12 EMN October 2009

By James R. Roberts, MD

Author Credentials andFinancial Disclosure: JamesR. Roberts, MD, is the Chair-

man of the Department of EmergencyMedicine and the Director of the Divi-sion of Toxicology at Mercy HealthSystems, and a Professor of Emer-gency Medicine and Toxicology at theDrexel University College of Medicine,both in Philadelphia.

All faculty and staff in a position tocontrol the content of this CME activityhave disclosed that they have no finan-cial relationships with, or financial in-terests in, any commercial companiespertaining to this educational activity.

Learning Objectives: After reading thisarticle, the physician should be able to:1. Discuss the EKG findings of hyper-kalemia.2. Summarize the progression of EKGfindings based on serum potassiumlevels.3. Identify those patients requiring em-piric therapy for hyperkalemia.

Release Date: October 2009

Some EKG findings foretell signifi-cant morbidity and even mortality,and some subtle yet serious resultsescape even seasoned cardiologists. LikeQTC prolongation and Brugada andWellens syndromes, discussed in previ-ous columns, hyperkalemia is an EKGstandout.

ElectrocardiographicManifestations of HyperkalemiaMattu A, et alAm J Emerg Med2000;18(6):721

This erudite paper with spectacu-lar EKG tracings by practicing emer-gency medicine EKG aficionados andexperts is a concise review of the mul-tiple EKG manifestations of hyper-kalemia. Because hyperkalemia is alife-threatening acute emergency anda frequent denizen of the ED, it is im-perative to be cognizant of the classicEKG findings of this metabolic abnor-mality. Hyperkalemia usually occurs in dialysis patients, but may be seen in DKA, adrenal insufficiency, acutedigoxin poisoning, severe dehydrationwith renal insufficiency, and prescribeddrugs that cause hyperkalemia. Medica-tion-wise, especially consider spirono-lactone, NSAIDs, Bactrim, and ACEinhibitors.

The medical school adage of hy-perkalemia is that the EKG manifeststall, sharply peaked T waves in theprecordial leads, perhaps a commonand omnipresent finding, albeit onewith minimal sensitivity (about 40%)and far from perfect specificity(about 85%). The classic EKG portend-ing imminent cardiac arrest demon-strates a severely wide QRS complex,and a sine wave appearance, harbin-gers of a soon-to-occur cardiac cata-strophe (asystole or VF). The majorityof patients also demonstrate brady-cardia. More subtle changes includeprolonged PR interval and absent Pwaves.

The authors augment their discus-sion with a review of five case historieswith accompanying EKGs. It would beinstructive to pull the original articlebecause the tracings are quite illustra-tive. The first case is a classic pre-sentation. A dialysis patient missedtwo appointments, and presented withmalaise and myalgias. Vital signs werenormal, and the physical examinationwas non-revealing. An EKG demon-strated prominent peak T waves (V1 toV3) and minimal widening of the QRS.This patient was empirically treatedfor hyperkalemia, and the serumpotassium level was 8.4 mEq/L. Thepharmacologic intervention was alsostandard, including 20 ml of 10% cal-cium gluconate, 2 amps of sodium bi-carbonate, 10 units of IV regular insulinwith 1 amp of D50, and 50 grams of

oral Kayexalate. EKG amelioration wasseen within a few minutes of empiricintervention.

Other cases were similar, and in-cluded patients with known renal insuf-ficiency who presented with malaiseand diffuse weakness as the garden-va-riety clinical manifestations of their hy-perkalemia. EKGs demonstrated absentP waves, irregular rhythms, peaked Twaves, and a widened QRS complex. All

cases demonstrated a rather marked de-crease in serum potassium levels fol-lowing treatment. In one case thepotassium level went from 8.1 mEq/Lto 6.6 mEq/L following calcium, insulin,bicarbonate, and Kayexalate therapy.Additional cases demonstrated moresevere EKG findings that exemplifiedthe classic sine wave morphology. In allcases, the clinicians appeared clairvoy-ant enough to institute empiric therapyagainst hyperkalemia based on EKGfindings alone. Bravo to these brave andgusty souls.

