Eclamptic convulsions are almost always prevented or arrested by plasma magnesium levels maintained at 4 to 7 mEq/L, 4.8 to 8.4 mg/dL, or 2.0 to 3.5 mmollL. But, one review of magnesium pharmacokinetics showed that most regimens result in much lower serum magnesium levels (Okusanya, 2016). This was especially true if only 1 g/hr was infused (Yefet, 2017). Importantly, the obesity epidemic has afected these observations (Cunningham, 2016). Tudela and colleagues (2013) described our observations from Parkland Hospital with magnesium administration to obese women. More than 60 percent of women whose body mass index (BMI) exceeded 30 kg/mrand who were receiving the 2 g/hr dose had sub therapeutic levels at 4 hours. hus, obese women would require 3 gl hr to maintain efective plasma levels. That said, most currently do not recommend routine magnesium level measurements (American College of Obstetricians and Gynecologists, 2013; Royal College of Obstetricians and Gynaecologists, 2006).
Patellar reRexes disappear when the plasma magnesium level reaches 10 mEq/L-about 12 mgl dL-presumably because of a curariform action. This sign serves to warn of impending magnesium toxicity. When plasma levels rise above 10 mEq/L, breathing becomes weakened. At 12 mEq/L or higher levels, respiratory paralysis and respiratory arrest follow (Somjen, 1966). Treatment with cacium gluconate or cacium chloride, 1 g intravenousy, along with discontinuation of forther manesium suate, usualy reverses mid-to-moderate respiratory depression. One of these agents should be readily available whenever magnesium is being infused. Unfortunately, the efects of intravenously administered calcium may be short-lived if there is a steady-state toxic level. For severe respiratory depression and arrest, prompt tracheal intubation and mechanical ventilation are lifesaving. Direct toxic efects on the myocardium from high levels of magnesium are uncommon (McCubbin, 1981; Morisaki, 2000).
Because magnesium is cleared almost exclusivey by renal excre . tion, the dosages described wil become excessive if glomerular il tration is substantialy decreased. The initial 4-g loading dose of magnesium sulfate can be safely administered regardless of renal function. It is important to administer the standard load ing dose and not to reduce it under the mistaken conception that diminished renal function requires it. This is because after distribution, a loading dose achieves the desired therapeutic level, and the infusion maintains the steady-state level. Thus, ony the maintenance infusion rate should be altered with dimin ished glomerular iltration rate. Renal function is estimated by measuring plasma creatinine. Whenever plasma creatinine lev els arer> 1.0 mg/mL, serum magnesium levels are determined to guide the infusion rate.
After a 4-g intravenous dose administered over 15 minutes, mean arterial pressure falls slightly, accompanied by a 13-percent rise in cardiac index (Cotton, 1986b). Thus, magnesium lowers systemic vascular resistance and mean arterial pressure. At the same time, cardiac output is increased. These indings are coincidental with transient nausea and Rushing, and the cardiovascular efects persist for only 15 minutes despite continued magnesium infusion.
Thurnau and associates (1987) showed that magnesium therapy led to a small but signiicant rise in the total magnesium concentration in the cerebrospinal Ruid. The magnitude of the elevation was directly proportional to the corresponding serum concentration.