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Am J Med Case Rep. Author manuscript; available in PMC 2020 August 25.
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Published in final edited form as:

Am J Med Case Rep. 2020 ; 8(10): 341–347.

Subarachnoid Hemorrhage Presenting with Second-Degree Type

I Sinoatrial Exit Block: A Case Report
Pramod Theetha Kariyanna1, Ruchi Yadav1, Vivek Yadav2, Samuel Apple1, Naseem A.
Hossain1, Neema Jayachamarajapura Onkaramurthy3, Apoorva Jayarangaiah4, Ayesha
Saad1, Isabel M. McFarlane1,*
1Division
of Cardiovascular Disease and Department of Internal Medicine, State University of
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New York, Downstate Medical Center, Brooklyn, New York, USA

2Department of Internal Medicine, Brookdale University Hospital and Medical Center, 1 Brookdale
Plaza, Brooklyn, New York- 11212, USA
3Department of Internal Medicine, Columbia College of Physicians and Surgeons, NYC Health
and Hospitals/Harlem Hospital Center, New York 10037, USA
4Department of Internal Medicine, Albert Einstein College of Medicine, NYC Health and
Hospitals/Jacobi Medical Center, Bronx, New York-10461, USA

Abstract
The understanding of neural regulation of the cardiovascular function and the implications of a
“Heart-Brain Axis “has been a topic of interest for clinicians for many years. Electrocardiographic
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(ECG) and structural cardiac changes, ranging from mild, asymptomatic, transient alteration in
cardiovascular function to severe, irreversible, and potentially life-threatening injury, can actually
be a manifestation of several neurological disorders. When managing cardiac disorders, a high
index of clinical suspicion, detailed history-taking and physical examination skills, and an
extensive workup that covers both cardiac and non-cardiac causes should be utilized. It is
important to consider that cardiovascular dysfunction of an underlying neurological etiology may
lead to difficulty in diagnosing and optimizing treatment of the latter. We report the case of a
middle-aged female with the chief complaint of syncope preceded by a headache with no focal
neurological deficits, originally diagnosed with- and whose syncope was attributed to sinus
bradycardia and type I sinoatrial (SA) exit block on ECG. Subsequently, when the patient became
altered, however, computer tomography (CT) angiography revealed subarachnoid hemorrhage
(SAH) with middle cerebral artery aneurysm. This presentation emphasizes the importance of
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tabulating neurological injury as one of the differential diagnoses while managing ECG changes in
cardiovascular disease (CVD), as missing and delaying the former can result in disastrous
consequences.

This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license
(http://creativecommons.org/licenses/by/4.0/).
*
Corresponding author: [email protected].
 Kariyanna et al. Page 2

Keywords
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subarachnoid hemorrhage (SAH); electrocardiography (ECG); type 1 sinoatrial (SA) exit block;
syncope; neurological injury; heart brain axis

1. Introduction
Syncope, defined as an abrupt and transient loss of consciousness due to cerebral
hypoperfusion, accounts for 1–1.5% of emergency department (ED) visits [1]. It is
categorized into neurally-mediated, cardiac, and orthostatic syncope according to the
underlying cause. Neurally-mediated syncope is the most common cause of syncope in the
general population and has a benign course, while cardiac syncope tends to correlate with an
increased mortality and morbidity [1]. One trigger that can lead to electrocardiography
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(ECG) changes in patients is aneurysmal subarachnoid hemorrhage (SAH), a type of

hemorrhagic stroke affecting approximately 30,000 persons per year in the United States
[2,3]. ECG changes are the most studied and widely recognized abnormalities following
SAH, seen in 25–90% of SAH patients [4,5,6,7,8]. In addition, rhythm and conduction
abnormalities either can occur alone or in combination with other ECG changes. Several
prospective and retrospective clinical studies on SAH have reported arrhythmias such as
sinus bradycardia (15%), sinus tachycardia (13%), premature ventricular beats (13%), atrial
fibrillation and ventricular tachycardia (2%), AV block (1.5%), and asystole (1%)
[9,10,11,12,13,14]. Neurogenic heart disease is defined as the brain’s effects on the heart,
with underlying mechanisms including excessive catecholamine activity, acute stressors,
autonomic disturbances, and reperfusion injury [15]. To the best of our knowledge, to date,
there is no published literature revealing second degree type I sinoatrial (SA) exit block as a
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manifestation of aneurysmal SAH. Higher risk of rebleeding and related mortality is

associated with a delay in the diagnosis and treatment of SAH [16]. Therefore, to avoid any
catastrophic consequences, neurological injury must be considered a part of the list of
potential etiological conditions causing cardiac conduction disorders.

