European Resuscitation Council Guidelines for Resuscitation 2010 Section 8. Cardiac arrest in special circumstances: Electrolyte abnormalities, poisoning, drowning, accidental hypothermia, hyperthermia, asthma, anaphylaxis, cardiac surgery, trauma, pregnancy, electrocution
Published online 19 October 2010, pages 1400 - 1433
- Electrolyte disorders
- Accidental hypothermia
- CA and cardiac surgery
- Traumatic CA
- Pregnancy CA
8a. Life-threatening electrolyte disorders
Electrolyte abnormalities can cause cardiac arrhythmias or cardiopulmonary arrest. Life-threatening arrhythmias are associated most commonly with potassium disorders, particularly hyperkalaemia, and less commonly with disorders of serum calcium and magnesium. In some cases therapy for life-threatening electrolyte disorders should start before laboratory results become available.
The electrolyte values for definitions have been chosen as a guide to clinical decision-making. The precise values that trigger treatment decisions will depend on the patient's clinical condition and rate of change of electrolyte values.
There is little or no evidence for the treatment of electrolyte abnormalities during cardiac arrest. Guidance during cardiac arrest is based on the strategies used in the non-arrest patient. There are no major changes in the treatment of these disorders since Guidelines 2005. 1 x J. Soar, C.D. Deakin, J.P. Nolan, et al.. European Resuscitation Council guidelines for resuscitation 2005. Section 7. Cardiac arrest in special circumstances. Resuscitation 67 (2005) (S135 - S170)
Prevention of electrolyte disorders
Identify and treat life-threatening electrolyte abnormalities before cardiac arrest occurs. Remove any precipitating factors (e.g., drugs) and monitor electrolyte values to prevent recurrence of the abnormality. Monitor renal function in patients at risk of electrolyte disorders (e.g., chronic kidney disease, cardiac failure). In haemodialysis patients, review the dialysis prescription regularly to avoid inappropriate electrolyte shifts during treatment.
Extracellular potassium concentration is regulated tightly between 3.5 and 5.0 mmol l−1. A large concentration gradient normally exists between intracellular and extracellular fluid compartments. This potassium gradient across cell membranes contributes to the excitability of nerve and muscle cells, including the myocardium. Evaluation of serum potassium must take into consideration the effects of changes in serum pH. When serum pH decreases (acidaemia), serum potassium increases because potassium shifts from the cellular to the vascular space. When serum pH increases (alkalaemia), serum potassium decreases because potassium shifts intracellularly. Anticipate the effects of pH changes on serum potassium during therapy for hyperkalaemia or hypokalaemia.
This is the most common electrolyte disorder associated with cardiopulmonary arrest. It is usually caused by increased potassium release from cells, impaired excretion by the kidneys or accidental potassium chloride administration.
There is no universal definition. We have defined hyperkalaemia as a serum potassium concentration higher than 5.5 mmol l−1; in practice, hyperkalaemia is a continuum. As the potassium concentration increases above this value the risk of adverse events increases and the need for urgent treatment increases. Severe hyperkalaemia has been defined as a serum potassium concentration higher than 6.5 mmol l−1.
There are several potential causes of hyperkalaemia, including renal failure, drugs (angiotensin converting enzyme inhibitors (ACE-I), angiotensin II receptor antagonists, potassium sparing diuretics, non-steroidal anti-inflammatory drugs (NSAIDs), beta-blockers, trimethoprim), tissue breakdown (rhabdomyolysis, tumour lysis, haemolysis), metabolic acidosis, endocrine disorders (Addison's disease), hyperkalaemic periodic paralysis, or diet (may be sole cause in patients with advanced chronic kidney disease). Abnormal erythrocytes or thrombocytosis may cause a spuriously high potassium concentration. 2 x W.S. Smellie. Spurious hyperkalaemia. BMJ 334 (2007) (693 - 695) The risk of hyperkalaemia is even greater when there is a combination of factors such as the concomitant use of ACE-I and NSAIDs or potassium sparing diuretics.
