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Case Report:

Left bundle branch block: a rare ECG manifestation of hyperkalemiaM. Venkata Madhav,1 G.Anvesh,1 K.V.Seshaiah,2 G.Eswar,1 Ajith Mohammad1

Department of 1General Medicine, Dr Pinnamaneni Siddhartha Institute of Medical Sciences and ReasearchFoundation, Chinoutpalli and Department of 2Medicine, Government Siddhartha Medical college, Vijayawada

ABSTRACTA 20-year-old female patient with chronic kidney disease was brought to our emergency medical department withsymptoms of pain in chest and abdomen, vomitings. Laboratory testing revealed serum potassium 7.7 mEq/L, serumcreatinine 9.1 mg/dL. Electrocardiogram (ECG) showed left bundle branch block (LBBB) pattern with left axis deviation,tall T waves and ST elevation. Among ECG alterations in hyperkalemia, LBBB is rare and is being reported in ourcase.

Key words: Electrocardiogram, Hyperkalemia, Left bundle branch blockVenkata Madhav M, Anvesh G, Seshaiah KV, Eswar G, Mohammad A. Left bundle branch block: a rare ECG manifestation ofhyperkalemia J Clin Sci Res 2015;4:159-63.DOI: http://dx.doi.org/10.15380/2277-5706.JCSR.13.075.

Corresponding author: Dr G. Eswar,Professor, Department of General Medi-cine, Dr Pinnamaneni Siddhartha Institute ofMedical Sciences and Reasearch Foun-dation, Chinoutpalli, India.e-mail: eswar1952@gmail.com

Online accesshttp://svimstpt.ap.nic.in/jcsr/apr-jun15_files/cr215.pdf

DOI: http://dx.doi.org/10.15380/2277-5706.JCSR.13.075

Received: 12 December 2013; Revised manuscript received: 03 July 2014; Accepted: 16 August 2014

INTRODUCTION

Extracellular potassium concentration isnormally maintained between 4.0-4.5 mEq/ L.Hyperkalemia, defined as serum potassiumgreater than 5.0 mEq/L, is a common metabolicdisturbance with potentially lifethreateningconsequences. While the incidence o fhyperkalemia in the general population is notwell documented, it is 1% to 10% inhospitalized patients, with a mortality ratio of1 per 1000 patients.1 Electrocardiogram (ECG)may provide the first evidence of hyperkalemia,but patient-to-patient variability is high. Eventhough most common ECG findings in hyper-kalemia include peaked T waves and widenedQRS complexes, hyperkalemia can causeseveral characteristic abnormalities which areoften progressive. Poor correlation has beenobserved between serum potassium levels andany specific ECG finding and the sensitivityof ECG for diagnosis of hyperkalemia ispoor.1-3 At the same time, any ECG change inthe clinical background of hyperkalemia should

alert the clinician for carrying out the work-upfor diagnostic confirmation. We report theoccurrence of LBBB caused by hyperkalemiain a young lady with Chronic kidney disease(CKD).

CASE REPORT

A 20-year-old female patient was brought toour emergency department with complaints ofpain abdomen, vomiting, and retrosternal chestpain of acute onset. Abdominal pain and chestpain were dull aching in character and were notrelated to any known precipitating factors. Shewas known to have CKD and was on mainte-nance haemodialysis since 3 months. Her pasthistory, birth and developmental history,childhood history were unremarkable. Patientdenied taking any medications known toprecipitate her clinical condition. She was notknown to have hypertension, diabetes mellitus.

General and systemic physical examination wasunremarkable. Laboratory values werehemoglobin 8.3g/dL; total leukocyte count

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13,100 cells/ mm3; neutrophils 80%. Blood ureanitrogen 40 mg/dL; serum creatinine 9.1 mg/dL; random plasma glucose 120 mg/dL;serum sodium 146 mEq/L; and serumpotassium 7.7 mEq/L. Antistreptolysin O titers,troponin I levels, and calcium were withinnormal range. Arterial blood gas analysisshowed pH 7.20; PaO2 109 mm Hg; PaCO2 55mm Hg; bicarbonate 16.2 mEq/L. ECG showedLBBB with left axis deviation, secondary ST-T changes and tall T waves in chest leads(Figure 1). A 2D-echocardiogram was un-remarkable. Chest radiograph showed mildcardiomegaly with normal lung fields.

She was initially treated with intravenouscalcium gluconate, insulin with glucose,salbutamol nebulization, and sodium poly-styrene sulfonate. Drug treatment did notnormalize her serum potassium levels.Haemodialysis was initiated, with which herserum potassium levels as well as ECG changesbecome normal (Figure 2).

In the clinical background of CKD and ab-sence of known precipitating factors forincreased serum potassium levels, her hy-perkalemia was attributed to CKD. With normalcardiac evaluation and absence of risk factorsfor coronary arterial disease, her ECG findings,were attributed to be due to hyperkalemia.

DISCUSSION

Under normal circumstances renal excretionaccounts for approximately 90% of dailypotassium elimination. As renal functiondeclines, a greater fraction of the filtered loadis excreted and serum potassium levels do notrise until renal function declines to less than25% of normal.2

Hyperkalemia decreases the resting membranepotential (RMP), the magnitude of the actionpotential, and maximum rate of rise of phase 0in the cardiac muscle. Hyperkalemia producesa biphasic effect on arterio-venous (AV)conduction system, with mild hyperkalemia

Figure 1: Pre-treatment electrocardiogram showing changes of hyperkalemia

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accelerating the AV conduction, and severehyperkalemia (7.5 mEq/L) depressing it.3 Ahigh concentration of extracellular potassiumslows impulse conduction through all cardiactissue, which accounts for a number of ECGfindings.

