Hyperkalemia-like ECG changes simulating acute myocardial infarction in a patient with hypokalemia undergoing potassium replacement

Hyperkalemia-like ECG Changes Simulating Acute Myocardial Infarction in a Patient With Hypokalemia Undergoing Potassium Replacement

John E. Madias, MD, FACC,* and Nicolaos E. Madias, MD+

Abstract: A

pseudoinfarctional ECG pattern, previously noted to occur rarely in association with hyperkalemia, was observed in a patient with severe hypokalemia in the course of I<+ replacement but while she was still hypokalemic. It is inferred that this puzzling ECG feature reflected a reduction of intracellular/ extracellular [K+ ] ratio in a patient with decreased intracellular I(+ concentration undergoing rapid K’ repletion. Key words: hypokalemia, hyperkalemia, potassium, myocardial infarction.

ST-segment elevation ( + ST) has not been reported in association with hyperkalemia. On the other hand, transient + ST and Q waves simulating acute myocardial infarction (MI) have rarely been noted in association with hypokalemia.‘-5 Such pseudoinfarctional ECG alterations have been recorded in patients with serum Kf concentrations ranging from 7.8 to 8.7 mJZq/l.1,‘,4 We report a patient with severe hypokalemia who developed transient, marked + ST in the course of K+ replacement but while she was still hypokalemic. We suggest that this paradox was due to “relative hyperkalemia” and consequent reduction of intracellular/extracellular [K + ] ratio effected by ongoing K + replacement in the likely presence of depressed intracellular K’ concentration.

Case Report

A 6%year-old woman was admitted to the hospital for evaluation of weakness, weight loss, and symptoms suggestive of urinary tract infection of 2 months’ duration. Physical examination revealed a cachectic (37.4-kg) woman in mild distress. Her temperature was 39.8”C, pulse 120 beats/min, respirations 36/min, and blood pressure 142/88 mm Hg. Other positive findings included a faint fourth heart sound, a grade II/VI systolic ejection murmur at the cardiac apex and lower left sternal border, diffuse lymphadenopathy, a slightly firm and tender liver with a total span of 13 cm, and mild bilateral pedal edema. Stool guaiac was negative. Laboratory tests included normal chest and abdominal radiographs; Hb, 8.5 g/dl; WBC, 11,400/mm3; platelet count, 140,000/mm3; BUN, 17 mg/dl; creatinine, 0.9 mg/ dl; glucose, 96 mg/dl; albumin, 2.2 g/dl; Na+ , 137; K’, 4.2; Cl-, 101; total CO*, 20.1 mmol/l; and prothrombin time, 17.1 seconds (control, 12.2 seconds). ECG revealed sinus tachycardia at a rate of 137 beats/ min, normal QRS axis, QRS of 0.09 seconds, flat T waves in leads I and aVL, and a QS pattern in leads

* From the Department of Medicine, Mount Sinai School of Medicine of the City University of New York, and the Cardiology Division, Mount Sinai-City Hospital Center, Elmhurst, New York. f From the Department ofMedicine, Tufts University School of Medicine, and the Division of Nephrology. New England Medical Center, Boston, Massachusetts. Reprint requests: John E. Madias, MD, Cardiology Division, Mount Sinai-City Hospital Center, 79-01 Broadway, Elmhurst, NY 11373.

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Table 1. Serum Composition Prior to and During the Patient’s Admission to the CCU

Day 6 9 11 12 14 14 14 15 15 15 18 22

Time (Hours) 8:00 8:00 8:00 8:00 4:00 6:00 8:30 3:00 10:00 2:00 8:00 8:00

am am am am pm pm pm am am pm am am

Kf (mmol/l)

Na+ (mmol/l)

cl(mmoV1)

Ca’+

Albumin

BUN

Creatinine

(mmol/l)

(mg/dl)

(gW

(mg/dl)

(mgW

4.4 3.7 3.6 2.6 2.0 2.0 3.0 5.4 5.2 4.7 4.1 3.9

148 145 135 135 133 135 138

96 112 105 99 94 96 101

29 25 23 20 23 24 22

7.5 6.9 8.4 7.2 6.6

2.2 2.3 2.5

145 140 144

112 107 114

26 27 24

co2

8.1

A

K+ 1 9 8:OOa.m.3.7 TIME

IL

m

aVR

1.5 1.3 1.1 1.2

31 29 11

2.2

1.0 0.9

ah

aVF

VI

V2

V3

V4

8 14 8z30p.m.3.0

C 14 8~45p.m.