Recognition of hyperkalaemia
Exclude hyperkalaemia in patients with an arrhythmia or cardiac arrest. 3 x J.T. Niemann, C.B. Cairns. Hyperkalemia and ionized hypocalcemia during cardiac arrest and resuscitation: possible culprits for postcountershock arrhythmias?. Ann Emerg Med 34 (1999) (1 - 7) Patients may present with weakness progressing to flaccid paralysis, paraesthesia, or depressed deep tendon reflexes. Alternatively, the clinical picture can be overshadowed by the primary illness causing hyperkalaemia. The first indicator of hyperkalaemia may also be the presence of ECG abnormalities, arrhythmias, cardiopulmonary arrest or sudden death. The effect of hyperkalaemia on the ECG depends on the absolute serum potassium as well as the rate of increase. Most patients will have ECG abnormalities at a serum potassium concentration higher than 6.7 mmol l−1. 4 x J. Ahmed, L.S. Weisberg. Hyperkalemia in dialysis patients. Semin Dial 14 (2001) (348 - 356) The use of a blood gas analyser that measures potassium can reduce delay in recognition.
The ECG changes associated with hyperkalaemia are usually progressive and include:
- first degree heart block (prolonged PR interval) [>0.2 s];
- flattened or absent P waves;
- tall, peaked (tented) T waves [T wave larger than R wave in more than 1 lead];
- ST-segment depression;
- S and T wave merging (sine wave pattern);
- widened QRS [>0.12 s];
- ventricular tachycardia;
- cardiac arrest (pulseless electrical activity [PEA], ventricular fibrillation/pulseless ventricular tachycardia [VF/VT], asystole).
Treatment of hyperkalaemia
There are three key treatments for hyperkalaemia 5 x A.V. Alfonzo, C. Isles, C. Geddes, C. Deighan. Potassium disorders – clinical spectrum and emergency management. Resuscitation 70 (2006) (10 - 25) :
- 1. cardiac protection;
- 2. shifting potassium into cells;
- 3. removing potassium from the body.
Intravenous calcium salts are not generally indicated in the absence of ECG changes. Monitor effectiveness of treatment, be alert to rebound hyperkalaemia and take steps to prevent recurrence of hyperkalaemia. When hyperkalaemia is strongly suspected, e.g., in the presence of ECG changes, start life-saving treatment even before laboratory results are available. The treatment of hyperkalaemia has been the subject of a Cochrane review. 6 x B. Mahoney, W. Smith, D. Lo, K. Tsoi, M. Tonelli, C. Clase. Emergency interventions for hyperkalaemia. Cochrane Database Syst Rev (2005) (CD003235)
Patient not in cardiac arrest
Assess ABCDE (Airway, Breathing, Circulation, Disability, Exposure) and correct any abnormalities. Obtain intravenous access, check serum potassium and record an ECG. Treatment is determined according to severity of hyperkalaemia.
Approximate values are provided to guide treatment.
Mild elevation (5.5–5.9 mmol l−1)
- Remove potassium from body: potassium exchange resins – calcium resonium 15–30 g OR sodium polystyrene sulfonate (Kayexalate) 15–30 g in 50–100 ml of 20% sorbitol, given either orally or by retention enema (onset in 1–3 h; maximal effect at 6 h).
- Address cause of hyperkalaemia to correct and avoid further rise in serum potassium (e.g., drugs, diet).
Moderate elevation (6–6.4 mmol l−1) without ECG changes
- Shift potassium intracellularly with glucose/insulin: 10 units short-acting insulin and 25 g glucose IV over 15–30 min (onset in 15–30 min; maximal effect at 30–60 min; monitor blood glucose).
- Remove potassium from the body as described above.
- Haemodialysis: consider if oliguric; haemodialysis is more efficient than peritoneal dialysis at removing potassium.
Severe elevation (≥6.5 mmol l−1) without ECG changes. Seek expert help and
- Use multiple shifting agents.
- Glucose/insulin (see above).
- Salbutamol 5 mg nebulised. Several doses (10–20 mg) may be required (onset in 15–30 min).