2. Case Report
A 63-year-old African American female with apast medical history of hypertension, asthma
and hyperlipidemia presented to the emergency department with a chief complaint of
syncope preceded by headache. In the ED, the patient was noted to have regained
consciousness shortly after her syncopal episode, but she complained of persistent headache
and dizziness. On physical examination, no focal neurologic deficits were found. Her vitals
at that time showed a blood pressure of 141/82 mmHg, heart rate of 48 beats per minute,
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temperature of 34.5°C (94.1°F), and respiratory rate of 19 cycles per minute. Her ECG
showed sinus rhythm and pauses with junctional escape beats and atrial premature
contractions with a ventricular rate of 46 beats per minute (Figure 1 and Figure 2).
Laboratory investigations were within normal limits (Table 1). Cardiology was consulted for
management of sinus bradycardia, sinoatrial block, and junctional escape. A transvenous
pacemaker was placed with good capture (Figure 3).

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The patient was initially admitted to the critical care unit for management of the
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bradyarrhythmia. Soon after admission to the critical care unit, she became altered, agitated,
and unable to follow commands. Neurology recommended a head CT to rule out intracranial
pathology. The imaging study revealed a diffuse SAH with hydrocephalus. An emergent
extra-ventricular drain was placed by Neurosurgery. The bradyarrhythmia and the altered
mental status then resolved. A follow up CT angiography of the brain showed a right middle
cerebral artery (MCA) aneurysm (Figure 4). She was transferred to the surgical intensive
care unit for further management of her SAH and right MCA aneurysm. The patient was
started on intravenous tranexamic acid, levetiracetam, and nimodipine. She underwent
cerebral angiography with Neuro-interventional Radiology. Cerebral angiography showed a
ruptured posterior communicating artery aneurysm (Figure 5, left image) which was
subsequently embolized with coil placement (Figure 5, middle image), resulting in near-
complete aneurysm occlusion and preservation of the adjacent arteries (Figure 5, right
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image). The patient was transferred back to the surgical intensive care unit neurologically
intact with mild functional limitations.

3. Discussion
Cardiac manifestations of SAH [17] are a well-known entity, ranging from mild ECG
variability, reversible left ventricular dysfunction (Takotsubo), non-ST-elevation myocardial
infarction (NSTEMI), ST-elevation myocardial infarction (STEMI), to cardiac arrest
[18,19,20,21,22,23]. As per a systematic review analysis, the crude global incidence of SAH
declined from 10.2 per 100000 person-years in 1980 to 6.1 in 2010, with large variation
according to region, age, and sex [24]. In the United States, the annual incidence of
aneurysmal SAH is 6–16 cases per 100,000 population, with approximately 30,000 episodes
occurring each year [25]. Out of all strokes, 20% are hemorrhagic, with SAH and
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intracerebral hemorrhage each accounting for 10% [26]. 75–85% of non-traumatic SAH is
caused by ruptured cerebral aneurysms [27]. The major cardiac manifestations resulting
from SAH are arrhythmias [13] (35%), myocardial injury seen as troponin elevations in the
first 24 hours [28] (28%), wall motion abnormalities [29] (28%), and classic deep septal T-
wave inversion or QTc prolongation on ECG [30,31]. Most of the rhythm alterations are
benign, including sinus bradycardia or tachycardia; atrial fibrillation, ventricular ectopics,
and junctional rhythm have also been described in SAH patients [31]. To the best of our
knowledge, there has been no prior report describing SAH as the underlying cause of a
second-degree type 1 SA nodal exit block; such a scenario is being reported for the first time
in this case report. The possible risk factors for arrhythmia occurrence include female
gender, QTc prolongation, excessive sympathetic discharge, coronary vasospasm, electrolyte
disturbances, and pre-existing hypertension [32]. Life-threatening arrhythmias occur in
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about 5% of cases [13]. Extensive myocardial injury following SAH can result in severely
depressed global cardiac function, as well as reduction particularly in the left ventricular
function. This condition is known as neurogenic stunned myocardium (NMS), recently
restyled as stress-related cardiomyopathy syndrome [33].

