [95% CI, 1.506–1.977, P<0.001]). Yanagawa et al. (2009) conducted a medical chart review including non-traumatic OHCA patients admitted to an emergency department (n=135). Potassium was significantly lower in patients with FNO (CPC1-2: K+=4.2±3.0 [n=16]; CPC 3-5: K+=5.6±1.6 [n=112], P=0.003).9 Choi (2020), analyzed data from a trial registry including 914 OHCA patients in which electrolyte information was available and that arrived at ED with ongoing CPA/CPR.10 After adjusting the covariates, hypokalemia was associated with FNO (OR = 4.45; 95% CI = 1.67–11.91; p = 0.0012), while hyperkalemia had no statistically significant association with FNO (OR = 0.79; 95% CI = 0.31–2.02). Similar results were found by Shida (2019) in a prospective, multicenter observational study that included 1516 patients with OHCA of cardiac origin with pre-hospital ROSC.11 The population was grouped according to potassium concentrations at presentation to the emergency department into Q1 (K ⩽3.8 mEq/L), Q2 (3.8< K⩽4.5 mEq/L), Q3 (4.5< K⩽5.6 mEq/L) and Q4 (K >5.6 mEq/L). One month survival with FNO (CBC 1-2) was best for Q1 (44.8%) and worst for Q4 (4.5%, P<0.001). The adjusted odds for survival with good neurologic outcome were 3 times worse for those patients in Q4 compared to those in Q1 (OR=0.31; 95% CI, 0.15–0.66). Thus, taken together, higher potassium concentrations were associated with worse outcomes. Outcome 2: Survival to discharge and 3: ROSC The results of the studies reporting the next most important outcomes of survival to discharge (4 observational studies; very low quality of evidence downgraded for serious risk of bias and very serious indirectness)7,11–13 and ROSC (5 observational studies; very low evidence downgraded for serious risk of bias and very serious indirectness)4,8,13–15 are similar to those reported for outcome 1. Of note, in 8 cats and 16 dogs in which samples were collected during ongoing CPR at a veterinary teaching hospital, potassium and sodium concentrations in animals with and without ROSC were not different.15 Only one study was identified that examined the association of treatment on ROSC in patients with hyperkalemia. Wang and colleagues (2016) conducted a retrospective study including 109 adults with IHCA and a serum potassium concentration > 6.5 mmol/L.10 In patients with serum potassium concentrations of 6.5 mmol/L to 7.9 mmol/L, sodium bicarbonate administration was positively associated with sustained ROSC (OR 10.51; 95% CI, 1.50-112.89; P=0.03). Likewise, calcium administration was associated with sustained ROSC in patients with serum potassium concentrations between 6.5 mmol/L and 9.4 mmol/L (OR 51.11; 95% CI, 3.12-1639.16; P=0.01). One retrospective observational study of trauma victims undergoing open chest CPR found that patients that did not experience ROSC had higher serum sodium and potassium concentrations than those who did regain ROSC.14 Two further observational studies, one in people and one in dogs and cats, did not find an association between intra-arrest sodium concentrations and survival to discharge (Shin, 2017) or ROSC (Hopper 2014).7,15 We did not find any further clinical trials, observational or experimental studies that evaluated the effect of treatment of severe potassium or sodium changes during CPR. However, we identified a series of case reports that reported circumstances in which hypokalemia or hyperkalemia were considered the cause rather than the consequence of CPA, and that describe the interventions administered during CPR. Five case reports in people describe CPA associated with severe hypokalemia ranging from 0.9 mmol/L to 2.9 mmol/L, the administration of potassium and its contribution to recovery.16–20 Allen et al (2016) report the case of a dog with CPA due to severe hypokalemia (1.5 mmol/L) associated with leptospirosis; this dog received peri-arrest potassium at 0.9 - 2.0 mmol/kg/hr and survived to discharge with good neurologic function.21 Five further case reports or case series document successful CPR in individuals with severe hyperkalemia due to kidney disease, rhabdomyolysis and other conditions.22–26 Treatment in these cases consisted in varying combinations of calcium gluconate, sodium bicarbonate, insulin and dextrose administration, as well as hemodialysis in addition to standard basic and advanced life support measures.