- Sodium bicarbonate: 50 mmol IV over 5 min if metabolic acidosis present (onset in 15–30 min). Bicarbonate alone is less effective than glucose plus insulin or nebulised salbutamol; it is best used in conjunction with these medications.7 and 8 x N.N. Ngugi, S.O. McLigeyo, J.K. Kayima. Treatment of hyperkalaemia by altering the transcellular gradient in patients with renal failure: effect of various therapeutic approaches. East Afr Med J 74 (1997) (503 - 509) x M. Allon, N. Shanklin. Effect of bicarbonate administration on plasma potassium in dialysis patients: interactions with insulin and albuterol. Am J Kidney Dis 28 (1996) (508 - 514)
- Use removal strategies above.
Severe elevation (≥6.5 mmol l−1) WITH toxic ECG changes. Seek expert help and
- Protect the heart first with calcium chloride: 10 ml 10% calcium chloride IV over 2–5 min to antagonise the toxic effects of hyperkalaemia at the myocardial cell membrane. This protects the heart by reducing the risk of pulseless VT/VF but does not lower serum potassium (onset in 1–3 min).
- Use multiple shifting agents (see above).
- Use removal strategies.
- Prompt specialist referral is essential.
Patient in cardiac arrest
Modifications to BLS
There are no modifications to basic life support in the presence of electrolyte abnormalities.
Modifications to ALS
- Follow the universal algorithm. Hyperkalaemia can be confirmed rapidly using a blood gas analyser if available. Protect the heart first: give 10 ml 10% calcium chloride IV by rapid bolus injection.
Shift potassium into cells:
- ∘ Glucose/insulin: 10 units short-acting insulin and 25 g glucose IV by rapid injection.
- ∘ Sodium bicarbonate: 50 mmol IV by rapid injection (if severe acidosis or renal failure).
- Remove potassium from body: dialysis: consider this for cardiac arrest induced by hyperkalaemia that is resistant to medical treatment. Several dialysis modes have been used safely and effectively in cardiac arrest, but this may only be available in specialist centres.
Indications for dialysis
Haemodialysis (HD) is the most effective method for removal of potassium from the body. The principle mechanism of action is the diffusion of potassium ions across the membrane down the potassium ion gradient. The typical decline in serum potassium is 1 mmol l−1 in the first 60 min, followed by 1 mmol l−1 over the next 2 h. The efficacy of HD in decreasing serum potassium concentration can be improved by performing dialysis with a low potassium concentration in the dialysate, 9 x C. Zehnder, J.P. Gutzwiller, A. Huber, C. Schindler, D. Schneditz. Low-potassium and glucose-free dialysis maintains urea but enhances potassium removal. Nephrol Dial Transplant 16 (2001) (78 - 84) a high blood flow rate 10 x J.P. Gutzwiller, D. Schneditz, A.R. Huber, C. Schindler, E. Garbani, C.E. Zehnder. Increasing blood flow increases kt/V(urea) and potassium removal but fails to improve phosphate removal. Clin Nephrol 59 (2003) (130 - 136) or a high dialysate bicarbonate concentration. 11 x R.M. Heguilen, C. Sciurano, A.D. Bellusci, et al.. The faster potassium-lowering effect of high dialysate bicarbonate concentrations in chronic haemodialysis patients. Nephrol Dial Transplant 20 (2005) (591 - 597)
Consider haemodialysis early for hyperkalaemia associated with established renal failure, oliguric acute kidney injury (<400 ml day−1 urine output) or when there is marked tissue breakdown. Dialysis is also indicated when hyperkalaemia is resistant to medical treatment. Serum potassium frequently rebounds after initial treatment. In unstable patients continuous renal replacement therapy (CRRT) (e.g., continuous veno-veno haemofiltration) is less likely to compromise cardiac output than intermittent haemodialysis. CRRT is now widely available in many intensive care units.
Cardiac arrest in haemodialysis patients
Cardiac arrest is the most common cause of death in haemodialysis patients. 12 x P.H. Pun, R.W. Lehrich, S.R. Smith, J.P. Middleton. Predictors of survival after cardiac arrest in outpatient hemodialysis clinics. Clin J Am Soc Nephrol 2 (2007) (491 - 500) Events occurring particularly during haemodialysis treatment, pose several novel considerations.
