CARDIAC FUNCTION IN ANEURYSMAL SUBARACHNOID HAEMORRHAGE: A STUDY OF ELECTROCARDIOGRAPHS AND ECHOCARDIOGRAPHIC ABNORMALITIES

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1 British Journal of Anaesthesia 1991; 67: CARDIAC FUNCTION IN ANEURYSMAL SUBARACHNOID HAEMORRHAGE: A STUDY OF ELECTROCARDIOGRAPHS AND ECHOCARDIOGRAPHIC ABNORMALITIES K. R. DAVIES, A. W. GELB, P. H. MANNINEN, D. R. BOUGHNER AND D. BISNAIRE SUMMARY Electrocardiographic (ECG) changes are reported frequently after subarachnoid haemorrhage (SAH). The aim of this study was to investigate the functional significance of ECG changes by echocardiographic assessment of cardiac function. Forty-five patients with intracranial aneurysms were studied. All patients had a 12-lead ECG and a two-dimensional echocardiogram. After patients with an history of chronic cardiac disease (n = 4) were excluded, only four patients were found to have wall motion abnormalities. These patients had only minor ECG abnormalities, but severe neurological dysfunction. Conversely, patients with other ECG abnormalities including the deep inverted T waves associated usually with SAH, had normal echocardiograms. We conclude that the ECG is not an accurate predictor of myocardial function after SAH and that myocardial dysfunction is related more closely to severity of neurological condition. KEY WORDS Haemorrhage: subarachnoid. Heart: cardiac dysfunction. Monitoring: echocardiography, electrocardiograph^. Electrocardiographic changes have been well documented after subarachnoid haemorrhage (SAH). In addition to T wave, S-T segment and Q-T interval abnormalities, changes in P wave and U wave configuration may be found, and arrhythmias [1-4]. Although these changes are not regarded usually as of great clinical significance because most of the patients do not have ischaemic heart disease and survive the perioperative period without overt adverse cardiac events, postmortem examinations frequently show focal myocardial haemorrhages and myocytolysis [5, 6]. In view of the latter, the electrocardiographic changes may have functional significance and may create a dilemma for the anaesthetist who sees the patient immediately before operation [7, 8]. The aim of this study was to assess the relationship between the electrocardiographic changes and an echocardiographic assessment of cardiac function. PATIENTS AND METHODS Forty-five patients with intracranial aneurysms, SAH, or both, were assessed. All patients had a 12-lead electrocardiogram and a two-dimensional echocardiographic study before operation. If more than a single electrocardiogram record existed, the one in closest temporal proximity to the echocardiographic study was used for assessment. Electrocardiograms were considered abnormal if the T wave was inverted or flattened, the S-T segment was elevated or depressed, the Q-T interval prolonged or a pathological Q wave or U wave was present. The presence of an arrhythmia or conduction defect was noted also. Bradycardia was defined as a heart rate less than 60 beat min" 1 in patients not taking p"-blockers. Axis deviation coincident with hypertension or pulmonary disease was not considered an acute change consistent with SAH. The two-dimensional echocardiograms were recorded on a Panasonic Model Ag 6300 VHS K. R. DAVIES, M.D., A. W. GELB*, M.B., CH.B., D.A.(ENG.), F.H.C.P.C, P. H. MANNINEN, M.D., F.R.c.p.c. (Department of Anaesthesia); D. R. BOUGHNER, M.D., F.R.C.P.C. (Cardiac Investigation Unit); D. BISNATRE, B.SC.N. (Nursing Services); University Hospital, London, Ontario, Canada. Accepted for Publication: January 28, Address for correspondence: Department of Anaesthesia, University Hospital, 339 Windermere Road, London, Ontario, N6A 5A5 Canada.