Treatment recommendation

We suggest measuring potassium concentrations in all dogs and cats during CPR (weak recommendation, very low quality of evidence). We recommend measuring potassium concentrations as early as possible in dogs and cats during CPR in which severe potassium abnormalities are suspected (strong recommendation, expert opinion).

Justification of treatment recommendation

Evidence suggests that hyperkalemia can develop during prolonged CPR but in most cases does not require treatment. Accordingly, a weak recommendation is provided for the routine determination of potassium concentrations during CPR. Multiple case reports suggest circumstances in which severe hypo- or hyperkalemia was associated with onset of CPA and in which aggressive intra-arrest measures were undertaken to correct the electrolyte disorders. Survival to discharge with a favorable outcome was achieved in these cases. There are multiple disease processes in dogs and cats that can lead to hyperkalemia, including AKI and urethral obstruction, reperfusion injury in cats with aortic thromboembolism or accidental intravenous overdose with potassium. Likewise, ROSC and successful defibrillation were achieved in patients with CPA and hypokalemia after rapid normalization of serum potassium concentration. We therefore recommend the timely determination of potassium concentrations in cases in which a precipitating cause for hyper- or hypokalemia is known or suspected.

Knowledge gaps

While moderate hyperkalemia has been noted with prolonged CPR, no studies have been conducted regarding the effectiveness of treatment of this hyperkalemia. In addition, it remains unclear whether there is an association between hypo- or hyperkalemia and survival to discharge or ROSC in veterinary species.

References:

1. Weiss JN, Qu Z, Shivkumar K. Electrophysiology of Hypokalemia and Hyperkalemia. Circ Arrhythm Electrophysiol. 2017;10(3):e004667.

2. Yano K, Kapuku GK, Hirata T, Hayano M. Effects of hypokalemia and disopyramide on electrical induction of ventricular tachyarrhythmia in nonischemic heart. International Journal of Angiology. 1996;5(2):105-109.

3. Yano K, Hirata M, Matsumoto Y, et al. Effects of chronic hypokalemia on ventricular vulnerability during acute myocardial ischemia in the dog. Jpn Heart J. 1989;30(2):205-217.

4. Martin GB, Carden DL, Nowak RM, Foreback C, Tomlanovich MC. Hyperkalemia during cardiac arrest and resuscitation in the canine model. Crit Care Med. 1986;14(4):300-302.

5. Geddes LA, Roeder RA, Rundell AE, et al. The natural biochemical changes during ventricular fibrillation with cardiopulmonary resuscitation and the onset of postdefibrillation pulseless electrical activity. Am J Emerg Med. 2006;24(5):577-581.

6. Choi SS, Kim WY, Kim W, Lim KS. Unexpected fatal hypernatremia after successful cardiopulmonary resuscitation with therapeutic hypothermia: a case report. J Korean Med Sci. 2012;27(3):329-331.

7. Shin J, Lim YS, Kim K, et al. Initial blood pH during cardiopulmonary resuscitation in out-of-hospital cardiac arrest patients: a multicenter observational registry-based study. Crit Care. 2017;21(1):322.

8. Corral Torres E, Hernández-Tejedor A, Suárez Bustamante R, et al. Prognostic value of venous blood analysis at the start of CPR in non-traumatic out-of-hospital cardiac arrest: association with ROSC and the neurological outcome. Crit Care. 2020;24(1):60.

9. Yanagawa Y, Sakamoto T, Sato H. Relationship between laboratory findings and the outcome of cardiopulmonary arrest. Am J Emerg Med. 2009;27(3):308-312.

10. Wang CH, Huang CH, Chang WT, et al. The effects of calcium and sodium bicarbonate on severe hyperkalaemia during cardiopulmonary resuscitation: A retrospective cohort study of adult in-hospital cardiac arrest. Resuscitation. 2016;98:105-111.

