Cardiac Arrest Due to Oral Potassium Administration
HERBERT N. HULTGREN, M.D. ROBERT SWENSON,
M.D.
GEORGE WETTACH,
M.D.
Palo Alto, California
Cardiac arrest developed in two patients afler the administration of oral potassium. Neither patient had renal insufficiency, but both had underlying heart disease. In one patient fatal ventricular fibrillation developed 4 days after he received an aortic valve replacement for aortic stenosis and while he was receiving oral potassium supplements. The serum potassium level before cardiac arrest was 8.1 meq. The second patient had angina and was given 40 meq of potassium orally 15 minutes after an exercise test which produced chest pain and S-T segment depression. One hour later, ventricular fibrillation developed. Resuscitation was successful. Both patients had electrocardiographic evidence of hyperkalemia. Oral administration of potassium may produce severe cardiac toxicity in patients with heart disease even when renal function is clinically normal. Cardiac arrest due to hyperkalemia is usually associated with the intravenous administration of potassium in patients with renal insufficiency. In some instances the oral administration of potassium, the use of potassium-retaining diuretics, acidosis or multiple blood transfusions may be accompanied by lethal hyperkalemia in the presence of moderate renal impairment. Cardiac arrest due to oral potassium ingestion with clinically normal renal function is rare. Hyperkalemia is an important cause of cardiac arrest, and Burchell [l] has suggested that more lives have been lost than saved by potassium therapy. Our purpose is to describe two instances of hyperkalemic cardiac arrest due to oral potassium administration in patients without clinical evidence of renal disease and to evaluate some of the causative mechanisms involved. CASE
REPORTS
Case 1. A 56 year old farm worker (A.V.G.) with severe aortic stenosis underwent aortic valve replacement (fresh aortic homograft) on cardiopulmonary bypass on March 17, 1970. Preoperatively, a complete left bundle branch
block was present
m*. Angiography
revealed
(Figure 1). The aortic valve area was 0.6 cm*/ moderate
2-F (O-4) aortic regurgitation,
normal
proximal coronary arteries and normal ventricular contraction. The ejection fraction was 80 per cent. At surgery, the mitral valve and coronary From the Medical Service, Palo Alto Veterans Administration Hospital, Palo Alto, California; and the Department of Medicine, Stanford Medical School, Stanford, California. Requests for reprints should be addressed to Dr. Herbert N. Hultgren, Cardiology Service, Veterans Administration Hospital, 3801 Miranda Avenue, Palo Atto, California 94304. Manuscript accepted March 12, 1974.
arteries
were
cross clamp
normal.
units of packed The
Total perfusion
time was 52 minutes.
was
69 minutes,
and aortic
red cells were given during surgery.
immediate
postoperative
were no significant
course
electrocardiographic
that suggested myocardial damage erative days, occasional ventricular were suppressed
time
Six units of fresh whole blood and 4
by xylocaine
January 1975
was
uncomplicated,
changes
and there
or serum enzyme
rises
during surgery. On the first 2 postoppremature beats were present which
infusion.
The American Journal of Medicine
Volume 58
139
CARDIAC ARREST AND POTASSIUM ADMINISTRATION-HULTGEN
ET AL.
aVR
aVL
aVF Electrocardiogram recorded immediately beFigure 2. fore death. Wide 01% complexes and absence of atrial activity are compatible with hyperkalemia. Serum potassium was 8.4 meqlliter.
Figure 1. Case 1. Preoperative electrocardiogram showing left bundle branch block, left axis deviation and abnormal P waves, and ventricular premature beats. day, 100 meq of potassium The serum potassium level rose from 4.0 to 6.9 meq/liter; electrocardiographic signs of moderate hyperkalemia were noted, and potassium therapy was discontinued. The patient was given a 1.O g sodium diet. Electrolyte and laboratory data are summarized in Table I. On the 2nd postoperative day, the patient was ambulatory with assistance, and he was transferred to the ward. The serum potassium level was 5.1 meq/liter. The oral adOn the first postoperative
was
given
TABLE
I
parenterally.
