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The Journal of Emergency Medicine, Vol. 27, No. 2, pp. 153–160, 2004Copyright © 2004 Elsevier Inc.

Printed in the USA. All rights reserved0736-4679/04 $–see front matter

doi:10.1016/j.jemermed.2004.04.006

Selected Topics:Cardiology Commentary

ELECTROCARDIOGRAPHIC MANIFESTATIONS: ELECTROLYTE ABNORMALITIES

Deborah B. Diercks, MD,* George M. Shumaik, MD,† Richard A. Harrigan, MD,‡ William J. Brady,MD,§ and Theodore C. Chan, MD†

*Department of Emergency Medicine, University of California, Davis Medical Center, Sacramento, California; †Department ofEmergency Medicine, University of California, San Diego Medical Center, San Diego, California; ‡Department of Emergency Medicine,

Temple University Medical Center, Philadelphia, Pennsylvania; and §Department of Emergency Medicine, University of Virginia,Charlottesville, Virginia

Reprint Address: Theodore C. Chan, MD, Department of Emergency Medicine, University of California, San Diego, 200 West ArborDrive #8676, San Diego, CA 92103

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Abstract—Because myocyte depolarization and repolarzation depend on intra- and extracellular shifts in ionradients, abnormal serum electrolyte levels can have pro

ound effects on cardiac conduction and the electrocardioram (EKG). Changes in extracellular potassium, calciumnd magnesium levels can change myocyte membrane p

ential gradients and alter the cardiac action potential.hese changes can result in incidental findings on the 1

ead EKG or precipitate potentially life-threatening dys-hythmias. We will review the major electrocardiographicndings associated with abnormalities of the major cationicontributors to cardiac conduction—potassium, calciumnd magnesium. © 2004 Elsevier Inc.

Keywords—electrolyte abnormality; electrocardio-ram; EKG; dysrhythmias; cardiac conduction; cations;otassium; calcium; magnesium

INTRODUCTION

ardiac electrical activity is mediated by ionic shiftscross cellular membranes. Aberrations in normal elec-rolyte homeostasis are often associated with alterationsn cardiac conduction. These may be limited to clinicallynsignificant changes in the surface electrocardiogramEKG) or result in life-threatening dysrhythmias. Al-

Selected Topics: Cardiology Commentaryis cooDiego Medical Center, San Diego, California andVirginia

153

hough the laboratory is indispensable in making defin-tive diagnoses of fluid, acid-base, and electrolyte distur-ances, the bedside EKG can often provide immediatensight and prompt life-saving care.

The clinical syndromes that create hypo- and hyper-mic concentrations of potassium, calcium and magne-ium are associated with the most common and clinicallymportant disturbances of cardiac rhythm related to elec-rolyte abnormality. Although discussed individually, its important to remember that there is a dynamic phys-ologic interrelationship to electrolyte homeostasis andhat aberration in one “compartment” may have impactn another.

CASE REPORTS

ase 1

34-year-old man presented to the Emergency Depart-ent (ED) complaining of generalized, progressiveeakness and shortness of breath over the past 4 days.he patient’s shortness of breath had progressed fromyspnea on exertion to dyspnea at rest over the sameime. He also complained of lightheadedness, nausea,nd occasional vomiting, but denied chest pain, palpita-ions, or abdominal pain. The patient admitted to recent

d by Theodore Chan, MD, of the University of California Sanm Brady, MD, of the University of Virginia, Charlottesville,

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ethamphetamine use, but denied prior cardiac history,ospitalizations, or surgery.

