Journal of Postgraduate Medicine
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Year : 1978  |  Volume : 24  |  Issue : 4  |  Page : 209-213  

Electrocardiographic abnormalities in acute cerebro-vascular accidents and their correlation with cerebro-spinal fluid pressure and serum electrolytes

MS Gambhir, AH Hakim, BS Bomb, RC Gupta, DK Agarwal 
 Department of Medicine, R.N.T. Medical College, Udaipur, Rajasthan, India

Correspondence Address:
M S Gambhir
Department of Medicine, R.N.T. Medical College, Udaipur, Rajasthan


Electrocardiographic studies have been carried out in 50 patients with acute cerebrovascular accidents. These cases included 31 cases from non-haemorrhagic group and 19 cases from haemor­rhagic group. `T«SQ» or T-U wave abnormalities were seen in 63.1% of cases in haemorrhagic group and in 35.4% of cases from non-hae­morrhagic group. Abnormal prolongation of QTc interval (105% of normal i.e. 0.45 Secs.) was observed in 73.6% cases from haemorrhagic group and in 35.4% of cases from non-haemorrhagic group. On comparing these two groups it was found that QTc was signi­ficantly more prolonged in patiens of haemorrhagic group than non­-haemorrhagic group. The CSF pressure was found to be signi­ficantly more in patients with ECG abnormalities. However, there teas no correlation between serum electrolyte levels and ECG abnormalities. After 2 weeks, the ECG abnormalities disappeared, except in two cases from haemorrhagic group. There was no signi­ficant difference in the incidence of mortality between patient having ECG abnormalities and the patients without ECG abnormalities. In the light of these findings the probable mechanism of production of ECG changes in acute cerebrovascular accidents is discussed.

How to cite this article:
Gambhir M S, Hakim A H, Bomb B S, Gupta R C, Agarwal D K. Electrocardiographic abnormalities in acute cerebro-vascular accidents and their correlation with cerebro-spinal fluid pressure and serum electrolytes.J Postgrad Med 1978;24:209-213

How to cite this URL:
Gambhir M S, Hakim A H, Bomb B S, Gupta R C, Agarwal D K. Electrocardiographic abnormalities in acute cerebro-vascular accidents and their correlation with cerebro-spinal fluid pressure and serum electrolytes. J Postgrad Med [serial online] 1978 [cited 2023 Jun 2 ];24:209-213
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Full Text


Acute cerebrovascular accidents (C.V.A.) are quite often accompanied with characteristic electrocardiographic (E.C.G.) abnormalities. [1],[2],[4],[6],[12],[15] The findings may be summarised as: Prolong­ation of the Q-Tc interval and a large and wide T or T-U wave of the same general configuration as in myocardial ischaemia. [6]

Similar ECG changes have been describ­ed in nonvascular intracranial lesions like meningitis and intracranial tumours by Hersch. [7] The mechanism by which these changes are produced is not clear. The various mechanisms which have been suggested by different workers [2],[3],[10] in­clude actual damage to the myocardium in the form of sub-endocardial haemor­rhage, electrolyte imbalance, and raised intracranial tension and vagotonicity.

In view of these varied explanations for the ECG abnormalities in acute CVA the present study was undertaken to review the pattern of ECG changes and its correlation with serum electrolytes (Sodium and Potassium) and the cerebrospina fluid (CSF) pressure if any. Other aims, of this study were to find out any correla­tion between ECG changes and prognosis and reversibility of these changes.

 Material and Methods

The present study was carried out on 50 clinically diagnosed patients of acute cerebrovascular accidents admitted with­in 48 hours after the onset of stroke to the general hospital, attached to R.N.T. Medical College, Udaipur. The diagnosis depended on focal neurological signs and temporal profile. These patients were further divided into two groups (1) hae­morrhagic vascular lesions and (2) non­haemorrhagic vascular lesions, depending upon the presence or absence of grossly apparent blood (non traumatic) or xan­thochromia or both in the CSF.