Case 1. Laboratory
Time of Study 3112 3116 Postoperatively 2 hours 9 hours 1st day 2nd day 3rd day 4th day 5th day
140
January 1975
ministration of 60 meq potassium (potassium triplex) was started three times daily, along with 0.25 mg digoxin and 500 mg chlorothiazide daily. These are routine postoperative measures in the Department of Surgery for patients undergoing valve replacement surgery. Unfortunately, neither blood urea nitrogen nor serum creatinine levels were determined during the first 4 postoperative days. Digoxin had been discontinued 5 days before surgery. On the 4th postoperative day, the patient experienced vague abdominal pain, nausea and vomiting. An abdominal roentgenogram was normal. On the 5th postoperative day, pallor and hypotension developed. The serum potassium was 8.1 meq and the blood urea nitrogen was 34 mg/ 100 ml. The electrocardiogram revealed periods of nodal and ventricular rhythm, and signs of hyperkalemia (Figure 2). Ventricular fibrillation occurred and resuscitation attempts failed. At autopsy, the total heart weight was 710 g, there was marked left ventricular hypertrophy and moderate left atrial hypertrophy. The coronary arteries were normal. The homograft valve was intact. There was no evidence of myocardial infarction. Histologic examination of the myocardium revealed several small scattered areas of myocardial necrosis with hemorrhage, neutrophilic exudation and myocytolysis. Hypertrophy of myocardial fibers was present. On histologic examination, the kidneys were normal as were the lungs and other organs.
Data During Hospital Course Supplemental Potassium Intake
Serum Creatinine (mg/lOO ml)
Blood Urea Nitrogen (mg/lOO ml)
Serum Potassium (meq/liter)
1.3 1.0
26 27
3.7 4.4
138 138
90 90
... ... . . .,. ... ...
4.0 6.9 5.9 5.1
141 138 136 128
100
...
...
... ...
130/90 120/90 100/75
... ...
. .
34
8.1
129
105 103 103 103 101 101
... . ...
The American Journal of Medicine
Volume 58
Serum Sodium (meq/liter)
(meq/day)
180 180 180 180
Weight
Blood Pressure
(kg)
(mm Hg)
106 105
100/70 go/70
.. ... 100/70
CARDIAC ARREST AND POTASSIUM ADMINISTRATION-HULTGEN
Electrocardiogram obtained after Figure 4. sion shows widening of the QRS complexes. leads were not recorded. recorded just before exercise test. Inferior lateral infarction, abnormal T waves and one ventricular premature beat are present.
Figure 3.
Case 2. Electrocardiogram
Case
2. This 58 year old man (R.S.) had stable angina pectoris of 3 years’ duration. The electrocardiogram (Figure 3) was compatible with an old inferior and lateral myocardial infarction which had occurred 2 years previously. He was not taking digitalis. Coronary arteriography revealed complete occlusion of the proximal right coronary artery, partial proximal occlusion of the left anterior descending coronary artery and irregular diffuse disease of the left circumflex branch. An exercise test (cycle ergometry) was positive with flat S-T segment depression occurring at a heart rate of 160/min. Chest pain was present at the end of the test and lasted for 2 minutes after exercise. No ventricular premature beats occurred in the immediate post-exercise electrocardiogram. Three minutes after the completion of the test, the electrocardiogram had reverted to the preexercise appearance. As part of a study of the effect of potassium upon ST-T wave changes occurring during exercise, the patient was given 40 meq potassium orally 15 minutes after cessation of the exercise test. One hour later, the test was to be repeated. As the mouthpiece was being adjusted, ventricular fibrillation developed. Conversion to a sinus rhythm was accomplished with DC shock, and the patient was brought to the Coronary Care Unit where he recovered uneventfully. The electrocardiogram after defibrillation is shown in Figure 4. The evident widening of the QRS complex is compatible with hyperkalemia. Two weeks before cardiac arrest, the patient’s urinalysis had been normal, serum sodium 140 meq/liter, serum potassium 5.0 meq/liter and blood urea nitrogen 37 mg/ 100 ml. At that time he was placed on a low salt diet (1,500 mg sodium chloride) without diuretics or oral potassium. On the day after his resuscitation, his urinalysis was normal, blood urea nitrogen 38 mg/lOO ml, sodium 130 meq/liter and potassium 5.5 meq/llter. Electrolytes were not determined on the day of the cardiac arrest. Two days
January
ET AL.