Comment: Not all clinicians are as as-tute as these, and many of us will lookat the EKGs associated with a potas-sium level in the 6-7 mEq/L range, anddismiss the tracing as minimally abnor-mal or delay a decision pending labo-ratory confirmation. As it turns out, thenext article confirms that it is rare totreat hyperkalemia based on EKG find-ings alone, even in the academic ivorytowers of Boston. If one does not havebedside or point-of-care blood testing,the serum potassium can take one tothree hours to return, and invariablythe most important specimen is he-molyzed, creating spurious results. Ofinterest, the clinical manifestations ofhyperkalemia are similar to those ofhypokalemia. Hyperkalemic patientsusually complain of weakness andmuscle aches, symptoms that shouldnot be ignored when evaluating the ubiq-uitous hallway patient with a dialysis

Electrocardiograms You Needto Know: Hyperkalemia

InFocus

This dialysis graft, coupled with an easy-to-ignore complaint of weakness, are a setup for hyperkalemia. A hallway monitor strip is a poor way to diagnose hyperkalemia, but a wide QRS should get your attention. Readily obtaining venous blood in a dialysis patient can be a gargantuan task that can delay labresults even further.

The peaked T waves on this EKG are striking, best described as too sharp tosit on. But the vicissitudes and vagaries of the T wave, especially on a monitorstrip, make the EKG diagnosis of hyperkalemia tenuous at lower serum levels.This EKG is not predictive of life-threatening hyperkalemia so one can wait forlab confirmation, perhaps with a call to the lab tech to move things along. Ofcourse, bedside testing solves a whole passel of lab turnaround foibles.

October 2009 EMN 13InFocus

graft in his arm. Patients with hyper-tension, diabetes, renal failure, and aslew of other medical problems havemany reasons to be weak, tired, andachy, but hyperkalemia is one condi-tion that should be high on onesradar, even when the patient proffersyet another weak and dizzy complaintlist.

The EKG manifestations of hyper-kalemia generally parallel the serumpotassium level. Characteristic EKGfindings are promulgated in every text-book, but in my experience, a plethoraof nonspecific changes can be seen, sodont be locked into an intense analysisof any given pattern. I have found thatbradycardia is common, but have notseen that emphasized. The accompany-ing figure provides a general overviewof potassium levels and EKG abnormal-ities, although there is obviously someoverlap. Potassium levels above 8.0mEq/L generally call for immediateaction, as do the EKG abnormalitiesassociated with such levels, often mar-shalling the troops absent a criticalvalue call from the tardy lab. One maybe forced to treat empirically, based onEKG evidence alone, especially in codesituations. Expect to be wrong on manysuch clinical calls.

Last months column depicted a clas-sic EKG of severe TCA overdose, withsquiggles surprisingly similar to hyper-kalemia. My only pearl here is that al-though the QRS can be wide in TCAoverdose and hyperkalemia, its signifi-cant tachycardia and the terminal Rwave in AVR that distinctly herald TCAtoxicity. Fortunately, bicarbonate helpsboth conditions.

Effects of Presentation andElectrocardiogram on Time toTreatment of HyperkalemiaFreeman K, et al Acad Emerg Med 2008;15(3):239

This is a fascinating article fromsome prestigious New England univer-sity hospitals that essentially describesstandard of care for EKG-based empiric

treatment of hyperkalemia in the ED,and provides insight into the expectedturnaround time for laboratory analysis.The authors attempted to determinewhether EKG features were associatedwith a difference in time to treatmentfor patients ultimately determined tohave hyperkalemia (level above 6mEq/L). Excluded subjects were thosewho had a give-away chief complaintof hyperkalemia or needs dialysis,and those who had a cardiac arrest.The median potassium level was only6.5 mEq/L (6.3-7.1). More than a thirdof the patients were taking ACE in-hibitors, drugs well known to causehyperkalemia.

