Paroxysmal Ventricular Fibrillation in TwoPatients with Hypomagnesemia

Treatment by Transvenous Pacing

By HENRY S. LOEB, M.D., RAYMOND J. PIETRAS, M.D.,

ROLF M. GUNNAR, M.S., M.D., AND JOHN R. TOBIN, JR., M.S., M.D.

SUMMARYParoxysmal ventricular fibrillation unassociated with heart block occurred in two

patients with hypomagnesemia. In neither patient were other causes of the arrhythmiaapparent. Temporary transvenous pacing successfully suppressed the episodes afterdrug therapy failed. Prolongation of the Q-T interval was a prominent electrocardio-graphic feature in both patients and is postulated to have resulted from a loss of intra-cellular potassium secondary to hypomagnesemia.

Additional Indexing Words:Adams-Stokes attacks Electrocardiographic featuresArrhythmia

pAROXYSMAL ventricular fibrillation is a 1 day priorcommon cause of Adams-Stokes attacks in of excessive

patients with complete heart block1-9 and The patient I

has been observed occasionally in patients She had no lwithout heart block.5 6 10-16 Two such cases disease.are reported herein. Each patient presented On physicwith recurrent seizures due to ventricular ly nourishedfibrillation refractory to usual modes of ther- apparent disapy, but controlled by catheter pacing. ature was niHypomagnesemia was documented in both vealed findiipatients and suggests a mechanism for the regurgitationamination w.arrhythmias. of pelvic infl

yielded norReport of Cases sion the he]

Case 1 ml. Levels (

B. W., a 29-year-old Negro female, was admitted bumin, globtto the hospital because of convulsions beginning ase were n(

potassium wchloride 89 I

From the Hektoen Institute for Medical Research The serumof the Cook County Hospital and the Departments mEq/L onof Medicine of the University of Illinois College of day, and 0.Medicine and the Stritch School of Medicine of studies incluLoyola University, Chicago, Illinois. preparation,

This investigation was supported in part by Grants selected viraHE-08834-03 and HE-09666-02 from the NationalInstitutes of Health, U.S. Public Health Service, Hospital Couand Grant C66-45 from the Chicago Heart Associa- Serial eletion. next several

210

Potassium deficiency

to admission following several weeksintake of alcohol and malnutrition.had had "asthma" since childhood andddicted to alcohol for several years.past history of cardiac or neurological

al examination, the patient was poor-1, but alert, cooperative, and in no;tress. Blood pressure was 110/60 mm,as 90 beats/min and regular; temper-iormal. Examination of the heart re-ings consistent with minimal aortici. The remainder of the physical ex-ras unremarkable except for evidencelammatory disease. Lumbar puncturemal cerebrospinal fluid. On admis-moglobin value was 8.7 g per 100of blood glucose, urea nitrogen, al-ulin, protein-bound iodine, and amyl-ormal. The concentration of serum7as 3.5 mEq/L; sodium 126 mEq/L;mEq/ L; and calcium 9.6 mg/ 100 ml.magnesium concentrations were 0.5admission, 0.6 mEq/L the following.7 mEq/L 6 days later. Additionalding blood cultures, Kahn test, L.E.ASO titers, and antibody titers to

1 antigens were negative.

irse

-ctrocardiograms recorded over thehours (fig. 1) revealed a pattern

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PAROXYSMAL VENTRICULAR FIBRILLATION

B.W am. 5/27165 LEAD II

c. 12:25 d. 12:29a.12:04 b. 12:08

e.12.'35

9.12:45 h. 1 :47 i. 12:48 k. 12:52

1.12:54 m. 1:00 n. 1:03 1:06

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P. 1:10 i. :13 r. 1:1T

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Figure 1Case 1. Lead II of the electrocardiogram recorded from 12:04 to 1:22 a.m. (a-d) Sinus rhythmwith progressive increase in the Q-T interval is seen. There is no evidence of heart block. In(e) bigeminal rhythm appears and reappears (in f) following a brief episode of ventricularfibrillation. (g and h) A longer episode of ventricular fibrillation was associated with a grandmal seizure. Following the seizure sinus rhythm ensues (j) and the Q-T interval again in-creases (k-r) until bigeminal rhythm reappears (s-u).

characterized by sinus rhythm, followed by bigem-inal rhythm, multifocal ventricular complexes, andventricular fibrillation terminating spontaneouslyin sinus rhythm. It was noted that the Q-T inter-val lengthened progressively prior to the appear-Circulation, Volume XXXVII, February 1968

ance of bigeminy but returned to a near normalduration immediately following ventricular fibril-lation. Although several brief periods of ventricularfibrillation were unaccompanied by clinical se-quelae, longer episodes were observed during