cardioverPrecordial
after resuscitation, the blood urea nitrogen was 36 mg/ 100 ml, sodium 138 meq/liter and potassium 4.2 meq/ liter. The electrocardiogram had reverted to the precardllc arrest pattern. Four weeks after resuscitation the patient had a Vineberg operation from which he recovered without complications. Four years later he died of a myocardial infarct. Autopsy revealed severe coronary disease and a recent infarct. The kidneys were grossly normal and weighed 150 g each. Histologic study revealed many patchy areas of interstitial fibrosis and inflammatory cell infiltrate. Many glomeruli were seen in various stages of fibrosis and hyalinization. COMMENTS Cardiac arrest in the first patient was clearly due to hyperkalemia. Characteristic electrocardiographic findings were present, the serum potassium level was elevated, and an excessive amount of potassium had been administered. There was no clinical evidence of other causes for the cardiac arrest. No evidence of renal disease was present. The preoperative blood urea nitrogen was 25 mg/lOO ml, the serum creatinine was 1 .O mg/ 100 ml, and the urinalysis was normal. No evidence of renal insufficiency was present during the immediate postoperative period. Urine output and the urinalysis were normal. Shortly before the cardiac arrest, the blood urea nitrogen was 34 mg/ 100 ml. At that time the patient had low blood pressure, periods of nodal rhythm and hyperkalemia. At autopsy, the kidneys and urinary tract were normal on gross and microscopic examination. Several factors probably accounted for the arrest in addition to the elevated serum potassium level. These include (1) rapid rise in serum potassium level, (2) low serum sodium or sodium depletion, (3) underlying cardiac disease and conduction defect (left bundle branch block) and (4) digitalis administration. The increase in serum potassium was not only due
1975
The American
Journal
of Medicine
Volume
58
141
CARDIAC ARREST AND POTASSIUM ADMINISTRATION-HULTGREN ET AL.
to an increased oral intake but also to probable potassium release from tissue cells as a consequence of surgery as well as potassium release from red cells due to hemolysis. The low sodium diet contained potassium chloride salt substitutes with a daily potassium content of approximately 5.5 g [2]. Sodium depletion and cardiac disease reduce the kidney’s ability to excrete potassium [ 3-61. p! low serum sodium enhances the cardiac toxicity of potassium [4]. Patients with cardiac disease and conduction defects may have an increased susceptibility to toxic effects of potassium [4,6,7], and digitalis may also enhance potassium cardiotoxicity [3,8]. The rapidity of the rise in serum potassium levels and individual susceptibility to potassium also influence cardiotoxicity [4,6,7,9-l 1,191. An important factor contributing to ventricular fibrillation in the second patient could have been exercise-induced myocardial ischemia with consequent local release of myocardial potassium. It has been shown that as little as 0.13 meq of potassium chloride infused into a dog’s coronary artery can result in ventricular fibrillation [ 121. Other factors were also important in producing cardiac arrest in this patient. Mild elevation of the blood urea nitrogen to 37 mg/lOO ml was present. He had been on a low sodium diet for 2 weeks prior
to the cardiac arrest and after resuscitation his serum sodium was 130 meq/liter. His serum potassium was 5.0 meq/liter 2 weeks before cardiac arrest. The mild elevation of the blood urea nitrogen level and the autopsy findings of interstitial and glomerular fibrosis suggested the presence of moderate renal dysfunction that probably impaired the patient’s ability to rapidly excrete the potassium load. A similar instance of hyperkalemic cardiac arrest following the oral administration of 15.0 g of potassium chloride was reported by Dodge and associates [ 71. Oral potassium administration has also been reported to result in ventricular tachycardia [ 131, atrioventricular block [ 141 and fatal cardiac arrest [ 151. Additional observations on the toxicity of oral potassium salts have been reported by Keith [ 161, Hullemann [ 171 and Bedford [ 181. It should be recognized that the oral administration of potassium may produce severe cardiac toxicity in patients with heart disease even when renal function is clinically normal. Potassium toxicity is enhanced by sodium depletion, underlying cardiac disease, digitalis administration and the rapidity of rise in serum potassium. Potassium-induced cardiac arrest is a common complication of medical therapy, and this problem deserves careful consideration by the medical profession.
REFERENCES
5.
6.
7.
8. 9. 10.
