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Second degree type II and complete atrioventricular block due to hyperkalemia
J. ELECTROCARDIOLOGY 19 (4), 1986, 393·396
Second Degree Type II and Complete Atrioventricular Block Due to Hyperkalemia BY JOSEPH MICHAELI, M.D.,* MAYER
M. BASSAN,
M.D.t AND MEIR BREZIS,
M.D.**
SUMMARY An 83-year-old woman was hospitalized with complete atrioventricular block and a pulse of 20/min. Three days earlier an electrocardiogram had revealed right bundle branch block with classic type II second degree atrioventricular block. Admission potassium was 7.8 meq/L; within 24 hours the potassium was lowered to 4.9 meq/L and the atrioventricular block disappeared. The patient was followed for nineteen months and remained normokalemic without recurrence of atrioventricular block, although the right bundle branch block persisted. She was then readmitted with bradycardia due to complete atrioventricular block despite normokalemia. We conclude that hyperkalemia can produce the classic picture of progressive bilateral bundle branch disease leading to high degree atrioventricular block, although this seems to occur in patients with extensive intrinsic disease of the conduction system.
In the past decade numerous reports have documented the ability of hyperkalemia to depress intraventricular conduction causing either diffuse QRS widening or the more specific patterns of bundle branch block or left hemifascicular block.>? Although acute administration of large doses of K + to dogs" or humans" was known to be capable of inducing advanced atrioventricular block, in 1973 Fisch stated that in "hyperkalemia due to the disease process per se and not due to administration of K +, A-V block greater than simple prolongation of the P-R is yet to be recorded." Wepresent a case of typical acute type II second degree atrioventricular block followed by complete heart block and syncope which were caused by hyperkalemia.
CASE REPORT An 83-year-old woman was admitted to the cardiac care unit after a syncopal episode, with an electrocardiogram which demonstrated complete atrioventricular block (Fig. IA). She was receiving a combination tablet containing hydrochlorothiazide 50 mg and the potassium-sparing diuretic amiloride 5 mg twice daily, as well as a low-sodium, high-potassium diet. Routine examinations nine months prior to admission had shown incomplete right bundle branch block (Fig. IB), serum potassium 4.4 meq/L, and urea 7.1 mmol/L. Three days prior to admission the patient was seen in the emergency room because of weakness, dizziness, palpitations, anorexia and vomiting of a week's duration. The serum potassium was 5.7 meq/L, the urea 22.4 mmol, and an electrocardiogram showed complete right bundle branch block with type II second degree atrioventricular block (Fig. Ie). Unexplainably, the patient was sent home with no change in therapy. On admission, blood pressure was 120/70 and pulse 22 beats/min. A temporary pacemaker was inserted immediately. Initial blood examinations revealed a serum potassium of 7.8 meq/L (repeat exam 8.0 meq/L), sodium 124 meq/L, urea 32.7 mmollL and creatinine 360 micromollL. Treatment was begun with intravenous glucose and insulin, and Kayexalate enemas. 'len hours after admission the potassium was 6.8 meq/L, and the patient was still pacemaker dependent with advanced atrioventricular block. By sixteen hours after admission the patient was in first degree atrioventricular block
... Lecturer, Department of Medicine, Hadassah University Hospital, Mount Scopus, Jerusalem. t Head, Cardiac Care Unit, Hadassah University Hospital, Mount Scopus, Jerusalem. ...... Senior Lecturer, Department of Medicine, Hadassah University Hospital, Mount Scopus, Jerusalem. From the Cardiac Care Unit and the Department of Internal Medicine, Hadassah University Hospital, Mount Scopus, Jerusalem, IsraeL The costs of publication of this article weredefrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.c. § 1734 solely to indicate this fact. Reprint requests to: J. Michaeli, M.D., Department of Hematology, Hadassah University Hospital, Ein Karem, P.O.B. 12000, Jerusalem 91 120, Israel.
393
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MICHAELI ET AL
with right bundle branch block. Serum potassium 22 hours after admission was 4.9 meq/L; the Kayexalate was discontinued. The patient was observed for another twelve days in the cardiac care unit without recurrence of advanced atrioventricular block. Followinghydration, serum potassium remained normal, and the urea fell gradually to 7.5 mmol/L. The right bundle branch block and borderline first degree atrioventricular block persisted (Fig. lD) . There was no enzyme rise or electrocardiographic finding to suggest acute myocardial infarction. The patient was discharged without a pacemaker and was followed without any signs or symptoms suggestive of advanced atrioventricular block. An electrocardiogram fifteen months after discharge showed right bundle branch block with a borderline PR interval. Serum potassium was 4.7 meq/L and urea 6.8 mmol/L. Nineteen months after the initial hospitalization, the patient was admitted again due to weakness and bradycardia. The electrocardiogram revealed complete atrioventricular block alternating with type II second degree atrioventricular block.