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LOEB ET AL.

which the patient lost consciousness and de-veloped tonic convulsions. Therapy includingprocainamide, diphenylhydantoin, potassium, cal-cium chloride, and 50% solution of glucose failedto prevent the arrhythmia. Although each epi-sode appeared to terminate spontaneously, thepossibility of a single fatal episode prompted in-stitution of artificial cardiac pacing as a means ofcontrolling the rhythm. A bipolar pacing catheterwas inserted without difficulty and pacing fromthe right ventricle appeared to be effective inpreventing further episodes of ventricular fibrilla-tion. Yet, several hours after pacing had beenstarted, the patient again lost consciousness andconvulsed. An electrocardiogram revealed ab-sence of artificial pacing which was found to bedue to battery failure. Upon battery replacement,pacing was reinstituted and continued for 24hours during which no further arrhythmia orseizures occurred. Pacing was then discontinued,and sinus rhythm without ventricular ectopicbeats ensued. Recovery was uneventful.

F.R.

Prior to discharge, myocardial biopsy was per-formed at open operation which revealed onlyminimal edema of the myocardium on light mi-croscopy. When last seen, the patient felt well,cardiac findings were unchanged, and the elec-trocardiogram showed a normal Q-T interval. Theserum magnesium concentration was 1.0 mEq/L.

Case 2F. R., a 24-year-old Negro female, was ad-

mitted because of loss of consciousness associatedwith convulsive seizures. Prior to admisssion thepatient had been taking digoxin and hydrochloro-thiazide for what was considered to be mildrheumatic heart disease. On the day of admissionshe had felt well except for slight fatigue afterreturning from a shopping trip. On awakeningfrom a brief nap, the first of several seizuresoccurred. Ingestion of more than her daily dosageof digoxin was denied.

Examination revealed an alert, anxious Negrofemale who was hyperventilating and vomiting.

LEA D 1

a.

b.

C.

Figure 2Case 2. Lead I of the electrocardiogram. (a and b) A continuous tracing taken shortly beforepacing. Sinus rhythm is present and the Q-T interval measures 0.52 sec. A few multifocalventricular complexes lead into ventricular fibrillation which after a few seconds terminatesspontaneously with resumption of sinus rhythm. Similar but longer episodes were associatedwith seizures. (c) Recorded during a clinic visit 6 months later. The Q-T interval measures0.4 sec.

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Blood pressure was 110/40, pulse 80 with bigem-iny, and rectal temperature 100 F. Auscultationof the heart disclosed a loud apical third heartsound and murmurs characteristic of mitral andaortic regurgitation. Physical examination wasotherwise negative. Since digitalis intoxicationwas suspected, potassium chloride was admin-istered parenterally prior to withdrawal of bloodfor electrolyte determination. Several hours later,values for the serum potassium were 3.9 mEqfL,sodium 137 mEq/L, and chloride 100 mEq/L.The serum magnesium concentration was 0.7mEq/L, increasing to 1.6 mEq/L by the sixthhospital day. Serum glutamic oxaloacetic trans-aminase (SGOT) values were 38, 78, 38, and 26units and values for lactic dehydrogenase (LDH)were 525, 1,575, and 930 units. Hemoglobin,white blood cell count, urea nitrogen, glucose,and icteric index were normal. Two L.E. prepara-tions were negative, and an ASO titer was 166Todd units.

Hospital CourseShortly after admission and coincident with the

appearance of ventricular fibrillation on the elec-trocardiogram, the first of many grand mal seiz-ures was observed. Between episodes, the rhythmwas sinus and regular or bigeminal. Treatmentwith potassium chloride, procainamide, and di-phenylhydantoin did not prevent the episodes(fig. 2a and b). Transvenous pacing was insti-tuted, and ventricular capture was accomplishedby pacing at 120/min preventing further ar-rhythmia. After 16 hours of pacing, the pacingunit was turned off, and normal sinus rhythmensued. Although the Q-T interval remained pro-longed for several days, the patient was asymp-tomatic and made an uneventful recovery.When last seen, although episodes of "ner-

vousness" and "hyperventilation syndrome" con-tinued, she had no cardiac symptoms and was nolonger taking digoxin or diuretics. Serum mag-nesium levels have been consistently normal sincedischarge. An electrocardiogram taken 6 monthsafter discharge (fig. 2c) showed a Q-T intervalof 0.4 sec.