142
Burchell H: Dilemmas in potassium therapy. Circulation 47: 1144, 1973. Levinsky NG: Management of emergencies. Vi. Hyperkalemia. N Engl J Med 274: 1076, 1966. Surawicz B: The role of potassium in cardiovascular therapy. Med Clin North Am 52: 1103, 1968. Larr ~w CT, Carver ST, Peterson RE, Horwith M: Hypoalronism as a cause of hyperkalemia and syncopal r ks in patients with complete heart block. Am J Med 2 1, 1951. 8 Reln 3 AS, Schwartz WB: Renal Disease, 2nd ed (Black D, ed), Philadelphia, F. A. Davis, 1967, p 763. Brown H, Tanner GL, Hecht HH: The effects of potassium salts in subjects with heart disease. J Lab Clin Med 37: 506, 1951. Dodge HT, Grant RP, Seavey PW: The effect of induced hyperkalemia on the normal and abnormal electrocardiogram. Am Heart J 45: 725, 1953. Lown B, Black H, Moore FD: Digitalis, electrolytes and the surgical patient. Am J Cardiol 6: 309, 1960. Swales JD: Hypokalemia and the electrocardiogram. Lancet 2: 1365, 1964. Williams R: Potassium overdosage: a potential hazard of non-rigid parenteral fluid containers. Br Med J 1: 714, 1973.
January 1975
The American Journal of Medicine
11. 12.
13.
14.
15. 16.
17.
18. 19.
Volume 58
Keith N, Osterberg A, Burchell H: Some effects of potassium in man. Ann Intern Med 16: 879, 1942. Surawicz B: Role of electrolytes in etiology and management of cardiac arrhythmias. Prog Cardiovasc Dis 10: 553. 1968. Wasserburger R, Corliss R: Value of oral potassium salts in differentiation of functional and organic T wave changes. Am J Cardiol 10: 673. 1962. Schlachman M, Rosenberg B: The effect of potassium on inverted T waves in organic heart disease. Am Heart J 40: 81, 1950. Kaplan M: Suicide by oral ingestion of a potassium preparation. Ann Intern Med 71: 363, 1969. Keith NM, Osterberg AE, Burchell HB: Some effects of potassium salts in man. Ann Intern Med 16: 879. 1942. Hullemann: Suicide due to consumption of bananas. Death of a bilateral nephrectomized female patient due to hyperkalemia after consumption of bananas. Dtsch Med Wochenschr 94: 1765, 1969. Bedford P, Leeds 0: Acute potassium intoxication. Lancet 2: 268, 1954. Mercer C, Logic J: Cardiac arrest due to hyperkalemia following intravenous potassium administration. Chest 64: 358, 1973.
HERBERT N. HULTGREN, M.D. ROBERT SWENSON,
M.D.
GEORGE WETTACH,
M.D.
Palo Alto, California
Cardiac arrest developed in two patients afler the administration of oral potassium. Neither patient had renal insufficiency, but both had underlying heart disease. In one patient fatal ventricular fibrillation developed 4 days after he received an aortic valve replacement for aortic stenosis and while he was receiving oral potassium supplements. The serum potassium level before cardiac arrest was 8.1 meq. The second patient had angina and was given 40 meq of potassium orally 15 minutes after an exercise test which produced chest pain and S-T segment depression. One hour later, ventricular fibrillation developed. Resuscitation was successful. Both patients had electrocardiographic evidence of hyperkalemia. Oral administration of potassium may produce severe cardiac toxicity in patients with heart disease even when renal function is clinically normal. Cardiac arrest due to hyperkalemia is usually associated with the intravenous administration of potassium in patients with renal insufficiency. In some instances the oral administration of potassium, the use of potassium-retaining diuretics, acidosis or multiple blood transfusions may be accompanied by lethal hyperkalemia in the presence of moderate renal impairment. Cardiac arrest due to oral potassium ingestion with clinically normal renal function is rare. Hyperkalemia is an important cause of cardiac arrest, and Burchell [l] has suggested that more lives have been lost than saved by potassium therapy. Our purpose is to describe two instances of hyperkalemic cardiac arrest due to oral potassium administration in patients without clinical evidence of renal disease and to evaluate some of the causative mechanisms involved. CASE
REPORTS
Case 1. A 56 year old farm worker (A.V.G.) with severe aortic stenosis underwent aortic valve replacement (fresh aortic homograft) on cardiopulmonary bypass on March 17, 1970. Preoperatively, a complete left bundle branch
block was present
m*. Angiography
revealed
(Figure 1). The aortic valve area was 0.6 cm*/ moderate
2-F (O-4) aortic regurgitation,
normal
proximal coronary arteries and normal ventricular contraction. The ejection fraction was 80 per cent. At surgery, the mitral valve and coronary From the Medical Service, Palo Alto Veterans Administration Hospital, Palo Alto, California; and the Department of Medicine, Stanford Medical School, Stanford, California. Requests for reprints should be addressed to Dr. Herbert N. Hultgren, Cardiology Service, Veterans Administration Hospital, 3801 Miranda Avenue, Palo Atto, California 94304. Manuscript accepted March 12, 1974.
