ALTERACIONES DEL POTASIO 2006.pdf

7/29/2019 ALTERACIONES DEL POTASIO 2006.pdf

1/16

Resuscitation (2006) 70, 1025

REVIEW PAPER

Potassium disordersclinical spectrum and

emergency management

Annette V.M. Alfonzo a,, Chris Isles b, Colin Geddes c, Chris Deighan a

a Renal Unit, Glasgow Royal Infirmary, Castle Street, Glasgow G4 0SF, UKb Renal Unit, Dumfries & Galloway Royal Infirmary, Bankend Road, Dumfries DG1 4AP, UKc Renal Unit, Western Infirmary, Dumbarton Road, Glasgow G11 6NT, UK

Received 12 August 2005 ; received in revised form 28 October 2005; accepted 3 November 2005

KEYWORDS

Hyperkalaemia;

Hypokalaemia;

Renal failure;

Dialysis;

Arrhythmias;

Cardiac arrest

Summary Potassium disorders are common and may precipitate cardiac arrhyth-mias or cardiopulmonary arrest. They are an anticipated complication in patientswith renal failure, but may also occur in patients with no previous history of renaldisease. They have a broad clinical spectrum of presentation and this paper willhighlight the life-threatening arrhythmias associated with both hyperkalaemia andhypokalaemia. Although the medical literature to date has provided a foundationfor the therapeutic options available, this has not translated into consistent medicalpractice. Treatment algorithms have undoubtedly been useful in the managementof other medical emergencies such as cardiac arrest and acute asthma. Hence, we

have applied this strategy to the treatment of hyperkalaemia and hypokalaemiawhich may prove valuable in clinical practice. 2005 Elsevier Ireland Ltd. All rights reserved.

Contents

Introduction.................................................................................................. 11Hyperkalaemia............................................................................................... 11

Clinical spectrum of presentation of hyperkalaemia ... ... .... ... ... .... ... ... .... ... ... ... .... ... ... .... 12Symptoms......................................................................................... 12ECG abnormalities........ ....... ...... ....... ....... ...... ....... ....... ...... ....... ...... ....... 12Arrhythmias associated with hyperkalaemia .... ... ... .... ... ... .... ... ... .... ... ... .... ... ... ... .. 14

Pseudohyperkalaemia ....... ....... ...... ....... ...... ....... ....... ...... ....... ....... ...... ....... ... 15Emergency treatment of hyperkalaemia ...... ....... ...... ....... ....... ...... ....... ....... ...... ...... 15

Abbreviations: K, potassium; ARF, acute renal failure; CRF, chronic renal failure; ESRF, end-stage renal failure A Spanish translated version of the summary of this article appears as Appendix in the online version at

10.1016/j.resuscitation.2005.11.002. Corresponding author. Tel.: +44 141 211 4842; fax: +44 141 211 4843.

E-mail address: [email protected] (A.V.M. Alfonzo).

0300-9572/$ see front matter 2005 Elsevier Ireland Ltd. All rights reserved.doi:10.1016/j.resuscitation.2005.11.002
http://dx.doi.org/10.1016/j.resuscitation.2005.11.002mailto:[email protected]://localhost/var/www/apps/conversion/tmp/scratch_2/dx.doi.org/10.1016/j.resuscitation.2005.11.002http://localhost/var/www/apps/conversion/tmp/scratch_2/dx.doi.org/10.1016/j.resuscitation.2005.11.002mailto:[email protected]://dx.doi.org/10.1016/j.resuscitation.2005.11.002


2/16

Potassium disordersclinical spectrum and emergency management 11

Protecting the heart....... ....... ...... ....... ....... ...... ....... ...... ....... ....... ...... ...... 16Shifting of potassium into cells....... ....... ....... ...... ....... ....... ...... ....... ...... ....... . 16Removing potassium from the body......... ...... ....... ...... ....... ....... ...... ....... ....... .. 17

Influence of degree of renal impairment on management.. ... .... ... ... .... ... ... ... .... ... ... .... ... ... 17Interventions in cardiopulmonary arrest... ....... ...... ....... ....... ...... ....... ...... ....... ....... .. 18

Haemodialysis during resuscitation..... ....... ...... ....... ....... ...... ....... ...... ....... ...... 18Post-resuscitation care..... ....... ....... ...... ....... ....... ...... ....... ....... ...... ....... .... 18

Development of an emergency treatment algorithm .... ... ... .... ... ... .... ... ... .... ... ... .... ... ... ... 19

Acute severe hyperkalaemia ...... ....... ....... ...... ....... ...... ....... ....... ...... ....... .... 20Life-threatening hyperkalaemia ...... ....... ....... ...... ....... ....... ...... ....... ...... ....... . 20Cardiac arrest..................................................................................... 20Principles of treatment algorithm ....... ....... ...... ....... ....... ...... ....... ....... ...... ..... 20

Prevention of hyperkalaemia ...... ....... ....... ...... ....... ....... ...... ....... ...... ....... ....... ... 20Hypokalaemia................................................................................................ 20

Clinical spectrum of hypokalaemia ...... ....... ....... ...... ....... ...... ....... ....... ...... ....... .... 21Symptoms......................................................................................... 21ECG abnormalities........ ....... ....... ...... ....... ...... ....... ....... ...... ....... ....... ...... 21Arrhythmias associated with hypokalaemia... .... ... ... .... ... ... .... ... ... .... ... ... ... .... ... ... 21

Treatment of hypokalaemia........... ....... ...... ....... ....... ...... ....... ....... ...... ....... ....... 22Developing a treatment algorithm for hypokalaemia.... .... ... ... ... .... ... ... .... ... ... .... ... ... .... .. 22

Patients with no symptoms....... ....... ...... ....... ...... ....... ....... ...... ....... ....... ..... 22Life-threatening arrhythmias... ...... ....... ....... ...... ....... ....... ...... ....... ....... ...... . 22

Cardiac arrest..................................................................................... 22Prevention of hypokalaemia ....... ...... ....... ....... ...... ....... ....... ...... ....... ....... ...... .... 22

Summary..................................................................................................... 24Conflict of interest........ ....... ...... ....... ...... ....... ....... ...... ....... ....... ...... ....... ....... ... 24Acknowledgement........ ....... ...... ....... ....... ...... ....... ...... ....... ....... ...... ....... ....... .... 24References................................................................................................... 24

Introduction

Potassium (K) is the most abundant cation in thebody. Under normal circumstances, only 2% of totalbody potassium stores are found in the extracellularspace and serum potassium concentration is tightlyregulated between 3.5 and 5.0 mmol/l.1 Therefore,there is normally a large potassium concentrationgradient between intracellular and extracellularfluid compartments and it is the magnitude of thepotassium gradient across cell membranes that con-tributes to the excitability of nerve and musclecells, including the myocardium.2

Potassium homeostasis is largely regulated bythe kidney accounting for excretion of 90% of daily

potassium loss.1 Therefore patients with renal fail-ure, acute or chronic, who have impaired regulatorymechanisms are prone to hyperkalaemia. Patientswith normal renal function eliminate only 510%of their daily potassium load through the gut.However, in patients with end-stage renal failure(ESRF), gut elimination is increased and accountsfor up to 25% of daily potassium elimination.3

Potassium disorders are common in clinical prac-tice and may be life-threatening. Before approach-ing the treatment of these conditions, it is impor-

tant to understand the basis of potassium home-ostasis and to recognise that these disorders maypresent with a diverse clinical spectrum includingsymptoms, ECG abnormalities and/or arrhythmias.There remains little consistency in treatment ofhyperkalaemia and hypokalaemia, therefore treat-ment algorithms have been developed to assistemergency management.

