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Resuscitation from transfusion-associated hyperkalaemic ventricular fibrillation.


Evidence to guide resuscitation from transfusion-related hyperkalaemic ventricular fibrillation is sparse. This case report describes a 29 kg patient undergoing scoliosis surgery who developed hyperkalaemic ventricular tachycardia/fibrillation following the replacement of over two blood volumes with banked blood in 90 minutes. Rapid reversion to sinus rhythm followed administration of 1.4 mmol of calcium chloride and two units of insulin (Actrapid, Novo Nordisk). The relevant literature is reviewed, indicating that an elevated serum ionised calcium level protects against hyperkalaemia, by an intracellular mechanism. Evidence supports the use of lignocaine, but not amiodarone, as additional treatment.

Key Words: massive transfusion, hyperkalaemia, calcium, resuscitation


Clinically significant hyperkalaemia is reported to be rare with blood transfusion and requires administration of at least 120 ml/min (in an adult) (1). A study of rapid blood transfusion found only transient and mild hyperkalaemia (average serum potassium level: 5.2[+ or -]0.3 mmol/1) and no serious arrhythmia (2). Hyperkalaemic ventricular fibrillation has been reported in association with massive transfusion of irradiated blood (3). Irradiated blood has an increased rate of rise of potassium level during further storage. A recent Cochrane review of emergency interventions for hyperkalaemia found no study addressing clinically relevant hyperkalaemia nor any reporting clinically important outcomes such as mortality or cardiac arrhythmias (4). Salbutamol, nebulised or inhaled, and intravenous (IV) insulin-and-glucose were found to be first-line therapies supported by the evidence, with a "wealth of anecdotal and animal data" suggesting that calcium is effective in treating arrhythmias associated with hyperkalemia. There are few case reports of successful resuscitation from transfusion-associated hyperkalaemia causing ventricular fibrillation.


A 16-year-old male was scheduled for elective correction of severe scoliosis, involving a thoracotomy and anterior spinal release, and a posterior instrumented spinal fusion. He suffered from severe cerebral palsy, probably due to intrauterine cytomegalovirus infection, and weighed 29.6 kg. The indication for operation was severe pain on sitting, caused by his costal margin impinging on his iliac crest. Previous general anaesthesia for tenotomies of hands and relocation of a submandibular duct to prevent drooling were uneventful. After the salivary duct relocation, exploration of a haematoma was necessary, but a discrete bleeding vessel was identified and routine coagulation tests were normal. His current medications were carbemazipine 400 mg morning, 300 mg nightly, diazepam 10 mg nightly, baclofen 20 mg twice a day, omeprazole 20 mg daily and alendronate 70 mg every two weeks. He had become agitated on hyoscine administration, but had no other adverse reaction to drugs. The preoperative haemoglobin level was 148 g/l.

Induction was at 0900 h and maintenance was with nitrous oxide/oxygen, a propofol infusion with a target plasma concentration of 4-6 microgram/ml and an atracurium infusion, with supplementary fentanyl boluses. Blood pressure was monitored with a 22-gauge catheter in a radial artery. Temperature was maintained with a forced-air warming blanket. The thoracotomy and anterior spinal release was uneventful and the patient was repositioned prone at 1500h for the posterior fusion. Between 1500 and 1700h sodium nitroprusside was infused at a rate of 1400 [micro]g/h, reducing to 800 and then 400 [micro]g/h (approximately 0.8-0.2 [micro]g/kg/min) to maintain the mean blood pressure between 50 and 60 mmHg. At 1615h there was 250 ml of blood in the cell-saver reservoir and this was washed and re-infused. Other intravenous fluids to this time had been two litres of Hartmann's solution and 1.5 litres of succinylated gelatin (Gelofusine; B Braun, Bella Vista, N.S.W).

During processing of the blood, the disposable set in the cell-saver separated at the top of the centrifuge, flooding the machine's electronics with blood. A technician was called to clean it and collection continued in the interim. At 1730h, 60 mg phenytoin was given IV as the patient would not be able to take oral carbamazepine postoperatively.