Serum K + was normal. The electrocardiogram further revealed the Q waves of an anteroseptal myocardial infarction not present nineteen months earlier, but present, in retrospect, on the electrocardiogram taken four months prior to the second admission (Fig. IE). After the atrioventricular block had persisted for seven days, a permanent pacemaker was inserted.
DISCUSSION The following factors weigh heavily in favor of a cause and effect relationship between the hyperkalemia and the atrioventricular block: (1) The temporal contiguity between the hyperkalemia and the appearance and disappearance of the block, (2) The absence of any other acute cause for atrioventricular block (e.g, acute myocardial infarction), and (3) The failure of atrioventricular block to recur during an observation period in excess of one year. Despite the circumstantial evidence favoring the etiologic role of hyperkalemia in our patient's conduction disturbance, the absence of the other expected manifestations of hyperkalemia, i.e. diffuse
B
c \I
o
E
Fig. 1. A. Admission: Complete A-V block with slowidioventricular rhythm. B. Nine months prior to admission: IRBBB. C. Three days prior to admission: 'Iypical Mobitz II second degree A-V block with fixed PR interval. D. Fourteenth hospital day: RBBB. E. Fifteen months later: RBBB.
J. ELEGrROCARDIOLOGY 19 (4), 1986
AN BLOCK DUE TO HYPERKALEMIA
QRS widening and disappearance of P waves, raises doubt concerning this explanation. Indeed, most of the reported cases of hyperkalemia-induced bundle branch block have been accompanied by evidence of diffuse depression of myocardial conduction in both atria and ventricles. Bashour et al. however, have shown that hyperkalemia can produce at least left fascicular blocks without concomitant severe myocardial tissue conduction depression,' and hyperkalemic block has been induced in animal without P wave abnormalities.t? In addition, we have personal knowledge of at least one patient, described by Leor and Stalnikowitz," who developed reversible left bundle block in association with hyperkalemia. Whenever the serum K + level was lowered with Kayexalate the bundle branch block disappeared. In this case the bundle branch block was of the classic type with no P wave abnormality. In our patient the right bundle branch block was most likely unrelated to the hyperkalemia, since at least incomplete right bundle branch block was known to be present well before the hyperkalemia, and complete right bundle branch block persisted after the latter was corrected. We assume that the hyperkalemia produced intermittent and then fixed left bundle branch block, which in the presence of right bundle branch block caused type II second degree and then complete atrioventricular block. Since Fisch's statement in 1973 several observers have reported transient advanced atrioventricular block in "spont aneous hyperkalemia': Cohen et al.3 described three cases of advanced atrioventricular block, one nodal and two apparently infranodal. These authors noted that all their cases of atrioventricular block had pre-existent bundle branch or fascicular block, and that the hyperkalemia aggravated these or caused additional delays. This observation holds true in our case also. Bashour et al.' described a patient with a severalsecond period of advanced atrioventricular block and a serum potassium of 8.2 meq/L. Ohmae and Rabkin" presented a patient with atrial fibrillation who developed transient right bundle branch block .and then apparent complete heart block due to hyperkalemia. Finally Przybojewski and KnottCraig described a case similar to our own of an 81-year-old male with renal failure and temporary complete atrioventricular block due to transient hyperkalemia.P
J. ELECTROCARDIOLOGY 19 (4), 1986
395
We believe the uniqueness, and hence clinical significance of our case lies in the fact that, except for the hyperkalemia, the patient seemed to represent a typical case ofprogressivedisease of the bundle branches culminating in a Stokes- Adams attack due to complete atrioventricular block. The usual findings of severe hyperkalemia, such as extreme widening of the QRS or disappearance of the P waves, were not seen. It is possible that the second and apparently permanent development of atrioventricular block was related to an intercurrent silent anterior M·I although it seems more likely to represent a progression of the initial process. Assuming the latter to be true, it confirms Rosen's observation that ''hyperkalemia is most likely to produce advanced conduction defects in patients with preexistent conduction diseasa?" In fact, it may be advisable for the patient with residual conduction defects to receive a permanent pacemaker despite the disappearance of atrioventricular block upon correction of the hyperkalemia.
