Alegbeleye Journal of Medical Case Reports (2018) 12:144

https://doi.org/10.1186/s13256-018-1648-5

CASE REPORT Open Access

Sudden cardiac arrest under spinal

anesthesia in a mission hospital:
a case report and review of the literature
Bamidele Johnson Alegbeleye

Abstract
Background: Sudden cardiac arrest following spinal anesthesia is relatively uncommon and a matter of grave
concern for any anesthesiologist as well as clinicians in general. There have been, however, several reports of such
cases in the literature. Careful patient selection, appropriate dosing of the local anesthetic, volume loading, close
monitoring, and prompt intervention at the first sign of cardiovascular instability should improve outcomes. The
rarity of occurrence and clinical curiosity of this entity suggest reporting of this unusual and possibly avoidable
clinical event.
Case presentation: We report the occurrence of unanticipated delayed cardiac arrest following spinal anesthesia in
a 25-year-old Cameroonian man. Incidentally, the index patient was successfully resuscitated with timely and
appropriate cardiopulmonary resuscitative measures. He went ahead to have emergency open appendectomy
with good post-operative outcome and recovery.
Conclusions: The management of such cardiac arrest under spinal anesthesia is very challenging in resource- limited
settings such as ours. Anesthetists and clinicians need to be well informed of this grave complication. A good
understanding of the physiologic changes caused by spinal anesthesia and its complications, adequate patient
selection, respecting the contraindications of the procedure, adequate monitoring, and constant vigilance are of
paramount importance to the eventual outcome.
Keywords: Anesthesia-spinal, Cardiac arrest, Intraoperative complications, Resuscitation