Hyperkalaemia

Hyperkalaemia is the most common electrolyte dis-order associated with potentially life-threateningarrhythmias and cardiopulmonary arrest. It is

defined as a serum potassium concentration above5.0 mmol/l2 and may be classified as mild (K5.05.9 mmol/l), moderate (K 6.06.4 mmol/l) orsevere (K6.5 mmol/l). A potassium concentra-tion above 10.0mmol/l is usually fatal unlessemergency treatment is readily instituted, how-ever survival with extreme hyperkalaemia (K14 mmol/l) has been reported.4 There are a num-ber of potential causes of hyperkalaemia whichare listed in Table 1, but most commonly itis the result of impaired excretion by the kid-


3/16

12 A.V.M. Alfonzo et al.

Table 1 Causes of Hyperkalaemia

Drugs ACE-inhibitors e.g. ramipril, captoprilAngiotensin Receptor Blockers e.g. losartanNSAIDs e.g. ibuprofen, diclofenacBeta-blockers e.g. atenololK+ supplements e.g. oral or IV replacementK+ sparing diuretics e.g. spironolactone

Antibiotics e.g. trimethoprimAnaesthetic agents e.g. suxamethonium

Renal and metabolic diseases Acute renal failureChronic renal failureType 4 renal tubular acidosisMetabolic acidosis

Diet Foods with high potassium contentFasting relative lack of insulinSalt substitute Lo salt

Endocrine disorders Addisons DiseaseHyporeninaemiaInsulin deficiency/Hyperglycaemia

Haematological disorder/Massive Cell Death Tumour lysis syndromeRhabdomyolysisMassive blood transfusionMassive haemolysis mechanical cell damage

Others Hyperkalaemic periodic paralysisPseudo-hyperkalaemia

Abnormal erythrocytesThrombocytosisLeucocytosis

ACE: angiotensin converting enzyme; K+: potassium; NSAIDs: non-steroidal anti-inflammatory drugs; IV: intravenous.

neys or increased release of potassium fromcells.2

Clinical spectrum of presentation ofhyperkalaemia

Symptoms

Patients may present with weakness progressing toflaccid paralysis, paraesthesia, depressed deep ten-don reflexes or respiratory difficulties.13 However,these symptoms usually only occur in severe cases,are not specific to hyperkalaemia and are oftenover-shadowed by the primary illness precipitating

hyperkalaemia. On the other hand, the absence ofthese symptoms should not lead to a false sense ofsecurity if the clinical history suggests a high riskof an electrolyte disturbance. In any event, moreinformation is required to guide medical manage-ment and the most useful tests are serum biochem-istry and ECG.

ECG abnormalities

The first indicator of hyperkalaemia may bethe presence of ECG abnormalities, arrhythmias,

or cardiac arrest. The effect of hyperkalaemiaon the ECG depends on the absolute serumpotassium as well as the rate of increase.3,5,6

There is great variability in the level of serumpotassium which results in ECG changes, butmost patients appear to show ECG abnormalitiesat a serum potassium level above 6.7 mmol/l.3

In rare instances, the ECG may be normaleven in extreme hyperkalaemia and this shouldraise the possibility of pseudo-hyperkalaemia.7,8

In the context of diabetic ketoacidosis, hyper-kalaemia may also present with ECG changessuggestive of myocardial ischaemia or pseudo-

infarction.9 The presence of other metabolic dis-turbances, such as hypocalcaemia, hyponatraemia,and acidaemia, may exacerbate the effects ofhyperkalaemia.3

Cardiac sensitivity to hyperkalaemia is maxi-mal in the atrium, and later in decreasing order,the ventricular cells, His cells, sinoatrial node andinter-atrial tracts.10 This may help to explain theprogressive changes seen in the ECG with increas-ing severity of hyperkalaemia (Table 2). As serumpotassium rises above 5.56.5 mmol/l, tall peaked


4/16


Table 2 ECG changes associated with the severity of hyperkalaemia

There is some degree of overlap of ECG features in hyperkalaemia. As serum potassium rises above 7 mmol/l, more than oneabnormality may be present. The risk of cardiac arrest increases with rising serum potassium and the presence of ominous ECGsigns indicated above.

Figure 1 Life-threatening ECG changes in hyperkalaemia. (a) Illustrates tented T waves, loss of P waves and a wideQRS complex in a patient presenting with paralysis and acute renal failure (serum K 9.3 mmol/l). (b) Illustrates a sine-wave pattern in a patient with acute renal failure and digoxin toxicity (serum K 9.3 mmol/l). (c) Illustrates a severebradycardia at a rate of 28 beats/min in a haemodialysis patient presenting with syncope (serum K 8.1mmol/l). (d) Illus-trates ventricular tachycardia in a haemodialysis patient presenting with generalised weakness (serum K 9.1 mmol/l).The paper speed is 25 mm/s.


5/16


T waves may appear. However, only 20% of hyper-kalaemic patients show the classical symmetricallynarrow peaked T waves, while the others showlarge amplitude T waves.11 As serum potassiumrises to 6.57.5 mmol/l, the PR interval becomesprolonged and the P wave becomes flattened andeventually lost. This is followed by prolongation of

the QRS complex when serum potassium rises to7.08.0 mmol/l. In severe hyperkalaemia, many ofthese features may occur simultaneously as shownin Figure 1a. Untreated, the QRS complex mergeswith the T wave to form a sine-wave pattern withimpending cardiac arrest (Figure 1b).

The effect of hyperkalaemia on the ECG inpatients with end-stage renal failure is less wellunderstood. Early investigators suggested thatpatients with ESRF have a tolerance to hyper-kalaemia and thereby do not manifest the usualneuromuscular and cardiac features.7,12 Morerecently, it has been postulated that the absence

of typical ECG changes may be partly explainedby changes in serum calcium.6 Nevertheless, theECG remains central to the management of hyper-kalaemia in all patients, including those with renalfailure.

Arrhythmias associated with hyperkalaemia

In addition to the ECG changes, virtually anyarrhythmia or conduction disturbance can occur inthe presence of hyperkalaemia. In some instances,treatment may be delayed as the rhythm distur-bance may not be immediately related to the elec-

trolyte disorder. The following is a review of thespectrum of arrhythmias associated with severehyperkalaemia.Bradycardia. Bradycardia is an ominous complica-tion of hyperkalaemia, but there are few reportsin the literature.1315 Patients presenting witha severe bradycardia in the context of hyper-kalaemia, as shown in Figure 1c, pose several dilem-mas. Firstly, there is no widely available guidancefor the use of calcium salts for bradycardia inducedby hyperkalaemia. As bradycardia is listed as apotential adverse effect of calcium salts, there maybe further reluctance to use calcium salts even in

the context of severe hyperkalaemia. However, theadministration of calcium to patients with AV blockmay avert progression to asystole while potassiumlowering drugs take effect and definitive treatmentis being planned.16

Secondly, the response to atropine is usually poorand a cardiology opinion is often sought. In this sit-uation, it may seem compelling to pace the heartprior to haemodialysis. Indeed there is one report oftemporary pacing for complete heart block inducedby hyperkalaemia (K 7.99 mmol/l), in which pacing

improved the haemodynamic status and appearedto facilitate an uneventful haemodialysis.15 In thiscase report, the ECG returned to normal sinusrhythm after haemodialysis. However, temporarypacing is not without risk, may not be effective anddelays definitive treatment of the underlying dis-order. Furthermore, proceeding with haemodialysis

without pacing may have led to the same outcome,which is often the case in our own clinical experi-ence.