Of the 168 patients treated for hy-perkalemia, 12 (12%) were treatedwithin 30 minutes of triage, and 26(16%) were treated empirically beforethe lab reported the potassium values.About a third of the EKGs demon-strated abnormalities of the T wave, al-though many were nonspecific. Only 35percent were considered textbook trac-ings. In retrospect, only half of thecases had an EKG abnormality consis-tent with hyperkalemia. Importantly,

none of the EKG abnormalitiesprompted early treatment. Two casesof cardiac arrest may have been sec-ondary to hyperkalemia, despite stan-dard therapy.

In this study, the median time fromED arrival to treatment for hyper-kalemia was an amazingly long 117minutes (range: 59-196). Even whenthe laboratory results were available,it required an additional 67 minutes(range: 49-82) to initiate treatment.So-called critical values from the labrequired a mean of 42 minutes (range:20-95) to receive specific therapy. Inthis study the most common present-ing complaints were dyspnea (20%),weakness (19%) or altered mental sta-tus (8%). Despite having knowledgeof the potential for hyperkalemia andhaving the EKG prior to serum potas-sium level, even rapid sleuthing of theEKG did not appear to shorten thetime from ED arrival to specific anti-potassium intervention. The authorsspeculate that this may be due to the nonspecific abnormalities seen in many EKGs in the presence of hyperkalemia.

The bottom line is that the EKG didnot spur early or empiric treatment ofhyperkalemia in this study. Essentially,no EKG finding prompted early ther-apy. The potassium levels were actu-ally modest (6.3-7.1 mEq/L) however,so it is not certain that more ominouscardiograms would have been metwith similar clinical indifference orclinician ennui.

Comment: This is indeed a discourag-ing report from a university hospital. Ithought my ED had a slug-like mental-ity when it came to hyperkalemia. Thelevel of hyperkalemia was probablynot life-threatening in the majority ofcases, and therefore the EKG was notas provocative or attention-grabbing asthe tracing seen when potassium levelsare well above 8.0 mEq/L, and the pa-tient is circling the drain leading to car-diac arrest. This article actually setsthe standard of care as a rather modestone, particularly with regard to recog-nition and treatment of hyperkalemiain the ED in comparison with the EKG.It appears that the clinicians fromBoston did not believe that empirictreatment for hyperkalemia should bebased solely on nonspecific EKG find-ings. I agree, but would hasten to addthat a sine wave should garner an em-piric intervention. While waiting forlab confirmation is a reasonable ap-proach in the nonacute circumstance,a widened QRS or sine wave prognos-ticates a poor outcome, and should obviously get ones full pharmacologicattention. Unless I am missing some-thing, this article is the poster child for point-of-care blood testing in theED.

Management of SevereHyperkalemiaWeisberg LSCrit Care Med 2008;36(12):3246

This is a literature-based summary ofhyperkalemia management, termed a po-tentially lethal electrolyte abnormality bythese authors. A serum potassium level of6.5 mEq/L or specific EKG abnormalitieswere considered emergency action pointsfor treatment. The standard regimen toantagonize the effects of potassium oncardiac depolarization is a threefold ap-proach: redistributing potassium into thecell (bicarbonate and insulin/glucose), en-hancing potassium elimination (dialysisor Kayexalate), and stabilizing cardiaccell membranes (calcium infusion). Thetreatment of severe hyperkalemia is med-ical student dogma, and it should befamiliar to all emergency physicians.

The authors nicely detail the sciencebehind calcium, insulin, bicarbonate,beta-agonist, and Kayexalate therapies.As a summary, calcium is the preferred

This EKG, obviously demonstrating a slow, wide bizarre QRS pattern with an almost sine wave appearance, is a harbinger of imminent cardiac arrest. Thepotassium level is likely well over 8 mEq/L. It calls for an astute clinician whohas the chutzpah to treat empirically with the entire drug regimen aimed atrapidly decreasing serum potassium levels and stabilizing cardiac depolarization.