Background and prompt intervention in the management of sud-

Ever since August Bier administered the first clinical den cardiac arrest under spinal anesthesia in a low-
spinal anesthesia more than a century ago, it has become resource setting.
an integral part of the modern day anesthesia practice.
Although considered simple to perform and a relatively Case presentation
safe technique, life-threatening complications do occur The patient was a 25-year-old Cameroonian man weigh-
under spinal anesthesia [1, 2]. In the literature, the re- ing 65 kg who was recently operated on for acute appen-
ported incidence of cardiac arrest is 1.3–18 in 10,000 dicitis in Banso Baptist Hospital, Northwest Cameroon.
patients [3–5]. All the preoperative investigations, including routine
We are reporting the occurrence of unanticipated de- blood biochemistry, chest X-ray posterior and anterior
layed cardiac arrest following spinal anesthesia in a view, and 12-lead electrocardiograms were normal. The
young and healthy patient. This communication is to abdominal ultrasound scan was essentially normal. In
bring to the fore the importance of vigilant monitoring the operating theater (OT), routine monitoring included
heart rate 78 beats/min, electrocardiogram, noninvasive
blood pressure (BP) 120/78 mmHg, and pulse oximetry
with SpO2 at 99% in room air, and these baseline param-
Correspondence: drbalegbeleye@gmail.com
Department of Surgery, Banso Baptist Hospital, P.O Box 9, Nso-Kumbo, eters were recorded and were essentially normal. An
Northwestern Region, Cameroon intravenous (IV) access was secured with a cannula and
© The Author(s). 2018 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0
International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and
reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to
the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver
(http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
Alegbeleye Journal of Medical Case Reports (2018) 12:144
our patient was preloaded with 500 mL of normal saline
solution. Under all aseptic precautions, a subarachnoid
block was performed at L3/L4 space in the left lateral
position with a 25-gauge Quincke needle and 3.2 mL of
hyperbaric bupivacaine was injected into the subarach-
noid space after confirming a clear and free flow of
cerebrospinal fluid (CSF). Five minutes after turning
the patient to the supine position, the sensory level of
block was found to be at T10. During skin preparation
of the abdomen, and almost 25 min after the subarach-
noid injection, our patient started complaining of
difficulty in breathing and this was followed with a con-
vulsion. Sensory level was rechecked and was found to
be at T10. A bolus of atropine 0.6 mg was administered
as his heart rate suddenly dropped to 40 beats/min,
SpO2 to 65%, while his BP became unrecordable and
peripheral pulses could not be palpated. Owing to
diminishing consciousness, our patient was immedi-
ately intubated with a cuffed endotracheal tube (ETT)
of 7.5 mm and positive pressure ventilation initiated
with Bain circuit and 100% oxygen was administered.
His heart arrested and cardiopulmonary resuscitation
(CPR) was started immediately with pharmacologic
intervention with adrenaline and dopamine and intra-
venous normal saline infusion. (Other vasopressors like
mephenteramine, noradrenaline etc. were not available.)
Within 4 min, our patient responded with a heart rate
of 140 bpm, SpO2 of 90%, and BP of 90/60 mmHg. Our
patient was restless even after administration of injec-
tion of diazepam 10 mg, and phenytoin 1.5 g in IV infu-
sion. Considering his slow response to resuscitative
measures, our patient was administered 150 mg propo-
fol and was paralyzed with 6 mg vecuronium and
electively ventilated in the OR. Apart from sinus tachy-
cardia, all investigations results including serum elec-
trolytes, complete blood counts and chest X-ray were
normal. Arterial blood gas analysis (ABG) was not
available in our facility. Our patient was adjudged by
both the anesthetist and attending surgeon as being fit
enough to proceed for the emergency open appendicec-
tomy via a Lanz incision with uneventful postoperative
course. After 2 h of elective ventilation and achieve-
ment of hemodynamic stability, our patient became
conscious and started responding to verbal commands
with good respiratory efforts, and extubation was done
after reversing the relaxant effect with standard doses
of neostigmine and glycopyrrolate. His postextubation
hemodynamic parameters were normal, and he was
transferred to the high dependency unit (HDU) for fur-
ther observation. Our patient was discharged on the
4th postoperative day with an uneventful course in
HDU. The follow-up visits at the 2nd, 4th, and 10th
week in the postoperative period showed satisfactory
clinical status.
Page 2 of 5
Discussion
Spinal anesthesia is considered to be a safe procedure
but complications rarely can occur in the clinical scene
[1, 2]. Ever since Caplan et al. [6] reported 14 cases of
cardiac arrest during spinal anesthesia in an American
Society of Anesthesiologists closed claim analysis, numer-
ous case reports and reviews have been published [7, 8].
The mechanism that triggers severe bradycardia [7–10]
and the etiology of cardiac arrest under spinal anesthesia
remain controversial and unclear. Oversedation, respira-
tory arrest, unintentional total spinal, myocardial infarc-
tion, and local anesthetic toxicity have all been suggested
as the causative factors. However, contribution of intrinsic
cardiac mechanisms and autonomic imbalance with the
background of parasympathetic predominance may pro-
vide a more convincing and physiologic explanation for
the occurrence of abrupt severe bradycardia and cardiac
arrest under spinal anesthesia [6–9]. It is established that
the final pathway is the absolute or relative increase in ac-
tivity of the parasympathetic nervous system [11]. Cardiac
