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

EE A N D C H E A H

1

II

AVR

IlI

AVL

VI

AVF

V2

V4

V5

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

ECG CHANGES IN THYROTOXlC PERIODIC PARALYSIS

265

t~

-~

.~

'~-"~. "N.

"N. "N. '~. 'N. "~. "~. "N. "N.

"~. "N.

"~. '~. "~. ' 5 - ' N .

' ~ - ' ~ . 'N. "~. "~- ~ '~. ~

+ + +

+ + + + + + + +

++

+ + + + +

+ + + + + + + + +

+ + +

+ + + + + + + +

++

++

~ ,. ,.-4.

~5~

t~

o

I

I

+

I

I

I

~.~

~-~ ~E

W

X c~ c~.- E

I-e~

Z

I

++

I

++

I

+

I

I

I

I

Z

~,=~" 111

~.

Z

f,g

.

,~ 9 ,.4

5 ~. I ~

~. ~. , ~ , ,-4

.

~ ,:5 I

.

I

I

~. ' ' .. I

'-:.

.

=

.

.~5 .

i~ ,.-4 =

.~

. ~. "~.

I

I

t

,

. , I

~

I

"

~

I~

. , ~ ..~ I

~

~;~

~" ~" ~5.

~5

~

, , ~

.

'

I

"':

~"

J = ~ = ~

~5~5~.:. I

I ~

"

I ~.

I ~.

~ I

~.

I ~.

i

ul ,,,J

I.L

$ ~Em~

E ~o ~"&.= r E

c~ c ~

J.

ELECTROCARDIOLOGY,

~=

e = = e ~

E

VOL

12,

NO.

3,

1979

.,-4

,.4.N,.4,.4

,~,..q~=~~

~u

266

EE AND CHEAH

V!

V2

v3

v~

vs

vs

r-F~Hi!ii~:

ii~

I

I

I;1

'?:4

:t

~,,~ : 2 : ~ ; --+-