Thirdly, there is some evidence to suggest areduced efficacy of temporary pacing. In severehyperkalaemia, there is elevation of the stimu-lation threshold at the electrode tissue interfaceduring cardiac pacing which can lead to failureof ventricular depolarisation.17 This was evidentin a case report of a post-operative patient whoprogressed to asystole due to hyperkalaemia (K10.2 mmol/l) despite the presence of a function-ing temporary pacemaker inserted at the time of

cardiac surgery.18 Similarly, transvenous pacing wasunsuccessful in a 16-year-old patient with severehyperkalaemia (K 9.8 mmol/l) despite good wireposition on screening.19 In terms of safety, in addi-tion to the usual risks of central venous cannu-lation, temporary pacing may be complicated byarrhythmias as hyperkalaemia increases myocardialexcitability.

Lastly, patients with permanent pacemakersare not protected from the cardiac consequencesof hyperkalaemia. Loss of atrial capture hasbeen reported in patients with dual-chamber pac-

ing devices who become hyperkalaemic.17,20

Itis postulated that the high atrial myocardialsensitivity to hyperkalaemia may be responsi-ble for the atrial unresponsiveness observed dur-ing dual-chamber pacing.17 In another report,hyperkalaemia-induced 2:1 AV block in a patientwith a dual-chamber pacemaker.21 Other mech-anisms by which hyperkalaemia may affect thepaced heart include prolongation of intraventric-ular conduction manifesting as a very wide QRScomplex17,22 and pacemaker latency which is anincrease in the interval between the pacemakerstimulus artefact and the onset of the paced beat.23

Treatment of hyperkalaemia leads to resolution ofconduction abnormalities and narrowing of the QRScomplex.

A universal recommendation is difficult in theface of little evidence, but haemodialysis per-formed without initial ultrafiltration and withappropriate cardiac monitoring, usually resolvesthe bradycardia without the need for cardiac inter-vention. A defibrillator with external pacing facil-ities should be available although this is rarelyneeded. Persistent bradycardia when the serum


6/16


potassium becomes normal requires further inves-tigation and management.Asytole. The outcome of asystolic cardiac arrestdue to hyperkalaemia is usually fatal unless theserum potassium can be returned to normal.One explanation is that severe hyperkalaemiacauses myocardial conductivity and excitability

to decrease eventually, thereby blocking car-diac conduction globally and maintaining cardiacstandstill.10 Despite this, there are several reportsof successful resuscitation in patients present-ing with or developing asystole as a result ofsevere hyperkalaemia.13,18,19,24 Dialysis was neces-sary during the course of cardiopulmonary resusci-tation (CPR) in most of these cases to lower theserum potassium. All of the resuscitation attemptswere prolonged and notably, the only patient man-aged medically without dialysis was reported tomake a spontaneous recovery 8 min after termi-nation of resuscitation.24 This suggests that the

effects of medical therapy may be delayed in thecontext of a cardiac arrest. Hyperkalaemia-inducedasystole is thought to be more common in chronicthan in acute hyperkalaemia,11 however, one ofthe above cases illustrated acute hyperkalaemia (K9.8 mmol/l) induced by suxamethonium in the pres-ence of otherwise normal renal function.19

Ventricular tachycardia. Ventricular tachy-cardia (VT) is a recognised manifestation ofhyperkalaemia,25,26 but it is more commonlyreported in association with hypokalaemia.11 Ithas also been suggested that the presence of a

broad complex tachycardia induced by hyper-kalaemia may be misinterpreted as VT instead ofa sine-wave pattern.24 However, pulseless VT hasbeen documented as the presenting cardiac arrestrhythm4,2729 or may occur during the resuscitationattempt of another primary rhythm19,24,30 in thepresence of hyperkalaemia. VT in the presenceof a cardiac output may also be a manifestationof severe hyperkalaemia in children31 as wellas adults,32 and this is confirmed by our ownobservations as shown in Figure 1d.Ventricular fibrillation. Ventricular fibrillation(VF) is often presented as the natural transi-

tion from a sine-wave pattern in the presenceof extreme hyperkalaemia (K > 8.0 mmol/l).1,3,11,32

However, in another report, ventricular arrhyth-mias or cardiac arrest was said to occur at any timepoint along the transition from peaked T waves tothe sine-wave pattern.6 In reality, a sine-wave pat-tern is a rare phenomenon probably because it givesrise to VF fairly rapidly, although it can also progressto VT or asystole.24 Additionally, the threshold forVF in hyperkalaemic patients is likely to be vari-able and may be influenced by the presence of

other electrolyte disorders. Therefore to pre-emptcardiac arrest, it is important to recognise all warn-ing signs (Table 2), institute treatment early andto be vigilant at all times. Analogous to resuscita-tion for hypothermia, it is important to recognisethat defibrillation is frequently unsuccessful untilthe serum potassium is controlled and CPR should

be prolonged.Pulseless electrical activity (PEA). Any elec-trolyte disorder may present as PEA, includinghyperkalaemia. There are few reports in the liter-ature of successful resuscitation with PEA as thepresenting rhythm of cardiac arrest. In each case,prolonged resuscitation was required.24,33,34

Pseudohyperkalaemia

Pseudohyperkalaemia, also known as spuri-ous hyperkalaemia, is defined as a differencebetween serum and plasma potassium greater

than 0.4mmol/l.35 It should be suspected inpatients with hyperviscosity syndromes such aspolycythemia rubra vera,35 in the absence ofECG changes despite severe hyperkalaemia,7,8

and when sample storage has been prolonged orinadequate.36 Arterial blood sampling is commonpractice in intensive care settings, but rarely pseu-dohyperkalaemia may occur due to malpositionof the arterial cannula resulting in a high shearrate and haemolysis.37 Recognition of pseudo-hyperkalaemia may avoid potentially hazardousmedical intervention, but the rapid detection

and treatment of true hyperkalaemia remains ofparamount importance.

Emergency treatment of hyperkalaemia

There is currently no standardised treatment strat-egy for the emergency management of hyper-kalaemia in clinical practice largely because thereis no agreement on a treatment threshold. This hasresulted in much confusion, over or under treat-ment, late specialist referral and patient deaths.Despite its clinical importance, the first systematicreview of the treatment of hyperkalaemia was pub-

lished only this year.26 To date, management hasbeen recommended on the basis of the severity ofhyperkalaemia and the effect on the ECG, but clearguidelines on the basis of the clinical circumstanceshas been lacking, particularly in the event of car-diac arrest. Before developing a treatment algo-rithm, several factors have been considered includ-ing the evidence for the therapeutic strategies cur-rently available, the influence of the degree ofrenal impairment on management and the approachto resuscitation in the event of cardiac arrest.


7/16


Table 3 Summary of therapeutic agents for the management of hyperkalaemia

Therapy Dose Mechanism Onset (min) Duration (h)

Calcium chloride 10 ml of 10% IV Antagonise 13 0.51Insulin/50% glucose 10 units in 25 g IV Shift 1530 46Salbutamol 0.5 mg IV 20 mg Neb Shift 1530 46Sodium bicarbonate 1 mmol/kg IV Shift 1530 SeveralCalcium resonium 1530 g PO/PR Removes Variable 46

IV: intravenous; Neb: nebulised; PO: oral; PR: per rectum; min: minute.

The drugs available to treat hyperkalaemia havenot changed for several decades and despite exten-sive investigation of their individual and combinedefficacy, their remains much variability in howthese agents are used in clinical practice. In gen-eral, the choice of agents is influenced by theseverity of hyperkalaemia and the presence ofECG changes or concurrent metabolic disturbances.In most instances, more than one agent is oftenrequired for adequate control and some agents(salbutamol and sodium bicarbonate) are not suit-able as monotherapy. A brief summary of the impor-tant drugs used to treat hyperkalaemia is givenbelow and the mechanism of action, rate of onsetand duration of action of these agents are shown inTable 3.