EKG Changes Associated with Increasing Potassium Levels

Typical ECG Appearance

Serum Potassium Mild: 5.5-6.5 mEq/L Moderate: 6.5-8.0 mEq/L Severe: >8.0 mEq/L

Possible ECG Abnormalities Peaked T waves, Loss of P wave, prolonged Progressive widening ofprolonged PR segment QRS complex, ST-segment QRS complex, sine

elevation, ectopic beats and wave, ventricular escape rhythms fibrillation, asystole,

axis deviations, bundle branch blocks, fascicularblocks

Continued on next page

14 EMN October 2009

emergency bullet for cardiac conduc-tion issues; insulin is best for translo-cating potassium back into the cell;Kayexalate has debatable efficacy andis slow; and dialysis is the most reli-able tool for removing potassium fromthe body. Beta-agonists are iffy, and bi-carbonate is minimally helpful. Theempiric treatment of hyperkalemiagenerally can be supported under theproper scenario, and such innocuousinterventions dont usually wreakhavoc even if ones diagnosis is off themark. But merely finding weaknessand an abnormal EKG can result inrather serious consequences if the pa-tient happens to have the rare case ofhypokalemic paralysis. The only down-side of the treatment of most patientswith standard hyperkalemia regimensis hypokalemia. Hyperglycemia, hyper-osmolality, and hypercalcemia are oflittle clinical consequence. These au-thors note that a benefit of nebulized

albuterol (such as 20 mg inhaled over10 minutes) is seen in only about 60percent of patients, with the most com-mon side effect being tachycardia.

Comment: I learned the general treat-ment protocol for severe hyper-kalemia, the quintessential shotgunapproach, as an intern. One aims topush potassium back into the cell, ex-tract it from the serum, and keep theheart beating and contracting. Thereare little data in the literature that anyspecific regimen causes any specificor quantitative result. Some questionany real value of sodium bicarbonate.When one decides to treat hyper-kalemia in the ED, a cornucopia oftherapies is simultaneously initiated.Most interventions have few down-

sides, and are well worth the poten-tial risks given the lethal potential forsevere untreated hyperkalemia. Im-portantly, all ED interventions, evencalcium, last only a few hours.

The usual ultimate treatment is he-modialysis, a necessity in the patientwith end-stage renal disease. I person-ally have minimal regard for nebulizedalbuterol. About 40 percent experienceno benefit, and the subset likely to im-prove is enigmatic so far. It doesntseem to produce clinically significanthypokalemia in the asthmatic patient.In fact, we never even check potassiumunder such circumstances. Albuterolcan make one very tremulous given thefourfold dose for hyperkalemia vs.asthma.

The Holy Grail for life-threatening

hyperkalemia is intravenous calcium.Calcium gluconate can be given via aperipheral vein as long as one is care-ful not to allow extravasation. Calciumchloride always burns, and while itcan be given through a dialysiscatheter (Quinton), the best choice isa central line. Occasionally I havegiven calcium chloride via a large pe-ripheral vein, but stand at the bedsideto make sure that it does not ex-travasate. Calcium chloride in the sub-cutaneous tissue is usually associatedwith some degree of tissue slough ornecrosis, and there is no antidote.When it has to be done, it has to bedone. Some clinicians prefer to usecalcium gluconate under all circum-stances calling for calcium supple-mentation, not a bad fail-safe mantra.

Kim (Nephron 1996;72[3]:476) studiedthe effect of simultaneously administeredinsulin/glucose and bicarbonate for treat-ing hyperkalemia. This synergic effect iscommonly sought, but efficacy is poorlyquantified. For patients with end-stagerenal disease, the treatment regimen con-sisted of 2 amps of bicarbonate, 1 amp of

The EKG generally parallels the serum potassium levels.

Improving Medication ComplianceThere is no proven way to ensure pa-tients follow medication directions forextended periods of time, according to anew report in the Cochrane Database ofSystematic Reviews.