Fig. 1. Serial ECG tracings

and serum

165 158 192 349 612 566 495 265 191 164 117

serum K+ to 2.6 mEq/l and the rise in glucose to 349 mg/dl and attributed the hypokalemia to ongoing osmotic diuresis. Repeat testing on day 14 (4:00 p.m. and 6:00 p.m.) revealed severe hypokalemia (2.0 mEq/l) and hyperglycemia (Table 1). Arterial blood gases on room air showed a pH of 7.48; PaCoz, 38 mm Hg; HCOs-, 28 mEq/l; and PaOz, 88 mm Hg. As soon as the results of the 4:00 p.m. tests became available, the patient received 40 mm01 of KC1 by mouth, the glucose-containing hyperalimentation solution was discontinued, and infusion of half-normal saline containing 60 mm01 of KC1 per liter was started at a rate of 100 ml/hour. A second oral dose of 40 mm01 of KC1 was adminis-

V1 and Vz with poor R wave progression in the right and midprecordial leads. A urine culture grew greater than 100,000 colonies/ml of Escherichia coli. She was treated for the urinary tract infection and was diagnosed with Hodgkin’s disease (stage 4B). She received blood transfusions and on day 8 was started on central hyperalimentation. On day 9, a modified MOPP regimen was initiated. The results of follow-up tests are shown in Table 1. Serial ECGs (Fig. 1A) were unchanged from the one performed on admission. Due to an administrative error, results of tests performed on day 12 (Table 1) were received on day 14. The treating physicians noted the decrease in

DAY

25 25 27 38 39 42 43

Glucose (mgW

potassium

concentration

values

of the patient.

V5

V6

Hyperkalemia-like

A

6

C

K+ TIME 14 tik3Op.m.

DAY

I

Ill ah

ah

ah

ECG Changes

V2

l

V3

Madias and Madias

V4

V5

95

V6

153:OOa.m.5.4

22

8:OOa.m.

Fig. 2.

3.9

Serial ECG tracings and serum potassium concentration values of the patient.

tered at 8:20 p.m. The patient did not offer any complaints and was clinically stable. An ECG and a repeat serum I<’ were obtained at 8:30 p.m. (Fig. lB, Table 1). The ECG revealed a heart rate of 100 beats/ min and marked + ST in leads VI-V4 consistent with an acute anterior MI. The T waves were peaked in the precordial leads and merged with the + ST. In addition, there was some widening and an increase in the amplitude of the QRS complexes. The P waves and the P-R interval were normal and the QT, was prolonged at 0.56 seconds. The value of serum K’ corresponding to this ECG became available later and was 3.0 mEq/l (Table 1). An ECG obtained 15 minutes after the previous tracing (8:45 p.m., Fig. 1C) showed a heart rate of 100 beats/min, further widening of the QRS complexes, and essentially unchanged + ST segments and T waves. Again, the P waves and the P-R interval were normal and the QT, was 0.57 seconds. An ECG obtained at 9:30 p.m. (Fig. 2A) revealed a heart rate of 100 beats/min, less widening of the QRS complexes, and some reduction of the magnitude of the + ST. The P waves and P-R interval were normal and the QT, was 0.58 seconds. Despite the absence of symptoms suggestive of myocardial ischemia, the patient was transferred to the coronary care unit (CCU) at 9:45 p.m. She continued to be clinically stable and had no complaints. Her serum I<+ at 3:00 a.m. of day 15 was 5.4 mEq/l (Table 1). A simultaneous ECG revealed a heart rate

