- Email: [email protected]
Hypokalemia in acute myocardial infarction
1534
Letters
to the Editor
American
REFERENCES
1. Belhassen B, Danon L, Shoshani D, Laniado S: Paroxysmal atrioventricular block triggered by orthostatic hypotension. AM HEART J 1986;112:1107.
2. Schwela H, Oltmanns G, Fiehring H. Orthostase-syndrom und bradykarde Herzrhythmusstorungen. Dtsch Gesundh Wesen 1979;34:498. 3. Schwela H, Lukoseviciute A, Oltmanns G, Bischoff KH, Franke T. Bipolares oesophagus-EKG zur Herzrhythmusanalyse bei Belastungsuntersuchungen. Herzschrittmacher 1986;6:142. 4. Athanasiu CJ. Zerebrale anfalle verborgener kardialer Genese. Munchen Med Wochenschr 1974,116:1281.
REPLY To the Editor:
I thank Drs. Schwela and Oltmanns for their comments. Their patient obviously represents another case of postural-induced complete atrioventricular (AV) block which, to the best of my knowledge, was first described in 1919 by Lutembacher.’ However, in the case of Drs. Shwela and Oltmanns as well as in other reports in the literature, 1.2 there is no mention of postural hypotension associated with occurrence of AV block. Our case is apparently unique in that postural hypotension, by inducing a reflex sinus tachycardia, triggered a phase 3 AV block that perpetuated due to a phase 4 AV block most probably located in the proximal portion of the His bundle. Bernard Department Tel-Aviv
Belhassen, M.D. of Cardiology Medical Center Tel-Aviv, Zsrael
REFERENCES
1. Lutembacher R. Bradycardie orthostatique; intermittence de conduction du faisceau de His. Arch Ma1 Coeur 1919;12:145.
2. Gallemaeits V. Dissociation auricplo-ventriculaire par I’orthostatisme (bradycardie orthostatique). Coeur 1923:16:332.
provoquee Arch Ma1
occurred. According to Nernst’s equation, the dangerous electrical instability that occurs in the ischemic area is caused by an alteration of the local distribution of potassium. Such alteration is due to a reduced activity of the Na/K pump, which in turn causes an increase in the extracellular K-ion concentration as well as a reduction in the intracellular concentration. The consequences of this local condition can be significantly worsened by a limited reduction in hematic potassium. The purpose of our study was to determine the reasons why spontaneous hypokalemia takes place after acute myocardial infarction. Such a study was carried out on 18 consecutive patients (of both sexes), hospitalized with a diagnosis of acute myocardial infarction in the Coronary Care Unit of the II Medical Clinic of Rome. None of the patients had been treated with diuretics or other potassium depleting drugs before hospitalization. In 11 patients the levels of hematic potassium were well below normal: 3.36 * .05 mM/L, as compared with normal levels of 4.4 t .03 mM/L (p < 0.001). The following red cell tests were also carried out on all patients: Na/K pump, Na/K co-transport, Na/Li contra-transport, passive permeability to Na and K, intracellular concentration of Na and K. The most interesting result of our study was the observation in 14 patients of increased activity of the Na/K pump, with an average index of 3680 & 1502 Na MiL of cells/hr, as compared with normal values of 1000 to 2000 Na M/L of cell&n. Those patients were further subdivided into two groups according to the level of their intracellular potassium: in 14 patients, the average concentration was 113 i 10 mM/L, while in the remaining six patients it was well above normal, with average values of 235 * 65 mM/L. This phenomenon can be interpreted in the first group as an inadequate effort to compensate and in the second group as the normal result of increased pump activity. Other studies’,’ have explained primary hypokalemia in the acute stage of myocardial infarction as the consequence of an altered distribution of potassium between the intra- and extracellular compartments, due to an increase in the hematic catecholamines that stimulate beta-2-receptors.’ Therefore, our objective for the future is to be able to measure hematic catecholamines while studying the Na/K pump in order to have a better understanding of their hyperactivity during the acute stage of myocardial infarction.