Following decortication of the spinous processes and laminae in preparation for instrumentation, bleeding increased greatly, requiring nine units of packed cells up to 1800h to maintain blood pressure. By this time the technician had arrived and was attempting to clean the inside of the cell saver, and the surgeon had placed a number of sublaminar wires. These had not yet been secured around the rods and projected approximately 15 cm out of the wound. The patient then developed a coarse ventricular tachycardia (VT), with a blood pressure of 60 to 65 mmHg. A bolus of 200 mg (1.4 mmol) Ca[Cl.sub.2] was immediately injected into the intravenous line which did not have blood running, ventilation was changed to 100% oxygen, help was sent for and two units of IV Actrapid insulin were given as a bolus. Dextrose 5% 500 ml was commenced and 150 mg amiodarone given. The blood pressure decreased over several minutes and the rhythm deteriorated towards ventricular fibrillation. However, just as cardiac output was being lost, the patient suddenly reverted to sinus rhythm with a rate of 65 bpm and a systolic blood pressure of 80 mmHg. Blood was sent for biochemical analysis. Coarse VT developed again about two minutes later and again reverted to sinus rhythm with a further 200 mg Ca[Cl.sub.2] and two units of insulin. Table 1 shows the blood biochemistry results immediately following the cardiac arrest and 22 minutes later. When the results were obtained, 100 mEq sodium bicarbonate was given and NaCl 0.9% commenced intravenously.

The systolic blood pressure remained around 80 mmHg for the rest of the case. Four units of platelets and two units of fresh frozen plasma (FFP) were given and 8 [micro]g desmopressin.

The operation was completed satisfactorily and the patient transferred ventilated to ICU at 1915h with a systolic blood pressure of 100 mmHg. At the end of the operation there were 2200 ml of blood in the cell saver and this was discarded as the machine was still non-functional.

Postoperatively, three units of FFP, two units of albumin and one unit of packed cells were given overnight. Further recovery was uneventful and the patient was extubated and returned to the ward on day two.


Use of a cell saver, for washing both banked units and salvaged blood, avoids infusing a potassium load with large blood transfusions, although late hypekaaemia is likely (5). Even when blood is not washed, arrhythmias due to hyperkalaemia are rare. In a study of hyperkalaemia in association with rapid blood transfusion in children during resuscitation from cardiac arrest, no child required specific treatment for hyperkalaemia. The authors concluded that once an effective circulation was established, the potassium-rich blood in the central compartment was circulated and the potassium distributed within total body water (6).

Experiments in isolated rat hearts indicate that increasing the ionised calcium concentrate to 2.7 mmol/l protects against most of the adverse effects of raising perfusate potassium concentration to as high as 11.8 mmol/1. This protection is prevented by the presence of verapamil, indicating that calcium acts intracellularly to block the electrocardiographic effects of hyperkalaemia (7). Experiments in rats suggest that pretreatment with calcium would not be effective. In this study, rats anaesthetised with halothane were pretreated with 15 mg/kg of calcium chloride, which was considered to be the maximum clinically acceptable dose, and subjected to an infusion of potassium chloride to raise serum potassium to about 10 mmol/1. The time to circulatory collapse and serum potassium when arrhythmias appeared were not increased by calcium pretreatment, but the serum calcium levels remained the same in both groups. This reflects the tight control of the ionised calcium level in plasma by the three main calciotropic hormones: parathyroid hormone, calcitriol and calcitonin (9). While restoring the ionised calcium level to normal would probably be beneficial and readily achievable, prophylactically raising the level above normal to achieve protection against hyperkalaemia seems impractical.

The Australian Advanced Paediatric Life Support Guidelines recommend 15 mg/kg of calcium chloride as an appropriate dose for treatment of hyperkalaemia. A relatively small dose was chosen initially on this occasion as the injection was a rapid bolus in the hope of achieving a rapid effect. The two doses in total approximate the recommendation. In this patient, 1.4 mmol calcium chloride would be expected to raise the plasma ionised calcium level acutely by approximately 1 mol/l assuming a haematocrit of 30%. Extravasation of calcium-containing solutions must be avoided as significant tissue necrosis is likely (10).

The hypogalcaemia seen in this case was probably caused by dilution and did not appear to have any direct clinical adverse effects. Life-threatening complications can be expected at ionised calcium levels below 0.5 mmol/l (9). The Australian Blood Bank uses 1660 mg sodium citrate dihydrate in the anticoagulant for each 450 ml of whole blood collected (11). Little of this citrate remains in the final presentation of packed red cells, as the whole blood is centrifuged and the red cells are then separated from the plasma and suspended in 100 ml of a solution which contains sodium chloride, mannitol, adenine and 900 mg dextrose monohydrate. The plasma portion produced by centrifugation retains most of the citrate.

