Inferior Wall Pseudoinfarction Pattern Due to Hyperkalemia ANDRAS VERECKEI From the 3 rd Department of Medicine, Semmelweis University, School of Medicine, Budapest, Hungary VERECKEI, A.: Inferior Wall Pseudoinfarction Pattern Due to Hyperkalemia. Pseudoinfarction pattern is a rare ECG manifestation of marked hyperkalemia. Case reports characteristically describe the oc- currence of anteroseptal pseudoinfarction pattern and four cases of anteroseptal together with inferior wall pseudoinfarction pattern associated with hyperkalemia. We report a case with isolated inferior wall pseudoinfarction pattern due to hyperkalemia. (PACE 2003; 26:2181–2184) hyperkalemia, pseudoinfarction pattern, electrocardiogram Introduction The well-known ECG manifestations of hyper- kalemia are shortened QT interval, symmetric, tall, peaked T waves and as the serum potassium con- centration progressively rises the QRS complex be- comes widened (which may result in various forms of intraventricular conduction disturbances) and blends with T wave producing a wide, bizarre, biphasic deflection (“sine wave” ECG). There is also a lengthening of the PR interval and diminu- tion in the amplitude of the P wave, which even- tually disappears. This latter event may coexist with preserved conduction of the impulses from the sinoatrial node to the atrioventricular node (“sinoventricular rhythm”), and ultimately ven- tricular fibrillation closes the picture. 1,2 However, pseudoinfarction pattern associated with hyperkalemia is a rare ECG manifestation. The few publications on pseudoinfarction patterns associated with hyperkalemia usually reported ECG abnormalities mimicking acute anteroseptal myocardial infarction. 3–8 Only four cases with an inferior wall and an anteroseptal pseudoinfarction pattern due to hyperkalemia were reported. 9–11 This case reports of an isolated inferior wall pseu- doinfarction pattern due to hyperkalemia. Case Report A 71-year-old woman presented with dysp- nea, ankle swelling, hypotension (blood pressure (BP) 85/65 mmHg), and no chest pain. On admis- sion the ECG (Figs. 1 and 2) showed sinus rhythm with horizontal QRS axis, pathological Q waves in leads III and aVF (the pathological Q waves in lead aVF are better seen in Fig. 2), Q waves in lead II, ST segment elevation in the inferior leads, in- verted T waves in leads III and aVF, and recip- rocal ST depression in leads I and aVL, suggest- ing evolving acute inferior myocardial infarction Address for reprints: Andras Vereckei, M.D., 3 rd Department of Medicine, Semmelweis University, School of Medicine, Bu- dapest, Kutvolgyi ´ ut 4, Hungary 1125. Fax: 36-1-225-0196; e-mail: vereckei@kut.sote.hu Received January 17, 2003; accepted February 1, 2003. and a slight ST segment elevation in leads V 1 and V 3 . The QRS was widened at 110 to 120 ms. The ST elevation in the inferior leads and T wave in- version in leads III and aVF cannot be attributed to secondary ST-T changes associated with wide QRS complexes, however, the slight ST elevation in leads V 1 and V 3 is probably a secondary ST elevation. The myocardial enzymes were repeat- edly normal. Echocardiography did not reveal any wall motion disturbance, ruling out acute myocar- dial infarction. The serum potassium concentra- tion was 8.9 mmol/L at the time of admission due to acute renal insufficiency induced by nons- teroid anti-inflammatory drug abuse for joint pain. Other pertinent laboratory values on admission were: serum calcium, 1.48 mmol/L; serum phos- phate, 1.84 mmol/L; serum sodium, 130 mmol/L; BUN, 46.9 mmol/L; serum creatinine, 357 μmol/L; pH, 7.27; pCO2, 11.8 mmHg; pO2, 113.9 mmHg; serum bicarbonate, 5.2 mmol/L; and oxygen sat- uration, 97%. Four days later when the serum potassium was normalized (4.0 mEq/L), the ECG (Fig. 3) showed sinus rhythm with narrow QRS complexes, the pseudoinfarction pattern disap- peared, ST elevation was no longer present, Q wave was seen only in lead III, and a slight T wave inversion was seen in the inferior leads. Discussion The ST elevations seen with marked hyper- kalemia often have a distinctive saddle-back ap- pearance and a terminal inversion of the T wave may also be present. 11 These features were present in this case as well. Transient Q waves associated with marked hyperkalemia are probably caused by the direct effect of marked increases in serum potassium concentration on the resting potential of myocardial cells. Normally the ratio of intra- cellular to extracellular potassium is about 30:1 and this ratio is the primary determinant of the negative resting potential of normal cardiac fibers. An increase in extracellular potassium concentra- tion will result in a decreased resting potential and consequently, a decrease in the amplitude of ac- tion potential. When there is a marked increase PACE, Vol. 26 November 2003 2181