of 106 beats/min, substantial resolution of the QRS widening and + ST, normal P waves and P-R interval, and a slightly prolonged QT, of 0.48 seconds (Fig. 2B). When the latest value of serum K + became available, the KCI-containing infusion was discontinued. Several determinations of serum K’ obtained over the course of the next few hours were within normal limits (Table l), as were numerous values obtained over subsequent days of hospitalization. No arrhythmias or conduction abnormalities were noted in the ECG monitor or a large number of ECGs recorded during the patient’s 3-day stay in the CCU. An acute MI was ruled out on the basis of absence of suggestive clinical clues and evolutionary changes in multiple ECGs recorded, as well as negative enzymatic screening. Creatine kinase (CK) values in three specimens were 83, 46, and 43 III/l with less than 1% myocardial CK isoenzyme (MB-CK). The upper normal values for CK and MB-CK were 75 IU/l and 4%, respectively. An echocardiogram performed in the CCU was normal. Serum K+ on day 22 was 3.9 mEql1, and a corresonding ECG tracing revealed a heart rate of 107 beats/min, normal P wave and P-R interval, and a QT, of 0.46 seconds (Fig. 2C). This ECG tracing was virtually identical to those obtained early in the patient’s clinical course. She received further therapy for Hodgkin’s disease and was discharged to the care of the hematologyoncology clinic.

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Discussion This patient presented us with the paradox of + ST lasting for a few hours in the absence of symptoms or clinical and laboratory signs suggestive of acute MI. Indeed, the latter was convincingly ruled out by the absence of development of QRS changes in the ECG and of enzymatic alterations, a clinical course not suggestive of acute MI, and the absence of ventricular ectopy during the CCU monitoring. The quite remote possibility that the observed ECG alterations represented an episode of painless variant angina can easily be discounted, since it would be difficult to explain the lack of progression to MI after such ECG changes persisted for several hours.6*7 Pericarditis can easily be ruled out, since the + ST was transient and of large magnitude, unlike the changes typically observed in patients with pericarditis, and no changes in the polarity of the P-R segment were noted.’ Moreover, there was no clinical evidence of pericarditis from either history or physical examination. The hypergIycemia noted in our patient could produce some ECG changes. However, such changes usually include nonspecific ST-segment and T wave alterations’ or transient, marked ST-segment depression. lo What, then, was the cause of our patient‘s marked + ST documented over a period of several hours, during which the patient was undergoing Kf replacement and the serum K + ranged from 3.0 to 5.4 mEq/l? Although never reported in association with hypokalemia, + ST simulating acute MI has been noted rarely in hyperkalemic patients in the setting of severe renal decompensation and/or diabetic ketoacidosis or in the courseofK + administration. ‘p-5. ’ l-l3 Had our patient been hyperkalemic during the time the ECG tracings revealed marked + ST, this could well have been a case of hyperkalemia-induced pseudoinfarctional ECG pattern. Such a possibility had to be entertained, considering the patient’s weight (40 kg) and the substantial amount of Kf administered (80 mEq orally and about 50 mEq intravenously, or 3.3 mEq/kg) over a period of 8 hours. Although absolute hyperkalemia cannot explain the ECG pattern observed in our patient, insights into its mechanism can be derived from ati examination of the pathophysiology of hyperkalemia-induced pseudoinfarctional ECG changes. The isoelectric status of the ST-segment depends on the stability of the intraceIlular/extracellular [K’ ] ratio. Upward or downward shifts of the ST-segment are due to alterations of this ratio, with a reduction causing + ST and a rise resulting in ST-segment depression.14,‘5 Thus, absolute hyperkalemia could generate + ST by

1989

effecting a decrease in the intracellular/extracellular [Kf ] ratio. Although we regard the + ST observed with hyperkalemia to be primary in nature, Surawicz et al. maintain that such changes are secondary to an intraventricular conduction delay.16,” According to these workers, both the widened QRS complex and the + ST noted with hyperkalemia are analogous to those observed with left bundle branch block. In the latter conduction abnormality, + ST in the right precordial leads may often simulate acute anterior MI.” Based on the above concepts,14,15 one could surmise that, under certain circumstances, KC replacement administered to K+ -depleted subjects might effect a substantial decrement in the intracellular/ extracellular [K+] ratio such that hyperkalemia-like + ST might evolve despite the prevailing normokaIemia or even hypokalemia. The rate of K+ replacement and the ease with which administered K* enters the intracellular compartment are among the factors of possible importance in mediating a decreased intracellular/extracellular [K’] ratio in the presence of only relative hyperkalemia. It is notable that in dog experiments and in work with isolated perfused hearts increasing extracellular [K+] rapidly from hypokalemic to normal levels resulted in more pronounced ECG changes than when the same change in [I<+ ] was produced more slowly or when the I<+ infusion commenced at a normokalemic level. l6 Ample reports have documented that hypocalcemia potentiates the effects of hyperkalemia on the ECG. 4,11-13,17,19 Our patient was hypocalcemic when the K+ administration commenced, and the hypocalcemia could be only partially attributed to the prevailing hypoalbuminemia (Table 1) . Thus, the setting of the hypokalemic or normokalemic patient undergoing K + replacement should be considered in the differential diagnosis of transient + ST in the ECG. Certainly, honoring established guidelines for the rate of potassium replacement therapy2’ and exercising special caution in patients with defects in cellular potassium uptake*’ should allow administration of the requisite, often large, potassium loads with impunity.