arteries
were
cross clamp
normal.
units of packed The
Total perfusion
time was 52 minutes.
was
69 minutes,
and aortic
red cells were given during surgery.
immediate
postoperative
were no significant
course
electrocardiographic
that suggested myocardial damage erative days, occasional ventricular were suppressed
time
Six units of fresh whole blood and 4
by xylocaine
January 1975
was
uncomplicated,
changes
and there
or serum enzyme
rises
during surgery. On the first 2 postoppremature beats were present which
infusion.
The American Journal of Medicine
Volume 58
139
CARDIAC ARREST AND POTASSIUM ADMINISTRATION-HULTGEN
ET AL.
aVR
aVL
aVF Electrocardiogram recorded immediately beFigure 2. fore death. Wide 01% complexes and absence of atrial activity are compatible with hyperkalemia. Serum potassium was 8.4 meqlliter.
Figure 1. Case 1. Preoperative electrocardiogram showing left bundle branch block, left axis deviation and abnormal P waves, and ventricular premature beats. day, 100 meq of potassium The serum potassium level rose from 4.0 to 6.9 meq/liter; electrocardiographic signs of moderate hyperkalemia were noted, and potassium therapy was discontinued. The patient was given a 1.O g sodium diet. Electrolyte and laboratory data are summarized in Table I. On the 2nd postoperative day, the patient was ambulatory with assistance, and he was transferred to the ward. The serum potassium level was 5.1 meq/liter. The oral adOn the first postoperative
was
given
TABLE
I
parenterally.
Case 1. Laboratory
Time of Study 3112 3116 Postoperatively 2 hours 9 hours 1st day 2nd day 3rd day 4th day 5th day
140
January 1975
ministration of 60 meq potassium (potassium triplex) was started three times daily, along with 0.25 mg digoxin and 500 mg chlorothiazide daily. These are routine postoperative measures in the Department of Surgery for patients undergoing valve replacement surgery. Unfortunately, neither blood urea nitrogen nor serum creatinine levels were determined during the first 4 postoperative days. Digoxin had been discontinued 5 days before surgery. On the 4th postoperative day, the patient experienced vague abdominal pain, nausea and vomiting. An abdominal roentgenogram was normal. On the 5th postoperative day, pallor and hypotension developed. The serum potassium was 8.1 meq and the blood urea nitrogen was 34 mg/ 100 ml. The electrocardiogram revealed periods of nodal and ventricular rhythm, and signs of hyperkalemia (Figure 2). Ventricular fibrillation occurred and resuscitation attempts failed. At autopsy, the total heart weight was 710 g, there was marked left ventricular hypertrophy and moderate left atrial hypertrophy. The coronary arteries were normal. The homograft valve was intact. There was no evidence of myocardial infarction. Histologic examination of the myocardium revealed several small scattered areas of myocardial necrosis with hemorrhage, neutrophilic exudation and myocytolysis. Hypertrophy of myocardial fibers was present. On histologic examination, the kidneys were normal as were the lungs and other organs.
Data During Hospital Course Supplemental Potassium Intake
Serum Creatinine (mg/lOO ml)
Blood Urea Nitrogen (mg/lOO ml)
Serum Potassium (meq/liter)
1.3 1.0
26 27
3.7 4.4
138 138
90 90
... ... . . .,. ... ...
4.0 6.9 5.9 5.1
141 138 136 128
100
...
...
... ...
130/90 120/90 100/75
... ...
. .
34
8.1
129
105 103 103 103 101 101
... . ...
The American Journal of Medicine
Volume 58
Serum Sodium (meq/liter)
(meq/day)
180 180 180 180
Weight
Blood Pressure
(kg)
(mm Hg)
106 105
100/70 go/70
.. ... 100/70
CARDIAC ARREST AND POTASSIUM ADMINISTRATION-HULTGEN
Electrocardiogram obtained after Figure 4. sion shows widening of the QRS complexes. leads were not recorded. recorded just before exercise test. Inferior lateral infarction, abnormal T waves and one ventricular premature beat are present.
Figure 3.