Coronary
HYPOKALEMIA INFARCTION
December 1987 Heart Journal
IN ACUTE MYOCARDIAL
Maria Clotilde Borg& M.D. Alessandro Pasquale, M.D. Via Catania, 99 Care Unit, Clinica Medica ZZ Universitci ‘Za Sapienza” 00161 Roma, Ztaly
To the Editor:
In the first hours after a myocardial infarction, the highest number of casualties can be attributed to malignant ventricular arrhythmias caused by increased automaticity of latent pacemakers, by reentry phenomena, and basically by changes in cellular excitability. After a myocardial infarction, electrical instability is due to a number of local and general mechanisms, directly or indirectly related to necrosis or myocardial hypoxia. The alterations of the electrolytic homeostasis’ are one of the most common of those mechanisms. In patients with or without myocardial infarction but suffering from hypokalemia, there is a well-known risk of malignant arrhythmias. The most common causes of hypokalemia are the administration of diuretics or of corticosteroids. It should also be pointed out that malignant arrhythmias are more frequent in patients where hypokalemia is accompanied by hypomagnesemia or by acid-base imbalance. Experimental* and clinical’ assays have demonstrated that malignant arrhythmias are caused by hypokalemia, even though the electrolytic alterations were still absent when the myocardial infarction
REFERENCES
1. Papademetriou V. Hypokalemia and malignant arrhythmias during acute myocardial infarction. AM HEART J 1985; 111:1220. 2.
Hohnloser SH, Verrier RL, Lown B, Reader E. Effect of hypokalemia on susceptibility to ventricular fibrillation in the normal and ischemic canine heart. AM HEART J 1985;112:32.
Nordrehaug JE, Johannesen KA, Von Der Lippe G. Serum potassium concentration as a risk factor of ventricular arrhythmias early in acute myocardial infarction. Circulation 1985;71:645. 4. Struthers AD, Reid JL, Whitesmith R, Rodger JC. Effect of intravenous adrenaline on electrocardiogram, blood pressure, and serum potassium. Br Heart J 1983;49:90. 5. Morgan DB, Young RM. Acute transient hypokalemia. New interpretation of a common event. Lancet 1983;2:751. 3.
Letters
to the Editor
American
REFERENCES
1. Belhassen B, Danon L, Shoshani D, Laniado S: Paroxysmal atrioventricular block triggered by orthostatic hypotension. AM HEART J 1986;112:1107.
2. Schwela H, Oltmanns G, Fiehring H. Orthostase-syndrom und bradykarde Herzrhythmusstorungen. Dtsch Gesundh Wesen 1979;34:498. 3. Schwela H, Lukoseviciute A, Oltmanns G, Bischoff KH, Franke T. Bipolares oesophagus-EKG zur Herzrhythmusanalyse bei Belastungsuntersuchungen. Herzschrittmacher 1986;6:142. 4. Athanasiu CJ. Zerebrale anfalle verborgener kardialer Genese. Munchen Med Wochenschr 1974,116:1281.
REPLY To the Editor:
I thank Drs. Schwela and Oltmanns for their comments. Their patient obviously represents another case of postural-induced complete atrioventricular (AV) block which, to the best of my knowledge, was first described in 1919 by Lutembacher.’ However, in the case of Drs. Shwela and Oltmanns as well as in other reports in the literature, 1.2 there is no mention of postural hypotension associated with occurrence of AV block. Our case is apparently unique in that postural hypotension, by inducing a reflex sinus tachycardia, triggered a phase 3 AV block that perpetuated due to a phase 4 AV block most probably located in the proximal portion of the His bundle. Bernard Department Tel-Aviv
Belhassen, M.D. of Cardiology Medical Center Tel-Aviv, Zsrael
REFERENCES
1. Lutembacher R. Bradycardie orthostatique; intermittence de conduction du faisceau de His. Arch Ma1 Coeur 1919;12:145.
2. Gallemaeits V. Dissociation auricplo-ventriculaire par I’orthostatisme (bradycardie orthostatique). Coeur 1923:16:332.