REFERENCES 1. BASHOUR, T, Hsu, I , GORFINKEL, H J, WICKRAMESEKARAN, RAND Bros, J C: Atrioventricular and intraventricular conduction in hyperkalemia. Am J Cardiol35: 199, 1975 2. COHEN, H C, Gozo, E G AND PICK, C:The nature and type of arrhythmias in acute experimental hyperkalemia in the intact dog. Am HeartJ 82: 777, 1971 3. COHEN, H C, ROSEN, K M AND P ICK, A: Disorders of impulse conduction and impulse formation caused by hyperkalemia in man. Am Heart J 89: 501, 1975 4. LICHSTEIN, E, GUPTA, P K AND GRUNWALD, A A: Hyperkalemic fascicular block. Chest 70: 290,1976 5. OHMAE, M AND RABKIN, S W: Hyperkalemiainduced bundle branch block and complete heart block. Clin Cardiol 4: 43, 1981 6. O'NEIL, J P AND CHUNG, E: Unusual electrocardiographic finding- bifascicular block due to hyperkalemia. Am J Med 61: 537, 1976 7. PUNJA, M M, SCHNEEBAUM, R AND COHEN, J: Bifascicular block induced by hyperkalemia J Electrocardiol 6: 71, 1973 8. ENSELBERG, C D, SIMMONS, H G AND MINTZ, A A: The effects of potassium upon the heart with special reference to the possibility of treatment of toxic arrhythmias due to digitalis. Am Heart J 39: 713, 1950 9. FISCH, C: Relation of electrolyte disturbances to cardiac arrhythmias. Circulation 47: 408, 1973
396 10.
MICHAELI ET AL
FISCH, C, GREENSPAN, K AND EDWARDS, R E: Complete atrioventricular block due to potassium. Cire Res 19: 373, 1966 11. LEOR, RAND STALNIKOWICZ, R: Hyperkalemic left bundle branch block and hyporeninemic hypoaldosteronism (hyperkalemic left bundle branch block). J Electrocardiol19: 93, 1986
12.
PnZYBOJEWSKI, J Z AND KNOTT-CRAIG , C J: Hyperkalemic complete heart block. A report of 2 unique cases and a review of the literature. SA Med J 63: 413, 1983
13.
RoSEN,
K M: Hyperkalemic conduction disturbances. JAMA 230: 90, 1974
J. ELECTROCARDIOLOGY 19 (4),1986
Second Degree Type II and Complete Atrioventricular Block Due to Hyperkalemia BY JOSEPH MICHAELI, M.D.,* MAYER
M. BASSAN,
M.D.t AND MEIR BREZIS,
M.D.**
SUMMARY An 83-year-old woman was hospitalized with complete atrioventricular block and a pulse of 20/min. Three days earlier an electrocardiogram had revealed right bundle branch block with classic type II second degree atrioventricular block. Admission potassium was 7.8 meq/L; within 24 hours the potassium was lowered to 4.9 meq/L and the atrioventricular block disappeared. The patient was followed for nineteen months and remained normokalemic without recurrence of atrioventricular block, although the right bundle branch block persisted. She was then readmitted with bradycardia due to complete atrioventricular block despite normokalemia. We conclude that hyperkalemia can produce the classic picture of progressive bilateral bundle branch disease leading to high degree atrioventricular block, although this seems to occur in patients with extensive intrinsic disease of the conduction system.
In the past decade numerous reports have documented the ability of hyperkalemia to depress intraventricular conduction causing either diffuse QRS widening or the more specific patterns of bundle branch block or left hemifascicular block.>? Although acute administration of large doses of K + to dogs" or humans" was known to be capable of inducing advanced atrioventricular block, in 1973 Fisch stated that in "hyperkalemia due to the disease process per se and not due to administration of K +, A-V block greater than simple prolongation of the P-R is yet to be recorded." Wepresent a case of typical acute type II second degree atrioventricular block followed by complete heart block and syncope which were caused by hyperkalemia.
