Posters
Presentation Type
Poster
Discipline Track
Clinical Science
Abstract Type
Case Report
Abstract
Background: Conduction disorders are common cardiac complications during pregnancy in women with and without structural heart disease. Sinus bradycardia has been described in few case reports secondary to increased vagal tone. Prevalence of newly acquired sinus node dysfunction without structural heart disease is unknown. In this case, we present a post-partum female with symptomatic acquired sinus node dysfunction who presented with severe sinus bradycardia.
Case Presentation: A 32-year-old Hispanic lady with a past medical history of obesity and obstetric formula of G4P4, who recently delivered her 4th child via C-section 4 weeks prior, presented to the Women´s Hospital as a transfer due to 4-day history of abdominal pain and subjective fever. Patient stated that her delivery was uneventful, and she was discharged 3 days later with iron pills due to recently diagnosed iron deficiency anemia. She complained of sudden onset episodes of subjective fever, that were associated with chills, diaphoresis, and abdominal pain on the incision site. These episodes were not associated with any foul discharge. She denied any history of heart disease in the past. She presented to an urgent care clinic and CT abdomen and pelvis without contrast revealed a collection anterior to the left uterine wall, suspicious for an abscess. She was later transferred to Women´s hospital and her vital signs were T 98.4, HR 65 BPM, RR 18 and BP 122/87 mm Hg. Her physical exam was remarkable for tenderness at the incision site, with no redness, pus expression, rebound or guarding. She was started on broad spectrum antibiotics and underwent emergent CT guided fluid collection with Fentanyl for pain management. Minimal drainage of dark blood was collected. Four days after procedure, patient suddenly became bradycardic. Her vitals were HR 37 bpm, BP 77/51 mm Hg and EKG was consistent with sinus bradycardia. Labs did not reveal any electrolyte abnormalities, cardiac enzymes, TSH and chest radiograph were within normal limits. Due to lack of response to atropine, the patient was transferred to ICU after placement of transvenous pacemaker. Emergent echocardiogram revealed normal left ventricular function, ejection fraction between 60-70% and normal RVSP. Two days later, her pacemaker was turned off and her baseline was sinus rhythm with a rate in the 60s. Leads of transvenous pacemaker were then removed and she was later discharged with close follow up with Cardiology and OBGYN.
Conclusions: Sinus bradycardia can be due to various medical conditions, including secondary to vasovagal response. This is called hypervagotonic sinus node dysfunction (HSND). HSND can be due to intrinsic abnormalities as well as secondary causes such as infections or drugs. Usually, HSND can be treated with conservative management. In our case, four days after the patient underwent interventional procedure, the patient presented symptoms consistent with sinus bradycardia. Holter monitoring and echocardiogram did not reveal significant abnormalities and after 24-48 hours it improved with conservative measures. This is an uncommon and unexpected presentation; however, further studies are required to understand if there is presence of predisposing factors in such population to present this abnormality.
Recommended Citation
Gomez Casanovas, Jose; Baird Borja, Andreina; Rincon-Rueda, Laura; Bartl, Mery; and Hernandez, Daniela, "Transient Sinus Node Dysfunction in a Postpartum Female with Sinus Bradycardia: A Case Report" (2024). Research Symposium. 24.
https://scholarworks.utrgv.edu/somrs/2023/posters/24
Included in
Transient Sinus Node Dysfunction in a Postpartum Female with Sinus Bradycardia: A Case Report
Background: Conduction disorders are common cardiac complications during pregnancy in women with and without structural heart disease. Sinus bradycardia has been described in few case reports secondary to increased vagal tone. Prevalence of newly acquired sinus node dysfunction without structural heart disease is unknown. In this case, we present a post-partum female with symptomatic acquired sinus node dysfunction who presented with severe sinus bradycardia.
Case Presentation: A 32-year-old Hispanic lady with a past medical history of obesity and obstetric formula of G4P4, who recently delivered her 4th child via C-section 4 weeks prior, presented to the Women´s Hospital as a transfer due to 4-day history of abdominal pain and subjective fever. Patient stated that her delivery was uneventful, and she was discharged 3 days later with iron pills due to recently diagnosed iron deficiency anemia. She complained of sudden onset episodes of subjective fever, that were associated with chills, diaphoresis, and abdominal pain on the incision site. These episodes were not associated with any foul discharge. She denied any history of heart disease in the past. She presented to an urgent care clinic and CT abdomen and pelvis without contrast revealed a collection anterior to the left uterine wall, suspicious for an abscess. She was later transferred to Women´s hospital and her vital signs were T 98.4, HR 65 BPM, RR 18 and BP 122/87 mm Hg. Her physical exam was remarkable for tenderness at the incision site, with no redness, pus expression, rebound or guarding. She was started on broad spectrum antibiotics and underwent emergent CT guided fluid collection with Fentanyl for pain management. Minimal drainage of dark blood was collected. Four days after procedure, patient suddenly became bradycardic. Her vitals were HR 37 bpm, BP 77/51 mm Hg and EKG was consistent with sinus bradycardia. Labs did not reveal any electrolyte abnormalities, cardiac enzymes, TSH and chest radiograph were within normal limits. Due to lack of response to atropine, the patient was transferred to ICU after placement of transvenous pacemaker. Emergent echocardiogram revealed normal left ventricular function, ejection fraction between 60-70% and normal RVSP. Two days later, her pacemaker was turned off and her baseline was sinus rhythm with a rate in the 60s. Leads of transvenous pacemaker were then removed and she was later discharged with close follow up with Cardiology and OBGYN.
Conclusions: Sinus bradycardia can be due to various medical conditions, including secondary to vasovagal response. This is called hypervagotonic sinus node dysfunction (HSND). HSND can be due to intrinsic abnormalities as well as secondary causes such as infections or drugs. Usually, HSND can be treated with conservative management. In our case, four days after the patient underwent interventional procedure, the patient presented symptoms consistent with sinus bradycardia. Holter monitoring and echocardiogram did not reveal significant abnormalities and after 24-48 hours it improved with conservative measures. This is an uncommon and unexpected presentation; however, further studies are required to understand if there is presence of predisposing factors in such population to present this abnormality.