Keywords
electrocardiographic - intracranial - hemorrhage
Introduction
Electrocardiographic (ECG) changes after ischemic stroke and subarachnoid hemorrhage
are well documented.[1] Nonmyocardial causes of ECG changes have also been well documented.[2] However, ECG changes after spontaneous intracerebral hemorrhage (SICH) have been
infrequently studied. In many cases, the changes that occur due to neurogenic causes
may be misinterpreted as primary cardiac events. The management will then be directed
toward cardiac causes rather than medical or surgical reduction in intracranial pressure
(ICP). Various studies have also shown a relationship between presence of neurogenic
ECG changes and mortality.[3]
[4] This study is hence undertaken to study ECG changes after SICH. This will help in
timely interventions to reduce ICP and may also help in patient prognostication.
Materials and Method
This study was conducted at a tertiary care center, prospectively over 1 year. Patients
with SICH (supra- and infratentorial) were included. Exclusion criteria were subarachnoid
or intraventricular hemorrhage (IVH) without parenchyma bleed, doubtful traumatic
bleeds, and patients on anticoagulation. A detailed history and examination was done.
All patients were admitted to neurosurgical intensive care unit (ICU) and managed
as per standard protocol. All patients had and ECG at time of admission and were monitored
continuously. ECG changes occurring were recorded by critical care team and confirmed
by the senior consultant. Echocardiography (ECHO) was done in all patients. All changes
detected on monitors were confirmed using a 12-lead ECG. The cardiologist was consulted
initially and as per clinical requirement. Neurosurgical management was aimed at lowering
of ICP and guided by clinical status in terms of surgery or conservative treatment.
The ECG changes were tabulated corresponding to different cerebral areas based on
findings of computed tomographic (CT) scan. CT was interpreted jointly by a neurosurgeon
and radiologist.
Results
Total 47 SICH patients were admitted to the neurosurgical ICU over 1 year. In this
study, 80.2% of the patients were males and 93.6% of patients were older than 40 years.
At the time of admission, one or more ECG abnormalities were seen in 66% of the patients
([Table 1]). The most common finding was a prolonged QTc interval (39%), followed by sinus
tachycardia or bradycardia and ST-segment changes ([Fig. 1]). All patients with brainstem and intraventricular bleed had changes in ECG, whereas
62% had basal ganglia (BG) bleed, 43% thalamic bleeds, and 57% had cortical bleeds
had ECG changes ([Table 2]). Concomitant ECHO changes were seen in 13% of patients (thalamic 2, IVH 1, and
brainstem 1). One patient had global hypokinesia, one patient had a right wall motion
defect, and left ventricular hypertrophy was seen in three patients. The most common
change in BG lesion was T-wave inversion as well as QTc prolongation in thalamic lesions
([Table 3]). ECG changes were seen in an equal percentage in males and females ([Table 1]). ECG changes were seen in all patients younger than 40 years whereas 75% of patients
in the age group of 61 to 70 were found to have changes on ECG ([Table 4]). Changes regarding side of bleed were not analyzed. Correlation with mortality
could not be done as few patients were shifted to other centers. In one IVH patient,
global hypokinesia was reversed after insertion of ventricular drain and normalization
of ICP.
Fig. 1 Distribution of ECG changes. AF, Atrial fibrillation; AV, atrioventricular; PSVT,
paroxysmal supraventricular tachycardia; RBBB, right bundle branch block
Table 1
Age and sex distribution of cases
|
Age (y)
|
M
|
F
|
|
|
< 40
|
3
|
0
|
3
|
|
41–50
|
11
|
0
|
11
|
|
51–60
|
12
|
4
|
16
|
|
61–70
|
8
|
4
|
12
|
|
> 70
|
4
|
1
|
5
|
|
38
|
9
|
47
|
Table 2
Percentage distribution of electrocardiographic changes
|
Region
|
Change
|
No
|
|
%
|
|
Thalamus (Th)
|
3
|
4
|
7
|
43
|
|
Basal ganglia (BG)
|
13
|
8
|
21
|
62
|
|
Frontal
|
2
|
2
|
4
|
50
|
|
Temporal
|
0
|
0
|
0
|
0
|
|
Parietooccipital
|
2
|
1
|
3
|
66
|
|
Intraventricular hemorrhage (IVH) with bleed
|
2
|
0
|
2
|
100
|
|
Brainstem
|
4
|
0
|
4
|
100
|
|
Subarachnoid hemorrhage (SAH)
|
4
|
1
|
5
|
80
|
|
Cortical venous thrombosis (CVT) with bleed
|
1
|
0
|
1
|
100
|
|
31
|
16
|
47
|
|
Table 3
Region-wise distribution of electrocardiographic changes
|
BG
|
Th
|
Cortical
|
SAH
|
IVH
|
Brainstem
|
CVT with bleed
|
|
Abbreviations: AF, Atrial fibrillation; AV, atrioventricular; BG, basal ganglia; CVT,
cortical venous thrombosis; IVH, intraventricular hemorrhage; PSVT, paroxysmal supraventricular
tachycardia; RBBB, right bundle branch block; SAH, subarachnoid hemorrhage; Th, thalamus.
