Electrocardiographic changes in thyrotoxic periodic paralysis

J. ELECTROCARDIOLOGY 12 (3), 1979, 263-279

Electrocardiographic Changes in Thyrotoxic Periodic Paralysis BY BERNARD EE, M.B., B.S. (MALAYA), M. MED. (SINGAPORE), M.R.C.P. (U.K.)* AND JIN-SENG CHEAH, M.D. (SINGAPORE), M.B., B.S. (SINGAPORE), F.R.A.C.P.t

SUMMARY The e l e c t r o c a r d i o g r a m s ( E C G s ) o f 30 p a t i e n t s w i t h h y p o k a l a e m i c t h y r o t o x i c p e r i o d i c p a r a l y s i s d u r i n g a n d a f t e r p a r a l y s i s w e r e studied. D u r i n g p a r a l y s i s , t y p i c a l f e a t u r e s o f h y p o k a l a e m i a w e r e seen in all p a t i e n t s w i t h s e r u m p o t a s s i u m levels o f 2.8mmol/1 o r less; above this level, the E C G s varied f r o m n o n - d i a g n o s t i c to t h o s e s h o w i n g t y p i c a l f e a t u r e s o f h y p o k a l a e m i a . I t was n o t possible to accur a t e l y p r e d i c t the s e r u m p o t a s s i u m level f r o m t h e E C G e x c e p t w h e n e i t h e r sinus a r r e s t o r h e a r t b l o c k was p r e s e n t . A l t h o u g h e x t r a s y s t o l e s have b e e n r e p o r t e d to be c o m m o n in h y p o k a l a e m i a , n o n e o f the p a t i e n t s in this s t u d y h a d e x t r a s y s toles. Sinus a r r e s t o c c u r r e d in two p a t i e n t s and s e c o n d d e g r e e a t r i o - v e n t r i c u l a r b l o c k o c c u r r e d in t h r e e p a t i e n t s , a f i n d i n g w h i c h has n o t been r e p o r t e d in hypokalaemia.

MATERIALS AND METHODS

T h y r o t o x i c p e r i o d i c p a r a l y s i s is a h y p o k a l a e m i c periodic p a r a l y s i s due to t h y r o t o x icosis w h i c h h a s a m a r k e d p r e d i l e c t i o n for m a l e s and t h e Mongoloid races, especially the C h i n e s e and J a p a n e s e . 1-5 W h i l e t h e r e is cons i d e r a b l e l i t e r a t u r e on t h e e l e c t r o c a r d i o g r a p h i c f e a t u r e s of h y p 0 k a l a e m i a , ~~ and on f a m i l i a l periodic paralysis, 1~15 t h e r e is little i n f o r m a t i o n on t h e d e t a i l e d e l e c t r o c a r d i o graphic changes in thyrotoxic periodic paralysis.2,3,11 In o u r e x p e r i e n c e w i t h t h y r o t o x i c periodic p a r a l y s i s in Singapore, we found several feat u r e s in t h e E C G s d u r i n g p a r a l y s i s which diff e r e d f r o m those r e p o r t e d in h y p o k a l a e m i a f r o m o t h e r causes. T h i s is d u e to t h e combination of h y p o k a l a e m i a and thyrotoxicosis. T h e p u r p o s e of this p a p e r is t h e r e f o r e to r e p o r t our e x p e r i e n c e of t h e e l e c t r o c a r d i o g r a p h i c abn o r m a l i t i e s in t h y r o t o x i c periodic paralysis.

Thirty patients with thyrotoxic periodic paralysis, seen at the U n i v e r s i t y D e p a r t m e n t of Medicine (I) of the Singapore General Hospital, were included in this study. Each was admitted to hospital following an attack of paralysis. A diagnosis of thyrotoxicosis was made at that time and confirmed by total thyroxine levels. They were all male Chinese whose ages ranged from 21 to 50 years, with a mean age of 31.7 years. None of them had any associated diseases including hypertension, diabetes mellitus and ischaemic heart disease and were not on any drug therapy, e.g. digitalis or quinidine. All had normal ECGs after correction of hypokalaemia. During an attack of paralysis, their serum potassium levels and ECGs were done simultaneously. Their severity of muscle weakness was graded as 0 to 5,12 and they ranged from total paralysis (Grade 0) to minimal weakness (Grade 4). Their serum p o t a s s i u m levels r a n g e d from 1.6mmol/1 to 3.3mmol/1 and they were put into four groups, A to D according to their serum potassium levels. As shown in Table 1, there were 11 patients in Group A (serum potassium 1.6 - 2.0mmol/1), five patients in Group B (serum potassium 2.1 - 2.5mmol/1), 12 patients in Group C (serum potassium 2.6 3.0mmol/1) and two patients in Group D (serum potassium 3.1-3.4mmol/1). A quantitative analysis of their ECGs for features of hypokalaemia was done according to a method previously described, s In each ECG, two leads (lead II and a praecordial lead with the tallest U wave) were analysed for the following signs: 1. U wave amplitude greater than lmm; 2. U wave amplitude g r e a t e r than T wave amplitude in the same lead; and 3. ST segment depression greater than 0.5mm.