2 CARDIAC FUNCTION IN SUBARACHNOID HAEMORRHAGE 59 recorder using a Hewlett-Packard phased-array ultrasound imaging system, model 77020A. Studies were performed with a 2.5-MHz transducer. Standard parasternal long axis, short axis, apical four chamber and two chamber views were obtained for analysis of left ventricular function [9]. The left ventricular short axis was recorded at the level of the base, mid ventricle and apical region. The basal region included both mitral valve leaflets and chordal structures, while the mid ventricular region was at the level of the papillary muscles and the apex was denned as the region extending from the most distal aspects of the papillary muscles to the ventricular apex. The videotape recordings were reviewed by an experienced echocardiographer (D.R.B.) without knowledge of the patient's neurological state. For purposes of analysis, the left ventricle was considered as divided into five segments consisting of the septum, anterolateral wall, posterolateral wall, posterior wall and apex. Wall motion in each segment was classified as normal, hypokinetic, akinetic or dyskinetic on the basis of a visual assessment of wall thickening and endocardial movement during systole. Normal myocardium showed inward movement of the endocardium with accompanying systolic wall thickening. Hypokinetic myocardium was defined as a reduction in wall thickening equal to or greater than 50% compared with normal segments. Akinetic segments had no systolic thickening and dyskinetic segments were denned as having paradoxical outward extension with systolic thinning [10]. The echocardiographic findings of mitral valve prolapse or ventricular hypertrophy were not considered as acute changes related to SAH. Patient records were reviewed for age, sex, acute or chronic neurological deficits, acute or chronic cardiac disease and serum electrolytes. The Botterell classification of clinical status after SAH was used [11]. cardiogram was 7.9 (SD 8.0) days (range 0-30 days). All echocardiograms were obtained after an electrocardiogram; mean time between the two tests was 2.8 (2.4) days. Table I shows the distribution of patients according to the presence and absence of electrocardiographic and echocardiographic changes. Four patients (9%) with SAH had electrocardiographic or echocardiographic changes that were consistent with their history of chronic ischaemic cardiac disease, that is, Q waves on the electrocardiogram and an history of previous myocardial infarction. Table II shows the results with these patients excluded. In the group with no history of cardiac disease (table II), 23(56%) had no electrocardiographic or echocardiographic abnormalities. Eighteen patients (44%) had electrocardiographic changes, consisting of T wave inversion (four patients), T wave flattening (four patients), sinus tachycardia (four patients), sinus bradycardia (five patients), P TABLE I. Number of patients with abnormalities of the ECG and echocardiogram (ECHO) as defined in text. ^Includes a patient who died ECG normal ECHO motion abnormality Total Neurological grade Total * 18 3* 1* TABLE II. Number of patients without heart disease with abnormalities of the ECG and echocardiogram (ECHO) as defined in the text. * Includes a patient who died RESULTS Forty-three patients had angiographic evidence of at least one intracranial aneurysm. Two patients had suffered SAH, but no aneurysm was found on angiography. Thirty-five patients (28 females, seven males; ages yr) had SAH (neurological grade 1-4). The remaining 10 (seven females, three males; ages yr) did not bleed from their aneurysm (neurological grade 0) (table I). The mean time between ictus and the electro- ECG normal ECHO motion abnormality Total Neurological grade * 3* 1* Total

3 BRITISH JOURNAL OF ANAESTHESIA but without echocardiographic abnormalities (median Botterell class = 1.0). There were no deaths in the 23 in whom both electrocardiogram and echocardiogram were normal. Neurologica] Both anterior and posterior circulation aneugrade ECG ECHO rysms were well represented in our study, yet bleeds associated with echocardiographic changes Akinetic apex and Inverted T waves in I, AVL, V M anterolateral wall appeared confined to the anterior circulation (one Hypokinetic apex Flattened T waves carotid, three anterior communicating), whereas the majority with only electrocardiographic Sinus tachycardia Hypokinetic septum changes had posterior circulation aneurysms. Flattened T waves I V None of the electrocardiographic changes was.4* Akinetic posterior Sinus tachycardia associated with abnormal electrolyte concenintraventricular lateral wall trations. Hypokinetic apex conduction delay All echocardiographic abnormalities occurred in patients with either severe SAH (Botterell wave enlargement, ectopy and small inferior Q