New progress in neuroanatomic studies, pathological assessments, and imaging modalities

have have helped illuminate the neural regulation of cardiovascular functions [34], a design
that involves a complex network of cortical and subcortical brain regions [35] along with the

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intrinsic cardiac system. Figure 6 elucidates the role of the central nervous system (CNS) in
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regulating the cardiovascular system (CVS) functions.

The orbitofrontal cortex and dorsal cingulate cortex process afferent information and control
efferent autonomic outflow to the CVS. The insular cortex is the main center regulating the
‘Heart-Brain Axis’ [36]. Some studies hypothesize that the right insula controls sympathetic
actions, and when damaged, can effect ECG changes and lead to increased mortality [37,38].
Others postulate the same for the left insula [39]. The amygdala receives inhibitory inputs
from the prefrontal and orbitofrontal cortices and processes them with the hypothalamus and
the brain stem nuclei [40,41]. In this way, it modulates the effect of emotional stimuli on the
heart [42]. The nucleus tractus solitarius (NTS), located in the posterior medulla, receives
hemodynamic inputs and sends efferents to the rostral ventrolateral medulla (RVLM) and
dorsal motor nucleus (DMN) of the vagus, which control the sympathetic and
parasympathetic outflow, respectively, to the heart [34]. The CNS regulates the CV function
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through cardiomotor sympathetic and parasympathetic outflow of the autonomic nervous

system (ANS) to the myocardium and cardiac conduction system [43]. In addition, there is
an intrinsic cardiac nervous system, composed of interconnected ganglionated plexi in
epicardial fat tissue, innervating the SA node, AV node, and pulmonary veins [44]. Oxidative
stress, nitric oxide levels, and abnormal baroreceptor and chemoreceptor signals are
conveyed to NTS, paraventricular nucleus, and RVLM through cardiac afferent fibers, which
results in fatal arrhythmias and ischemia [45,46].

The neuronal control of the CVS undergoes major alterations in different circumstances and
may contribute to progression of the underlying heart disease. Immediately after SAH, there
is intense activity in the hypothalamus, insula, and brain stem, causing significant activation
of sympathetic nerve endings, with release of norepinephrine [32]. In patients with SAH,
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repolarization abnormalities, caused by an increase in sympathetic activity in SAH, are the

most common ECG finding [47]. The SA node acts as the normal pacemaker of the heart,
generating action potentials that travel through the conduction system to cause myocardial
contraction [48]. SA nodal exit block is a condition in which the impulse fired by the SA
node is unable to reach the neighboring atrial tissue [49]. It is divided into three degrees of
block, similar to AV blocks. On ECG, SA nodal exit block can be inferred from the P wave
activity, but only a second degree SA block can be detected in the ED using a 12-lead ECG
[50]. Second degree SA nodal exit block is of two types: type I Wenckebach and type II.
Type I has a P-P interval that progressively shortens in duration until there is a dropped P
wave [49].

At times, it can be difficult to establish neurological injury as the cause or the consequence
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of cardiovascular dysfunction due to the high prevalence of coexistent cardiac disorders and
shared risk factors in these patients. Electrocardiographic alterations and conduction defects,
both benign and fatal, are commonly seen after brain injury even without a preexisting heart
disease. However, when the cardiovascular presentation of the symptoms are not correlated
with their neurological cause, it can result in delayed or missed diagnosis of neurological
diseases.

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4. Conclusion
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Between 50 to 100% of patients experience cardiac rhythm disturbances during the acute
phase of SAH, but only 1–4% of patients experience a clinically significant arrhythmia.
SAH is a serious condition that frequently leads to neurological impairment and death;
therefore, its timely diagnosis and management is of utmost significance. The current article
is an effort at consolidating the information available in an attempt to avoid errors in the
diagnosis of neurological disease presenting in an atypical manner. Recently, the ‘Heart-
Brain Axis’ concept, which acknowledges a complex network of neural regulation of
cardiovascular functions, has gained much popularity. More collaborative studies and
research are likely to further advance our understanding of the neural control of the cardiac
tissue.