*Lecturer, Department of Medicine, Faculty of Medicine, University of Singapore. t Professor, Department of Medicine, Faculty of Medicine, University of Singapore. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked " a d v e r t i s e m e n t ~' in accordance with 18 U.S.C. w 1734 solely to indicate this fact. Reprint requests to: Dr. Bernard Ee, University Department of Medicine (I), Singapore General Hospital, Singapore 3, Republic of Singapore. 263

264

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The ECGs were i n t e r p r e t e d as: 1. "Typical" of h y p o k a l a e m i a if 3 out of t h e possible 6 signs were p r e s e n t (see Fig. 1); 2. "Compatible" w i t h h y p o k a l a e m i a if 1 or 2 signs r e l a t e d to t h e U wave were present; and 3. "Non-diagnostic" of h y p o k a l a e m i a i f only ST s e g m e n t depression was p r e s e n t or if none of t h e signs were present, The PR, QT, QTc a n d QU i n t e r v a l s were measured. The absolute h e i g h t s of t h e T a n d U waves and ST s e g m e n t depression were a n a l y s e d to see if t h e y c o r r e l a t e d w i t h t h e i r s e r u m p o t a s s i u m levels. Cardiac a r r h y t h m i a s were also looked for. Table 1 SERUM POTASSIUM LEVELS DURING THYROTOXIC PERIODIC PARALYSIS GROUP A B C D TOTAL

SERUM POTASSIUM (MMOL/L) 1.6 2.1 2.6 3.1

-

2.0 2.5 3.0 3.4

NUMBEROF CASES (%) 11 (36.7%) 5 (16.6%) 12 (40.0%) 2 (6.7%) 30 (100.0%)

RESULTS 1. E C G s i g n s o f h y p o k a l a e m i a , s As s h o w n in Table 2, all 16 p a t i e n t s in Groups A a n d B (serum p o t a s s i u m 1.6-2.5mmol/1) h a d ECGs which were "typical" of h y p o k a l a e m i a , a l t h o u g h 12 of the 16 p a t i e n t s h a d a h e a r t r a t e of 100/min. or more. In Group C (serum potassium 2.6 - 3.0mmol/1), 9 of the 12 p a t i e n t s (75.0%) h a d "typical"ECGs, two p a t i e n t s h a d "compatible" ECGs (serum p o t a s s i u m 2.9 and 3 . 0 m m o l / 1 respectively) and one p a t i e n t

V3

V6

F i g . I E C G of a p a t i e n t w i t h thyrotoxic periodic paralysis ( s e r u m p o t a s s i u m 2.2 mmol/1) showing ~typical" features of h y p o k a l e m i a w i t h t a l l U waves in leads V2 to V4 and ST depression in leads II, III, V4 to V~. The P w a v e s a r e fused w i t h t h e p r e c e d i n g U w a v e s giving a ~titted" a p p e a r a n c e to t h e P waves.