Immediately after hospitalisation a detailed neurological examination was carried out to assess the neurological deficit. In addition to routine investiga­tions, following special investigation were also carried out:

ECG on the day of admission and after two weeks.Serum sodium and potassium esti­mation at the time of admission by flame photometry.CSF pressure estimation by mano­meter.

In all ECG's the QTc interval was cal­culated according to the method described by Kissin. [9]

The QTc interval was compared bet­ween the haemorrhagic and nonhaemor­rhagic group by the Students `t' test. The CSF pressure and serum electrolyte levels were also compared between pati­ents showing ECG abnormalities and patients without any ECG abnormalities by the same statistical method.


The results of the present study are summarised in [Table 1] and[Table 2]. As evident from the tables, 19 patients belonged to haemorrhagic group and 31 patients, to non-haemorrhagic group. QTc was found to be prolonged (more than 105% of normal) in 14 out of 19 patients from the haemorrhagic group and 11 out of 31 patients from the non-haemorrhagic group. The average QT( was 123.3% of normal in the haemorrhagic group, and 114.6% of nor­mal in the non-haemorrhagic group. Or statistical analysis the QTc interval in haemorrhagic group was significantly longer than the non-haemorrhagic group (p [6]

On follow up it was seen that in most of the cases the ECG changes reverted to normal within a period of two week; except in two cases from the haemor­rhagic group, in whom slight prolonga­tion of the Q-Tc duration persisted, al­though in these the T or T-U wave ab­normality disappeared. This indicates that ECG abnormalities in acute CVA is produced by some pathophysiology which does not produce permanent damage to the heart.

There was no significant difference in the incidence of mortal ty between patients of acute CVA with ECG abnor­malities and those without ECG abnor­malities. This further indicates that there is no significant structural damage to heart in majority of the patients of acute CVA with ECG abnormalities as suggested by Koskelo et al [10] otherwise one would expect higher mortality in these patients than those who are not having any ECG abnormality. In agree­ment with our view while contrary to the observation of Koskelo et al [10] other workers [1],[4],[14] were unable to find any histopathological changes in the myocar­dium of the patients dying from sub­arachnoid haemorrhage.

From the present study it is clear that there is no correlation between the serum sodium and potassium levels and ECG abnormalities encountered in patients of acute CVA suggesting that ECG abnor­malities encountered in patients of acute CVA are not because of alteration in the serum sodium and potassium levels. This observation is in confirmation with those of Huganholetz [8] and Shuster, [11] while con­trary to the suggestion of Burch et al. [2]

Another point which is clear from the present study is that the mean CSF pres­sure was significantly higher in patients of acute CVA who had ECG abnormali­ties than those who had no ECG abnor­malities; this indicates that raised CSF pressure by some mechanism may be pro­ducing the ECG abnormalities. This possibility is further supported by the observation of Hersch [7] who has reported similar ECG abnormalities in patients of raised intracranial tension because of nonvascular causes. How the raised in­tracranial tension produces the ECG ab­normalities, is yet speculative. Cushing 5 demonstrated the dysfunction of autonomic nervous system to be due to increased intracranial pressure in dogs, which could be eliminated by vagotomy. This sug­gests that raised intracranial tension does have an effect on vagol tone. This view is supported by Chetri and De, [3] who cor­related intracranial hypertension with vagal hyperactivity and have shown that the administration of intravenous atropine tends to reverse the non-specific ST and T or TU wave abnormalities of acute CVA to normal, while similar alteration due to coronary artery disease remained unaffected. Smith and Ray [13] have also implicated autonomic dysfunction as a probable mechanism responsible for E.C.G. changes and arrhythmia in patients having raised intracranial ten­sion.


The authors are thankful to the Princi­pal and Controller and Superintendent R.N.T. Medical College and attached groups of hospitals for their kind permis­sion to publish this work.


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