Protecting the heart

Calcium chloride. Although there are no clinicalstudies assessing the efficacy of calcium salts in theemergency management of hyperkalaemia, there

remains little doubt of their importance in emer-gency management even in patients with normalserum calcium. Both calcium salts, calcium chlo-ride and calcium gluconate, antagonise the car-diac membrane excitability and have been widelyrecommended for the treatment and prophylaxisof arrhythmias due to hyperkalaemia when life-threatening ECG changes (absent P waves, wideQRS, sine-wave pattern) are present2426 or whencardiac arrest occurs. Some reports also suggestthe use of calcium salts for isolated peaked Twaves which is an early ECG manifestation ofhyperkalaemia.16,25,38 This approach seems appro-

priate since the transition period from peaked Twaves to broad QRS complex is unknown and islikely to be highly variable from patient to patient.As peaked T waves are a frequently recollected signof hyperkalaemia, it may also prompt earlier recog-nition and treatment.

The decision of which calcium salt should beused, chloride or gluconate, is largely guided bypracticalities such as availability and local practice.Calcium chloride contains more calcium (6.8 mmolin 10ml) than calcium gluconate (2.2 mmol in 10 ml)

and has greater bioavailability, but is more likelyto cause tissue injury if extravasation occurs. Insome institutions, calcium gluconate is the pre-ferred option in a non-arrested patient, but it isimportant to bear in mind that a higher dose maybe necessary to block the toxic effects of hyper-kalaemia on the heart.

Efficacy: calcium chloride and calcium gluconatedo not lower serum potassium.

Cautions: known or suspected digoxin toxicity.Rate of administration should be slower (over30 min) in patients taking digoxin as calcium saltsmay contribute to toxicity.38,39

Adverse effects: bradycardia, arrhythmias, tis-sue necrosis if extravasation occurs.

Shifting of potassium into cells

Insulinglucose therapy. Several studies haveevaluated the efficacy of insulin with glucosefor the treatment of hyperkalaemia.4042 Insulinenhances cellular uptake of potassium by stim-

ulating the sodiumpotassium (NaK) adenosinetriphosphatase (ATP) pump.38 This effect is inde-pendent of its effect on cellular glucose uptake.3

Administration of glucose without insulin is not rec-ommended in non-diabetics as endogenous insulinrelease may be insufficient and paradoxically couldincrease serum potassium further.43 It is importantto note that the potassium lowering effect of insulinis preserved in renal failure, but uraemia attenu-ates the hypoglycaemic response.38

Efficacy: insulin reduces potassium by 0.651mmol/l within 60 min of administration.3,16,38,40

Cautions: regular (soluble) insulin should beused. Adverse effects: hypoglycaemia. This may be

delayed (3060min post-infusion) if less than30 g glucose is given.38

Sodium bicarbonate. Sodium bicarbonatedecreases the concentration of H+ in the extra-cellular fluid compartment which increasesintracellular Na+ via the Na+/H+ exchanger andfacilitates K+ shift into cells via the NaKATPasepump. However, bicarbonate does not lower serum


8/16


potassium in the absence of metabolic acidosis.43

Disappointingly, there is limited evidence for theuse of sodium bicarbonate in the treatment ofhyperkalaemia.3,41,42,44,45

Efficacy: no study has shown an independentpotassium lowering effect within 60 min,26 butwhen used in combination with insulinglucose

or salbutamol, it lowered potassium by0.47 0.31 mmol/l at 30 min.42

Cautions: calcium salts and sodium bicarbonateshould not be administered simultaneously viathe same route to avoid precipitation of calciumcarbonate.

Adverse effects: hypernatraemia; pulmonaryoedema due to large sodium load; tetany inpatients with coexistent hypocalcaemia.

Salbutamol. Beta agonists have been widely stud-ied for the treatment of hyperkalaemia.4051 Salbu-tamol binds to beta-2 receptors stimulating adeny-

lase cyclase which converts ATP to 35 cyclic adeno-sine monophospate. This results in stimulation ofthe NaK ATP pump and intracellular potassiumuptake.38

Efficacy: salbutamol lowers serum potas-sium by 0.871.4 mmol/l after intravenousadministration46,50 and by 0.530.98 mmol/lafter administration in the nebulised form.40

The response is dependent on the dose admin-istered as greater efficacy was reported inpatients receiving 20 mg versus 10 mg of neb-ulised salbutamol.26 It is important to notethat beta-blockers may affect the response totreatment and up to 40% of patients with ESRFdo not respond to salbutamol.3

Cautions: beta-agonists may exacerbate tachy-cardia in patients with tachyarrhythmias.

Adverse effects: tachycardia, tremor, anxietyand flushing.

Removing potassium from the body

Exchange resins. Cation exchange resins arecross-linked polymers with negatively chargedstructural units which exchange calcium (cal-

cium resonium) or sodium (sodium polystyrenesulphonate; Kayexalate) for potassium across theintestinal wall.

Efficacy: resins do not appear to increase faecalpotassium excretion above the effect of induc-tion of diarrhoea with laxatives.52,53 These stud-ies have reported no reduction in serum potas-sium at 4 h.26,53

Cautions: slow acting, therefore unsuitablefor urgent management of hyperkalaemia. Co-administration of laxative is recommended.

Adverse effects: constipation, intestinal necro-sis.

Diuretics. The theoretical basis for the use ofdiuretics in the treatment of hyperkalaemia isto enhance urinary potassium excretion. However,there are no clinical trials to support their use inthe treatment of hyperkalaemia.26

Intravenous fluids. Although there is no clinicaltrial to support fluid replacement,26 it is advisableto administer 0.9% saline intravenously if there isclinical evidence of volume depletion with the aimof improving renal perfusion and enhancing urinarypotassium excretion.Dialysis. Dialysis is the most immediate and reli-able way of removing potassium from the body.The principle mechanism of action is the diffu-sion of potassium across the transmembrane gra-dient. Haemodialysis can remove 2540 mmol/h ofpotassium54 and is more effective than peritoneal

dialysis. The typical decline in serum potassium is1 mmol/l in the first 60 min, followed by 1 mmol/lover next 2h.3 The efficacy of haemodialysis inlowering serum potassium can be improved by per-forming dialysis with a low potassium concentrationin the dialysate,55 a high blood flow rate56 or a highdialysate bicarbonate concentration.57

Influence of degree of renal impairment onmanagement

Hyperkalaemia may occur in the context of acute

(ARF), chronic (CRF) or end-stage renal failure(ESRF). The aetiology may vary depending on thedegree of renal impairment. Drugs are the mostcommon cause of hyperkalaemia in ARF and CRF.In patients with severe CRF (GFR < 30 ml/min) orESRF, additional factors including dietary potassiumintake become important. Non-compliance with thehaemodialysis schedule can also result in lethalhyperkalaemia. Hyperkalaemia has been reportedto be the indication for emergency dialysis 24% ofthe time in patients on maintenance haemodialysisin one centre.58

The clinical sequelae of hyperkalaemia may

be influenced by the rate of onset of hyper-kalaemia and the frequency of its occurrence. InARF, hyperkalaemia often develops rapidly and isusually poorly tolerated, therefore prompt aggres-sive treatment is warranted. It has been suggestedthat the slower onset of hyperkalaemia in CRFis better tolerated and ECG signs may be absentdespite a serum potassium of 7.07.5 mmol/l.24

A relative tolerance to hyperkalaemia has alsobeen postulated in patients with ESRF who expe-rience frequent mild hyperkalaemia,12 however


9/16


there remains little evidence to support this the-ory as 35% of deaths in dialysis patients maybe attributable to hyperkalaemia.59 Therefore, theeffects of hyperkalaemia should not be underesti-mated in patients with advanced renal impairment.