had a non-diagnostic ECG (serum potassium 3.0mmol/1). I n Group D ( s e r u m p o t a s s i u m 3.1 - 3.4mmol/1), one h a d a "compatible" E C G and t h e other a ~nondiagnostic'one. Therefore, E C G s '~typical" of h y p o k a l a e m i a were found in all p a t i e n t s w i t h a s e r u m p o t a s s i u m of 2.8mmol/1 or less. However, t h e "typical" ECGs h a d corresponding s e r u m levels r a n g i n g from 1.6 to 3.0 m m o l / 1 . 2. U wave. U w a v e s of more t h a n l m m in h e i g h t a n d t a l l e r t h a n t h e i r corresponding T waves, were seen in all 23 p a t i e n t s w i t h s e r u m p o t a s s i u m levels of 2.8mmol/1 or less. T h e i r absolute heights, however, correlated poorly w i t h t h e i r corresponding s e r u m p o t a s s i u m levels. The t a l l e s t U wave was 10mm and the p a t i e n t h a d a h e a r t r a t e of 115/min. In several p a t i e n t s , the U wave was fused w i t h the following P wave, or was fused w i t h the preceding T wave. (see Fig. 2). In one p a t i e n t who h a d a t r i a l flutter-fibrillation C i m p u r e flutter"), t h e h e i g h t of the U w a v e v a r i e d according to t h e l e n g t h of the p r e c e d i n g R-R interval, being t a l l e r following a long R-R i n t e r v a l and s h o r t e r following a short R-R i n t e r v a l . (see Fig. 3). Tachycardia, therefore, has a t e n d e n c y to decrease t h e h e i g h t of t h e U wave. 3. T Wave. The T w a v e s were of lower a m p l i t u d e t h a n t h e i r corresponding U w a v e s in all 23 pat i e n t s with w e r u m p o t a s s i u m levels of 2.8mmot/1 or less. W h e n c o m p a r e d w i t h t h e i r c o r r e s p o n d i n g E C G s after correction of the h y p o k a l a e m i a , all 30 p a t i e n t s had T w a v e a m p l i t u d e s which were less t h a n h a l f of t h e i r n o r m a l T waves. There was no correlation b e t w e e n the h e i g h t of t h e T waves a n d t h e s e r u m p o t a s s i u m levels. 4. T/U ratio. A l t h o u g h a T/U r a t i o of less t h a n 1.0 was p r e s e n t in all p a t i e n t s w i t h a s e r u m potassium level of 2.8mmol/1 or less, no correlation was found between the T/U r a t i o and t h e s e r u m p o t a s s i u m level. J. ELECTROCARDIOLOGY, VOL 12, NO. 3, 1979

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2 Fig. 2 ECG of a p a t i e n t with thyrotoxic periodic paralysis (serum potassium 2.5 mmol/1) with tall U waves b u t no ST depression. The P waves are fused with the preceding U waves (shown more clearly i n the e n l a r g e m e n t of lead %72). 5. ST s e g m e n t depression. ST s e g m e n t depression was p r e s e n t i n p a t i e n t s with s e r u m p o t a s s i u m levels r a n g i n g from 1.6 to 3.0mmol/1 and the presence or absence of ST segment depression did not correlate with the serum potassium level. 6. P R interval and P wave. It was difficult to measure the PR i n t e r v a l s in 11 of the 30 patients because of the fusion of the P wave with the precedi n g T wave. This caused the P wave to be either completely buried w i t h i n the U wave or caused the P wave to b e g i n above the baseline a n d to end at the baseline, giving a characteristic "tilted" appearance to the P wave. (See Figs. 1 and 2).

I n the 19 p a t i e n t s whose P R intervals could be measured, the PR intervals n e v e r exceeded 0.20 sec., except i n three p a t i e n t s who had a second degree a t r i o - v e n t r i c u l a r block of the W e n k e b a c h type. 7. QT, QTc intervals. The QT i n t e r v a l could be m e a s u r e d i n 16 cases only because of the p a r t i a l fusion of the T and P waves i n the other 14 cases. These were all normal, i.e. 0.42 sec. or less. 13 8. C a r d i a c r h y t h m a n d c a r d i a c a r r h y t h m i a s . F o u r t e e n of the 30 p a t i e n t s were in sinus r h y t h m , and most had a sinus tachycardia. One p a t i e n t had atrial flutter-fibrillation ("impure" flutter) which

J. ELECTROCARDIOLOGY, VOL 12, NO. 3, 1979

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Fig. 3 ECG of a patient with thyrotoxic periodic paralysis (serum potassium 2.6 mmol/l) showing atrial flutter-fibrillation and features of hypokalemia (U waves in leads II V3 to V~). In lead V4, the U wave following a long R-R interval was much taller than the U wave following a shorter R-R interval. The flutter-fibrillation persisted after correction of the hypokalemia. persisted after correction of the hypokalaemia. Periods of sinus arrest were present in two patients, one of whom had an escape r h y t h m arising from another atrial focus (see Fig. 4). In both patients, the sinus arrest disappeared after correction of the hypokalaemia. Three patients had a second degree atrio-ventricular block of the Wenkebach type, showing progressive prolongation of the PR interval followed by a dropped beat. Their ventricular rates, however, ranged from 100/min. to l l5/min, and after correction of the hypokalaemia, the atrio-ventricular block disappeared (see Fig. 5). The two patients with sinus arrest and the three patients with second degree atrio-ventricular block were very m a r k e d l y hypokalaemic, t h e i r serum p o t a s s i u m level being 2.1mmol/1 and less. The presence of sinus arrest or heart block therefore indicates very severe hypokalaemia. None of the 30 patients studied had either supraventricular or ventricular extrasystoles. There were also none with intraventricular blocks.