11. Shida H, Matsuyama T, Iwami T, et al. Serum potassium level on hospital arrival and survival after out-of-hospital cardiac arrest: The CRITICAL study in Osaka, Japan. Eur Heart J Acute Cardiovasc Care. Published online 2019:2048872619848883.

12. Choi DS, Shin SD, Ro YS, Lee KW. Relationship between serum potassium level and survival outcome in out-of-hospital cardiac arrest using CAPTURES database of Korea: Does hypokalemia have good neurological outcomes in out-of-hospital cardiac arrest? Adv Clin Exp Med. 2020;29(6):727-734.

13. Okada Y, Kiguchi T, Irisawa T, et al. Predictive accuracy of biomarkers for survival among cardiac arrest patients with hypothermia: a prospective observational cohort study in Japan. Scand J Trauma Resusc Emerg Med. 2020;28(1):75.

14. Schnüriger B, Talving P, Inaba K, et al. Biochemical profile and outcomes in trauma patients subjected to open cardiopulmonary resuscitation: a prospective observational pilot study. World J Surg. 2012;36(8):1772-1778.

15. Hopper K, Borchers A, Epstein SE. Acid base, electrolyte, glucose, and lactate values during cardiopulmonary resuscitation in dogs and cats. J Vet Emerg Crit Care (San Antonio). 2014;24(2):208-214.

16. Ten Bos LM, Veenstra TC, Westerhof BD, Bosch FH. A case of extreme hypokalaemia. Neth J Med. 2016;74(9):406-409.

17. Groth KA, Kelsen J, Løfgren B. Cardiac arrest due to lymphocytic colitis: a case report. J Med Case Rep. 2012;6:80.

18. Struck MF, Nowak A. Cardiac arrest during elective orthopedic surgery due to moderate hypokalemia. Middle East J Anaesthesiol. 2011;21(3):435-436.

19. Muhammad Ali S, Shaikh N, Shahid F, Shah A, Zafar HB. Hypokalemia Leading to Postoperative Critical Arrhythmias: Case Reports and Literature Review. Cureus. 2020;12(5):e8149.

20. Liu JK, Sim SS, Hsieh FC, Wu YH. Intravenous potassium solution boluses save a life from hypokalemic cardiac arrest. Am J Emerg Med. 2020;38(1):162.e1-162.e2.

21. Allen AE, Buckley GJ, Schaer M. Successful treatment of severe hypokalemia in a dog with acute kidney injury caused by leptospirosis. J Vet Emerg Crit Care (San Antonio). 2016;26(6):837-843.

22. Offman R, Paden A, Gwizdala A, Reeves JF. Hyperkalemia and cardiac arrest associated with glucose replacement in a patient on spironolactone. Am J Emerg Med. 2017;35(8):1214.e1-1214.e3.

23. Romano M, Boesch JM, Peralta S, Parker C, Kollias G. HYPERKALEMIA IN TWO JAGUARS ( PANTHERA ONCA) ANESTHETIZED WITH DEXMEDETOMIDINE, KETAMINE, AND ISOFLURANE. J Zoo Wildl Med. 2018;49(2):505-507.

24. Lin JL, Lim PS, Leu ML, Huang CC. Outcomes of severe hyperkalemia in cardiopulmonary resuscitation with concomitant hemodialysis. Intensive Care Med. 1994;20(4):287-290.

25. Nanda U, Willis A. A successful outcome of prolonged resuscitation of cardiac arrest with pulseless electrical activity (PEA) due to severe hyperkalaemia. N Z Med J. 2009;122(1293):3561.

26. Ochoa-Gómez J, Villar-Arias A, Aresti I, Marco-Aguilar P. A case of severe hyperkalaemia and compartment syndrome due to rhabdomyolysis after drugs abuse. Resuscitation. 2002;54(1):103-105.