Call the resuscitation team and seek expert help immediately. Whilst BLS is underway, a trained dialysis nurse should be assigned to the dialysis machine. The conventional practice is to return the patient's blood volume and take off haemodialysis, although this approach is not the most time-efficient. 13 x A.V. Alfonzo, K. Simpson, C. Deighan, S. Campbell, J. Fox. Modifications to advanced life support in renal failure. Resuscitation 73 (2007) (12 - 28)
A shockable cardiac rhythm (VF/VT) is more common in patients undergoing haemodialysis14 and 15 x T.R. Davis, B.A. Young, M.S. Eisenberg, T.D. Rea, M.K. Copass, L.A. Cobb. Outcome of cardiac arrests attended by emergency medical services staff at community outpatient dialysis centers. Kidney Int 73 (2008) (933 - 939) x J.P. Lafrance, L. Nolin, L. Senecal, M. Leblanc. Predictors and outcome of cardiopulmonary resuscitation (CPR) calls in a large haemodialysis unit over a seven-year period. Nephrol Dial Transplant 21 (2006) (1006 - 1012) than in the general population.16 and 17 x C. Sandroni, J. Nolan, F. Cavallaro, M. Antonelli. In-hospital cardiac arrest: incidence, prognosis and possible measures to improve survival. Intensive Care Med 33 (2007) (237 - 245) x P.A. Meaney, V.M. Nadkarni, K.B. Kern, J.H. Indik, H.R. Halperin, R.A. Berg. Rhythms and outcomes of adult in-hospital cardiac arrest. Crit Care Med 38 (2010) (101 - 108)
The safest method to deliver a shock during dialysis requires further study. Most haemodialysis machine manufacturers recommend disconnection from the dialysis equipment prior to defibrillation. 18 x S. Bird, G.W. Petley, C.D. Deakin, F. Clewlow. Defibrillation during renal dialysis: a survey of UK practice and procedural recommendations. Resuscitation 73 (2007) (347 - 353) An alternative and rapid disconnect technique for haemodialysis has been described. Disconnection during continuous venovenous haemofiltration is not required. 13 x A.V. Alfonzo, K. Simpson, C. Deighan, S. Campbell, J. Fox. Modifications to advanced life support in renal failure. Resuscitation 73 (2007) (12 - 28) The use of automated external defibrillators in dialysis centres can facilitate early defibrillation. 19 x R.W. Lehrich, P.H. Pun, N.D. Tanenbaum, S.R. Smith, J.P. Middleton. Automated external defibrillators and survival from cardiac arrest in the outpatient hemodialysis clinic. J Am Soc Nephrol 18 (2007) (312 - 320)
In life-threatening circumstances and cardiac arrest, vascular access used for haemodialysis can be used to give drugs. 13 x A.V. Alfonzo, K. Simpson, C. Deighan, S. Campbell, J. Fox. Modifications to advanced life support in renal failure. Resuscitation 73 (2007) (12 - 28)
Potentially reversible causes
All of the standard reversible causes (4 Hs and 4 Ts) apply to dialysis patients. Electrolyte disorders, particularly hyperkalaemia, and fluid overload (e.g., pulmonary oedema) are most common causes.
Hypokalaemia is common in hospital patients. 20 x A. Rastegar, M. Soleimani. Hypokalaemia and hyperkalaemia. Postgrad Med J 77 (2001) (759 - 764) Hypokalaemia increases the incidence of arrhythmias, particularly in patients with pre-existing heart disease and in those treated with digoxin.
Hypokalaemia is defined as a serum potassium < 3.5 mmol l−1. Severe hypokalaemia is defined as a K+ < 2.5 mmol l−1 and may be associated with symptoms.
Causes of hypokalaemia include gastrointestinal loss (diarrhoea), drugs (diuretics, laxatives, steroids), renal losses (renal tubular disorders, diabetes insipidus, dialysis), endocrine disorders (Cushing's Syndrome, hyperaldosteronism), metabolic alkalosis, magnesium depletion, and poor dietary intake. Treatment strategies used for hyperkalaemia may also induce hypokalaemia.