CASE REPORT An 83-year-old woman was admitted to the cardiac care unit after a syncopal episode, with an electrocardiogram which demonstrated complete atrioventricular block (Fig. IA). She was receiving a combination tablet containing hydrochlorothiazide 50 mg and the potassium-sparing diuretic amiloride 5 mg twice daily, as well as a low-sodium, high-potassium diet. Routine examinations nine months prior to admission had shown incomplete right bundle branch block (Fig. IB), serum potassium 4.4 meq/L, and urea 7.1 mmol/L. Three days prior to admission the patient was seen in the emergency room because of weakness, dizziness, palpitations, anorexia and vomiting of a week's duration. The serum potassium was 5.7 meq/L, the urea 22.4 mmol, and an electrocardiogram showed complete right bundle branch block with type II second degree atrioventricular block (Fig. Ie). Unexplainably, the patient was sent home with no change in therapy. On admission, blood pressure was 120/70 and pulse 22 beats/min. A temporary pacemaker was inserted immediately. Initial blood examinations revealed a serum potassium of 7.8 meq/L (repeat exam 8.0 meq/L), sodium 124 meq/L, urea 32.7 mmollL and creatinine 360 micromollL. Treatment was begun with intravenous glucose and insulin, and Kayexalate enemas. 'len hours after admission the potassium was 6.8 meq/L, and the patient was still pacemaker dependent with advanced atrioventricular block. By sixteen hours after admission the patient was in first degree atrioventricular block
... Lecturer, Department of Medicine, Hadassah University Hospital, Mount Scopus, Jerusalem. t Head, Cardiac Care Unit, Hadassah University Hospital, Mount Scopus, Jerusalem. ...... Senior Lecturer, Department of Medicine, Hadassah University Hospital, Mount Scopus, Jerusalem. From the Cardiac Care Unit and the Department of Internal Medicine, Hadassah University Hospital, Mount Scopus, Jerusalem, IsraeL The costs of publication of this article weredefrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.c. § 1734 solely to indicate this fact. Reprint requests to: J. Michaeli, M.D., Department of Hematology, Hadassah University Hospital, Ein Karem, P.O.B. 12000, Jerusalem 91 120, Israel.
393
394
MICHAELI ET AL
with right bundle branch block. Serum potassium 22 hours after admission was 4.9 meq/L; the Kayexalate was discontinued. The patient was observed for another twelve days in the cardiac care unit without recurrence of advanced atrioventricular block. Followinghydration, serum potassium remained normal, and the urea fell gradually to 7.5 mmol/L. The right bundle branch block and borderline first degree atrioventricular block persisted (Fig. lD) . There was no enzyme rise or electrocardiographic finding to suggest acute myocardial infarction. The patient was discharged without a pacemaker and was followed without any signs or symptoms suggestive of advanced atrioventricular block. An electrocardiogram fifteen months after discharge showed right bundle branch block with a borderline PR interval. Serum potassium was 4.7 meq/L and urea 6.8 mmol/L. Nineteen months after the initial hospitalization, the patient was admitted again due to weakness and bradycardia. The electrocardiogram revealed complete atrioventricular block alternating with type II second degree atrioventricular block.
Serum K + was normal. The electrocardiogram further revealed the Q waves of an anteroseptal myocardial infarction not present nineteen months earlier, but present, in retrospect, on the electrocardiogram taken four months prior to the second admission (Fig. IE). After the atrioventricular block had persisted for seven days, a permanent pacemaker was inserted.
DISCUSSION The following factors weigh heavily in favor of a cause and effect relationship between the hyperkalemia and the atrioventricular block: (1) The temporal contiguity between the hyperkalemia and the appearance and disappearance of the block, (2) The absence of any other acute cause for atrioventricular block (e.g, acute myocardial infarction), and (3) The failure of atrioventricular block to recur during an observation period in excess of one year. Despite the circumstantial evidence favoring the etiologic role of hyperkalemia in our patient's conduction disturbance, the absence of the other expected manifestations of hyperkalemia, i.e. diffuse
B
c \I
o
E
Fig. 1. A. Admission: Complete A-V block with slowidioventricular rhythm. B. Nine months prior to admission: IRBBB. C. Three days prior to admission: 'Iypical Mobitz II second degree A-V block with fixed PR interval. D. Fourteenth hospital day: RBBB. E. Fifteen months later: RBBB.