arrest has been reported within 12–72 min of spinal
anesthesia, while other cardiovascular side effects have
been reported as late as 3–5 h after the administration of
spinal anesthesia [12].
Our patient was hemodynamically stable and well oxy-
genated prior to the administration of spinal anesthesia.
No ischemic changes were noticed in the electrocardio-
gram. Causative factors like myocardial infraction, re-
spiratory depression, local anesthetic toxicity, subdural
injection, and high level of spinal anesthesia were con-
sidered and excluded by the sequence of events and la-
boratory investigations. Our patient had acute appendicitis
with right iliac fossa pain, leading to sympathetic stimula-
tion to maintain BP and cardiac output with normocardia
or relative tachycardia. Once the spinal analgesia was
established, our patient became pain free and the sympa-
thetic drive was aborted. Subsequently, the resulting
bradycardia and hypotension occurred. The other con-
tributory factor is that this patient with abdominal pain,
nausea, and a few bouts of vomiting might have been
avoiding fluids or food for some unspecified period. Hence
our patient was probably in negative fluid balance. The
500 mL of fluid loading at spinal anesthesia might be
inadequate to counter the vasodilator effect of the spinal
anesthesia. These two factors, including aborted sympa-
thetic overdrive and negative fluid balance, must have
been the cause for sudden cardiac arrest.
Thus, contributing to autonomic imbalance was a pos-
sible primary trigger resulting in bradycardia and asys-
tole in our patient [13–15].
Reports from the literature also implicate autonomic
imbalance with a background of vagal dominance may
intensify any tendency to bradycardia that might other-
wise have been more benign, transient, or possibly
Alegbeleye Journal of Medical Case Reports (2018) 12:144
unnoticed [16]. There exist a number of risk factors
(Table 1) with variable impact on the occurrence of
severe bradycardia and cardiac arrest under spinal
anesthesia. These factors may identify vulnerable pa-
tients. However, presence of two or more listed factors
may place these patients at high risk for bradycardia and
cardiac arrest under spinal anesthesia [16]. Due to in-
consistent reporting, risk factor association with the oc-
currence of bradycardia and cardiac arrest under spinal
anesthesia still remains uncertain and contradictory [16].
The other mechanisms involved in cardiac arrest after
spinal anesthesia include administration of excessive
doses of local anesthetics in a previously hypovolemic
patient, which can be secondary to preoperative fasting,
malnutrition, dehydration, use of diuretics or vasodila-
tors [17]. Even the perioperative events such as bleeding,
changes in patient’s positioning, placement of bone ce-
ment, light nature of anesthesia on a background of co-
morbidities and others can be responsible for cessation
of cardiac activity [17]. It is generally recommended that
the level of blockade should be limited to T6 and
hemodynamic reserves should be evaluated and moni-
tored for any complication [17]. The degree of bleeding
should be observed regularly and replaced with blood
whenever necessary, so as to reduce morbidity and mor-
tality [17]. The present case report pertains to young
ASA grade I patient who was preloaded with about 500
mL of fluid before administration of anesthesia. The pre-
loading might be inadequate to offer a plausible etiology,
especially with a background of vomiting and inadequate
oral intake, even though the patient had been on
intravenous fluids prior to the procedure. The spinal
anesthesia also might have aborted the sympathetic over-
drive provided by pain stimulation in a patient with ab-
dominal pain from acute appendicitis. The resultant
outcome was vagal predominance, which was a major
contributor to the cardiac arrest [18–20].
Specific strategies to anticipate and prevent vagal predom-
inance forms the mainstay in the management of severe
bradycardia and cardiac arrest under spinal anesthesia are
presented in Table 2. Appropriateness of spinal anesthesia
Table 1 Risk factors for bradycardia and cardiac arrest during
spinal anesthesia
1. Age < 50 years
2. Baseline heart rate < 60/min
3. ASA physical status I and II
4. Use of beta blockers
5. Sensory level blockade above T6
6. Prolonged PR interval
7. Vagotonia
Min Minute, ASA American Society of Anesthesiologists, T6 Intervertebral disc
space no 6, PR P and R wave as per Electrocardiogram (ECG) waves
Page 3 of 5
Table 2 Management strategies for bradycardia and cardiac
arrest during spinal anesthesia
Prevention:
1. Appropriate patient selection for spinal anesthesia when two or
more risk factors are present (Table 1)
2. Maintaining adequate preload
3. Prompt replacement of fluid and blood loss.
4. Vigilance during patient positioning
Treatment of bradycardia:
1. Mild to moderate bradycardia (HR 30–60/min) - stepwise
escalation of therapy
a. Atropine 0.4–0.6 mg, IV
b. Ephedrine 25-50 mg, IV
c. Epinephrine 0.2–0.3 mg, IV
2. Severe bradycardia or cardiac arrest
a. Advanced Cardiac Life Support guidelines to be followed
b. Early administration of epinephrine known to improve
outcome
Management of associated factors:
1. Rapid fluid infusion
2. Patient repositioning
3. Avoid surgical manipulation.
HR Heart Rate, IV Intravenous Route, Min Minute, Mg Milligram
in patients at risk must be evaluated carefully. Alternative
anesthetic techniques should be considered whenever intra-
operative massive blood loss or vasodilatation is anticipated.
Adequate preloading and replacement of volume loss has
been emphasized in a number of studies [18–20].
Local anesthetics are widely used in modern medical
procedures. Though the incidence of reported adverse
effects of local anesthetics is low, occasional severe tox-
icity and deaths have been reported [21]. Among all,