References

Levine HD, Wanzer SH, Merrill JP: Dialyzable currents of injury in potassium intoxication resembling acute myocardial infarction or pericarditis. Circulation 13:29, 1956

Hyperkalemia-like 2. Castleman L, Goldberg M, Zuckerman S et al: Selected electrocardiographic changes during acute renal failure and hemodialysis. Am J Cardiol 12:841, 1963 D: Electrocardiographic 3. Gelzayd EA. Holzman changes of hyperkalemia simulating acute myocardial infarction: report of a case. Dis Chest 51:21 1, 1967 4. Chawla KK, Cruz J, Kramer NE, Towne WD: Electrocardiographic changes simulating acute myocardial infarction caused by hyperkalemia: report of a patient with normal coronary arteriograms. Am Heart J 95:637, 1978 5. Meyers GB: Other QRS-T patterns that may be mistaken for myocardial infarction. Circulation 2:75, 1950 6. Madias JE: The syndrome of variant angina culminating in acute myocardial infarction. Circulation 59:297, 1979 7. Maseri A, Severi S. De Nes M et al: “Variant” angina: one aspect of a continuous spectrum of vasospastic myocardial ischemia. Am J Cardiol 42:1019, 1978 8. Spodick DH: Diagnostic electrocardiographic sequences in acute pericarditis: significance of PR segment and PR vector changes. Circulation 48:575, 1973 9. Rose G: Diabetes, hyperglycemia and coronary heart disease. Prev Med 12:70, 1983 10. Allegro G, Pilati G, Ciavarella A, Vannini P: Transitory ECG changes of an ischemic type during hyperosmolar non-ketoacidotic coma. G ltal Cardiol 12:83 1, 1982 I 1. Burris AC, Chung EK: Pseudomyocardial infarction associated with acute bifascicular block due to hypcrkalemia. Cardiology 65: 115, 1980

ECG Changes

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and Madias

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12. Cohen A, Utarnachitt RV: Electrocardiographic changes in a patient with hyperkalemia and diabetic acidosis associated with acute anteroseptal pseudomyocardial infarction and bifascicular block. Angiology 32:361, 1981 13. Chaithiraphan S, Sahasakul Y: Electrocardiographic changes of hyperkalemia simulating acute myocardial infarction: a report of two cases. J Med Assoc Thailand 60:389, 1977 14. Logic JR: Electrophysiologic effects of regional hyperkalemia in the canine heart. Proc Sot Exp Biol Med 141:725, 1972 15. Kwoczynski JK, Ekmekci A, Toyoshima H, Prinzmetal M: Electrocardiographic ischemic patterns without coronary artery disease. Dis Chest 39:305, 1961 16. Surawicz B, Chlebus H, Mazzoleni A: Hemodynamic and electrocardiographic effects of hyperpotassemia: differences in response to slow and rapid increases in concentration of plasma K+. Am Heart J 73:647, 1967 17. Surawicz B: Relationship between electrocardiogram and electrolytes. Am Heart J 73:814, 1967 18. Scott RC: Left bundle branch block: a clinical assessment (II). Am Heart J 70:691, 1965 19. Surawicz B, Lepeschkin E: The electrocardiographic pattern of hypopotassemia with and without hypocalcemia. Circulation 8:801, 195 3 20. Cohen JJ, Gennari FJ, Harrington JT: Disorders of potassium balance. p. 908. In Brenner BM, Rector FC Jr (eds): The kidney, 2nd ed. WB Saunders, Philadelphia, 198 1 21. Perez GO, Oster JR, Pelleya R et al: Hyperkalemia from single small oral doses of potassium chloride. Nephron 36:270, 1984