Open Access Case

Report DOI: 10.7759/cureus.32798

Bradycardia as a Rare Sign of Pulmonary

Embolism: A Case Report of Pulmonary Embolism
Review began 12/04/2022
Diagnosis in Cardiac Arrest Using Point-of-Care
Review ended 12/12/2022
Published 12/21/2022 Ultrasound
© Copyright 2022 Muhammad Awais Cheema 1 , Salman Naeem 2 , Amir Alzarrad 2 , Tony Joy 2 , Haythem Jarad 2
Cheema et al. This is an open access
article distributed under the terms of the
Creative Commons Attribution License CC- 1. Emergency Department, Worthing Hospital, University Hospitals Sussex NHS Foundation Trust, Worthing, GBR 2.
BY 4.0., which permits unrestricted use, Emergency Department, Barts Health NHS Trust, London, GBR
distribution, and reproduction in any
medium, provided the original author and
Corresponding author: Muhammad Awais Cheema, awaischeema47@gmail.com
source are credited.

Abstract
We describe a case of cardiac arrest with pulmonary embolism and deep venous thrombosis diagnosed by
point-of-care ultrasound, which resulted in a favorable outcome. In this article, we have also delineated
bradycardia as an atypical sign of pulmonary embolism and explained the potential mechanism behind it.

Categories: Emergency Medicine

Keywords: cardiac arrest outcome, point-of-care-ultrasound, pulmonary embolism, emergency medicine
resuscitation, emergency medicine, drugs and medicine, respiratory system, venous thromboembolism <
cardiovascular medicine

Introduction
Acute pulmonary embolism (PE) can be a life-threatening disorder with mortality as high as 30% in
untreated cases [1]. With an annual incidence of around 60-70 cases per 100,000 people, it is one of the
common emergencies presenting to the emergency department (ED) [2]. Patients usually present with
tachycardia, dyspnea, cough, hemoptysis, and chest pain. Dyspnea is reported by more than 75% of patients;
however, PE can also present as syncope, abdominal pain, and seizures [3]. Wells criterion for PE [4] is a
validated tool to determine the estimated pre-test probability of PE, but the diagnosis relies heavily on the
clinical gestalt of the physician. As a result of variability in the clinical presentation, a PE diagnosis in the
ED can be challenging. This is a case report of an atypical presentation of PE in a patient who presented
with syncope and bradycardia.

Case Presentation
A 48-year-old woman with a history of end-stage renal disease (ESRD), epilepsy, and transplant
nephrectomy experienced a sudden collapse while awaiting her hemodialysis session. She was mildly
hypoxemic but otherwise hemodynamically stable (heart rate: 76, blood pressure: 111/74 mmHg, oxygen
saturation: 90% on room air, temperature: 35.6°C, and Glasgow Coma Scale [GCS]: 15/15). She was
transferred to ED for further management. Approximately, one-minute post-arrival, she became
unresponsive, with a heart rate of 20 bpm. The patient demonstrated jugular vein distension (JVD). She then
became pulseless and went into cardiac arrest. Cardiopulmonary resuscitation was commenced immediately.

Intra-arrest bedside ultrasound examination was performed, which showed a dilated right ventricle (RV)
(Figure 1), a septal bulge toward the left ventricle, and a hypertrophic left ventricle with a severely reduced
ejection fraction.

How to cite this article

Cheema M, Naeem S, Alzarrad A, et al. (December 21, 2022) Bradycardia as a Rare Sign of Pulmonary Embolism: A Case Report of Pulmonary
Embolism Diagnosis in Cardiac Arrest Using Point-of-Care Ultrasound. Cureus 14(12): e32798. DOI 10.7759/cureus.32798
 FIGURE 1: Apical four-chamber view of the heart showing massively
dilated right ventricle (RV) as compared to the left ventricle (LV)

The scan also showed clots in the right brachiobasilic arteriovenous fistula (BB-AVF) (Figure 2) and a deep
vein thrombosis (DVT) in the left common femoral vein (Figure 3). The patient was consequently
thrombolyzed with a 50-mg intravenous bolus of alteplase. This was followed by an intravenous infusion of
50 mg alteplase given over 30 minutes. She also received 5000 units of heparin.

FIGURE 2: Linear view of the right brachiobasilic fistula with

hyperechoic masses, likely clots, hanging by fibrinous band

2022 Cheema et al. Cureus 14(12): e32798. DOI 10.7759/cureus.32798 2 of 5

 FIGURE 3: Transverse view of the superficial tissue of the left inguinal
area with compression, showing the left superficial femoral artery
(SFA), left profunda femoris artery (PFA) underneath, and
noncompressible left femoral vein (FV) left lateral to SFA and PFA

She had a return of spontaneous circulation and underwent a computerized tomographic (CT) pulmonary
angiogram and CT of the abdomen and pelvis, which confirmed bilateral PE (Figure 4) and clots in both
common femoral veins. She was admitted to the intensive care unit (ICU) where she remained stable. She
was discharged on anticoagulation on hospital day 3 with no neurological deficit with further follow-up in
the outpatient hematology clinic.