Supplemental:

Case reports, Hypokalemia

• TenBos, 2016: A case of extreme hypokalaemia (0.9) identified after ROSC. No treatment intraarrest.
• Groth 2012: Case of OHCA due to severe hypokalemia, resuscitated for >1 hour with 16 shocks; sustained ROSC after correcting hypokalemia; good functional outcome.
• Stuck 2011: Geriatric intraop CPA with moderate hypokalemia, 2.9, considered to contribute to CPA. Recovered. No treatment for hypokalemia during arrest. Questionable association with hypokalemia.
• Ali 2020: Case report, including 2 human cases with hypokalemia associated with CPA. Case 1: A young healthy woman; perioperative severe hypokalemia (2.2 mmol/L); repeated episodes of VF requiring cardiopulmonary resuscitation (CPR), direct current (DC) shock and anti-arrhythmic therapy, intravenous potassium. Good functional recovery. Case 2: A 78-year-old male patient, postoperative repeated VF due to hypokalemia (2.4 mmol/L); 210 mmol of potassium chloride, antiarrhythmic therapy, DC shock, and CPR. Good functional outcome.
• Liu 2020: Case report on a case of severe hypokalemia (1.5 mmol/L) due to thyrotoxic periodic paralysis (TPP) in a young Asian male. KCl administration during CPR (60 mEq total, 68 kg bodyweight). ROSC after 35 minutes of CPR. Good functional outcome.
• Allen 2015: Case of a dog (dachshund) with cardiac arrest due to severe hypokalemia (K=1.5 mmol/L) associated with leptospirosis, CPR for 5 minutes until ROSC; good functional outcome

Case reports, hyperkalemia

• Offman 2017: Hyperkalemia (6.6 mmol/L) was observed in elderly women with a long list of comorbitities, and hyperkalemia was connected to CPA. Was treated with NaBic and calcium gluconate (no dose reported). Recovery.
• Romano 2018: 2 jaguars anesthetized, hyperkalemia associated with CPA in both animals, CPR and full functional recovery. Potassium moderately elevated at 6.2 mmol/L and 6.8 mmol/L; no specific treatment. Uncertain pathophysiology, but apparently previously reported in other large felids other than Jaguars.
• Lin 1993: Case series including 3 cases of severe hyperkalemia (9.6, 8.5 and 8.5 mmol/L) due to chronic renal failure (2 cases) and acute kidney disease (1 case), in which hyperkalemia was resolved by means of hemodialysis. All achieved ROSC, 2 with good functional outcome, one died for severity of illness (AKI)
• Ochoa-Gomez 2002: Hyperkalemia due to rhabdomyolysis (K=9.2 mmol/L) with drug abuse, CPA and treatment with standard ALS plus CaGluc and NaBic. ROSC achieved, no survival to discharge.
• Nanda 2009, A case of extreme hyperkalaemia. Cardiac arrest due to kidney disease; 9.5 mmol/L K pre-arrest, 7.3 mmol/L after ROSC. Ten ml of 10% calcium chloride x 2; Glucose-insulin infusion

Case reports, sodium

• Choi 2012: Post-cardiac arrest increase in a woman with diabetes insipidus in which the serum sodium concentration increased by 45 mmol/L to 192 mmol/L within 24 hours and who died from cerebral edema as a consequence.