Most studies investigating the therapeuticeffects of pharmacological agents for the treat-

ment of hyperkalaemia have been performedin patients with ESRF as this model provides asignificant cohort of patients with mild hyper-kalaemia who pass little urine, thereby makinginterpretation of treatment efficacy much easier.26

The therapeutic options are the same irrespectiveof the nature and severity of the underlying renaldisease. However in ESRF, sodium bicarbonate hasbeen found to be less effective,3,26 and medicalmeasures only provide temporary relief until dial-ysis can be initiated. Overall, the main differencein approach to treatment may be the urgency forcorrection of serum potassium of mild-moderate

severity, but prompt treatment is warranted forsevere hyperkalaemia irrespective of the degreeof renal impairment.

Interventions in cardiopulmonary arrest

The focus so far has been averting cardiac arrestwith prompt treatment of hyperkalaemia. However,cardiac arrest may occur if treatment of knownhyperkalaemia has been sub-optimal or ineffective.In other cases, hyperkalaemia is discovered onlyafter the resuscitation is underway. When hyper-

kalaemia is suspected to be the primary precipitantof cardiac arrest, resuscitation should not be termi-nated until serum potassium is controlled, by anymeans necessary, unless there are extenuating cir-cumstances. Hyperkalaemia may also arise duringthe resuscitation attempt as a result of metabolicchanges and hypoxia but does not usually requirespecific intervention.39

During CPR, adrenaline (epinephrine) should bethe first drug to be administered irrespective of thecause of cardiac arrest. Adrenaline is a powerfulsympathomimetic amine with both alpha- and beta-adrenergic activity which helps to drive potassium

into cells, thereby lowering serum potassium.24Next, calcium chloride should be administered toantagonise the toxic effects of hyperkalaemia.Sodium bicarbonate should be considered in thecontext of a metabolic acidosis. Insulinglucose isthought to be ineffective during CPR,39 however itis unlikely to cause harm and should begin to haveeffect with minutes of return of spontaneous circu-lation. There is no literature available on the use ofintravenous salbutamol in this scenario. Optimisingventilation during CPR can avoid compounding aci-

dosis and further extracellular shift of potassium.This approach is summarised in Figure 2.

Haemodialysis during resuscitation

In cardiac arrest, dialysis modalities have beenused effectively for the rewarming of hypother-mic patients, but there is relatively little experi-

ence in its use for hyperkalaemia. It seems ironicthat the indication for which dialysis is intendedis rarely implemented during resuscitation, partic-ularly when medical therapy may be less effec-tive. The hesitancy to initiate dialysis during CPRis largely because technique failure is anticipated.The general perception is that haemodialysis can-not be achieved during CPR as the extracorporealcircuit will clot due to inadequate blood pres-sure. However, there is evidence to suggest thatdialysis can be effective despite reduced circula-tion. With the aid of the blood pump, a bloodflow rate of up to 150 ml/min can be achieved

with external chest compressions at a rate of60/min27 and up to 200 ml/min at a rate of80100/min.28

There are several reports of patients treated suc-cessfully with dialysis during CPR for cardiac arrestsecondary to hyperkalaemia.13,18,19,29,30,60,61,62 Inmany of these reports, resuscitation combinedwith dialysis has been successful even after pro-longed CPR (in excess of 90 min) with no neu-rological sequelae. The dialysis mode used wasdependent on local availability and practice,but success has been reported with haemodial-

ysis, veno-venous haemofiltration or veno-venoushaemodiafiltration,62 and also with peritonealdialysis.19 This growing series of reports over thelast two decades suggests that external cardiaccompression can support adequate blood flow forhaemodialysis. Ultimately, if the blood clots in thecircuit, it would be reasonable to try again asthere is little to lose. Haemodialysis is undoubt-edly the most effective treatment for managinglife-threatening hyperkalaemia.

Post-resuscitation care

If the resuscitation attempt is successful, atten-

tion should turn to maintaining the circulation,performing further investigations, deciding on thetiming for haemodialysis and planning after-care.Insulinglucose may be more effective for persis-tent hyperkalaemia.39 If vascular access for dialysishas not been achieved during resuscitation, thismay now be possible with the return of sponta-neous circulation. Femoral access is usually fast anduncomplicated. Early specialist input will ensurethe preparation of a dialysis machine to avoid fur-ther delay.


10/16


Figure 2 Emergency treatment algorithm for hyperkalaemia in adults.

Development of an emergency treatmentalgorithm

It has been previously noted that there is great vari-ability in treatment of hyperkalaemia from patientto patient even within the same centre, withouta clear rationale.63 This is not an isolated phe-

nomenon and suggests a need for a consistent pro-tocol. The main objectives in designing such a pro-tocol are to provide a level of serum potassium atwhich action should be initiated, to prompt earlyrecording of an ECG to guide management and tooutline a structured approach depending on theclinical setting. Emergency treatment is likely to


11/16


be required for patients with moderate to severehyperkalaemia, therefore the recommended treat-ment threshold of serum potassium has been set at6.0 mmol/l (Figure 2). The ECG features and clinicalcondition of the patient then guide immediate clin-ical decisions. Analogous to acute asthma, we havedefined similar treatment categories which incor-

porate the severity of hyperkalaemia, as reflectedby level of serum potassium, ECG features and theclinical setting.

Acute severe hyperkalaemia

Acute severe hyperkalaemia is defined as a raisedserum potassium in the presence of a normal ECG.As these patients do not show evidence of cardiactoxicity, calcium chloride is not indicated. In thesepatients, the intensity of treatment is guided by thelevel and rate of rise of serum potassium and thelikelihood or re-establishing good urine output.

Life-threatening hyperkalaemiaLife-threatening hyperkalaemia is defined as hyper-kalaemia which is sufficiently severe to cause ECGabnormalities ranging from tented T waves toarrhythmias. The level of serum potassium causingthese abnormalities is highly variable, but is likelyto exceed 6.5 mmol/l. Life-saving treatment shouldbe initiated immediately, even before laboratoryresults are available, in the presence of the ECGchanges outlined in Figure 2.

Cardiac arrest

Patients may suffer cardiac arrest as the initialpresentation or following life-threatening hyper-kalaemia. Standard ALS should be initiated, fol-lowed by the administration of calcium chloride andshifting agents (Figure 2). Haemodialysis should beconsidered if hyperkalaemia is resistant to initialmedical therapy.

Principles of treatment algorithm

The treatment of hyperkalaemia in all of the abovesettings is based on five key principles:

1. Cardiac protection by antagonising the effects

of hyperkalaemia.2. Shifting K+ into cells.3. Removing K+ from the body.4. Monitoring serum K+ for rebound hyperkalaemia.5. Prevention of recurrence of hyperkalaemia.

These steps follow a logical sequence and suc-cessful treatment is also dependent on seekingexpert advice as early as possible. It is important tore-assess the effects of initial treatment by mon-itoring the serum potassium. Rebound is a well-recognised phenomenon, even after haemodialysis,

with 70% of potassium reduction being abolished at6 h after dialysis.3

Prevention of hyperkalaemia

A treatment strategy is incomplete unless pre-ventative measures are taken to avoid develop-

ment or recurrence of hyperkalaemia. Patientswith advanced renal failure are most susceptibleto hyperkalaemia and care should be taken withdrug prescribing and diet in this patient group.Patients with other chronic illnesses including pro-teinuric kidney diseases, cardiac failure, diabetesmellitus and portal hypertension are also suscep-tible to hyperkalaemia. This risk may be com-pounded by the presence of even mild renal fail-ure in association with other co-morbidity. How-ever, medicines which may increase serum potas-sium levels such as ACE inhibitors, angiotensin II

antagonists, NSAIDs, and potassium sparing diuret-ics, especially if combined, are the most commonpreventable cause of hyperkalaemia. Severe hyper-kalaemia was reported in 2% of patients in theRALES study despite multiple exclusion criteria.64

Hyperkalaemia may also occur in the setting ofacute illness in patients taking these agents, espe-cially if there is a degree of volume depletion.

