Resuscitation 81 (2010) 1400–1433 Contents lists available at ScienceDirect Resuscitation journal homepage: www.elsevier.com/locate/resuscitation 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 Jasmeet Soar a,∗, Gavin D. Perkins b, Gamal Abbas c, Annette Alfonzo d, Alessandro Barelli e, Joost J.L.M. Bierens f, Hermann Brugger g, Charles D. Deakin h, Joel Dunning i, Marios Georgiou j, Anthony J. Handley k, David J. Lockey l, Peter Paal m, Claudio Sandroni n, Karl-Christian Thies o, David A. Zideman p, Jerry P. Nolan q a Anaesthesia and Intensive Care Medicine, Southmead Hospital, North Bristol NHS Trust, Bristol, UK b University of Warwick, Warwick Medical School, Warwick, UK c Emergency Department, Al Rahba Hospital, Abu Dhabi, United Arab Emirates d Queen Margaret Hospital, Dunfermline, Fife, UK e Intensive Care Medicine and Clinical Toxicology, Catholic University School of Medicine, Rome, Italy f Maxima Medical Centre, Eindhoven, The Netherlands g EURAC Institute of Mountain Emergency Medicine, Bozen, Italy h Cardiac Anaesthesia and Critical Care, Southampton University Hospital NHS Trust, Southampton, UK i Department of Cardiothoracic Surgery, James Cook University Hospital, Middlesbrough, UK j Nicosia General Hospital, Nicosia, Cyprus k Honorary Consultant Physician, Colchester, UK l Anaesthesia and Intensive Care Medicine, Frenchay Hospital, Bristol, UK m Department of Anesthesiology and Critical Care Medicine, University Hospital Innsbruck, Innsbruck, Austria n Critical Care Medicine at Policlinico Universitario Agostino Gemelli, Catholic University School of Medicine, Rome, Italy o Birmingham Children’s Hospital, Birmingham, UK p Imperial College Healthcare NHS Trust, London, UK q Anaesthesia and Intensive Care Medicine, Royal United Hospital, Bath, UK 8a. Life-threatening electrolyte disorders no major changes in the treatment of these disorders since Guide- lines 2005.1 Overview Prevention of electrolyte disorders Electrolyte abnormalities can cause cardiac arrhythmias or car- diopulmonary arrest. Life-threatening arrhythmias are associated Identify and treat life-threatening electrolyte abnormalities most commonly with potassium disorders, particularly hyper- before cardiac arrest occurs. Remove any precipitating factors (e.g., kalaemia, and less commonly with disorders of serum calcium and drugs) and monitor electrolyte values to prevent recurrence of the magnesium. In some cases therapy for life-threatening electrolyte abnormality. Monitor renal function in patients at risk of elec- disorders should start before laboratory results become available. trolyte disorders (e.g., chronic kidney disease, cardiac failure). In The electrolyte values for definitions have been chosen as a haemodialysis patients, review the dialysis prescription regularly guide to clinical decision-making. The precise values that trigger to avoid inappropriate electrolyte shifts during treatment. treatment decisions will depend on the patient’s clinical condition and rate of change of electrolyte values. Potassium disorders There is little or no evidence for the treatment of electrolyte abnormalities during cardiac arrest. Guidance during cardiac arrest Potassium homeostasis is based on the strategies used in the non-arrest patient. There are 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 ∗ Corresponding author. compartments. This potassium gradient across cell membranes E-mail address: [email protected] (J. Soar). contributes to the excitability of nerve and muscle cells, including 0300-9572/$ – see front matter © 2010 European Resuscitation Council. Published by Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.resuscitation.2010.08.015 J. Soar et al. / Resuscitation 81 (2010) 1400–1433 1401 the myocardium. Evaluation of serum potassium must take into • cardiac arrest (pulseless electrical activity [PEA], ventricular fib- consideration the effects of changes in serum pH. When serum rillation/pulseless ventricular tachycardia [VF/VT], asystole). pH decreases (acidaemia), serum potassium increases because potassium shifts from the cellular to the vascular space. When Treatment of hyperkalaemia serum pH increases (alkalaemia), serum potassium decreases There are three key treatments for hyperkalaemia5: because potassium shifts intracellularly. Anticipate the effects of pH changes on serum potassium during therapy for hyperkalaemia 1. cardiac protection; or hypokalaemia. 