Observational studies: ROSC

• Schnueriger 2012: 22 humans with open chest CPR after traumatic CPA. The sodium and potassium levels were higher for those who never regained a heartbeat than for those who did regain a pulse (sodium: 155 ± 14 vs. 147 ± 9 mmol/L, p = 0.094; potassium: 6.0 ± 1.1 vs. 4.6 ± 1.0 mmol/L, p = 0.014). Severe hyperkalemia (potassium >5.5 mmol/L) occurred significantly more often in patients who did not regain a heartbeat/any ROSC (p = 0.030).
• Torres 2020: Prospective observational study in human non-traumatic OHCA including 1552 patients. Venous sample obtained when initially placing IV catheter (arm). Potassium was significantly higher in those that failed to achieve ROSC: K+ (mmol/l) 4.22±1.01 (ROSC) versus 4.55±1.28 (no ROSC), OR 1.293 (95% CI, 1.180–1.416), P=0.001, OR represent reduction in ROSC per 1 mmol/L increment in potassium concentration. No significant association of Na concentration and ROSC was found: Na+ (mmol/l) 138.53±12.97 (ROSC) versus 139.57±8.04 (no ROSC), OR 1.010 (95% CI, 0.999–1.021) P=0.083.
• Hopper 2014: 24 of blood gases and electrolyte samples collected during CPR (8 cats and 16 dogs) in a veterinary teaching hospital. The median (range) potassium concentration was 5.4 (2.6–12.2) and the sodium concentration 144 mmol/L (113–171). In 3 animals hyperkalemia was considered the cause of CPA. In this small patient cohort, potassium and sodium concentrations were not different from each other: Sodium (mmol/L): ROSC (n=15) 145 (131–160), no-ROSC (n=9) 142.5 (113–171); Potassium (mmol/L): ROSC, 5.5 (2.6–10), no-ROSC: 5.0 (3.8–12.2)
• Choi 2017: Observational trial registry data used for this study, including 914 OHCA patients in which electrolyte information was available and that arrived at ED with ongoing CPA/CPR; K concentrations at arrival to ED; according to the serum potassium level, the patients were divided into a hypokalemia group (K+ < 3.5 mEq/L), normokalemia group (K+ = 3.5–5.4 mEq/L) and a hyperkalemia group (K+ ≥ 5.5 mEq/L). ROSC rates were higher in the hypokalemia group (35/46; 76.1%) compared to normokalemia (185/370; 50%) and the hyperkalemia group (192/497; 38.6%; P<0.0001)
• Martin 1986: 14 dogs with experimental VF arrest and 5 min down time, followed by 30 minutes of closed chest CPR: K levels significantly increased as CPR progressed (from 3.5±0.4 mmol/L to 4.6±0.5 mmol/L after 5 minutes of CPR; P<0.001), and then stayed at the level until the end of CPR), and resolved rapidly after ROSC (3.5±0.9 mmol/L after 15 minutes of ROSC). Defibrillation was started after 30 minutes of CPR. There was no difference between dogs achieving ROSC (4.4±0.9 mmol/L) versus those that did not (5.1±1.2 mmol/L, no P value provided), nor did K have a significant association with ROSC on regression analysis (data not provided).
• Wang 2015[EF1]: Observational retrospective study including 109 adults with IHCA and a potassium plasma concentration of higher than 6.5 mmol/L. In patients with serum potassium concentrations of <7.9 mEq/L sodium bicarbonate administration was positively associated with sustained ROSC (odds ratio [OR]: 10.51; 95% confidence interval [CI]: 1.50-112.89; p: 0.03). Likewise, calcium administration was associated with sustained ROSC in patients with serum potassium concentrations <9.4 mEq/L (OR: 51.11; 95% CI: 3.12-1639.16; p: 0.01).

Observational studies: Survival to discharge

• Shin 2017: Observational study in people from registry data including 2229 OHCA patients. Looking at first electrolyte value examined. No patients who survived to hospital discharge had potassium levels > 10 mEq/L. None of the patients with good neurological recovery had potassium levels > 8.5 mEq/L. Adjusted OR for potassium 0.89 (95% CI, 0.82–0.96) P=0.003.
• Choi 2020: Observational trial registry data used for this study, including 914 OHCA patients in which electrolyte information was available and that arrived at ED with ongoing CPA/CPR; K concentrations at arrival to ED; according to the serum potassium level, the patients were divided into a hypokalemia group (K+ < 3.5 mEq/L), normokalemia group (K+ = 3.5–5.4 mEq/L) and a hyperkalemia group (K+ ≥ 5.5 mEq/L). After adjusting the covariates, hypokalemia had a significantly positive correlation with survival discharge (OR = 2.25; 95% CI = 1.05– 4.82; p = 0.0011). Hyperkalemia had a significantly negative association with survival discharge (OR = 0.40; 95% CI = 0.22–0.72; p < 0.0001)
• Shida 2019: Prospective, multicenter observational study, including OHCA of cardiac origin with pre-hospital ROSC (n=1516); K at arrival to ED. Four groups: Q1 (K ⩽3.8 mEq/L), Q2 (3.8< K⩽4.5 mEq/L), Q3 (4.5< K⩽5.6 mEq/L) and Q4 (K >5.6 mEq/L). One month survival was best for Q1 (59.2%) and worst for Q4 (8.4%), P<0.001
• Okada 2020: Human OHCA presenting to ED with hypothermia; n=754 for which 458 had K available (5.5% survival rate); primary outcome was 1-month survival; blood samples taken on hospital arrival. The median [IQR] of temp was 30.0 °C [26.4–31.3]. High sensitivity (96%) if K>7.0 mmol/L for non-survival to 1 month.