DISCUSSION It has been reported previously t h a t the electrocardiographic features of hypokalaemia do not correlate well with the serum potassium level, 14-16 and may be only of limited value in predicting the serum p o t a s s i u m level. It has been previously shown t h a t in the absence of a tachycardia, when the serum potassium level was less than 2.7mmol/1, ECGs "typical" of hypokalaemia were consistently seen. s Our findings in this study concur with previous studies in that "typical" ECGs were consist e n t l y s e e n w i t h s e r u m p o t a s s i u m l e v e l s of 2.8mmol/1 or less. Weaver and Burchell (1960) stressed the presence of a T/U ratio of less t h a n 0.5, T wave inversion and ST segment depression as

J. ELECTROCARDIOLOGY, VOL 12, NO. 3, 1979

indicating severe hypokalaemia2 Our study, however, showed no correlation between these features and the serum potassium levels. It is only possible to conclude t h a t an ECG which is "typical" of hypokalaemia is associated with a serum potassium level of 3.0mmol/1 or less, and it is not possible to predict how much lower it is. The presence of a tachycardia has been reported to produce "non-diagnostic" ECGs despite severe hypokalaemia.8 In our study, despite the presence of a sinus tachycardia in most of the patients, there was no effect on the interpretation of the ECGs, "non-diagnostic" or %ompatible" ECGs being seen only when the serum potassium level was 3.0mmol/1 or more. However, a tachycardia undoubtedly has the effect of making the U wave amplitude lower than it would have been if the heart rate was slower. This fact was shown quite clearly in the patient with atrial flutter-fibrillation, in whom t a l l e r U waves occurred following longer R-R intervals. The long R-R interval following an extrasystole also explains the phenomenon of post-extrasystolic alternans of the U wave which has been previously reported. 17 The PR intervals in this study never exceeded the normal upper limit of 0.20 sec., concurring with p r e v i o u s s t u d i e s . 9'1s The QTc i n t e r v a l s were also w i t h i n n o r m a l l i m i t s as h a s been shown previously. TM The findings in this study which differed markedly from previous studies were the types of cardiac a r r h y t h m i a s seen. None of the patients with t h y r o t o x i c p e r i o d i c p a r a l y s i s , d e s p i t e severe hypokalaemia, had supraventricular or ventricular extrasystoles, which are reported to occur freq u e n t l y in h y p o k a l a e m i a ? '~'18'1s In a study of

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Fig. 4 ECG of a patient with thyrotoxic periodic paralysis during paralysis (top) and after paralysis (bottom). During paralysis (serum potassium 1.9 mmol/1), several episodes of sinus arrest occurred (recorded in lead II) resulting in an escape rhythm of low atrial origin with a shorter PR interval. The typical features of hypokalemia are seen in leads V2 and V3. The EKG became normal after potassium therapy. 25 patients with thyrotoxic periodic paralysis, 2 it was reported that extrasystoles were common. The rarity of ectopic beats in this series may be due to the sinus tachycardia suppressing potential ectopic pacemakers. While bradycardia has been described in associa-

tion with hypokalaemia, ls'2~ sinus arrest or sinoatrial block has never been documented in patients with hypokalaemia. In our study, two patients with serum potassium levels of 1.9mmol/1, had periods of sinus arrest which disappeared when the hypokataemia was corrected, and this is the first

J. ELECTROCARDIOLOGY, VOL 12, NO. 3, 1979

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Fig. 5 ECG of a patient with thyrotoxic periodic paralysis during paralysis (top) and after paralysis (bottom). During paralysis (serum potassium 2.0 mml/L), the features of hypokalemia were present together with second degree atro-ventricular block (Wenkebach type). The EKG became normal after correction of the hypokalemia. report of its occurrence in hypokalaemia without the added effect of digitalis. Whereas conduction defects had been demonstrated in experimentally induced hypokalaemia, 21 no case of atrio-ventricular block has been previously reported. In our study, three patients had second degree atrio-ventricular block (Wenkebach type), and their serum potassium levels were J ELECTROCARDIOLOGY,

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2.1mmol/1 and less. This is believed to be the first report of atrio-ventricular block in hypokalaemia, a l t h o u g h it h a s b e e n r e p o r t e d to o c c u r in thyrotoxicosis. 22 The occurrence of such potentially dangerous arrhythmias would suggest that the hypokalaemia in thyrotoxic periodic paralysis should be promptly corrected.

270

EE AND CHEAH

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22.

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