On physical examination, vital signs were notable forpulse of 152 beats/min, blood pressure of 142/68 mmg, and respiratory rate of 24 breaths/min. Pulse oxim-

try was 95% oxygen saturation on room air. The patientas in moderate distress. His chest examination was

lear to auscultation and cardiac examination was nota-le for a regular tachycardia with a grade 2/6 systolicurmur. The abdomen was soft and nontender, and

eurologic examination was notable for mild diffuseeakness. An EKG was obtained, revealing a wide com-lex tachycardia of unclear etiology (Figure 1). Initialreatment included oxygen, intravenous fluids, and bolusntravenous lidocaine without change. After an arteriallood gas revealed a significant metabolic acidosis (pH.08, pO2 217, pCO2 22), sodium bicarbonate was ad-inistered. A repeat EKG 15 min later demonstrated

lowing of the heart rate, narrowing of the QRS width,nd the presence of “peaked” T waves primarily in therecordial leads consistent with hyperkalemia (Figure). The suspicion of hyperkalemia was confirmed by a

igure 1. Wide complex tachycardia consistent with a “sine-wevel of 8.1 mg/dL.

igure 2. Repeat 12-lead EKG in patient with hyperkalemia

aves most prominent in leads V2–V5.

erum potassium level of 8.1 mEq/L.The patient was diagnosed with metamphetamine-

nduced acute renal failure (creatinine 20.1 mEq/L) andas stabilized with calcium chloride, additional bicar-onate, insulin/glucose therapy, followed by hemodialy-is. A repeat EKG obtained the day after admissionevealed a return to sinus rhythm with normal QRSnterval and resolution of the peaked T-waves (Figure 3).he patient was subsequently discharged in good condi-

ion after a 5-day hospitalization.

ase 2

24-year-old woman with a history of type 1 renalubular acidosis presented to the ED complaining of 2ays of headache, generalized weakness, and diffuseuscle cramping. The patient also noted the onset of

ausea and vomiting over the last day. She denied anyhest pain, palpitations, shortness of breath, respiratoryifficulty, cough, fevers, chills, diarrhea, or urinary com-laints. She had run out of her usual medications, includ-

ppearance on 12-lead EKG in patient with serum potassium

fter initiation of treatment. Note the “tented” symmetric T

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Electrolyte Abnormalities 155

ng potassium supplementation, 4 days prior. Her tem-erature was 36.2°C (97.1°F), pulse 71 beats/min, bloodressure 98/68 mm Hg, and respiratory rate 18 breaths/in. Her examination revealed a well and non-toxic

ppearing young woman in no acute distress. The pul-onary and cardiac examinations were unremarkable.n neurologic examination, she demonstrated intact sen-

ation and motor strength, but had a slow gait.An initial 12-lead EKG was obtained (Figure 4) that

emonstrated a U wave deflection after the T wave, besteen in the precordial leads V3–V6. Serum potassiumas 2.1 mEq/L and the patient was admitted for aggres-

ive intravenous and oral potassium repletion. During therst day of admission, the patient’s serum potassium

evel dropped to as low as 1.9 mEq/L. A repeat EKGemonstrated further flattening of the T wave and in-rease in U wave size such that it masked the end of the

wave and beginning of the P wave (Figure 5). Theatient eventually developed so-called “giant” U wavesearly completely masking the T wave, especially in therecordial leads (Figure 6). With aggressive electrolyteorrection, the patient’s serum potassium normalizedver the next 48 h and the EKG abnormalities resolved.

igure 3. Follow-up 12-lead EKG in patient with hyperkalbnormalities seen in Figure 2.

igure 4. 12-lead EKG in patient with type 1 RTA presentin

recordial leads (particularly lead V4) consistent with the diagnosi

ase 3

55-year-old man with a history of bladder cancerresented to the ED complaining of weakness and con-tipation over the past week. He had recently completedcourse of radiation therapy for his cancer. He denied

alpitations, lightheadedness, chest pain, and shortnessf breath. He complained of mild intermittent abdominalain associated with his diffuse weakness. On examina-ion, his pulse was 98 beats/min, blood pressure 138/72m Hg, respiratory rate 16 breaths/min, and he was

febrile. The chest and cardiac examinations were unre-arkable. The patient had some mild diffuse abdominal

enderness to palpation, but no rebound tenderness oruarding. His neurologic examination revealed mild dif-use weakness, but no other focal findings.