For primary prevention, patients at risk of hyper-kalaemia should have close monitoring of serumbiochemistry and should discontinue drugs knownto potentiate serum potassium during acute illness.Patients with severe renal failure, acute or chronic,

should receive specialist attention as early as pos-sible. For secondary prevention after initial treat-ment of hyperkalaemia, it is important to monitorelectrolyte levels and to prevent recurrence of theabnormality by removing any precipitating factors(e.g. drugs).

Hypokalaemia

Low serum potassium is reported to be the mostcommon electrolyte abnormality in hospitalised

patients.1 There are many causes of hypokalaemiaas shown in Table 4, but drugs and gastrointestinaldisease account for a significant proportion. Potas-sium concentration in the blood is also affectedby the metabolic status of the patient. In thepresence of a metabolic alkalosis, potassium shiftsinto cells. Hypokalaemia can also contribute to themaintenance of a metabolic alkalosis by enhanc-ing bicarbonate absorption and increasing chlorideexcretion in the kidney.1 Hypokalaemia is definedas a serum potassium 3.5 mmol/l.1,2,65,66 It may


12/16


Table 4 Causes of hypokalaemia

Increase potassium lossDrugsdiuretics, laxative abuse, liquorice, steroidsGI lossesdiarrhoea, vomiting, ileostomy, intestinal fistula, villous adenomaRenalrenal tubular disorders, Bartters syndrome, Liddles syndrome, Gitelmans syndrome, nephrogenic

diabetes insipidousEndocrinehyperaldosteronism, Cushings syndrome, Conns syndrome

Dialysishaemodialysis on low potassium dialysate, peritoneal dialysisTranscellular shift

Insulin/glucose therapyBeta-adrenergic stimulatione.g. salbutamolAlkalosisHypokalaemic periodic paralysis

Decreased potassium intakePoor dietary intake (less than 1 g/day)

Magnesium depletion (increases renal potassium loss)Poor dietary intakeIncreased magnesium loss

be classified as mild (K 3.03.5 mmol/l), moderate(K 2.53.0 mmol/l) or severe (K < 2.5 mmol/l) andsymptoms are more likely with increasing severity.

Clinical spectrum of hypokalaemia

Symptoms

Patients with mild hypokalaemia usually have nosymptoms. As serum potassium level falls fur-ther, the nerves and muscles are predominantly

affected causing fatigue, weakness, leg cramps,and constipation. In severe cases, rhabdomyoly-sis, ascending paralysis and respiratory difficultiesmay occur. The probability of symptoms appears tocorrelate with the presence of pre-existing heartdisease (ischaemia, heart failure, left ventricu-lar hypertrophy), and the rapidity of the onset ofhypokalaemia.6567

ECG abnormalities

There are usually no ECG changes in patients withmild hypokalaemia, but these may become evidentin moderate to severe hypokalaemia including the

presence of U waves, T wave flattening, or ST seg-ment changes.2

Arrhythmias associated with hypokalaemia

Severe hypokalaemia predisposes to arrhythmiasand cardiac arrest. In patients treated with digoxin,hypokalaemia of any severity can increase theincidence of arrhythmias.65 Patients with estab-lished digoxin toxicity are particularly at risk. Thefollowing is a review of the common arrhyth-mias associated with hypokalaemia and the effect

of hypokalaemia in patients maintained on anti-arrhythmic agents.Ventricular tachycardia/fibrillation. Hypokalae-mia can predispose to ventricular tachycardia orventricular fibrillation.11 This risk is particularlyhigh following acute myocardial infarction andmaintaining the serum potassium above 3.9 mmol/lmay reduce the risk of early VF.66 The arrhyth-mia may not respond to electrical or chemical car-dioversion until the serum potassium is corrected.

Long QT syndrome and torsade de pointes. Thelong QT syndrome, which may be inherited oracquired, is caused by malfunction of the ion chan-nels responsible for ventricular repolarisation.68

Potassium and/or magnesium depletion are themain metabolic disorders associated with channelmalfunction and hence predispose to arrhythmias.The characteristic arrhythmia seen is torsade depointes which may present as syncope or cardiacarrest. This is recognised as a variant of ventricu-lar tachycardia in which the QRS complexes changeamplitude around the isoelectric line and is fre-quently preceded by pauses.68 The mainstay of

treatment is the correction of hypokalaemia andadministration of magnesium sulphate.Patients taking anti-arrhythmic drugs.

Hypokalaemia may also interfere with the benefi-cial effects of anti-arrhythmic drugs rendering thepatients susceptible to a recurrence of the under-lying arrhythmia.66 In addition, hypokalaemiacan compound the effects of Class III anti-arrhythmic agents such as sotalol predisposing toarrhythmias.66,68 Indeed, torsade de pointes hasbeen reported in 24% of patients treated with


13/16


sotalol and this risk is increased in older patientsand in the presence of renal impairment.68

Although this risk is also dose-dependent, thereare reported cases of torsade de pointes inducedby low doses of sotalol.69

Treatment of hypokalaemia

The treatment approach depends on the severityof hypokalaemia and the presence of symptomsand ECG abnormalities. As a guide to the deficit intotal body potassium, serum potassium decreasesby 0.3 mmol/l on average for every 100 mmol reduc-tion in total body potassium stores, but this isvariable depending on body mass.1,65 Hence, thedeficit can be considerable in moderateseverehypokalaemia and care should be taken duringreplacement. The administration of potassium, par-ticularly by the intravenous route is not without

risk. Gradual replacement of potassium is safer andavoids excessive replacement.Many patients who are potassium deficient are

also deficient in magnesium. Magnesium is impor-tant for potassium uptake and for the maintenanceof intracellular potassium levels, particularly in themyocardium. Combined deficiency may potentiatethe risk of cardiac arrhythmias. Repletion of magne-sium stores will facilitate more rapid correction ofhypokalaemia and is recommended in severe casesof hypokalaemia.66,70

Developing a treatment algorithm forhypokalaemia

A recent report has highlighted the inadequacyof treating this common medical problem.71 Thisreport assessing treatment adequacy showed thathypokalaemia was found in 2.6% of hospitalisationsover a one year period with inadequate manage-ment of hypokalaemia in 24% of these cases. Theseinadequacies included failure to measure serumpotassium subsequently in 6.4% of patients and fail-ure to correct hypokalaemia in 30% of patients priorto discharge. The mortality of the hypokalaemic

population was 10-fold higher than the generalhospitalised population. Hence, it is important todetect, monitor and treat hypokalaemia appropri-ately.

The main considerations in designing an emer-gency treatment algorithm for hypokalaemia areto establish the level of serum potassium whereintravenous replacement is indicated, the rate ofpotassium replacement according to the clinicalsetting and the need for co-administration of mag-nesium. Stable patients with mild hypokalaemia (K

3.03.5 mmol/l) are not included in the treatmentalgorithm as oral potassium replacement is usu-ally sufficient. Expert help should be considered forpatients with hypokalaemia of any severity whichis associated with arrhythmias or cardiac arrest.Continuous ECG monitoring is essential during IVadministration and the dose should be titrated after

repeated sampling of serum potassium levels. Theemergency management of hypokalaemia is sum-marised in Figure 3. Treatment is guided by thedegree of hypokalaemia and the clinical setting.

Patients with no symptoms

In the absence of digoxin toxicity or severe heartdisease, potassium should be gradually replaced ata rate of 10 mmol/h in asymptomatic patients. Mag-nesium replacement is required only if found to bemagnesium deficient.

