Impact of pre-spinal atropine on post spinal hemodynamic and cardiac output measured by electrical cardiometry in cesarean delivery, a randomized controlled trial

ABSTRACT

Background

Spinal anesthesia is a widely used technique for cesarean delivery, but it often results in hypotension, bradycardia, and reduced cardiac output (CO). Atropine has a potent muscarinic receptor antagonist activity in the heart. It may be a good choice to prevent post-spinal bradycardia and minimize the marked CO reduction.

Methods

Sixty pregnant women between the ages of 18 and 40 who were ASA-PS II and planned for elective cesarean delivery were divided into two equal groups at random. Both groups received spinal anesthesia. Atropine group (I) (n = 30): patients received 0.01 mg/kg atropine, while control group (II) (n = 30): patients received the same volume of saline. CO measured by electrical cardiometry (EC) was the primary outcome where, heart rate (HR), mean blood pressure (MBP), stroke volume (SV), systemic vascular resistance (SVR), and neonatal outcomes were the secondary outcomes.

Results

CO after the intervention was higher in the atropine (group I) than in the control (group II). Also, CO reduction at 5 and 10 min following spinal anesthesia was less in the group I than in the group II. Except for baseline reading, HR was significantly higher in the atropine group versus the control group. MBP was higher in the atropine group than in the control group in all readings. SV and SVR were similar in both groups. Neonatal outcomes were equivalent in both groups.

Conclusion

Pre-spinal atropine was effective in preventing post-spinal bradycardia and minimized CO reduction in patients undergoing elective cesarean delivery under spinal anesthesia.

KEYWORDS:

• Atropine
• cardiac output
• caesarean delivery
• electrical cardiometry
• spinal anesthesia

List of abbreviations

ASA-PS: American Society of Anesthesiologists Physical Status, BMI: Body mass index, CO: Cardiac output, EC: Electrical cardiometry, ECG: Electrocardiography, SV: Stroke volume, SVR: Systemic vascular resistance, MBP: Mean blood pressure NIBP: Non-invasive blood pressure, SpO2 Oxygen saturation, TEB: thoracic electrical bio-impedance.

Authors’ contributions

AMA designed the work and reviewed the manuscript. MAE revised the literature, performed the analysis, revised the statistical analysis, and wrote the manuscript. MMA design of the work revised literature and collected the data. AMA followed the patients and collected the data. All authors approved the final version of the manuscript. All authors have contributed intellectually to the manuscript and the manuscript has been read and approved by all the authors. The manuscript has not been published, simultaneously submitted, or accepted for publication elsewhere.

Disclosure statement

No potential conflict of interest was reported by the authors.

Availability of data and material

The datasets generated and/or analyzed during the current study are not publicly available due [publishing the clinical data about any study conducted in our hospitals and approved by the institutional ethical committee is against the policy of the Faculty of Medicine, Ain Shams University unless there is a reasonable request] but are available from the corresponding author on reasonable request.

Trial registration

Ethical committee approval of Faculty of Medicine, Ain-Shams University (FMASU R 216/2022)), and a Clinical Trials Registry (ID NCT05658380).

Additional information

Funding

There was no external funding in the preparation of this manuscript.