A 12-lead EKG was obtained demonstrating a sinushythm with an abnormally short QT interval (Figure 7).

hen corrected, the QTc interval measured 0.37 s. Se-um electrolyte levels confirmed the diagnosis of hyper-alcemia with a calcium level of 14.7 mg/dL. The pa-ient’s elevated calcium was attributed to his cancer ande was admitted for therapy. He received intravenous

day after treatment. Note the resolution in the T wave

weakness. Note the prominent U wave, best seen in the

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uid hydration, as well as furosemide to increase renalalcium loss and etidronate to reduce bone mineral loss.fter 3 days of hospitalization, the patient’s serum cal-

ium level was 9.2 mg/dL and his QTc interval normal-zed on repeat EKG.

DISCUSSION

he most common electrolyte abnormalities affecting theKG include disorders of potassium, calcium and mag-esium (Table 1). Electrolyte imbalances affect the de-olarization and repolarization phases of the cardiac cy-le action potential by altering potentials across cardiacyocyte cellular membranes. Although we will discuss

ach electrolyte and its associated abnormalities sepa-ately, it is important to remember that combined disor-ers do occur and there is a dynamic physiologic inter-ction between these cations.

otassium

otassium is predominantly an intracellular cation withnly 2% of the total body potassium in the extracellular

igure 6. 12-lead EKG in same patient demonstrating so-call

igure 5. 12-lead EKG in patient with worsening hypokalemiahe U waves.

he preceding T wave and after P wave.

pace. Although the mechanism of potassium regulationetween spaces is complex, there are two main transportrocesses. An active transport process involves the Na�-�-ATPase pump, insulin, beta-adrenergic agents, andineral corticosteroids; and passive transport results

rom alterations in the pH and extracellular cellular fluidsmolality. Homeostatic serum potassium concentrations maintained by the terminal nephron segments of theidney. Factors that lead to alterations in serum potas-ium regulation include renal failure and medicationsuch as non-steroidal anti-inflammatory agents, angio-ensin-converting enzyme inhibitors, diuretics, and digi-alis (1,2).

Potassium plays an important role in maintaining thelectrical potential across the cellular membrane, as wells in depolarization and repolarization of the myocytes.lterations in serum potassium levels can have dramatic

ffects on cardiac cell conduction and may lead to elec-rocardiographic (EKG) changes. Although in some pa-ients EKG changes do not accompany serum potassiumbnormalities, the electrocardiogram is a useful screen-ng tool for gauging the severity of the serum potassium

nt” U waves, particularly in V3–V5 where the U wave masks

the flattening of the T waves and increasing prominence of

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Electrolyte Abnormalities 157

bnormality and the urgency of therapeutic intervention3,4).

ypokalemia

ypokalemia is the result of renal loss, gastrointestinalosses, extracellular to intracellular shift, or inadequateotassium intake (1). Due to the high prevalence ofatients on medications that can result in hypokalemia,

igure 7. Patient with history of bladder cancer and marked hf 0.37 s in 12-lead EKG.

able 1. Electrocardiographic Findings Associated withDisturbances in Serum Electrolyte Levels

ElectrolyteAbnormality Electrocardiographic Findings

ypokalemia Decreased T wave amplitudeT wave inversionST segment depressionProminent U WaveProlongation of QT(U) IntervalVentricular tachycardiaTorsades de pointes

yperkalemiaMild Large amplitude T waves

“Peaked” or “tented” T wavesModerate PR interval prolongation

Decreased P wave amplitude,disappearance

QRS complex wideningConduction blocks with escape beats

Severe Sine-wave patternVentricular fibrillationAsystole

ypocalcemia Prolongation of QTc intervalVentricular dysrhythmiasTorsades de pointes

ypercalcemia Shortening of QTc intervalBradydysrhythmias

ypo/Hypermagnesemia

No unique electrocardiographicabnormalities, but often associated withcalcium abnormalities

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he diagnosis is relatively common. In addition to com-on medications, conditions such as diarrhea and vom-

ting may lead to low potassium levels. It can alsoccompany other metabolic abnormalities such as hypo-agnesemia.As serum potassium levels decline, the transmem-

rane potassium gradient is decreased. The effect on theell membrane is an elevation in the resting membraneotential and a prolongation of the action potential, par-icularly phase 3 repolarization and refractory periods5).