Life-threatening arrhythmias

In an emergency such as an arrhythmia, intra-venous potassium is required, but the rate of cor-rection of serum potassium causes uncertainty.The maximum recommended intravenous dose ofpotassium is 20 mmol/h, but more rapid adminis-tration (initial infusion of 2 mmol/min for 10 min,followed by 10 mmol over 510 min) is indicatedfor unstable arrhythmias when cardiac arrest isimminent.2 Rapid bolus injection of potassiumshould be avoided in all circumstances as thismay precipitate cardiac arrest. Magnesium shouldbe administrated early after initiating potassium

replacement, even before the serum magnesiumlevel is known.

Cardiac arrest

Cardiac arrest may occur in patients known tobe hypokalaemic. Alternatively, hypokalaemia mayonly be discovered after resuscitation is underway.Although the metabolic status after cardiac arrestusually favours an increase in serum potassium,total body potassium remains low. Prompt correc-tion of hypokalaemia may not only render defibrilla-tion more successful, but may reduce the incidenceof further arrhythmias in the post-arrest period as

the metabolic status of the patient improves andpotassium shifts back into cells.

Prevention of hypokalaemia

Hypokalaemia is frequently iatrogenic and hencepotentially avoidable. For primary prevention,electrolytes should be monitored in patients at risk.In the general population, this includes patientstreated with diuretics and those with high gastro-intestinal losses. For secondary prevention, it


14/16


Figure 3 Emergency treatment algorithm for hypokalaemia in adults.

is important to monitor serum potassium afterinitial treatment and to prevent recurrence ofhypokalaemia by removing any precipitating fac-tors.

Hypokalaemia may also occur in patients withrenal failure requiring renal replacement ther-apy. Non-renal specialists may be unaware of thedegree of potassium flux which occurs with differ-

ent dialysis modalities. Hypokalaemia is a frequentoccurrence in patients receiving peritoneal dialy-sis and potassium supplements are often required.In those receiving haemodialysis, hypokalaemia ismost likely toward the end or immediately after asession. Patients most at risk are those with a lowserum potassium before beginning a dialysis ses-sion, particularly if dialysed against an inappropri-


15/16


ately low potassium dialysate. Therefore, patientswith advanced renal failure are also potentially sus-ceptible to hypokalaemia and it is important to con-sider measures to prevent hypokalaemia in patientsat all levels of renal function.

SummaryPotassium disorders may have life-threatening con-sequences. It is important to recognise that bothhyperkalaemia and hypokalaemia are potentiallyavoidable complications of commonly prescribeddrugs. The clinician should be aware that both maypresent with a range of ECG changes, virtually anyarrhythmia or cardiac arrest. Treatment algorithmsprovide a stratified approach based on biochemical,clinical and pharmacokinetic criteria and may assistclinicians in the immediate care of these commonmedical emergencies.

Conflict of interest

The authors have no conflict of interest in relationto this paper.

Acknowledgement

The authors wish to thank Dr Keith Simpson, direc-tor of the Scottish Renal Registry Group, for his

valuable contributions to the treatment algorithms.

References

1. Rastergar A, Soleimani M. Hypokalaemia and hyperkalaemia.Postgrad Med J 2001;77:75964.

2. Guidelines 2000 for cardiopulmonary resuscitation and emer-gency cardiovascular care: International Consensus on Sci-ence. Part 8: Advanced Challenges in resuscitation: Section1: Life-threatening electrolyte abnormalities. Circulation2000;102:21722.

3. Ahmed J, Weisberg LS. Hyperkalaemia in dialysis patients.Semin Dial 2001;14:34856.

4. Tran HA. Extreme hyperkalaemia. South Med J2005;98:72932.

5. Fisch C. Relation of electrolyte disturbances to cardiacarrhythmia. Circulation 1973;47:40819.

6. Aslam S, Freidman EA, Ifudu O. Electrocardiography isunreliable in detecting potentially lethal hyperkalaemiain haemodialysis patients. Nephrol Dial Transplant2002;17:163942.

7. Szerlip HM, Weiss J, Singer I. Profound hyperkalaemia with-out electrocardiographic manifestations. Am J Kidney Dis1986;7:4615.

8. Bandyopadhyay S, Banerjee S. Severe hyperkalaemia withnormal electrocardiogram. Int J Clin Pract 2001;55:4867.

9. Moulik PK, Nethaji C, Khaleeli AA. Misleading electrocardio-graphic results in patient with hyperkalaemia and diabeticketoacidosis. Br Med J 2002;325:13467.

10. Ettinger PO, Regan TS, Olderwurtel HA. Hyperkalaemia, car-diac conduction, and the electrocardiogram: overview. AmHeart J 1974;88:36071.

11. Slovis C, Jenkins R. Conditions not primarily affecting theheart. Br Med J 2002;324:13204.

12. Frohnert PP, Giuliani ER, Friedberg M, Johnson WJ,

Tauxe WN. Statistical investigation of correlations betweenserum potassium levels and electrocardiographic findings inpatients on intermittent haemodialysis therapy. Circulation1970;41:66776.

13. Costa P, Visetti E, Canavese C. Double simultaneoushaemodialysis during prolonged cardiopulmonary resuscita-tion for hyperkalaemic cardiopulmonary arrest. Case report.Minerva Anaestesiol 1994;60:1434.

14. Walter RB, Bachli EB. Near fatal arrhythmia caused by hyper-kalaemia. Heart 2002;88:578.

15. Kim NH, Oh SK, Jeong JW. Hyperkalaemia induced completeatrioventricular block with a narrow QRS complex. Heart2005;91:e5.

16. Emmett M. Non-dialytic treatment of acute hyperkalaemiain the dialysis patient. Semin Dial 2000;13:27980.

17. Ortega-Carniecer J, Benezet J, Benezet-Mazuecos J. Hyper-kalaemia causing loss of atrial capture and extremelywide QRS complex during DDD pacing. Resuscitation2004;62:11920.

18. Torrecilla C, de la Serna JL. Hyperkalaemic cardiac arrest,prolonged heart massage and simultaneous haemodialysis.Inten Care Med 1989;15:3256.

19. Jackson MA, Lodwick R, Hutchison SG. Lesson of theweek: hyperkalaemic cardiopulmonary arrest successfullytreated with peritoneal dialysis. Br Med J 1996;312:128990.

20. Barold SS. Loss of atrial capture during DDD pacing: whatis the mechanism? Pacing Clin Electrophysiol 1998;21:19889.

21. Luzza F, Carerj S, Oreto G. An unusual hyperkalaemia

induced block. Heart 2001;86:686.22. Tomcsanyi J. J. Extremely wide QRS complex with VVI pac-

ing. Pacing Clin Electrophysiol 2002;25:11289.23. Kistler PM, Mond HG, Vohra JK. Pacemaker ventricular block.

Pacing Clin Electrophysiol 2003;26:19979.24. Quick G, Bastani B. Prolonged asystolic hyperkalaemic car-

diac arrest with no neurological sequelae. Ann Emerg Med1994;24:30511.

25. An advisory statement on conditions which may require mod-ifications in resuscitation procedures or techniques. Pre-pared by Members of the International Liaison Committeeon Resuscitation. Special resuscitation situations. Resuscita-tion 1997;34:12949.

26. Mahoney BA, Smith WAD, Lo DS. Emergency interven-tion for hyperkalaemia. Cochrane Database SystemRev 2005;2(Issue). Art. No.: CD003235.pub2. DOI:10.1002/14651858. CD003235. pub2.

27. Lin JL, Huang CC. Successful initiation of haemodialysisduring cardiopulmonary resuscitation due to lethal hyper-kalaemia. Crit Care Med 1990;18:423.

28. Strivens E, Siddiqi A, Fluck R, Hutton A, Bell D. Hyper-kalaemic cardiac arrest: may occur secondary to mis-use of diuretics and potassium supplements. Br Med J1996;313:693.