Case 2. Electrocardiogram
Case
2. This 58 year old man (R.S.) had stable angina pectoris of 3 years’ duration. The electrocardiogram (Figure 3) was compatible with an old inferior and lateral myocardial infarction which had occurred 2 years previously. He was not taking digitalis. Coronary arteriography revealed complete occlusion of the proximal right coronary artery, partial proximal occlusion of the left anterior descending coronary artery and irregular diffuse disease of the left circumflex branch. An exercise test (cycle ergometry) was positive with flat S-T segment depression occurring at a heart rate of 160/min. Chest pain was present at the end of the test and lasted for 2 minutes after exercise. No ventricular premature beats occurred in the immediate post-exercise electrocardiogram. Three minutes after the completion of the test, the electrocardiogram had reverted to the preexercise appearance. As part of a study of the effect of potassium upon ST-T wave changes occurring during exercise, the patient was given 40 meq potassium orally 15 minutes after cessation of the exercise test. One hour later, the test was to be repeated. As the mouthpiece was being adjusted, ventricular fibrillation developed. Conversion to a sinus rhythm was accomplished with DC shock, and the patient was brought to the Coronary Care Unit where he recovered uneventfully. The electrocardiogram after defibrillation is shown in Figure 4. The evident widening of the QRS complex is compatible with hyperkalemia. Two weeks before cardiac arrest, the patient’s urinalysis had been normal, serum sodium 140 meq/liter, serum potassium 5.0 meq/liter and blood urea nitrogen 37 mg/ 100 ml. At that time he was placed on a low salt diet (1,500 mg sodium chloride) without diuretics or oral potassium. On the day after his resuscitation, his urinalysis was normal, blood urea nitrogen 38 mg/lOO ml, sodium 130 meq/liter and potassium 5.5 meq/llter. Electrolytes were not determined on the day of the cardiac arrest. Two days
January
ET AL.
cardioverPrecordial
after resuscitation, the blood urea nitrogen was 36 mg/ 100 ml, sodium 138 meq/liter and potassium 4.2 meq/ liter. The electrocardiogram had reverted to the precardllc arrest pattern. Four weeks after resuscitation the patient had a Vineberg operation from which he recovered without complications. Four years later he died of a myocardial infarct. Autopsy revealed severe coronary disease and a recent infarct. The kidneys were grossly normal and weighed 150 g each. Histologic study revealed many patchy areas of interstitial fibrosis and inflammatory cell infiltrate. Many glomeruli were seen in various stages of fibrosis and hyalinization. COMMENTS Cardiac arrest in the first patient was clearly due to hyperkalemia. Characteristic electrocardiographic findings were present, the serum potassium level was elevated, and an excessive amount of potassium had been administered. There was no clinical evidence of other causes for the cardiac arrest. No evidence of renal disease was present. The preoperative blood urea nitrogen was 25 mg/lOO ml, the serum creatinine was 1 .O mg/ 100 ml, and the urinalysis was normal. No evidence of renal insufficiency was present during the immediate postoperative period. Urine output and the urinalysis were normal. Shortly before the cardiac arrest, the blood urea nitrogen was 34 mg/ 100 ml. At that time the patient had low blood pressure, periods of nodal rhythm and hyperkalemia. At autopsy, the kidneys and urinary tract were normal on gross and microscopic examination. Several factors probably accounted for the arrest in addition to the elevated serum potassium level. These include (1) rapid rise in serum potassium level, (2) low serum sodium or sodium depletion, (3) underlying cardiac disease and conduction defect (left bundle branch block) and (4) digitalis administration. The increase in serum potassium was not only due
1975
The American
Journal
of Medicine
Volume
58
141
CARDIAC ARREST AND POTASSIUM ADMINISTRATION-HULTGREN ET AL.