bupivacaine is considered to be 4–16 times more cardio-
toxic than lignocaine [22]. Delayed cardiac arrests have
been reported after 20 min of spinal anesthesia [21, 22].
This possibility was also being considered in the present
scenario as our patient developed breathlessness and
convulsions before cardiac arrest, almost 20 min after
administration of spinal anesthesia.
Circulatory or respiratory insufficiency can occur after
inducing sedation for the purpose of giving comfort
and relieving anxiety related to a surgical procedure.
The sedated state can result in loss of spontaneous
verbalization for a brief period of time before detection
of cardiac arrest. Major hypoxic events (SpO2 < 85% for
> 30 s) have been reported without apparent cyanosis
or changes in the respiratory pattern. Thus it is possible
that respiratory insufficiency may have been present
but clinically unrecognized [23]. It has been suggested
recently that the combination of sympathetic blockade
produced by high spinal anesthesia and the vagolytic
Alegbeleye Journal of Medical Case Reports (2018) 12:144
effect of fentanyl might account for the sudden appear-
ance of bradycardia [24]. Drugs such as droperidol can
also lead to severe hypotension and sudden cardiac ar-
rest during spinal anesthesia on account of their α-
blocking effect [25]. Patients on beta blockers and other
alternative medicines provide another challenging situ-
ation as the cardiac arrest in these patients can be refrac-
tory as vasoconstriction mechanisms in the peripheral
vasculature may be impaired [3, 11, 26]. But in the present
clinical situation, our patient did not receive any beta
blockers or other medications nor was any sedation ad-
ministered before the occurrence of cardiac arrest.
The term “vagotonia” describes the clinical situation
of resting bradycardia, atrioventricular (AV) block, or
complete AV dissociation that is normally present in
7% of the population [27]. In such population, inci-
dence of asystole is higher during performance of pro-
cedures, which can enhance vagolytic activity [28, 29].
Cardiac arrest is more common in young individuals
with an established fact that vagal tone is greater in the
patient and increase in parasympathetic activity further
enhances exaggerated vagal tone [11, 30]. This could be
one of the plausible causes in our patient. Unexpected
cardiac arrest has been reported after small postural
changes of the patient including placing a leg in the
holder and turning the patient to the left lateral or
prone position, and in some cases the arrest has been
reported even after the surgical procedure had already
finished [31]. It seems difficult to explain these situa-
tions based only on preload changes. Maybe they are
due to reflex phenomena similar to those of auto-
nomic dysfunction or hyperreflexia described in pa-
tients with a spinal cord section. Thus, there should
be minimal movement or mobilization of the patient
after spinal anesthesia [31]. However, in the present
clinical scenario, our patient had cardiac arrest in a
supine position, which excludes the above-mentioned
plausible cause, while the likely indicators have already
been described.
Conclusions
Finally, Banso Baptist Hospital is a mission hospital with
limited facilities. The hospital intensive care unit has
very limited facilities and therefore can best be described
as a high dependency unit (HDU). This index patient
had a good postoperative outcome. We must reiterate
that the significance and management of such clinical
situations depends upon the anesthesiologist’s acumen
and a high index of suspicion in order to detect early
that something is “going wrong”. The experience-based
empirical anesthesia practice should always consider the
evidence-based approach in such clinical situations [32].
The best clinical pearl in such situations is to believe and
to intervene immediately any detectable abnormalities are
Page 4 of 5
seen. Disbelief and insecurity are common patterns of this
situation and may influence the final outcome [1, 32].
Therefore, the knowledge of the physiologic changes
caused by spinal anesthesia and its complications, ad-
equate patient selection, respecting the contraindica-
tions of the procedure, adequate monitoring, and
constant vigilance are of paramount importance to the
eventual outcome.
Acknowledgments
Dr. Benjamin Kakule Malikidogo MD, PAACS, General Surgeon, Department of
General Surgery, Banso Baptist Hospital, Cameroon, who provided professional
support during the writing of this case report and also read and approved the
final manuscript.
Mr. Samuel Yengong SRN, Dip. Anaesthesia, Anaesthesiologist, Department
of Anaesthesia, Banso Baptist Hospital, Cameroon, who provided professional
support during the writing of this case report and also read and approved
the final manuscript.
Funding
No record of funding for this case report declared.
Availability of data and materials
All data generated or analysed during this study are included in this
published article and can also be accessed via http://dx.doi.org/10.6084/
m9.figshare.6220241.
Disclosures
The authors have no disclosures.
Author’s contributions
BJA conceived of the study and participated in its design and coordination,
helped to draft the manuscript, read and approved the final manuscript.
Ethics approval and consent to participate
Not applicable.
Consent for publication
Written informed consent was obtained from the patient for publication of
this case report and any accompanying images. A copy of the written
consent is available for review by the Editor-in-Chief of this journal.
Competing interests
The author declares that he has no competing interests.
Publisher’s Note
Springer Nature remains neutral with regard to jurisdictional claims in
published maps and institutional affiliations.
Received: 13 December 2017 Accepted: 7 March 2018
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