Acknowledgments
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This work is supported, in part, by the efforts of Dr. Moro O. Salifu M.D., M.P.H., M.B.A., M.A.C.P., Professor and
Chairman of Medicine through NIH Grant No. S21MD012474.

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Figure 1.
Electrocardiogram showing Mobitz type I sinus atrial node exit block with progression to
junctional rhythm
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Figure 2.
EKG showing sinus bradycardia
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Figure 3.
Portable chest X-ray showing transvenous pacer (indicated by arrows)
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Figure 4.
Computed tomography scan of the head showing right middle cerebral artery aneurysm
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Figure 5.
Cerebral angiogram showing an aneurysm in the right posterior communicating artery (left),
during endovascular coil placement (middle), and complete regression of aneurysm
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following endovascular coil placement (right)

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Figure 6.
This flow diagram outlines the Heart-Brain Axis (Legend: RVLM- rostral ventrolateral
medulla, DMN- dorsal motor nucleus, ANS-autonomic nervous system, CNS- central
nervous system, SA- sinus atrial, AV- atrioventricular)
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Table 1.

Complete Blood Count

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Lab Data Reference Range On Admission

COMPLETE BLOOD COUNT

White blood cell count (10×3/uL) 4.10 – 10.10 12

Neutrophils (%) 44.5 – 73.4 70.9

Lymphocytes (%) 17.8 – 42.0 19.8

Monocytes (%) 5.7 – 11.2 8.8

Eosinophils (%) 0.2 – 6.0 0.1

Basophils (%) 0.3 – 1.1 0.4

Neutrophils absolute (10×3/uL) 1.40 – 6.80 8.47

Lymphocytes absolute (10×3/uL) 1.10 – 2.90 2.37

Monocytes absolute (10×3/uL) 0.20 – 1.00 1.05

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Eosinophils absolute (10×3/uL) 0.00 – 0.40 0

Basophils absolute (10×3/uL) 0.00 – 0.10 0

Red blood cells (10×6/uL) 4.33 – 5.43 4.74

Hemoglobin (g/dL) 12.9 – 16.7 13.6

Hematocrit (%) 40.0 – 47.0 40.8

Mean corpuscular volume (fL) 80.8 – 94.1 85.9

Mean corpuscular hemoglobin (pg) 27.1 – 31.2 28.7

Mean corpuscular hemoglobin conc (g/dl) 31.0 – 34.4 33.4

Red cell distribution width (%) 12.3 – 14.6 13.8

Mean platelet volume (fL) 7.9 – 11.0 8.7

Platelets (10×3/uL) 153 – 328 223

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Troponin I (ng/mL) 0.012 – 0.034 0.4

P-Natriuretic Peptide (pg/mL) 11.1 – 125.0 80.7

Ferritin (ng/mL) 17.90 – 464.00 95.4

CHEMISTRY
Glucose (mg/dL) 70 – 99 140

Blood urea nitrogen (mg/dL) 9.0 – 20.0 10

Creatine (mg/dL) 0.66 – 1.25 0.90

Sodium (mEq/L) 133 – 145 136

Potassium (mEq/L) 3.5 – 5.1 4.5

Chloride (mEq/L) 98 – 107 103

Calcium (mg/dL) 8.4 – 10.5 9.7

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Anion gap (mEq/L) 13

Total Protein (g/dL) 6.3 – 8.2 8.2

Albumin (g/dL) 3.5 – 5.0 4.1

Total Bilirubin (mg/dL) 0.2 – 1.3 0.7

Aspartate transaminase (U/L) 21 – 72 37

Am J Med Case Rep. Author manuscript; available in PMC 2020 August 25.
 Kariyanna et al. Page 15

Lab Data Reference Range On Admission

Alanine aminotransferase (U/L) 17 – 59 40
Author Manuscript

Alkaline Phosphatase (U/L) 38.0 – 126.0 74

Serum Bicarbonate, Co2 (mEq/L) 22 – 30 23

D-dimer (ng/mL) 0 – 230 50

Troponin I 0.00–0.2 0.01

Author Manuscript
Author Manuscript
Author Manuscript

Am J Med Case Rep. Author manuscript; available in PMC 2020 August 25.