J. ELEGrROCARDIOLOGY 19 (4), 1986
AN BLOCK DUE TO HYPERKALEMIA
QRS widening and disappearance of P waves, raises doubt concerning this explanation. Indeed, most of the reported cases of hyperkalemia-induced bundle branch block have been accompanied by evidence of diffuse depression of myocardial conduction in both atria and ventricles. Bashour et al. however, have shown that hyperkalemia can produce at least left fascicular blocks without concomitant severe myocardial tissue conduction depression,' and hyperkalemic block has been induced in animal without P wave abnormalities.t? In addition, we have personal knowledge of at least one patient, described by Leor and Stalnikowitz," who developed reversible left bundle block in association with hyperkalemia. Whenever the serum K + level was lowered with Kayexalate the bundle branch block disappeared. In this case the bundle branch block was of the classic type with no P wave abnormality. In our patient the right bundle branch block was most likely unrelated to the hyperkalemia, since at least incomplete right bundle branch block was known to be present well before the hyperkalemia, and complete right bundle branch block persisted after the latter was corrected. We assume that the hyperkalemia produced intermittent and then fixed left bundle branch block, which in the presence of right bundle branch block caused type II second degree and then complete atrioventricular block. Since Fisch's statement in 1973 several observers have reported transient advanced atrioventricular block in "spont aneous hyperkalemia': Cohen et al.3 described three cases of advanced atrioventricular block, one nodal and two apparently infranodal. These authors noted that all their cases of atrioventricular block had pre-existent bundle branch or fascicular block, and that the hyperkalemia aggravated these or caused additional delays. This observation holds true in our case also. Bashour et al.' described a patient with a severalsecond period of advanced atrioventricular block and a serum potassium of 8.2 meq/L. Ohmae and Rabkin" presented a patient with atrial fibrillation who developed transient right bundle branch block .and then apparent complete heart block due to hyperkalemia. Finally Przybojewski and KnottCraig described a case similar to our own of an 81-year-old male with renal failure and temporary complete atrioventricular block due to transient hyperkalemia.P
J. ELECTROCARDIOLOGY 19 (4), 1986
395
We believe the uniqueness, and hence clinical significance of our case lies in the fact that, except for the hyperkalemia, the patient seemed to represent a typical case ofprogressivedisease of the bundle branches culminating in a Stokes- Adams attack due to complete atrioventricular block. The usual findings of severe hyperkalemia, such as extreme widening of the QRS or disappearance of the P waves, were not seen. It is possible that the second and apparently permanent development of atrioventricular block was related to an intercurrent silent anterior M·I although it seems more likely to represent a progression of the initial process. Assuming the latter to be true, it confirms Rosen's observation that ''hyperkalemia is most likely to produce advanced conduction defects in patients with preexistent conduction diseasa?" In fact, it may be advisable for the patient with residual conduction defects to receive a permanent pacemaker despite the disappearance of atrioventricular block upon correction of the hyperkalemia.
REFERENCES 1. BASHOUR, T, Hsu, I , GORFINKEL, H J, WICKRAMESEKARAN, RAND Bros, J C: Atrioventricular and intraventricular conduction in hyperkalemia. Am J Cardiol35: 199, 1975 2. COHEN, H C, Gozo, E G AND PICK, C:The nature and type of arrhythmias in acute experimental hyperkalemia in the intact dog. Am HeartJ 82: 777, 1971 3. COHEN, H C, ROSEN, K M AND P ICK, A: Disorders of impulse conduction and impulse formation caused by hyperkalemia in man. Am Heart J 89: 501, 1975 4. LICHSTEIN, E, GUPTA, P K AND GRUNWALD, A A: Hyperkalemic fascicular block. Chest 70: 290,1976 5. OHMAE, M AND RABKIN, S W: Hyperkalemiainduced bundle branch block and complete heart block. Clin Cardiol 4: 43, 1981 6. O'NEIL, J P AND CHUNG, E: Unusual electrocardiographic finding- bifascicular block due to hyperkalemia. Am J Med 61: 537, 1976 7. PUNJA, M M, SCHNEEBAUM, R AND COHEN, J: Bifascicular block induced by hyperkalemia J Electrocardiol 6: 71, 1973 8. ENSELBERG, C D, SIMMONS, H G AND MINTZ, A A: The effects of potassium upon the heart with special reference to the possibility of treatment of toxic arrhythmias due to digitalis. Am Heart J 39: 713, 1950 9. FISCH, C: Relation of electrolyte disturbances to cardiac arrhythmias. Circulation 47: 408, 1973
396 10.
MICHAELI ET AL
FISCH, C, GREENSPAN, K AND EDWARDS, R E: Complete atrioventricular block due to potassium. Cire Res 19: 373, 1966 11. LEOR, RAND STALNIKOWICZ, R: Hyperkalemic left bundle branch block and hyporeninemic hypoaldosteronism (hyperkalemic left bundle branch block). J Electrocardiol19: 93, 1986
12.
PnZYBOJEWSKI, J Z AND KNOTT-CRAIG , C J: Hyperkalemic complete heart block. A report of 2 unique cases and a review of the literature. SA Med J 63: 413, 1983
13.
RoSEN,
K M: Hyperkalemic conduction disturbances. JAMA 230: 90, 1974
J. ELECTROCARDIOLOGY 19 (4),1986