Researchers led by R. Brian Haynes,MD, PhD, of McMaster University, up-dated a 2005 review summarizing ran-domized control trials of interventions tohelp patients follow prescriptions.

They found that four of 10 interven-tions reported in nine trials showed aneffect on adherence and at least oneclinical outcome for short-term treat-ments, which lasted one to three weeks.In those short-term trials, the re-searchers found one intervention thatsignificantly improved patient adher-ence but did not enhance clinical out-come. Some effective approachesincluded counseling and providingwritten instructions.

For long-term treatments, 36 of 81interventions reported in 69 trials wereassociated with improvements in adher-ence, but only 25 interventions led toimprovement in at least one treatmentoutcome. Some approaches with limitedsuccess included sending reminders to pa-tients and following up with phone calls.

First TB Cases May PredictOutbreakThe first two cases of tuberculosis in aregion may provide clues on the poten-

tial for an outbreak, according to theJuly 1 American Journal of Respiratoryand Critical Care Medicine.

Researchers from the KNCV Tuber-culosis Foundation in the Hague,Netherlands, led by Sandra Kik, MSc,analyzed data from the NetherlandsTuberculosis Register and the NationalInstitute of Public Health from morethan 18,200 patients with reported TBbetween 1993 and 2004. They dis-counted cases that were not culture-confirmed, could not be exactlymatched between the two databases,or were duplicates. Remaining caseswere divided into 622 cluster episodes,with 1,756 individual cases, 54 ofwhich were large clusters (five or morecases).

They found that if the first two pa-tients were diagnosed within threemonths of each other, lived in urbanareas, and if one or both were of sub-Saharan African nationality, there wasa 56 percent chance that the twocases will lead to a large outbreak ofTB. If the patients exhibit none ofthose characteristics, the odds are justone percent.

Rapid Response Teams IneffectiveRapid response teams in hospitals donot result in a reduced rate of cardiopul-monary arrests or deaths, according tothe December 3 issue of JAMA.

Researchers led by Paul S. Chan,MD, of the University of Missouri,Kansas City, examined the association

between a rapid response team inter-vention and long-term challenges inhospital-wide cardiopulmonary arrestsand mortality rates. The study includedadult inpatients admitted between Jan-uary 2004 and August 2007 at a 404-bed tertiary care academic hospital.Rapid response team education andprogram rollout occurred from Sept. 1to Dec. 31, 2005. A total of 24,193 pa-tient admissions were evaluated prior tothe intervention and 24,978 after.

The researchers found there were376 rapid response team activations af-ter intervention implementation. Themost common reasons for activationwere altered neurological status, tachy-cardia exceeding 130 beats per minute,tachypnea exceeding 30 breaths perminute, and hypotension assessed asblood pressure lower than 90 mmHg.

Case fatality rates after cardiopul-monary arrest were similar prior toand after the rapid response teamintervention (77.9% vs. 76.1%). Hos-pital-wide mortality rates did notmeaningfully change after the inter-vention: 3.22 prior to intervention vs.3.09 after intervention, per 100admissions. Secondary analyses re-vealed few instances of rapid re-sponse team undertreatment orunderuse that may have affected themortality findings.

EPs: Resuscitation Practices LackingAn overwhelming majority of emer-gency physicians say resuscitation prac-

tices in the United States are not veryeffective, according to a recent ACEPsurvey.

The college conducted the State ofResuscitation survey in September, re-leasing the results in November. A totalof 1056 online questionnaires werecompleted by ACEP members in se-lected sections. The survey was admin-istered by Saperstein Associates, anindependent opinion research com-pany, and was sponsored by ZOLL Med-ical Corporation.

The survey found almost all EPs(94%) believe a patient in sudden car-diac arrest is more likely to survive if aCPR-trained bystander administersCPR before professional rescuers ar-rive. More than half said the length oftime between patient collapse andfirst responder arrival is an importantfactor in determining the success ofresuscitation efforts. Other factorsviewed as having a positive impact in-cluded faster patient-to-doctor times(77%), data collection and sharing(73%), automated technologies (66%),and real-time feedback on compres-sions (65%).

