Rate Dependent Bundle Branch Block Inducedby HyperkalemiaNAVEEN MANOHAR and MING-LON YOUNGFrom the Department of Pediatrics, University of Miami, Florida

IntroductionAn increase in serum potassium can be fol-

lowed by severe and progressive cardiac electro-physiological derangement. In the surface elec-trocardiogram hyperkalemia is manifested withwidening of the QRS due to the conduction de-lay in the specialized conduction system and themyocardium. This article describes an unique caseof rate dependent bundle branch block caused byhyperkalemia.

Case ReportA.M. is a 14-day-old premature girl born at

29 weeks of gestation with a birth weight of 730 gand good Apgar scores (1 minute, 8; 5 minutes,9). Her blood urea nitrogen and creatinine startedto increase at the 7th day of life and remainedfairly constant until day 14. Her electrolytes on day13 showed a sodium of 132 meq/L, potassium of4.2 meq/L, CO2 of 23, urea nitrogen of 24 mg/dL,and creatinine of 1.3 mg/dL. She also developedepisodes of apnea and bradycardia requiring intu-bation and ventilatory support on the 13th day oflife.

On day 14 she developed a pnemothoraxthat prompted a chest tube insertion. Cardiac ar-rhythmias were noticed on the cardiac monitor.A rhythm strip (Fig. 1) showed sinus arrhyth-mia with varied P-P intervals (530–410 ms) anda relatively constant and prolonged P-R interval of180 ms (because some P waves fell into the QRS-Tcomplexes thus it was uncertain this was Mobitztype I atrioventricular block). Immediately follow-ing the ninth QRS-T complex after a long pauseof 740 ms, the next cardiac cycle had a relativelynarrow QRS (80 ms). This was followed by a ratedependent right bundle branch block; the R-R in-tervals decreased progressively from 740 to 380 mswith a gradual widening of the QRS complexes(80–150 ms). The arterial blood gas showed: pH6.8, pCO2 67, pO2 75, HCO3 12, and base excess- 22. The electrolytes drawn at this time showed:sodium 130 meq/L, potassium 8.8 meq/L, CO2 11,urea nitrogen 72 mg/dL, and creatinine 2.7 mg/dL.

Address for reprints: Ming Young, M.D., Department of Pedi-atrics, University of Miami, (R-76), P.O. Box 016960, Miami, FL33101. Fax: (305) 324-6012; e-mail: MYoung@miami.edu

Received January 14, 2003; revised March 21, 2003; acceptedApril 8, 2003.

The baby was managed with kayexelate,NaHCO3, calcium, insulin, and glucose. Theelectrolyte abnormalities were corrected within24 hours and her blood urea nitrogen and crea-tinine on day 20 were 28 mg/dL and 1.7 mg/dL.The cause for her sudden and profound metabolicacidosis, hyperkalemia, and renal failure hasnot been ascertained. After normalization of theelectrolytes her electrocardiogram became un-remarkable. There was no recurrence of therate dependent bundle branch block even whenshe had sinus tachycardia with a cardiac cyclelength that was <400 ms. The baby was stablethereafter.

DiscussionThe cardiac sensitivity to potassium is maxi-

mal in the atrium and the ventricle and least in thespecialized conduction system. There have beenseveral reports of left- or right-axis deviation ofthe QRS,1 bifascicular block,2,3 and right bundlebranch block that are normalized after treatmentof hyperkalemia.4 A rate dependent nature to thesebocks have not seen described in hyperkalemia.

Rate dependent bundle branch block occurswhen the cycle length falls below the refractory pe-riod of the bundle branch. Normally, the refractoryperiod of the bundle branch is shorter than the car-diac cycle length in a normal physiological rangeof heart rate. With a decrease in cycle length, the re-fractory period of the bundle branch normally de-creases.5 Therefore, rate dependent bundle branchblock might occur when there is an absence of thisexpected decrease in the refractory period of thebundle branch with the decrease in cardiac cyclelength, or due to an absolute increase in the bun-dle branch refractory period, or a combination ofthe two.6

In the present patient, below the cycle lengthof 440 ms there was a gradual progression intoa complete bundle branch block manifested by aprogressive widening of the QRS when the car-diac cycles were decreased further. The pause inthe rhythm strip might be caused by an impair-ment of the sinus node impulse generation sec-ondary to hyperkalemia, or a subtle progressivelengthening of PR intervals followed by a blockedP wave that was buried inside the widened QRS-Tcomplex (i.e., Mobitz type I atrioventricular con-duction block). This transient pause permitted thenext atrial impulse conduct to the ventricle in arelatively normal pattern.

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Figure 1. Rhythm strip showing rate dependent right bundle branch block (the middle third of this rhythm strip leadII is enlarged for clarity)(see Text for details).

References1. Pryor R, Blount SG Jr. The clinical significance of true left axis de-

viation, left intraventricular blocks. Am Heart J 1966; 72:391–413.2. Punja MM, Schneebaum R, Cohen J. Bifascicular block induced by

hyperkalemia. Electrocardiology 1973; 6:71–76.3. O’Neil JP, Chung EK. Unusual electrocardiographic finding—

bifascicular block due to hyperkalemia. Am J Med 1976; 61:537–540.4. Fisch C, Knoebel SB, Feigenbaum H, et al. Potassium and monopha-

sic action potentials, electrocardiogram, conduction and arrhyth-mias. Progr Cardiovasc Dis 1966; 8:387–418.

5. Denes P, Wu D, Dhingra R, et al. The effects of cycle length on cardiacrefractory periods in man. Circulation 1974; 49:32–41.

6. Denes P, Wu D, Dhingra RC, et al. Electrophysiological observationsin patients with rate dependent bundle branch block. Circulation1975; 51:244–250.

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