FIGURE 4: Axial view of computerized tomographic (CT) pulmonary

angiogram showing a radiolucent clot in the left pulmonary artery
depicted by the arrow

Discussion
This case report highlights an atypical manifestation of a massive PE. In this patient, syncope and sinus
bradycardia were two anomalous signs which are not commonly attributed to acute PE. The fact that the
patient was arrested soon after her admission to ED limited the history and examination. The obstructive
shock was clinically first suspected after noticing that the patient had distended jugular veins. Jugular
venous pressure (JVP) can be raised due to various reasons including an increase in right heart pressure,
volume, or occlusion of the superior vena cava (SVC). In acute PE, blood flow through the pulmonary
arteries is obstructed. Pulmonary artery occlusion causes elevated right ventricular pressure through several

2022 Cheema et al. Cureus 14(12): e32798. DOI 10.7759/cureus.32798 3 of 5

 mechanisms [5]. The acute rise in right ventricular pressure with resultant right heart failure in a massive PE
is reflected by a raised JVP.

Although PE has long been recognized as an important and serious cause of syncope, its prevalence in
patients presenting to the ED with syncope is actually rare, with a rate of diagnosis ranging from 0.06% to
0.55% [6]. It is proposed that PE causes syncope via three different mechanisms: (i) massive PE causing
reduction in cardiac output leading to decreased perfusion of the cerebrum, (ii) a complete heart block in
pre-existing left bundle branch block, and (iii) stimulation of vagal mechanosensory nerve endings in the
left ventricle leading to cardiogenic shock and bradycardia [7]. All of these mechanisms reduce cardiac
output that limits cerebral perfusion, causing loss of consciousness and syncope.

Contrary to the common clinical perception of acute PE being associated with persistent tachycardia, large
cohort clinical studies have shown that sinus bradycardia may be present in more than 2% of patients with
PE [8]. This bradycardia may be a result of a complete atrioventricular (AV) block due to an injury to the right
bundle branch that runs superficially in the RV wall and in the intraventricular septum and is sensitive to
acute RV dilatation in a patient with pre-existing electrical conduction system disease like left bundle
branch block (LBBB) [5]. Alternatively, bradycardia can occur due to RV dilation and pressure overload from
PE leading to excess vagal stimulation [9]. In this case, the patient first had an episode of syncope and then
developed profound sinus bradycardia just before losing cardiac output. It is postulated that extracellular
ATP could play a mechanistic role in syncope and bradycardia associated with PE. The mechanisms
suggested are localized release of ATP by platelet activation and ATP-induced pulmonary-pulmonary and
cardio-cardiac vagal stimulation [7]. The excess vagal stimulation causes negative chronotropic and
dromotropic effects on the heart. This phenomenon along with mechanical obstruction in blood flow can
lead to profoundly reduced cardiac output, resulting in syncope and subsequent cardiac arrest.

Patients with ESRD receiving hemodialysis are more at risk of having venous thromboembolism.
Königsbrügge et al. found that the incidence of venous thromboembolism (VTE) is 10.9/1000 patient-years
in ESRD patients [10] as compared to 0.9/1000 patient-years in the normal population [11]. Bedside echo has
been shown to aid in the diagnosis of PE. The typical signs on echo are increased RV to left ventricle ratio,
McConnell’s sign, tricuspid regurgitation, decreased tricuspid annular plane excursion, and D-sign [12].
Although these signs are non-specific, they help to raise the clinical suspicion of PE in a patient with high
pre-test probability. Most PEs originate from a lower limb [13]. Compression ultrasonography (CUS) for DVT
has a sensitivity of 90% and a specificity of 95% [14]. Right heart strain on echo and positive CUS in the
lower limbs of DVT in a high-risk hemodynamically unstable patient warrants systemic thrombolysis
according to the European Society of Cardiology guidelines for pulmonary embolism [15]. On subsequent
sonography of this patient's upper limb BB-fistula, further blood clots were visualized.

Conclusions
Point-of-care ultrasound in cardiac arrest can aid in the early diagnosis of the cause of cardiac arrest, which
might improve the patient's outcome. In high-risk patients receiving hemodialysis, PE should be considered
a differential diagnosis of syncope. In addition, bradycardia can be a confounding sign in the presentation of
acute PE.

Additional Information
Disclosures
Human subjects: Consent was obtained or waived by all participants in this study. Conflicts of interest: In
compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services
info: All authors have declared that no financial support was received from any organization for the
submitted work. Financial relationships: All authors have declared that they have no financial
relationships at present or within the previous three years with any organizations that might have an
interest in the submitted work. Other relationships: All authors have declared that there are no other
relationships or activities that could appear to have influenced the submitted work.

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