grades 3 and 4; P < 0.01 compared with grade 0-2 waves (one patient each) and conduction abnor- patients) or an history of chronic ischaemic heart mality (two patients). Elimination of patients who disease. No patient had echocardiographic abhad only rhythm or conduction abnormalities normalities associated with an entirely normal (seven patients) would remove one grade 4 patient electrocardiogram, but the abnormalities were with echocardiographic and electrocardiographic minor in three (flattened T waves or intrachanges (table III), one grade 3, one grade 0, and ventricular conduction delay, or both). However, four grade 1 patients from table II. Four of the 18 none of the patients with the deep inverted T patients (22 %) with electrocardiographic abnor- waves usually associated with SAH had echomalities also had echocardiographic changes. The cardiographic abnormalities (table III). changes were either hypokinesis or akinesis and Of 24 patients without a previous history of involved at least 30% of the heart (table III). hypertension, 10 were found on admission to Two of the four patients with electrocardiographic hospital to have sustained increases in arterial and echocardiographic changes died within 7 days pressure. Two patients with both electrocardiofrom complications of SAH (neurological grade 3 graphic and echocardiographic changes had severe and 4). There was one death among the 14 hypertension (systolic > 200 mm Hg and diapatients with electrocardiographic abnormalities stolic > 100 mm Hg) while the other eight, only TABLE III. ECG abnormalities in patients with abnormal echocardiogram (ECHO) (abnormalities as defined in text). *Indicates a patient who died rv-i J. i. r alieni i - i nc i MH>W ^ IK>I niiii M I I U > I I I \ r < *.. R s~ ^/ ~*"S uim in leads 1, 2, 3, avf, V5_<. The associated echocardiogram was normal.

4 CARDIAC FUNCTION IN SUBARACHNOID HAEMORRHAGE rmt FIG. 2. Patient 2. The electrocard.,^;.*;...,. /*.,..a.^ i-wijcarjia wuli ii,,,u i >,. echocardiogram showed hypokinesis of the intraventricular septum. three of whom had an electrocardiographic abnormality and none of whom had echocardiographic changes, had considerably smaller increases in arterial pressure. Illustrative cases Patient 1. A 31-yr-old woman in previously good health presented with an acute SAH from a ruptured posterior inferior cerebellar aneurysm. She was classified as grade 1. There was no acute cardiovascular instability or history of cardiac disease. Serum electrolyte concentrations were normal on admission. An electrocardiogram at that time showed normal sinus rhythm with very prominent T wave inversion in leads 1, 2, 3, avf and V ^ (fig. 1). The following day a twodimensional echocardiogram showed no abnormality. The patient was discharged 9 days later in good condition, following surgery. Patient 2. A 43-yr-old woman in previously good health presented with an acute SAH from an anterior communicating aneurysm. Her neurological grade was 1. There was no acute cardiovascular instability or history of cardiac disease. Serum electrolyte concentrations were normal. Electrocardiogram obtained at the time showed sinus rhythm without abnormality. A two-dimensional echocardiogram was normal. Ten days after admission, the same patient had another acute SAH. Her new neurological grade was 3. She had a sustained increase in systolic arterial pressure to more than 200 mm Hg. An electrocardiogram showed sinus tachycardia and minimal T wave flattening which was not present the previous week (fig. 2). A two-dimensional echocardiogram showed new localized hypokinesis of the intraventricular septum. The patient's neurological condition deteriorated over the next 3 days, at which time she died. Serum myocardial iso-enzyme concentrations did not support a diagnosis of myocardial infarction. Consent for an autopsy was not obtained. DISCUSSION Acute changes in the electrocardiogram are often indicative of cardiac disease which warrants a thorough but time consuming clinical investigation. However, the electrocardiographic changes after subarachnoid haemorrhage, which are usually regarded as not indicative of significant cardiac dysfunction, may cause urgent surgery to be delayed [7,8]. By echocardiographic examination, we attempted to determine if these electrocardiographic changes represent cardiac dysfunction. Appearing within the first 14 days after SAH, ECG changes may take up to 6 weeks to resolve [3]. Possible causes of these changes include abnormal electrolyte concentrations, vagal stimulation and hypothalamic dysfunction resulting in sympathetic stimulation [5, 12, 13]. Disturbances in serum electrolyte concentrations have been demonstrated after SAH and some of the electrocardiographic changes after SAH resemble those present in patients with such disturbances [12].