to an increased oral intake but also to probable potassium release from tissue cells as a consequence of surgery as well as potassium release from red cells due to hemolysis. The low sodium diet contained potassium chloride salt substitutes with a daily potassium content of approximately 5.5 g [2]. Sodium depletion and cardiac disease reduce the kidney’s ability to excrete potassium [ 3-61. p! low serum sodium enhances the cardiac toxicity of potassium [4]. Patients with cardiac disease and conduction defects may have an increased susceptibility to toxic effects of potassium [4,6,7], and digitalis may also enhance potassium cardiotoxicity [3,8]. The rapidity of the rise in serum potassium levels and individual susceptibility to potassium also influence cardiotoxicity [4,6,7,9-l 1,191. An important factor contributing to ventricular fibrillation in the second patient could have been exercise-induced myocardial ischemia with consequent local release of myocardial potassium. It has been shown that as little as 0.13 meq of potassium chloride infused into a dog’s coronary artery can result in ventricular fibrillation [ 121. Other factors were also important in producing cardiac arrest in this patient. Mild elevation of the blood urea nitrogen to 37 mg/lOO ml was present. He had been on a low sodium diet for 2 weeks prior
to the cardiac arrest and after resuscitation his serum sodium was 130 meq/liter. His serum potassium was 5.0 meq/liter 2 weeks before cardiac arrest. The mild elevation of the blood urea nitrogen level and the autopsy findings of interstitial and glomerular fibrosis suggested the presence of moderate renal dysfunction that probably impaired the patient’s ability to rapidly excrete the potassium load. A similar instance of hyperkalemic cardiac arrest following the oral administration of 15.0 g of potassium chloride was reported by Dodge and associates [ 71. Oral potassium administration has also been reported to result in ventricular tachycardia [ 131, atrioventricular block [ 141 and fatal cardiac arrest [ 151. Additional observations on the toxicity of oral potassium salts have been reported by Keith [ 161, Hullemann [ 171 and Bedford [ 181. It should be recognized that the oral administration of potassium may produce severe cardiac toxicity in patients with heart disease even when renal function is clinically normal. Potassium toxicity is enhanced by sodium depletion, underlying cardiac disease, digitalis administration and the rapidity of rise in serum potassium. Potassium-induced cardiac arrest is a common complication of medical therapy, and this problem deserves careful consideration by the medical profession.
REFERENCES
5.
6.
7.
8. 9. 10.
142
Burchell H: Dilemmas in potassium therapy. Circulation 47: 1144, 1973. Levinsky NG: Management of emergencies. Vi. Hyperkalemia. N Engl J Med 274: 1076, 1966. Surawicz B: The role of potassium in cardiovascular therapy. Med Clin North Am 52: 1103, 1968. Larr ~w CT, Carver ST, Peterson RE, Horwith M: Hypoalronism as a cause of hyperkalemia and syncopal r ks in patients with complete heart block. Am J Med 2 1, 1951. 8 Reln 3 AS, Schwartz WB: Renal Disease, 2nd ed (Black D, ed), Philadelphia, F. A. Davis, 1967, p 763. Brown H, Tanner GL, Hecht HH: The effects of potassium salts in subjects with heart disease. J Lab Clin Med 37: 506, 1951. Dodge HT, Grant RP, Seavey PW: The effect of induced hyperkalemia on the normal and abnormal electrocardiogram. Am Heart J 45: 725, 1953. Lown B, Black H, Moore FD: Digitalis, electrolytes and the surgical patient. Am J Cardiol 6: 309, 1960. Swales JD: Hypokalemia and the electrocardiogram. Lancet 2: 1365, 1964. Williams R: Potassium overdosage: a potential hazard of non-rigid parenteral fluid containers. Br Med J 1: 714, 1973.
January 1975
The American Journal of Medicine
11. 12.
13.
14.
15. 16.
17.
18. 19.
Volume 58
Keith N, Osterberg A, Burchell H: Some effects of potassium in man. Ann Intern Med 16: 879, 1942. Surawicz B: Role of electrolytes in etiology and management of cardiac arrhythmias. Prog Cardiovasc Dis 10: 553. 1968. Wasserburger R, Corliss R: Value of oral potassium salts in differentiation of functional and organic T wave changes. Am J Cardiol 10: 673. 1962. Schlachman M, Rosenberg B: The effect of potassium on inverted T waves in organic heart disease. Am Heart J 40: 81, 1950. Kaplan M: Suicide by oral ingestion of a potassium preparation. Ann Intern Med 71: 363, 1969. Keith NM, Osterberg AE, Burchell HB: Some effects of potassium salts in man. Ann Intern Med 16: 879. 1942. Hullemann: Suicide due to consumption of bananas. Death of a bilateral nephrectomized female patient due to hyperkalemia after consumption of bananas. Dtsch Med Wochenschr 94: 1765, 1969. Bedford P, Leeds 0: Acute potassium intoxication. Lancet 2: 268, 1954. Mercer C, Logic J: Cardiac arrest due to hyperkalemia following intravenous potassium administration. Chest 64: 358, 1973.