More than half the respondents saidpoor survival rates from sudden cardiacarrest is related to the aging population,while one-quarter said obesity has con-tributed most to poor survival rates.Though EPs said bystander CPR wouldimprove survival, efforts to teach layper-sons are scattered and often nonexis-tent, and respondents want civic leadersto be more engaged in the issue.

In Brief

HY P E R KA L E M I AContinued from previous page

InFocus

October 2009 EMN 15

D50, and 50 units of regular insulin, eitheralone or combined therapy. The bicar-bonate alone had little effect on serumpotassium. The glucose/insulin therapyhad a modest benefit, but a combinationof the two lowered serum potassiumfrom 6.2 to 5.2 mEq/L at 60 minutes.Plasma osmolality was not an issue, andthere was no hypoglycemia. Bottom line:Bicarbonate is of minimal importance,but it seems synergistic with insulin andmay have other benefits on the milieu ofrenal failure.

Allon et al (Ann Intern Med 1989;110[6]:426) studied the effect of nebu-lized albuterol for acute hyperkalemiain hemodialysis patients. This was arandomized prospective double blindplacebo controlled trial studying either10 or 20 mg of nebulized albuterol. Thebeta-agonist lowered serum potassiumlevels by approximately 0.6 to 0.9mEq/L, with a higher dose providing thegreater effect. The hypokalemic effectwas noted within one to two hours, andthere were no adverse cardiovasculareffects. Notably, some patients had nosignificant response, but the reason forthis was not known. This report wasone of the first articles to postulate apotassium-lowering effect of nebulizedalbuterol, an intervention that seems tohave gained popularity in the ED. In-haled beta-agonist may be a good alter-native when IV access is not readilyavailable.

The American Heart Associationrecommends immediate therapy forserum potassium levels greater than 6mEq/L, but this is hardly a lethal potas-sium level, or one that cannot await lab-oratory confirmation. Exactly whenpotassium levels become life-threaten-ing is unknown, but treating any levelover the AHA recommendations isreasonable. An exception to the usualtherapeutic cocktail may be severe de-hydration where saline alone will quicklylower potassium levels that are raisedsecondary to pre-renal azotemia.

In these days of the omnipresent six-to infinity-hour ED waits for dialysis oradmission, the return of hyperkalemiais not an uncommon issue for the EPwho may have moved on to other pa-tients, content that the inpatient teamhas taken control. No ED interventionlasts more than a few hours so the clin-ician must be vigilant to provide con-tinuing care after the initial bevy ofmedications saved the day. I prefer tocheck the potassium in about an hour to

gloat over my success, and again two tothree hours later if the patient is still inthe ED. An endocrinologist friend ofmine offered the following regimen forcontinuous calcium gluconate, the mostuseful immediate cardioprotective in-

tervention for severe hyperkalemia:Add 6 ampoules of calcium gluconate toa liter of normal saline, and infuse 1ml/kg per hour of this concoction. Cal-cium levels will not get excessivelyhigh, and continued myocardial self-

stabilization will occur. The fluid loadis minimal. In a dialysis patient, I wouldcontinue this for about three to fourhours, augmented with frequent call tothe dialysis center for the more defini-tive intervention.

October 2009Questions:

1. Tall peaked T waves on the EKG are nearly 100% sensitive and specific for hyperkalemia. True False

2. A slow, wide QRS pattern resembling a sine wave indicates impending cardiac arrest from hyperkalemia. True False

3. It is extremely dangerous to empirically administer medication therapy for hyperkalemia without confirming theserum potassium level. True False

4. Nebulized albuterol is contraindicated in the presence of hyperkalemia. True False

5. Once hyperkalemia has been treated in the ED, a repeat evaluation of potassium levels and additional therapy forthe next 24 hours is not required. True False

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