|
|
QTc prolonged
|
3
|
4
|
1
|
3
|
0
|
1
|
1
|
|
Sinus brady
|
2
|
1
|
1
|
1
|
0
|
0
|
|
|
Sinus tachy
|
2
|
1
|
0
|
0
|
1
|
1
|
|
|
ST elevation
|
2
|
1
|
1
|
0
|
0
|
2
|
|
|
ST depression
|
2
|
1
|
1
|
0
|
0
|
1
|
|
|
T inversion
|
4
|
0
|
0
|
0
|
0
|
1
|
|
|
RBBB
|
0
|
0
|
1
|
0
|
1
|
|
|
|
PSVT
|
1
|
0
|
1
|
0
|
0
|
|
|
|
AF
|
1
|
0
|
0
|
0
|
0
|
|
|
|
AV block
|
0
|
1
|
0
|
0
|
0
|
|
|
|
Junctional ectopic
|
0
|
1
|
0
|
0
|
0
|
|
|
Table 4
Distribution of cases with ECG changes
|
Age (y)
|
M
|
F
|
|
Percentage
|
|
< 40
|
3
|
0
|
3
|
100
|
|
41–50
|
6
|
0
|
6
|
54
|
|
51–60
|
8
|
2
|
10
|
62
|
|
61–70
|
6
|
3
|
9
|
75
|
|
> 70
|
2
|
1
|
3
|
60
|
|
25
|
6
|
31
|
66
|
Discussion
Electrocardiographic changes after ischemic stroke have been well documented.[1]
[2] However, ECG changes occurring after SICH have been infrequently studied. In many
cases, the changes that occur due to neurogenic causes may be misinterpreted as primary
cardiac events.[3]
[4]
[5] The authors found that a prolonged QTc interval was the most common abnormality
seen in SICH patients. This was in accordance with other studies. Similar to other
studies, BG and thalamic bleeds had a higher frequency of ECG changes.[3]
[4]
[5] There are various studies describing the pathophysiology of cardiac events after
SICH. It has been proposed that a cardiac cortical rhythm control site is probably
present within the middle cerebral artery territory or in the anterior cingulate cortex.[6]
[7] Vascular damage to these areas has been postulated to cause cardiac arrhythmias
due to a disinhibition of the right insular cortex with resulting increased sympathetic
tone. Ischemic involvement of the right hemisphere induces a higher risk for cardiac
arrhythmia occurrence than that of the left hemisphere. The autonomic nervous system
receives neural input from various parts of the cerebral cortex, hypothalamus, and
brainstem, which is extensively interconnected. Derangements of autonomic function
have also been shown to be responsible for the disturbances of rate, rhythm, and conduction.[6]
[7]
[8]
Tachycardia and pressor responses were more commonly seen after stimulation of the
right insular cortex and after experimental stimulation of the left vagus that innervates
the atrioventricular node and the cardiac conduction system. Bradycardia was found
to be more common after stimulation of the left insular cortex or the right vagus
nerve that innervates the sinoatrial node.[8] It has been demonstrated that ECG changes were present in more than 90% of unselected
patients with ischemic stroke and intracerebral hemorrhage; however, the prevalence
was much lower after exclusion of patients with preexisting heart disease. QT abnormalities
have been associated with a higher in-hospital mortality.[9]
[10]
QT prolongation after SICH was also found to be an independent risk factor for subsequent
stroke besides traditional risk factors.[11] Popescu et al have demonstrated that ECG changes are frequent in hemorrhagic stroke
and correlate with greater in-hospital mortality. They found that QTc and ST-segment
abnormalities were the only two factors associated with poor outcome.[4]
Conclusion
Electrocardiographic changes occurring after SICH need to be cautiously interpreted,
as the primary cause may be neurogenic and subsequent treatment would require lowering
of ICP either surgically or medically, rather than managing the changes as a primary
cardiac event.