The earliest EKG change associated with hypokale-ia is a decrease in the T wave amplitude. As potassium

evels decline further, ST segment depression and actualwave inversions can be seen. The PR interval can be

rolonged and there can be an increase in the amplitudef the P wave. With even lower serum potassium levels,he classic EKG change associated with hypokalemia ishe development of U waves. The U wave is described as

positive deflection after the T-wave that is often besteen in the mid-precordial leads, such as V2 and V3Figures 4, 5). These changes have been reported inlmost 80% of patients with potassium levels � 2.7Eq/L (6). With extreme hypokalemia, giant U wavesay often mask the smaller preceding T waves or after Paves (Figure 6) (7).The EKG correlates of hypokalemia can be confused

ith myocardial ischemia. In addition, it can be difficulto differentiate a U wave from a peaked T wave that isresent in hyperkalemia. In patients with hyperkalemia,he peaked T wave usually has a narrow base and theRS may or may not be widened.As a result of the increased duration of the action

otential and refractory period, patients with hypokale-ia are at increased risk for certain dysrhythmias (5).he prolongation of the QT, or more correctly QTU

lcemia demonstrating an abnormally shortened QTc interval

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achycardia. A pseudo-prolonged QT interval may beeen, which is actually the QU interval with an absent Tave. It has been reported that patients with hypokale-ia are at increased risk of ventricular fibrillation (8).reatment of hypokalemia focuses on parenteral and oralotassium supplementation, as well as identification andreatment of the source of the electrolyte abnormality.

yperkalemia

tudies validate a good correlation with hyperkalemiand EKG changes. The earliest EKG abnormalities haveeen reported in patients with serum potassium levels asow as 5.5 mEq/L (3). In addition, there is a predictableKG progression as the serum potassium becomes morelevated.

With the increased extracellular concentration of po-assium, transmembrane permeability is increased, caus-ng an influx of potassium into the cells. There is alter-tion of the transmembrane potential gradient, a decreasen magnitude of the resting potential, and a decrease inelocity of phase 0 of the action potential. The potassiumnflux causes a shortening of the action potential andesults in delayed conduction between the myocytes (3).ltimately, these changes produce a slowing of conduc-

ion. These conduction abnormalities result in a numberf electrocardiographic changes that are present in hy-erkalemia. The earliest EKG correlate is T wave tent-ng, classically described as symmetrically narrow oreaked, though the deflection is often wide and of largemplitude (Figure 2) (9). In addition, the inverted Taves associated with left ventricular hypertrophy canseudonormalize (i.e., flip upright) with hyperkalemia10). These T wave changes occur as a result of thecceleration of the terminal phase of repolarization andre most prominently seen in the precordial leads. This isften seen when potassium levels exceed 5.5 mEq/L.

With higher levels of serum potassium, cardiac con-uction between myocytes is suppressed. Reduction intrial and ventricular transmembrane potential causes annactivation of the sodium channel, decreasing the cel-ular action potential. Atrial tissue is more sensitive tohese changes earlier and, as a result, P wave flatteningnd PR interval prolongation may be seen before QRSnterval prolongation. These changes generally occurhen potassium levels exceed 6.5 mEq/L (5). As the

erum potassium level increases further, there is eventualoss of the P wave, attributable to the increased sensitiv-ty of the atrial myocytes to elevated potassium levels.