29. Kao KC, Huang CC, Tsai YH, et al. Hyperkalaemic cardiopul-monary arrest successfully reversed by haemodialysis dur-ing cardiopulmonary resuscitation: case report. ChanggengYiXue Za Zhi 2000;23:5559.
http://dx.doi.org/10.1002/14651858http://dx.doi.org/10.1002/14651858


16/16


30. Lin JL, Lim PS, Leu ML, et al. Outcomes of severe hyper-kalaemia in cardiopulmonary resuscitation with concomitanthaemodialysis. Intensive Care Med 1994;20:28790.

31. Virdi VS, Bharti B, Poddar B, Saus S, Parmar VR. Ventricu-lar tachycardia in congenital adrenal hyperplasia. AnaesthIntensive Care 2002;30:3802.

32. Grimm W, Alter P, Maisch B. Cardiac arrest due to severehyperkalaemia. Herz 2004;29:353.

33. Lawton JM. Hyperkalaemic electromechanical dissociation.

Wis Med J 1990;89:45961.34. Pang P, Look RB, Brown DFM. Wide complex rhythm and car-

diac arrest. J Emerg Med 2004;26:197200.35. The MM, Zaman MJS, Brooks AP, Li Voon Chong JSW. When

is a high potassium not a high potassium? J Roy Soc Med2003;96:3545.

36. Trull AK, Jackson C, Walsh S, et al. The perennial problemwith potassium. Ann Clin Biochem 2004;41:4752.

37. Mehta V, Ahmed Z. Apparent hyperkalaemia from blood sam-pled from an arterial cannula. Br J Anaesth 2004;93:4568.

38. Ahee PP, Crowe AV. The management of hyperkalaemiain the emergency department. J Accid Emerg Med2000;17:18891.

39. Kloeck W, Cummins RO, Chamberlain D, et al. Specialresuscitation situations: an advisory statement from the

international liaison committee on resuscitation. Circulation1997;95:2196210.

40. Allon M, Copkney C. Albuterol and insulin for treatmentof hyperkalaemia in haemodialysis patients. Kidney Int1990;38:86972.

41. Allon M, Shanklin N. Effect of bicarbonate administrationon plasma potassium in dialysis patients: interactions withinsulin and albuterol. Am J Kidney Dis 1996;28:50814.

42. Ngugi NN, McLigeiyo SO, Kayima JK. Treatment of hyper-kalaemia by altering the transcellular gradient in patientswith renal failure: effect of various therapeutic approaches.East Afr Med J 1997;74:5039.

43. Kamel SK, Wei C. Controversial issues in the treatment ofhyperkalaemia. Nephrol Dial Transplant 2003;18:22158.

44. Blumberg A, Weidman P, Shaw S, Gnadinger M. Effect of

various therapeutic approaches on plasma potassium andmajor regulating factors in terminal renal failure. Am J Med1988;85:50712.

45. Kim HJ. Combined effect of bicarbonate and insulin withglucose in acute therapy of hyperkalaemia in end-stage renaldisease patients. Nephron 1996;72:47682.

46. Lens XM, Montoliu J, Cases A, et al. Treatment of hyper-kalaemia in renal failure: salbutamol v insulin. Nephrol DialTransplant 1989;4:22832.

47. Montoliu J, Almirall J, Ponz E, et al. Treatment of hyper-kalaemia in renal failure with salbutamol inhalation. J InternMed 1990;228:357.

48. Liou HH, Chiang SS, Wu SC, et al. Hypokalaemic effects ofintravenous infusion or nebulisation of salbutamol in patientswith chronic renal failure: comparative study. Am J KidneyDis 1994;23:26671.

49. MandelbergA, Krupnik Z, Houri S, et al. Salbutamol metered-dose inhaler with spacer for hyperkalaemia: how fast? Howsafe? Chest 1999;115:61722.

50. McClure RJ, Prasad VK, Brocklebank JT. Treatment of hyper-kalaemia using intravenous and nebulised salbutamol. ArchDis Child 1994;70:1268.

51. Pancu D, LaFlamme M, Evans E, Reed J. Levalbuterol is aseffective as racemic albuterol in lowering serum potassium.J Emerg Med 2003;25:136.

52. Emmett M, Hootkins RE, Fine KD. Effect of three laxativesand a cation exchange resin on faecal sodium and potassiumexcretion. Gastroenterology 1995;108:75260.

53. Gruy-Kapral C, Emmett M, Santa Ana CA, Porter JL, Ford-tran JS, Fine K. Effect of single dose resin-cathartic ther-apy on serum potassium concentration in patients withend-stage renal failure. J Am Soc Nephrol 1998;10:192430.

54. Defronzo PA, Bia M. Clinical disorders of hyperkalaemia. Ann

Rev Med 1982;33:5212.55. Zehnder C, Gutzwiller JP, Huber A, Schindler C, Schneditz

D. Low-potassium and glucose-free dialysis maintains ureabut enhances potassium removal. Nephrol Dial Transplant2001;16:7884.

56. Gutzwiller JP, Schneditz D, Huber AR, Schindler C, Garbani E,Zehnder CE. Increasing blood flow increases kt/V (urea) andpotassium removal but fails to improve phosphate removal.Clin Nephrol 2003;59:1306.

57. Heguilen RM, Sciurano C, Bellusci AD, et al. The fasterpotassium-lowering effect of high dialysate bicarbonate con-centrations in chronic haemodialysis patients. Nephrol DialTransplant 2005;20:5917.

58. Sacchetti A, Stuccio N, Panebianco P, Torres M. Haemodialy-sis for treatment of renal failure emergencies. Am J Emerg

Med 1999;17:3057.59. Morduchowicz G, Winkler J, Drazne E, et al. Causes of death

in patients with end-stage renal disease treated by dialysisin a centre in Israel. Isr J Med Sci 1992;28:7769.

60. Gomez-Arnau J, Criado A, Martinez MV, et al. Hyperkalaemiccardiopulmonary arrest: prolonged heart massage and simul-taneous haemodialysis. Crit Care Med 1981;9:5567.

61. Josephs W, Lenga P, Odenthal HJ, et al. Rate of successand prognosis of cardiopulmonary resuscitation in patientson maintenance haemodialysis. Intensiv und Notfallmedizin1990;27:2159.

62. Schummer WJ, Schummer C. Hyperkalaemic cardiopul-monary arrest: the method chosen depends on the localcircumstances. Crit Care Med 2002;30:16745.

63. Acker C, Johnson JP, Palevsky PM, Greenberg A. Hyper-

kalaemia in hospitalised patients: causes, adequacy of treat-ment, and results of an attempt to improve physician com-pliance with published therapy guidelines. Arch Intern Med1998;158:91724.

64. The RALES investigators, Effectiveness of spironolactoneadded to an angiotensin-converting enzyme inhibitor and aloop diuretic for severe chronic congestive heart failure. AmJ Cardiol 1996;78:9027.

65. Gennari FJ. Hypokalaemia. New Eng J Med 1998;339:4518.66. Cohn JN, Kowey PR, Whelton PK, et al. New guidelines for

potassium replacement in clinical practice. Arch Intern Med2000;160:242936.

67. Schulman M, Nairns RG. Hypokalaemia and cardiovasculardisease. Am J Cardiol 1990;65:4E9E.

68. Viskin S. Long QT syndromes and torsade de pointes. Lancet1999;354:162533.

69. Tan HH, Hsu LF, Kam RM, Chua T, Teo WS. A case series ofsotalol-induced torsade de pointes in patients with atrialfibrillationa tale with a twist. Ann Acad Med Singapore2003;32:4037.

70. Loughrey CM. Serum magnesium must also be known in pro-found hypokalaemia. Br Med J 2002;324:103940.

71. Paltiel O, Salakhov E, Ronen I. Management of severehypokalaemia in hospitalised patients. Arch Intern Med2001;161:108995.

Documents

ALTERACIONES DEL POTASIO 2006.pdf