The patient had been taking alendronate, a member of the biphosphonate group of drugs, to treat osteoporosis. These drugs have complex actions, but a direct effect on mature osteoclasts to prevent bone mobilisation appears to be their major route of action (12). Only about 1% of the body's calcium stores are immediately available and there is little information about the details of the dynamics of this pool. It has been shown that recovery of serum calcium concentrations following an acute lowering with edetate calcium disodium (EDTA) is unaffected in patients taking pamidronate (a bisphosphonate similar to alendronate) chronically for osteoporosis (13). It is therefore unlikely that alendronate contributed to the calcium disturbance and arrhythmias seen in this case.

The nine units of packed cells infused contained 5.4g of dextrose. This does not account for the hyperglycaemia seen, which was probably caused by the stress response to the surgery. Even if the hyperglycaemia had been due to an exogenous glucose load, with concomitant endogenous insulin production, this would not be expected to decrease the serum potassium level (14). It is notable that, in normal individuals, the average decrease in serum potassium following a bolus of insulin of 0.15 units/kg is only 0.4 mmol/l (from 4 mmol/l to 3.6 mmol/1) after 15 minutes (15). Both hyper- and hypoglycaemia are detrimental to neurological outcomes after cerebral hypoxia and cardiac arrest. We elected to give dextrose with the insulin initially until the blood glucose level was confirmed.

Sodium bicarbonate was given when the pH was found to be low. Current Advanced Life Support Guidelines state that bicarbonate may be considered to treat pre-existing metabolic acidosis, but it is not recommended for resuscitation from cardiac arrest and the Cochrane review found equivocal evidence to support bicarbonate use in hyperkalaemia.

Salbutamol lowers serum potassium, but the effect does not occur for three to five minutes and is preceded by a small rise. This small rise could provoke arrhythmias and has caused the role of salbutamol as a first treatment to be questioned (16). Amiodarone was given in this case. Amiodarone's antiarrhythmic action is probably blocked by hyperkalaemia (17), so it is not suggested for use in arrhythmias associated with hyperkalaemia.

Thirty minutes prior to developing VT, the patient had received 60 mg phenytoin IV Phenytoin has effects on both sodium and potassium channels. It has a similar effect to the class lb antiarrhythmic drug lignocaine on voltage-gated sodium channels (18). Lignocaine protected anaesthetised dogs from ventricular fibrillation during infusion of potassium chloride into the left anterior descending coronary artery (19) and there is a report of a case in which ventricular tachycardia due to transfusion-associated hyperkalaemia reverted following administration of lignocaine (20). Phenytoin also inhibits the cardiac rapid rectifier potassium ion current channel expressed by the human ether-a-go-go related gene (21), resulting in acquired long QT syndrome. Hypokalaemia is one factor which can precipitate ventricular tachycardia with long QT syndrome (22), but hyperkalaemia would be expected to be protective. Overall the presence of phenytoin was probably neutral or beneficial in terms of arrhythmia control.

When VT developed, the surgeons commenced tightening the sublaminar wires as quickly as possible in case cardiac compression became necessary. Effective cardiac compression in the prone position is possible. In a similar situation a successful outcome was achieved after 15 minutes of cardiac massage (3). In the case described in this report, the presence of unsecured sublaminar wires and an open wound containing foreign material would have introduced major morbidity if cardiac compression had become necessary.

In conclusion, rapid injection of calcium chloride along with insulin rapidly reversed ventricular tachycardia/fibrillation caused by hyperkalaemia. There is evidence to support the use of lignocaine in this clinical scenario, while amiodarone is probably ineffective in the presence of hyperkalaemia.

Accepted for publication on October 14, 2006.


(1.) Miller RD. Transfusion therapy. In: Miller RD, ed. Anesthesia, 5th Ed. Churchill Livingston, Philadelphia 2000; 1626-1627.

(2.) Linko K, Saxelin I. Electrolyte and acid-base disturbances caused by blood transfusions. Acta Anaesthesiol Scand 1986; 30:139-144.

(3.) Buntain SG, Pabari M. Massive transfusion and hyperkalaemic cardiac arrest in craniofacial surgery in a child. Anaesth Intensive Care 1999; 27:530-533.

(4.) Mahoney BA, Smith WA, Lo DS, Tsoi K, Tonelli M, Clase CM. Emergency interventions for hyperkalaemia. Cochrane Review 2005.

(5.) Board J. Hyperkalaemia and massive transfusion. Anaesth Intensive Care 2000; 28:111.

(6.) Brown Karen A, Bissonnette B, Me Intyre B. Hyperkalaemia during rapid blood transfusion and hypovolaemic cardiac arrest in children. Can J Anaesth 1990; 37:747-754.