Disproportional effects of varying levels ofhyperkalemia on the resting membranepotential and the threshold potential (TP)explains the initial increase in excitability andconduction velocity followed by their decreaseas the potassium level increases further.Hyperkalemia is associated with increasedmembrane permeability to potassium, whichaccelerates repolarization and shortens theaction potential (AP) duration. Hyperkalemiapreferentially shortens the plateau of thePurkinje fibres, thereby decreasing the

dispersion of repolarization in the ventricle. Italso slows the diastolic depolarization of thePurkinje fibers.4 The effect of hyperkalemiadepends on the tissue involved, with the atrialmyocardium being the most sensitive, theventricular myocardium less sensitive, and thespecialized tissue (sinoatrial node and Hisbundle) the least sensitive. Atypical bundlebranch blocks, intraventricular conductiondelays, ventricular tachycardia, ventricularfibrillation and idioventricular rhythm are morecommonly seen in severe hyperkalemia (serumpotassium >10 mEq/L). Bundle branch blocksin hyperkalemia are atypical in the sense thatthey involve the initial and terminal forces ofQRS complex. Shifts in the QRS axis indicatedisproportionate conduction delays in the leftbundle fascicles.4

Figure 2: Post-treatment electrocardiogram showing normalization

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As hyperkalemia progresses, depolarizationmerges with repolarization, expressed in theECG with QT shortening and apparent STsegment elevation simulating acute injury. Thisdisappears with haemodialysis dialyzablecurrent of injury.

The disproportionate conduction delay in thebundle branch system occurs more often in theright than in the left, unlike in our patient whohad LBBB pattern.5 The hyperkalemic ECGchanges range from peaked T waves, loss of Pwaves, prolonged QRS complex, ST elevation,escape beats and escape rhythm to sine wave,ventricular fibrillation, asystole, axis devia-tions, bundle branch blocks, and fascicularblocks.6 Sinus node depression, and malignantventricular arrhythmias can also occur. Usualorder of appearance of ECG changes is tall Twaves, QRS widening, loss of P wave, STelevation with “pseudo infarction” pattern, sinewave and eventual asystole.7

In a study of 27 patients with ECG changes ofhyperkalemia, elevated serum potassium levelswere found in 22 patients (82%); On the otherhand in 39 patients with hyperkalemia, ECGshowed agreement in only 21 (54%).8 In aretrospective study, ECG changes were seen in43% of patients with serum K+ ranging from6.0-6.8 mEq/L, and in only 55% of patients withvalue of 6.8 mEq/L or greater.1 Another studydocumented that ECG changes were associatedwith serum K+ 6.8-7.6 mEq/L, and foundconsistent above levels of 7.8 mEq/L.9 In onemore study7 of 292 patients with hy-perkalemia, only 40 abnormal ECGs werefound. In this study7 peaked T waves, mostfrequent ECG change were seen in only twopat ients with mild (5.0-6.9 mEq/L)hyperkalemia and prolonged PR interval wasseen in all ranges of serum K+ levels.

In general, a correlation can be observedbetween increasing abnormality of ECG patternand increasing serum potassium concentrations.

However, patient-to-patient variability is high.ECG changes might be subtle or even absent,further complicating the diagnosis. Thus ECGfindings might not be sensitive in detecting mildand moderate hyperkalemia, as documented inmany studies.

It was documented that there was a lack ofconfirmity of ECG manifestations with serumpostassium levels and this disparity wasattributed to the presence of ECG alterationsfrom other causes or to concomitantabnormalities of other electrolytes. 8 Innephrectomized animals or in the presence ofrenal disease with acidosis, small increases inthe serum potassium concentration may quicklyalter the Ke / Ki (extracellular potassium/intracellular potassium) ratio resulting in earlyand typical changes of hyperkalemia. But in thepresence of alkalosis with intact renal regula-tory mechanism, a disturbance of the Ke/Ki ratiomay not occur until there is marked depletionof the body potassium and ECG changes canbe expected to be delayed. Thus, it isconceivable that the effects of the electrolytederangement on the ECG may depend to asignificant degree on the presence or absenceof renal regulation of serum electrolytes.8

Among hyperkalemic changes, LBBB wasreported as rare finding and was associated withsevere hyperkalemia (>8.0 mEq/L). In a study10

of atrioventricular and intraventricularconduction in hyperkalemia (n=12) the authorsreported isolated left posterior hemi-block(LPHB) in 4; isolated left anterior hemi-block(LAHB) in 2; RBBB with LAHB in 2; RBBBwith LPHB in 1; LBBB with abnormal left axisdeviation in 2; and advanced atrio-ventricularblock in 1 patient.

Two cases with hyperkalemic ECG changeswith RBBB with left axis deviation in one caseand complete heart block in second case, whichdisappeared with treatment of hyperkalemiahave been reported.5 Hyperkalemia appears to

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potentiate subclinical conduction abnormalitiesespecially in the His-Purkinje system.

ECG changes of hyperkalemia are frequentlyconsistent at higher levels of serum K+ ( 7.8mEq/L) and often progressive.11 Amonghyperkalemic ECG changes, conduction blocksare infrequent and also LBBB is rare comparedto RBBB. LBBB, which was a rare report inliterature, was documented in our patient, inaddition to the other ECG findings.

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