2. shifting potassium into cells; 3. removing potassium from the body. Hyperkalaemia Intravenous calcium salts are not generally indicated in the This is the most common electrolyte disorder associated with absence of ECG changes. Monitor effectiveness of treatment, cardiopulmonary arrest. It is usually caused by increased potassium be alert to rebound hyperkalaemia and take steps to prevent release from cells, impaired excretion by the kidneys or accidental recurrence of hyperkalaemia. When hyperkalaemia is strongly potassium chloride administration. suspected, e.g., in the presence of ECG changes, start life-saving treatment even before laboratory results are available. The treat- ment of hyperkalaemia has been the subject of a Cochrane review.6 Definition There is no universal definition. We have defined hyperkalaemia as a serum potassium concentration higher than 5.5 mmol l−1;in Patient not in cardiac arrest. Assess ABCDE (Airway, Breathing, practice, hyperkalaemia is a continuum. As the potassium con- Circulation, Disability, Exposure) and correct any abnormalities. centration increases above this value the risk of adverse events Obtain intravenous access, check serum potassium and record increases and the need for urgent treatment increases. Severe an ECG. Treatment is determined according to severity of hyper- hyperkalaemia has been defined as a serum potassium concentra- kalaemia. tion higher than 6.5 mmol l−1. Approximate values are provided to guide treatment. Mild elevation (5.5–5.9 mmol l−1): Causes There are several potential causes of hyperkalaemia, includ- • Remove potassium from body: potassium exchange resins – ing renal failure, drugs (angiotensin converting enzyme inhibitors calcium resonium 15–30 g OR sodium polystyrene sulfonate (ACE-I), angiotensin II receptor antagonists, potassium spar- (Kayexalate) 15–30 g in 50–100 ml of 20% sorbitol, given either ing diuretics, non-steroidal anti-inflammatory drugs (NSAIDs), orally or by retention enema (onset in 1–3 h; maximal effect at beta-blockers, trimethoprim), tissue breakdown (rhabdomyolysis, 6 h). tumour lysis, haemolysis), metabolic acidosis, endocrine disorders • Address cause of hyperkalaemia to correct and avoid further rise (Addison’s disease), hyperkalaemic periodic paralysis, or diet (may in serum potassium (e.g., drugs, diet). be sole cause in patients with advanced chronic kidney disease). Abnormal erythrocytes or thrombocytosis may cause a spuriously Moderate elevation (6–6.4 mmol l−1) without ECG changes: high potassium concentration.2 The risk of hyperkalaemia is even greater when there is a combination of factors such as the concomi- • Shift potassium intracellularly with glucose/insulin: 10 units tant use of ACE-I and NSAIDs or potassium sparing diuretics. 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). Recognition of hyperkalaemia • Remove potassium from the body as described above. Exclude hyperkalaemia in patients with an arrhythmia or • Haemodialysis: consider if oliguric; haemodialysis is more effi- cardiac arrest.3 Patients may present with weakness progress- cient than peritoneal dialysis at removing potassium. ing to flaccid paralysis, paraesthesia, or depressed deep tendon reflexes. Alternatively, the clinical picture can be overshadowed Severe elevation (≥6.5 mmol l−1) without ECG changes. Seek expert by the primary illness causing hyperkalaemia. The first indicator help and: of hyperkalaemia may also be the presence of ECG abnormali- ties, arrhythmias, cardiopulmonary arrest or sudden death. The • Use multiple shifting agents. effect of hyperkalaemia on the ECG depends on the absolute serum • Glucose/insulin (see above). potassium as well as the rate of increase. Most patients will have • Salbutamol 5 mg nebulised. Several doses (10–20 mg) may be ECG abnormalities at a serum potassium concentration higher than required (onset in 15–30 min). − 6.7 mmol l 1.4 The use of a blood gas analyser that measures potas- • Sodium bicarbonate: 50 mmol IV over 5 min if metabolic acidosis sium can reduce delay in recognition. present (onset in 15–30 min). Bicarbonate alone is less effective The ECG changes associated with hyperkalaemia are usually than glucose plus insulin or nebulised salbutamol; it is best used progressive and include: in conjunction with these medications.7,8 • Use removal strategies above. • first degree heart block (prolonged PR interval) [>0.2 s]; − • flattened or absent P waves; Severe elevation (≥6.5 mmol l 1) WITH toxic ECG changes. Seek • tall, peaked (tented) T waves [T wave larger than R wave in more expert help and: than 1 lead]; • ST-segment depression; • Protect the heart first with calcium chloride: 10 ml 10% calcium • S and