5 62 BRITISH JOURNAL OF ANAESTHESIA However, in our patients, we found no relationship between serum electrolyte concentrations (in particular potassium and calcium) and electrocardiographic changes. Other investigators also have found no relationship between serum potassium concentration and electrocardiographic aberrations [14, 15]. Only five patients had sinus bradycardia on electrocardiogram, but we cannot exclude vagal mechanisms at the time of the bleed. Hypothalamic lesions after SAH have been associated with myocardial damage [16]. It is postulated that microinfarcts from cerebral artery spasm form in the hypothalamus after SAH [17]. As the hypothalamus is a centre for autonomic control, this leads to derangement of the sympathetic nervous system with increased catecholamine stimulation of the myocardium, both directly via the cardiac nerves and indirectly via the adrenal medulla [12]. Pathological examination of the heart after SAH may be grossly normal, but microscopic subendocardial haemorrhages and myocytolysis are often present [5, 6]. From experimental studies in which animals had the heart denervated, the adrenal glands removed or were treated with P-blockers or reserpine, it appeared that direct neural input to the heart was the most important [18, 19]. There is also an associated increase in release of corticosteroid after SAH which potentiates the effects of catecholamines [20]. Fifty-two percent of our patients with an intracranial bleed had electrocardiographic abnormalities that were unexplained by chronic disease. This is consistent with other reports in the literature [3, 13, 14]. Of interest in our study is the fact that those patients with the prominent large inverted T waves associated usually with SAH had normal echocardiographic studies (for example our patient 1). In contrast with some other studies, we found no relationship between the type of electrocardiographic changes and the level of consciousness, hypertension or mortality [2, 21]. The four patients with abnormal echocardiograms had minor electrocardiographic alterations. Echocardiogram abnormalities appear to reflect the severity of subarachnoid bleeding. Patients with abnormal echocardiogram results averaged two Botterell grades worse, suggesting myocardial dysfunction is related to a worse neurological grade. In addition, their prognosis is poor, as two of the four succumbed to dieir disease. In contrast, all 28 of 29 patients with a normal echocardiographic study after SAH were discharged home from hospital. This is consistent widi an earlier smaller study in which wall motion abnormalities corresponded with increased neurological grade and poorer outcome [22]. The sensitivity of the echocardiogram is greatly enhanced if the study is performed while the subject is stressed, for example during exercise. We did not feel that it would be ethical deliberately to stress patients with a SAH, and so may have missed some patients with myocardial dysfunction. Conversely, those with the worst neurological grade were probably the most stressed, and this may partly or completely explain their incidence of echocardiographic changes. None of our patients died as a direct result of their cardiac dysfunction. This is consistent with other studies [23, 24]. Neurological status is the most important determinant of outcome and death is usually the direct result of the brain injury. Whereas cardiac dysfunction is not a direct cause of mortality after SAH, it may increase morbidity because of arrhythmias or pulmonary oedema [25]. Several methodological issues deserve comment. Some of our patients were not admitted until several days after SAH. There is the possibility that acute and quickly resolving changes in the electrocardiogram were missed in some subjects. Similarly, there was a delay between the electrocardiogram and the echocardiogram which may have resulted in us missing rapidly resolving echocardiographic changes. The definition of electrocardiographic abnormality we used was less precise than that used currently in relation to ischaemic heart disease, but is consistent with that used previously in relation to SAH [1-4]. Elimination of patients who had only rhythm or conduction abnormalities would not alter our conclusions. Although our sample size is substantially larger than the previous study of echocardiographic dysfunction in SAH [22], our sample is still too small to allow detailed statistical analysis. Confirmation of these results in a much larger study is desirable. In conclusion, we found a poor relationship between electrocardiographic changes after SAH and evidence of myocardial dysfunction on the echocardiogram. A better relationship existed between the echocardiogram and the severity of the neurological injury. We suggest that, in the absence of a history of cardiac disease, the

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