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Background <p>Maternal arterial hypotension occurs in 55–90% of cesarean sections performed under spinal anesthesia. While sympatholysis and aortocaval compression are conventional explanations, refractory cases suggest possible biochemical contributors beyond sympatholysis. We hypothesized that an acute deficit in ionized calcium coupled with endothelial mediator overproduction may constitute a “double lock” mechanism that contributes to hemodynamic decompensation. This prospective observational study examined these associations.</p> Methods <p>A prospective, single-center analytical study was conducted from June 2025 to February 2026 at the Centre Hospitalier d’Essos, Yaoundé, enrolling 80 ASA I–II parturients undergoing elective cesarean section under spinal anesthesia. Hemodynamic parameters (SBP, DBP, MAP, HR, SpO₂), plasma electrolytes (Na⁺, K⁺, Cl⁻, iCa²⁺), and vasoactive mediators (nitric oxide [NO], prostaglandin I₂ [PGI₂]) were measured at baseline (T0) and 10&#xa0;min post-induction (T1).</p> Results <p>Hypotension was confirmed in 78% of participants. MAP fell by 23% (92.4 ± 8.1 to 71.2 ± 9.5 mmHg; <i>p</i> &lt; 0.001). Ionized calcium dropped significantly below the critical threshold (1.18 ± 0.06 to 0.98 ± 0.04 mmol/L; <i>p</i> &lt; 0.01), correlating strongly with SBP decline (<i>r</i> = 0.72; <i>p</i> &lt; 0.01). NOₓ increased by 37.9% and PGI₂ by 25.3% (both <i>p</i> &lt; 0.01). Na⁺, K⁺, and Cl⁻ remained stable.</p> Conclusion <p>Spinal anesthesia-induced hypotension in parturients was associated with concurrent acute ionized calcium reduction and elevated vasoactive mediators (NOₓ and PGI₂), consistent with a “double lock” hypothesis. These findings are exploratory and hypothesis-generating. They support prospective interventional investigation of ionized calcium and vasoactive mediators as contributors to hemodynamic decompensation during spinal anesthesia for cesarean section.</p>

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Cardiovascular adaptation to spinal anesthesia-induced hypotension during scheduled cesarean section: the paradigm of ionized calcium and nitric oxide in a prospective cohort study

  • 期刊论文

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  • 发表日期：

    2026年8月1日

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  • Mpeyou Sani Mohamed,
  • Daniel Ewa Ikpi,
  • Ngokoh Ghislain Nyemji,
  • Nga Nomo Serge Vivier,
  • Ndam Gbetnkom Pascal,
  • Favour Nyoh Beshel,
  • Daniel Udofia Owu

摘要

Background

Maternal arterial hypotension occurs in 55–90% of cesarean sections performed under spinal anesthesia. While sympatholysis and aortocaval compression are conventional explanations, refractory cases suggest possible biochemical contributors beyond sympatholysis. We hypothesized that an acute deficit in ionized calcium coupled with endothelial mediator overproduction may constitute a “double lock” mechanism that contributes to hemodynamic decompensation. This prospective observational study examined these associations.

Methods

A prospective, single-center analytical study was conducted from June 2025 to February 2026 at the Centre Hospitalier d’Essos, Yaoundé, enrolling 80 ASA I–II parturients undergoing elective cesarean section under spinal anesthesia. Hemodynamic parameters (SBP, DBP, MAP, HR, SpO₂), plasma electrolytes (Na⁺, K⁺, Cl⁻, iCa²⁺), and vasoactive mediators (nitric oxide [NO], prostaglandin I₂ [PGI₂]) were measured at baseline (T0) and 10 min post-induction (T1).

Results

Hypotension was confirmed in 78% of participants. MAP fell by 23% (92.4 ± 8.1 to 71.2 ± 9.5 mmHg; p < 0.001). Ionized calcium dropped significantly below the critical threshold (1.18 ± 0.06 to 0.98 ± 0.04 mmol/L; p < 0.01), correlating strongly with SBP decline (r = 0.72; p < 0.01). NOₓ increased by 37.9% and PGI₂ by 25.3% (both p < 0.01). Na⁺, K⁺, and Cl⁻ remained stable.

Conclusion

Spinal anesthesia-induced hypotension in parturients was associated with concurrent acute ionized calcium reduction and elevated vasoactive mediators (NOₓ and PGI₂), consistent with a “double lock” hypothesis. These findings are exploratory and hypothesis-generating. They support prospective interventional investigation of ionized calcium and vasoactive mediators as contributors to hemodynamic decompensation during spinal anesthesia for cesarean section.