As the serum level continues to rise to levels abovewo times normal, there is suppression of sinoatrial andtrioventricular conduction, resulting in sinoatrial and

trioventricular blocks, often with escape beats. Other c

locks including intraventricular conduction delay, bun-le branch block, and fascicular blocks have been re-orted. Interestingly, bypass tracts are more sensitive toelayed conduction from potassium elevation, which canesult in the normalization of the EKG and loss of theelta wave in patients with Wolff-Parkinson-White syn-rome

With extremely high serum potassium levels, a mark-dly prolonged and wide QRS complex can fuse with thewave, producing a slurred, “sine-wave” appearance on

he EKG (Figure 1). This finding is a pre-terminal eventnless treatment is initiated immediately. The fatal events either asystole, as there is complete block in ventric-lar conduction, or ventricular fibrillation (5).

Although the above EKG progression is descriptive ofhe classic presentation of hyperkalemia, these changeso not always accompany elevated serum potassiumevels. Metabolic alterations such as alkalosis, hyper-atremia, or hypercalcemia can antagonize the trans-embrane effects of hyperkalemia and result in the

lunting of the EKG changes associated with elevatedotassium levels (11).

Treatment of life-threatening hyperkalemia focusesn blocking the effects on myocyte transmembrane po-ential and cardiac conduction, as well as decreasingxtracellular potassium levels. Response to therapy isften prompt with visualization noted on the EKG orlectrocardiographic monitor. Calcium can effectivelylock the effect of extracellular potassium elevation onardiac myocytes within minutes of administration byestoring a more appropriate electrical gradient acrosshe cellular membrane. Calcium is usually administeredn the form of calcium chloride or gluconate, thoughalcium chloride delivers a much larger amount of cal-ium per unit volume. However, calcium may induceoxic dysrhythmias such as asystole in digitalis toxicatients. Sodium bicarbonate, magnesium, beta-2 adren-rgic agonists, and the combination of glucose and insu-in all drive potassium intracellularly and lower the ex-racellular serum potassium level. Finally, excess bodyotassium can be removed with the use of sodium poly-tyrene sulfonate or dialysis.

alcium

he human body has a nearly inexhaustible reservoir ofalcium (Ca��) stored as hydroxyapatite in skeletalone. Of a total of 1 to 2 kg of adult total body Ca��,nly 1 gram of calcium is present in plasma. Approxi-ately half is protein bound primarily to albumin. A

mall fraction is complexed with phosphate, bicarbonate,itrate and lactate, with the remainder being ionized free

alcium. Extracellular Ca�� concentrations are tightly

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Electrolyte Abnormalities 159

ontrolled through a complex homeostatic mechanismediated primarily by parathyroid hormone and modu-

ated through effector cells in kidney, bone and intestine.he gradient between intracellular and extracellulara�� is 1000- to 10,000-fold, making rapid transmem-rane shifts through “gated” channels possible. Ca�� ismportant in a myriad of regulatory mechanisms, skeletaluscle contraction, control of enzymatic reactions, and

s a key ion in myocyte electrical activity and myocardialontraction (12).

ypocalcemia

ypocalcemia is classically seen with functional para-hyroid hormone deficiency, either as absolute hormoneeficiency (primary hypoparathyroidism), post-parathy-oidectomy, or related to a pseudo-hypoparathyroid syn-rome. Other causes of hypocalcemia include vitamin Deficiency, congenital disorders of calcium metabolism,hronic renal failure, acute pancreatitis, rhabdomyolysis,nd sepsis. Hypocalcemia is commonly seen in criticallyll patients, with a reported incidence of as high as 50%13). Furthermore, hypocalcemia is often associated withypomagnesemia. Neuromuscular irritability is the car-inal feature of hypocalcemia, with carpal-pedal spasmeing the classical physical sign that may progress torank tetany, laryngospasm or tonic-clonic seizure activ-ty.

