By using the FloTrac/Vigileo Monitoring System, the present study provides direct evidence regarding the attenuation of the changes in CO, SVR, CVP and MAP induced by pneumoperitoneum and maintenance of intraoperative hemodynamic stability by magnesium sulfate. Additionally, magnesium sulfate administered before pneumoperitoneum reduced the changes in vasopressin level associated with hemodynamic instability.
This is the first study to evaluate the direct effects of magnesium sulfate on CO and SVR using the FloTrac/Vigileo Monitoring System. Previous studies on the effects of magnesium sulfate on hemodynamic stability had used indirect or direct arterial pressure as a measure to indicate the peripheral circulatory resistance [1, 4, 5]. Compared to NIBP, both the thermodilution method and FloTrac / Vigileo can monitor SVR, but the thermometry measurement in clinical practice is limited, mainly because of the risks associated with pulmonary artery catheterization and it can not provide continuously monitor changes in SVR. In contrast, the FloTrac / Vigileo is a minimally invasive hemodynamic monitoring system, the hemodynamic parameters such as CVP, MAP, SVR and CO can be continuously measured.
The pneumoperitoneum lifts the diaphragm, causing an increase in intrathoracic pressure and venous resistance, thereby reducing CO. The body sympathetic excitement compensatory raises SVR to maintain arterial blood pressure. However, the increase in SVR further decreases the CO, forming a vicious circle [7, 8]. Younger patients can tolerate the decrease in CO under physiologic conditions. As the blood vessels progressively harden and cardiovascular compensatory function declines, their ability to adapt to changes in circulating blood volume is severely reduced in elderly. For example, a further decrease in CO induced by pneumoperitoneum might result in deleterious effects in elderly patients with hypertension or ischemic heart disease.
By using the FloTrac / Vigileo Monitoring System, our study demonstrated that pneumoperitoneum decreased CO, which was observed in previous studies [7]. Our results also showed that intravenous magnesium sulfate at a dose of 50 mg/kg could effectively alleviate the reduction in CO, by dilating the peripheral blood vessels and reducing the vascular tone.
During pneumoperitoneum for operative laparoscopy, impairment of hemodynamic status occurs mainly at the beginning of peritoneal insufflation [2]. It is well known that elevated intrapleural pressure significantly reduces the venous return and the circulating blood volume, which induces the elevated levels of vasopressin [1, 2, 10]. Adrenergic receptor blockers, calcium channel blockers, opioids, and vasodilators are routinely used to attenuate the pneumoperitoneum-related hemodynamic instability, but they are all accompanied with varying degrees of reduction in CO. In contrast, magnesium sulfate produces rapid and transient vasodilation by a direct action without causing a reduction in CO, and by indirectly blocking the sympathetic pathway and inhibiting the catecholamine and vasopressin release [1, 3]. Adjuvant analgesia with magnesium sulfate can significantly reduce the dose of remifentanil. Consistent with these findings, in the present study, at the initiation of pneumoperitoneum, and 5, 10minutes post-pneumoperitoneum are the most severe periods of hemodynamic fluctuations, and it was also the most effective time period for magnesium sulfate to inhibit pneumoperitoneum associated hypertension. Moreover, hemodynamic fluctuations at 30 and 60 minutes post-pneumoperitoneum were less pronounced, indicating that magnesium sulfate only reduced abnormally elevated blood pressure and had no effect on normal blood pressure. Jee D found that intravenous magnesium sulfate could improve the increased arterial pressure and inhibit the release of vasopressin caused by pneumoperitoneum at 5 and 10 min post-pneumoperitoneum [1]. Similarly, we found that magnesium sulfate at a dose of 50 mg/kg could effectively attenuate the release of vasopressin.
A minimum therapeutic level of 2 mmol/L magnesium sulfate has been proposed in the clinical management of eclampsia patients [11]. If the magnesium serum concentration is more than 3 mmol/L, the patients may develop tendinous reflexes [3]. Therefore, it is essential to select a safe and effective minimum dose of magnesium sulfate to ensure the safety of patients. Besides, taking into account the effect of magnesium sulfate on intraoperative muscle relaxation, the magnesium ion concentration was measured again before extubation to ensure patients’ safety. In the present study, the average serum concentration of magnesium sulfate in group H was between 2 - 3 mmol/L. In group L, the level of serum magnesium concentration was lower than 2 mmol/L at T3. Further, there were no statistically significant differences in the extubation time between the three groups, did not observed any reported serious adverse effects and the potentiation effect of magnesium on neuromuscular blockade as reported in other observations [12], which could be related to the surgery time and the metabolic duration of magnesium sulfate. These results indicate that 50 mg/kg magnesium sulfate may be a safe dose for attenuating the pneumoperitoneum-related hemodynamic changes during laparoscopic gastrointestinal surgery.
The analgesic effect of magnesium sulfate at a dose of 50 mg/kg was relatively obvious, which may be related to the higher concentration of magnesium ions after surgery (Serum magnesium concentration level in group H was1.38 ± 0.13 mmol/l after surgery). In contrast, the reason why the postoperative pain score in group L was higher was that the magnesium ion concentration was lower after surgery, so it did not play an analgesic role. (The level of serum magnesium concentration was 1.07 ± 0.11 mmol/l after surgery). Perioperative intravenous magnesium reduced opioid consumption and pain scores, which was believed to be caused by a physiological block of the ion channel on the N-methyl-D-aspartate receptor and inhibition of the intracellular Ca2+ mobility [6, 10, 13]. This analgesic effect may also contribute to the hemodynamic stability in the patient during surgery. However, further research is needed to determine the exact mechanisms causing the analgesia.