Observational studies: Functional outcome

• Shin 2017: Observational study in people from registry data including 2229 OHCA patients. Looking at first electrolyte value examined. None of the patients with good neurological recovery had potassium levels > 8.5 mEq/L.
• Torres 2020: Prospective observational study in human non-traumatic OHCA including 1552 patients. Venous sample obtained when initially placing IV catheter (arm). Potassium was significantly lower in those with good functional outcome (CPC I and II) compared to those with CPC>II: K+ (mmol/l) 3.95±0.79, versus 4.49±1.21, OR 1.725 (95% CI, 1.506–1.977) P<0.001; no association was identified for sodium: Na+ (mmol/l) 139.20±12.67, versus 138.88±10.68, OR 0.997 (95% CI, 0.986–1.008) P=0.620
• Yanagawa 2009: retrospective observational study by medical chart review. Non-traumatic OHCA treated in ED, n=135. Sodium was not associated with CPC, CPC3-5: 140±0 (n=112) CPC1-2: 139±1 (n=16) n.s. Potassium was associated with CPC: CPC3-5: 5.6±1.6 (n=112), CPC1-2: 4.2±3.0 (n=16) P=0.003. Multivariate analysis using a logistic regression did not identify factors independently associated with the outcome (but likely underpowered for this analysis).
• Choi 2020: Observational trial registry data used for this study, including 914 OHCA patients in which electrolyte information was available and that arrived at ED with ongoing CPA/CPR; K concentrations at arrival to ED; according to the serum potassium level, the patients were divided into a hypokalemia group (K+ < 3.5 mEq/L), normokalemia group (K+ = 3.5–5.4 mEq/L) and a hyperkalemia group (K+ ≥ 5.5 mEq/L). After adjusting the covariates, hypokalemia had a significantly positive correlation with neurologically favorable survival (OR = 4.45; 95% CI = 1.67–11.91; p = 0.0012). Hyperkalemia had no statistically significant correlation with neurologically favorable survival (OR = 0.79; 95% CI = 0.31–2.02; p = 0.0414)
• Shida 2019: Prospective, multicenter observational study, including OHCA of cardiac origin with pre-hospital ROSC (n=1516); K at arrival to ED. Four groups: Q1 (K ⩽3.8 mEq/L), Q2 (3.8< K⩽4.5 mEq/L), Q3 (4.5< K⩽5.6 mEq/L) and Q4 (K >5.6 mEq/L). One month survival with good functional outcome (CBC1-2) was best for Q1 and worst for Q4: Q1: 44.8%, Q2: 30.3%, Q3: 11.7%, Q4: 4.5%, P<0.001; Adjusted OR Q4 versus Q1: 0.31 (95% CI, 0.15–0.66)

Physiological studies

• Martin 1986: 14 dogs with experimental VF arrest and 5 min down time, followed by 30 minutes of closed chest CPR: K levels significantly increased as CPR progressed (from 3.5±0.4 mmol/L to 4.6±0.5 mmol/L after 5 minutes of CPR; P<0.001), and then stayed at the level until the end of CPR), and resolved rapidly after ROSC (3.5±0.9 mmol/L after 15 minutes of ROSC).
• Geddes 2006: Swine study, VF induced cardiac arrest undergoing mechanical chest compressions: There was a steady increase in K+ of nearly 10% per minute of VF with CPR.

[EF1]Online article published 2015 and volume issue published 2016—zotero lists 2016…..maybe incorrect??