Recognition of hypokalaemia
Exclude hypokalaemia in every patient with an arrhythmia or cardiac arrest. In dialysis patients, hypokalaemia occurs commonly at the end of a haemodialysis session or during treatment with peritoneal dialysis.
As serum potassium concentration decreases, the nerves and muscles are predominantly affected causing fatigue, weakness, leg cramps, constipation. In severe cases (K+ < 2.5 mmol l−1), rhabdomyolysis, ascending paralysis and respiratory difficulties may occur.
ECG features of hypokalaemia are:
- U waves;
- T wave flattening;
- ST-segment changes;
- arrhythmias, especially if patient is taking digoxin;
- cardiopulmonary arrest (PEA, pulseless VT/VF, asystole).
This depends on the severity of hypokalaemia and the presence of symptoms and ECG abnormalities. Gradual replacement of potassium is preferable, but in an emergency, intravenous potassium is required. The maximum recommended IV dose of potassium is 20 mmol h−1, but more rapid infusion (e.g., 2 mmol min−1 for 10 min, followed by 10 mmol over 5–10 min) is indicated for unstable arrhythmias when cardiac arrest is imminent. Continuous ECG monitoring is essential during IV infusion and the dose should be titrated after repeated sampling of serum potassium levels.
Many patients who are potassium deficient are also deficient in magnesium. Magnesium is important for potassium uptake and for the maintenance of intracellular potassium levels, particularly in the myocardium. Repletion of magnesium stores will facilitate more rapid correction of hypokalaemia and is recommended in severe cases of hypokalaemia. 21 x J.N. Cohn, P.R. Kowey, P.K. Whelton, L.M. Prisant. New guidelines for potassium replacement in clinical practice: a contemporary review by the National Council on Potassium in Clinical Practice. Arch Intern Med 160 (2000) (2429 - 2436)
Calcium and magnesium disorders
The recognition and management of calcium and magnesium disorders is summarised in Table 8.1 .
[Calcium] > 2.6 mmol l−1
|Primary or tertiary hyperparathyroidism||Confusion||Short QT interval||Fluid replacement IV|
|Malignancy||Weakness||Prolonged QRS Interval||Furosemide 1 mg kg−1 IV|
|Sarcoidosis||Abdominal pain||Flat T waves||Hydrocortisone 200–300 mg IV|
|Drugs||Hypotension||AV-block||Pamidronate 30–90 mg IV|
|Arrhythmias||Cardiac arrest||Treat underlying cause|
[Calcium] < 2.1 mmol l−1
|Chronic renal failure||Paraesthesia||Prolonged QT interval||Calcium chloride 10% 10–40 ml|
|Acute pancreatitis||Tetany||T wave inversion||Magnesium sulphate 50% 4–8 mmol (if necessary)|
|Calcium channel blocker overdose||Seizures||Heart block|
|Toxic shock syndrome||AV-block||Cardiac arrest|
|Tumour lysis syndrome|
[Magnesium] > 1.1 mmol l−1
|Renal failure||Confusion||Prolonged PR and QT intervals||Consider treatment when [Magnesium] > 1.75 mmol l−1|
|Iatrogenic||Weakness||T wave peaking|
|Respiratory depression||AV-block||Calcium chloride 10% 5–10 ml repeated if necessary|
|AV-block||Cardiac arrest||Ventilatory support if necessary|
|Cardiac arrest||Saline diuresis – 0.9% saline with furosemide 1 mg kg−1 IV|
[Magnesium] < 0.6 mmol l−1
|GI loss||Tremor||Prolonged PR and QT Intervals||Severe or symptomatic:|
|Polyuria||Ataxia||ST-segment depression||2 g 50% magnesium sulphate (4 ml; 8 mmol) IV over 15 min.|
|Starvation||Nystagmus||T-wave inversion||Torsade de pointes:|
|Alcoholism||Seizures||Flattened P waves||2 g 50% magnesium sulphate (4 ml; 8 mmol) IV over 1–2 min.|
|Malabsorption||Arrhythmias – torsade de pointes||Increased QRS duration||Seizure:|
|Cardiac arrest||Torsade de pointes||2 g 50% magnesium sulphate (4 ml; 8 mmol) IV over 10 min.|
References in context
The recognition and management of calcium and magnesium disorders is summarised in Table 8.1.