The primary electrocardiographic manifestation ofypocalcemia is lengthening of the QTc interval. Hy-ocalcemia prolongs phase 2 of the action potential withhe impact modulated by the rate of change of serumalcium concentration and function of the myocyte cal-ium channels. Prolongation of the QTc interval is asso-iated with early after-repolarizations and triggered dys-hythmias. Torsades de pointes potentially can beriggered by hypocalcemia but is much less commonhan with hypokalemia or hypomagnesemia.

Whereas electrocardiographic conduction abnormali-ies are common, serious hypocalcemia-induced dys-hythmias such as heart block and ventricular dysrhyth-ias are infrequent (13). The development of

ysrhythmias is often associated with other co-morbidi-ies such as structural heart disease, ischemia, or inssociation with drug therapy (e.g., digitalis, cat-cholamines). Severe symptoms and life-threateningysrhythmias mandate immediate treatment with paren-eral calcium salts. In addition, associated electrolytebnormalities, including hypomagnesemia, phosphatebnormalities and acidemia may need to be corrected.itamin D and oral calcium supplementation can be

dministered for chronic hypocalcemia. w

ypercalcemia

ypercalcemia is the cardinal feature of hyperparathy-oidism. It is typically chronic, mild and well tolerated.evere hypercalcemia with serum levels above 14mg/dLan be precipitated in these patients by dehydration fromastrointestinal losses, diuretic therapy, or ingestion ofarge amounts of calcium salts. The most common clin-cal presentation of hypercalcemia is in patients withetastatic non-parathyroid cancers. Accelerated bone re-

orption dramatically increases the load of filtered cal-ium and renal sodium reabsorption becomes impaired,reating a cascade of volume depletion and worseningypercalcemia. Symptoms of hypercalcemia can be rel-tively vague, including fatigue, lethargy, motor weak-ess, anorexia, nausea, constipation and abdominal pain.

The effect of hypercalcemia on the electrocardiograms the opposite of hypocalcemia with the hallmark ofbnormal shortening of the QTc interval (Figure 7).linically significant rhythm disturbances associatedith hypercalcemia are rare because elevation of extra-

ellular calcium is generally not associated with trig-ered dysrhythmias. Cardiac conduction abnormalitiesay occur, with bradydysrhythmias being the most com-on (14).Therapy for hypercalcemia is generally instituted

ased on clinical signs more than absolute serum levels,lthough empiric therapy is often started at levels of4mg/dL even in the asymptomatic patient. In patientsith hypoalbuminemia, measured serum calcium levelsay mask significant elevations in free ionized extracel-

ular calcium. The mainstays of treatment are intrave-ous volume repletion and bisphosphonate agents thatnhibit osteoclastic bone resorption. The use of loopiuretics to promote calciuresis is often recommendedut is problematic in the hypovolemic patient. Dialysisay be required in severe cases.

agnesium

agnesium, a primarily intracellular cation, participatesn hundreds of enzymatic reactions and in essential hor-onal regulation. It is important in the maintenance of

ellular ionic balance with the modulation of sodium,otassium and calcium. The average adult contains about4 g of magnesium, with only 1% found in the extracel-ular space. Ongoing dietary intake is required to main-ain normal levels (15).

The historical medical indication for magnesium ther-py has been in the management of the ecclamptic syn-romes of pregnancy. Magnesium also has a role in thecute management of wide-complex tachydysrhythmias

here therapy may be lifesaving. There is a burgeoning,

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hough inconclusive literature related to other potentialherapeutic uses in asthma, myocardial infarction, andcute cerebral ischemia (16).