(7.) Bisogno JL, Langley A, Von Dreele MM. Effect of calcium to reverse the electrocardiographic effects of hyperkalaemia in the isolated rat heart: a prospective, dose-response study. Crit Care Med 1994; 22:697-704.

(8.) Hollman MW, Strumper D, Salmons VA, Washington JM, Durieux ME. Effects of calcium and magnesium pretreatment on hyperkalaemic cardiac arrest in rats. Eur J Anaesthesiol 2003; 20:606-611.

(9.) Aguilera M, Vaughan RS. Calcium and the anaesthetist. Anaesthesia 2000; 55:779-790.

(10.) Yosowitz P, Ekland DA, Shaw RC, Parsons RW Peripheral intravenous infiltration necrosis. Ann Surg 1975; 182:553-556.

(11.) Blood Component Information 2005. Australian Blood Bank.

(12.) Rogers MJ. New insights into the molecular mechanisms of action of biphosphonates. Curr Pharm Des 2003; 9:2643-2658.

(13.) Landman JO, Schweitzer DH, Frolich M, Hamdy NA, Papapoulos SE. Recovery of serum calcium concentrations following acute hypogalcemia in patients with osteoporosis on long-term oral therapy with the biphosphonate pamidronate. J Clin Endocrinol Metab 1995; 80:524-528.

(14.) Muto S, Sebata K, Watanabe H, Shoji F, Yamamoto Y, Ohashi M et al. Effect of oral glucose administration on serum potassium concentration in hemodyalysis patients. Am J Kidney Dis 2005;46:697-705.

(15.) Fisher BM, Thomson I, Hepburn DA, Frier BM. Effects of adrenergic blockade on serum potassium changes in response to acute insulin-induced hypoglycemia in nondiabetic humans. Diabetes Care 1991; 14:548-552.

(16.) Mandelberg A, Krupnik Z, Houri S, Smetana S, Gilad E, Matas Z et al. Salbutamol metered-dose inhaler with spacer for hyperkalemia: how fast? How safe? Chest 1999; 115:617-622.

(17.) Akiyama J, Tomizawa T, Umezawa S, Morishima A. Hyperkalemia probably reverses the antiarrhythmic effects of amiodarone: a case report. Jpn Cite J 1999; 63:323-325.

(18.) Ragsdale DS, McPhee JC, Scheuer T, Catterall WA. Common molecular determinants of local anesthetic, antiarrhythmic, and anticonvulsant block of voltage-gated Na+ channels. Proc Natl Acad Sci USA 1996; 93:9270-9275.

(19.) Ettinger PO, Moore RJ, Calabro J, Oldewurtel HA, Regan TJ. Ventricular tachyarrhythmias in regional myocardial hyperkalemia: efficacy of three antiarrhythmic agents. J Electrocardiol 1980; 13:153-157.

(20.) Stoops CM. Acute hyperkalemia associated with massive blood replacement. Anesth Analg 1983; 62:1044-1052.

(21.) Danielsson BR, Lansdell K, Partmore L, Tomson T Phenytoin and phenobarbital inhibit human HERG potassium channels. Epilepsy Res 2003; 55:147-157.

(22.) Viskin S. Long QT syndromes and torsade de pointes. Lancet 1999; 354:1625-1633.


Sydney Children's Hospital, Sydney, New South Wales, Australia

* M.B., B.S., F.A.N.Z.C.A., Visiting Anaesthetist, Anaesthesia Department, Sydney Children's Hospital.

Reprints will not be available.
Arterial blood results immediately after return of sinus rhythm and
22 minutes later

Time 1800 h 1822 h Normal range

pH 7.19 7.42 (7.35-7.43)

[P.sub.a][O.sub.2] (mm Hg) 170 508 (69-116)

[P.sub.a][O.sub.2] (mm Hg) 36.6 34.5 (32-45)

Base excess -13.4 -1.7 (-2-2)

[Na.sup.+] (mmol/l) 131 133 (136-146)

[K.sup.+] (mmol/l) 7.3 4.4 (3.5-5.0)

[C1.sup.-] (mmol/l) 113 116 (98-106)

[Ca.sup.++] (mmol/l) 0.82 0.68 (1.1-1.3)

glucose (mmol/l) 20.9 26.6 (3.9-5.8)

lactate (mmol/l) 5.6 3.2 (0.5-1.6)

Hb (g/l) 181 88 (130-180)
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Article Details
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Title Annotation:Case Report
Author:Woodforth, I.J.
Publication:Anaesthesia and Intensive Care
Article Type:Clinical report
Geographic Code:8AUST
Date:Feb 1, 2007
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