Go to context
Electrolyte abnormalities are among the most common causes of cardiac arrhythmias. Of all the electrolyte abnormalities, hyperkalaemia is most rapidly fatal. A high degree of clinical suspicion and aggressive treatment of underlying electrolyte abnormalities can prevent many patients from progressing to cardiac arrest.
|J. Soar, C.D. Deakin, J.P. Nolan, et al..||European Resuscitation Council guidelines for resuscitation 2005. Section 7. Cardiac arrest in special circumstances.||Resuscitation 67 (2005) (S135 - S170)||2005|
|W.S. Smellie.||Spurious hyperkalaemia.||BMJ 334 (2007) (693 - 695)||2007|
|J.T. Niemann, C.B. Cairns.||Hyperkalemia and ionized hypocalcemia during cardiac arrest and resuscitation: possible culprits for postcountershock arrhythmias?.||Ann Emerg Med 34 (1999) (1 - 7)||1999|
|J. Ahmed, L.S. Weisberg.||Hyperkalemia in dialysis patients.||Semin Dial 14 (2001) (348 - 356)||2001|
|A.V. Alfonzo, C. Isles, C. Geddes, C. Deighan.||Potassium disorders – clinical spectrum and emergency management.||Resuscitation 70 (2006) (10 - 25)||2006|
|B. Mahoney, W. Smith, D. Lo, K. Tsoi, M. Tonelli, C. Clase.||Emergency interventions for hyperkalaemia.||Cochrane Database Syst Rev (2005) (CD003235)||2005|
|C. Zehnder, J.P. Gutzwiller, A. Huber, C. Schindler, D. Schneditz.||Low-potassium and glucose-free dialysis maintains urea but enhances potassium removal.||Nephrol Dial Transplant 16 (2001) (78 - 84)||2001|
|J.P. Gutzwiller, D. Schneditz, A.R. Huber, C. Schindler, E. Garbani, C.E. Zehnder.||Increasing blood flow increases kt/V(urea) and potassium removal but fails to improve phosphate removal.||Clin Nephrol 59 (2003) (130 - 136)||2003|
|R.M. Heguilen, C. Sciurano, A.D. Bellusci, et al..||The faster potassium-lowering effect of high dialysate bicarbonate concentrations in chronic haemodialysis patients.||Nephrol Dial Transplant 20 (2005) (591 - 597)||2005|
|P.H. Pun, R.W. Lehrich, S.R. Smith, J.P. Middleton.||Predictors of survival after cardiac arrest in outpatient hemodialysis clinics.||Clin J Am Soc Nephrol 2 (2007) (491 - 500)||2007|
|A.V. Alfonzo, K. Simpson, C. Deighan, S. Campbell, J. Fox.||Modifications to advanced life support in renal failure.||Resuscitation 73 (2007) (12 - 28)||2007|
|S. Bird, G.W. Petley, C.D. Deakin, F. Clewlow.||Defibrillation during renal dialysis: a survey of UK practice and procedural recommendations.||Resuscitation 73 (2007) (347 - 353)||2007|
|R.W. Lehrich, P.H. Pun, N.D. Tanenbaum, S.R. Smith, J.P. Middleton.||Automated external defibrillators and survival from cardiac arrest in the outpatient hemodialysis clinic.||J Am Soc Nephrol 18 (2007) (312 - 320)||2007|
|A. Rastegar, M. Soleimani.||Hypokalaemia and hyperkalaemia.||Postgrad Med J 77 (2001) (759 - 764)||2001|
|J.N. Cohn, P.R. Kowey, P.K. Whelton, L.M. Prisant.||New guidelines for potassium replacement in clinical practice: a contemporary review by the National Council on Potassium in Clinical Practice.||Arch Intern Med 160 (2000) (2429 - 2436)||2000|