Hypomagnesemia is the most common clinically en-ountered aberration of magnesium homeostasis and isaused by decreased intake, increased losses, or alteredntracellular-extracellular distribution. Unlike other elec-rolyte disturbances, there is no classical syndrome andeasurement of serum levels do not correlate well with

linical manifestations. Hypomagnesemia is associatedith far-reaching adversity across the physiologic spec-

rum, including central nervous system (CNS) effectsseizures, mental status changes), cardiovascular effectsdysrhythmias, vasospasm), endocrine effects (hypokale-ia, hypocalcemia), and muscle effect (bronchospasm,uscle weakness). Hypermagnesemia is primarily seen

n patients with renal failure who ingest large amounts ofagnesium salts and is usually well tolerated. Symptom-

tic hypermagnesemia is most often iatrogenic in origin,nd is associated with errors in intravenous dosing. Se-ere symptoms include CNS depression, areflexia, respi-atory failure, and rarely, cardiac arrest.

There are no unique electrocardiographic effects thatan be attributed specifically to either hypomagnesemiar hypermagnesemia. It is well known that both su-raventricular and ventricular dysrhythmias can be po-entiated if not directly caused by hypomagnesemia.

agnesium has been shown to be efficacious in theanagement of atrial tachydysrhythmias although there

s no correlation between rhythm conversion and plasmaoncentration. Magnesium sulfate is considered first-lineherapy by the American Heart Association ACLS guide-ines for torsades de pointe (17).

CONCLUSIONS

ntracellular and extracellular cations such as potassium,

alcium and magnesium critically affect the cardiac ac-

ion potential and myocyte depolarization and repolar-zation. Changes in extracellular levels of these electro-ytes can have profound effects on cardiac conduction.lectrocardiographic findings associated with these dis-

urbances can provide clues to the diagnosis, as well asuide therapeutic interventions.

REFERENCES

1. Brobst D. Review of the pathophysiology of alterations in potas-sium homeostasis. J Am Vet Med Assoc 1986;188:1019–25.

2. Brown RS. Potassium homeostasis and clinical implications. Am JMed 1984;77:3–10.

3. Yu AS. Atypical electrocardiographic changes in severe hyperka-lemia. Am J Cardiol 1990;77:906–8.

4. Martinez-Vea A, Bardaji A, Garcia C, Oliver JA. Severe hyperka-lemia with minimal electrocardiographic manifestations: a reportof seven cases. J Electrocardiol 1999;32:45–9.

5. Webster A, Brady W, Morris F. Recognising signs of danger: EKGchanges resulting from an abnormal serum potassium concentra-tion. Emerg Med J 2002;19:74–7.

6. Surawicz B. Electrolytes and the electrocardiogram. Postgrad Med1974;55:123–9.

7. Yan GX, Lankipalli RS, Burke JK, Musco S, Kowey PR. Ventric-ular repolarization components of the electrocardiogram: cellularbasis and clinical significance. J Am Coll Cardiol 2003;42:401.

8. Helfant RH. Hypokalemia and arrhythmias. Am J Med 1986;80:13–22.

9. Slovis C, Jenkins R. Conditions not primarily affecting the heart.BMJ 2002;324:1320–3.

0. Mattu A, Brady WJ, Robinson DA. Electrocardiographic manifes-tations of hyperkalemia. Am J Emerg Med 2000;18:721–6.

1. Campistol JM, Almirall J, Montoliu J, Revert L. Electrographicalterations induced by hyperkalaemia simulating acute myocardialinfarction. Nephrol Dial Transplant 1989;4:233–5.

2. Bushinsky DA, Monk RD. Electrolyte quintet: calcium. Lancet1998;352:306–11.

3. Carlstedt F, Lind L. Hypocalcemic syndromes. Crit Care Clin2001;17:139–53.

4. Ziegler R. Hypercalcemic crisis. J Am Soc Nephrol 2001;12(Suppl17):S3–9.

5. Agus ZS, Wasserstein A, Goldfarb S. Disorders of calcium andmagnesium homeostasis. Am J Med 1982;72:473–9.

6. Dacey M. Hypomagnesemic disorders. Crit Care Clin 2001;17:155–64.

7. Part 6: Advanced cardiovascular life support: section 5: pharma-cology I: agents for Arrhythmias. Circulation 2000;102(8 Suppl):

I112–28.