DiscussionThe management of patients with recur-

rent ventricular arrhythmias unassociatedwith heart block is frequently difficult. Whenfactors such as electrolyte imbalance, hy-poxia, or hypotension are present, their cor-rection may suffice. In other instances ven-tricular irritability may be suppressed bydrugs. All too frequently, however, thesemethods are either ineffective or require dan-Circulation, Volume XXXVII, February 1968

gerous dosages of myocardial depressantdrugs. Artificial cardiac pacing has recentlybeen found effective in preventing recurrentventricular arrhythmias in patients who, likeour two patients, had repeated episodes notresponsive to conventional drug therapy.'4-20Although the mechanisms by which pacingis able to suppress ventricular arrhythmiasunassociated with heart block are obscure,increasing the heart rate appears to be animportant factor.20 In addition, since rapidatrial pacing has been as effective as rapidventricular pacing,'5' 18 changing the direc-tion of myocardial depolarization probablyplays no role.

In neither of our patients could the par-oxysms of ventricular fibrillation be explainedby their mild valvular lesions, and in neitherwas there evidence of active carditis. Bothpatients had hypomagnesemia without sig-nificant abnormalities of other serum elec-trolytes.

In case 1, the low serum magnesium can beexplained by alcoholism and malnutrition.2' 28In case 2, the cause of hypomagnesemia isless certain, but may have been related tothiazide therapy.29 Since potassium was givento this patient before determination of serumelectrolytes, hypokalemia could not be ex-cluded; however, prolongation of the Q-Tinterval persisted after the serum potassiumconcentration was known to be normal. An-xiety and hyperventilation were prominentfeatures of case 2, and both may be as-sociated with ventricular fibrillation.6 30Although neuromuscular abnormalities are

commonly associated with clinical hypomag-nesemia,31, 32 consistent cardiovascular man-ifestations have not been described. In ninehypomagnesemic patients, Randall and asso-ciates26 found it difficult to interpret electro-cardiographic changes because of associateddiseases and other electrolyte deficiencies.Nonspecific ST-segment and T-wave abnor-malities were noted and, in two instances,these disappeared after magnesium replace-ment. In Fankushen and co-workers',25 studiesof hypomagnesemic alcoholics, one patient'selectrocardiograms showed a prolonged Q-T

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interval persisting after all serum electrolytesexcept magnesium had returned to normal.Electrocardiographic changes found in experi-mental magnesium deficiency have included adecrease in the P-R and QRS intervals and in-verted T waves.33' 34 Seta and associates 35found T-wave peaking to be an early mani-festation of magnesium depletion, but whenmagnesium deficiency was prolonged, theelectrocardiographic changes resembled thoseof hypokalemia. These investigators alsofound that by making animals magnesiumdeficient, the duration of digitalis intoxica-tion could be prolonged.36Any relationship between hypomagnesemia

and the ventricular arrhythmias occurring inour patients remains speculative. In both pa-tients prolongation of the Q-T interval was aprominent electrocardiographic feature. Oth-ers12 17, 37, 38 have noted association betweena prolonged Q-T interval and ventricular ar-rhythmias, but no single mechanism satisfac-torily explains these observations. In the ab-sence of overt hypokalemia or hypocalcemia,a prolonged Q-T interval might be explainedby abnormalities in the relationship betweenintracellular and extracellular potassium. Fail-ure of potassium to reenter the depolarizedcell (delayed repolarization) or a diastolicleak of potassium from cells already re-polarized (early depolarization) could, ifasymmetrical, be recorded by the surfaceelectrocardiogram as a prolongation of theQ-T interval. Asynchronous repolarization isthought by Palmer39 to promote aberrantconduction, reentry phenomenon, and ven-tricular fibrillation. The role played by mag-nesium in the above scheme is derived fromits influence upon cell membrane permeabil-ity. In magnesium deficiency a reduction inthe activity of the magnesium dependent en-zyme (adenosine-triphosphatase) leads to aloss of intracellular potassium.36' 40, 41 Thus,the magnesium deficiency in our patientsmay have caused a loss of intracellular po-tassium leading to prolongation of the Q-Tinterval, increased vulnerability, and par-oxysms of ventricular fibrillation.

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TOBIN, JR.HENRY S. LOEB, RAYMOND J. PIETRAS, ROLF M. GUNNAR and JOHN R.

Treatment by Transvenous PacingParoxysmal Ventricular Fibrillation in Two Patients with Hypomagnesemia:

Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 1968 American Heart Association, Inc. All rights reserved.

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