provoquee Arch Ma1
occurred. According to Nernst’s equation, the dangerous electrical instability that occurs in the ischemic area is caused by an alteration of the local distribution of potassium. Such alteration is due to a reduced activity of the Na/K pump, which in turn causes an increase in the extracellular K-ion concentration as well as a reduction in the intracellular concentration. The consequences of this local condition can be significantly worsened by a limited reduction in hematic potassium. The purpose of our study was to determine the reasons why spontaneous hypokalemia takes place after acute myocardial infarction. Such a study was carried out on 18 consecutive patients (of both sexes), hospitalized with a diagnosis of acute myocardial infarction in the Coronary Care Unit of the II Medical Clinic of Rome. None of the patients had been treated with diuretics or other potassium depleting drugs before hospitalization. In 11 patients the levels of hematic potassium were well below normal: 3.36 * .05 mM/L, as compared with normal levels of 4.4 t .03 mM/L (p < 0.001). The following red cell tests were also carried out on all patients: Na/K pump, Na/K co-transport, Na/Li contra-transport, passive permeability to Na and K, intracellular concentration of Na and K. The most interesting result of our study was the observation in 14 patients of increased activity of the Na/K pump, with an average index of 3680 & 1502 Na MiL of cells/hr, as compared with normal values of 1000 to 2000 Na M/L of cell&n. Those patients were further subdivided into two groups according to the level of their intracellular potassium: in 14 patients, the average concentration was 113 i 10 mM/L, while in the remaining six patients it was well above normal, with average values of 235 * 65 mM/L. This phenomenon can be interpreted in the first group as an inadequate effort to compensate and in the second group as the normal result of increased pump activity. Other studies’,’ have explained primary hypokalemia in the acute stage of myocardial infarction as the consequence of an altered distribution of potassium between the intra- and extracellular compartments, due to an increase in the hematic catecholamines that stimulate beta-2-receptors.’ Therefore, our objective for the future is to be able to measure hematic catecholamines while studying the Na/K pump in order to have a better understanding of their hyperactivity during the acute stage of myocardial infarction.
Coronary
HYPOKALEMIA INFARCTION
December 1987 Heart Journal
IN ACUTE MYOCARDIAL
Maria Clotilde Borg& M.D. Alessandro Pasquale, M.D. Via Catania, 99 Care Unit, Clinica Medica ZZ Universitci ‘Za Sapienza” 00161 Roma, Ztaly
To the Editor:
In the first hours after a myocardial infarction, the highest number of casualties can be attributed to malignant ventricular arrhythmias caused by increased automaticity of latent pacemakers, by reentry phenomena, and basically by changes in cellular excitability. After a myocardial infarction, electrical instability is due to a number of local and general mechanisms, directly or indirectly related to necrosis or myocardial hypoxia. The alterations of the electrolytic homeostasis’ are one of the most common of those mechanisms. In patients with or without myocardial infarction but suffering from hypokalemia, there is a well-known risk of malignant arrhythmias. The most common causes of hypokalemia are the administration of diuretics or of corticosteroids. It should also be pointed out that malignant arrhythmias are more frequent in patients where hypokalemia is accompanied by hypomagnesemia or by acid-base imbalance. Experimental* and clinical’ assays have demonstrated that malignant arrhythmias are caused by hypokalemia, even though the electrolytic alterations were still absent when the myocardial infarction
REFERENCES
1. Papademetriou V. Hypokalemia and malignant arrhythmias during acute myocardial infarction. AM HEART J 1985; 111:1220. 2.
Hohnloser SH, Verrier RL, Lown B, Reader E. Effect of hypokalemia on susceptibility to ventricular fibrillation in the normal and ischemic canine heart. AM HEART J 1985;112:32.
Nordrehaug JE, Johannesen KA, Von Der Lippe G. Serum potassium concentration as a risk factor of ventricular arrhythmias early in acute myocardial infarction. Circulation 1985;71:645. 4. Struthers AD, Reid JL, Whitesmith R, Rodger JC. Effect of intravenous adrenaline on electrocardiogram, blood pressure, and serum potassium. Br Heart J 1983;49:90. 5. Morgan DB, Young RM. Acute transient hypokalemia. New interpretation of a common event. Lancet 1983;2:751. 3.