Cardiovascular alterations in severe pregnancy-induced hypertension: Acute effects of intravenous magnesium sulfate

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The central hemodynamic effects of intravenous magnesium, sulfate were studied in five patients with severe pregnancy-induced hypertension. All five patients had a Swan-Ganz and a radial artery catheter placed prior to initiation of magnesium sulfate therapy. Four grams of magnesium sulfate was given over 15 minutes followed by a continuous infusion of 1.5 gm per hour. There was a 12.5% increase in cardiac index immediately after the infusion but cardiac index returned to pretherapy values by 15 minutes after infusion. The mean arterial pressure was significantly (p < 0.01.) decreased 30 minutes after the 4 gm loading dose but had returned to baseline values by 1 hour. There were no other significant changes in any of the hemodynamic or oxygen-related variables measured. Our data confirm previous hemodynamic studies in patients with severe pregnancy-induced hypertension indicating a hyperdynamic state with large fluctuations in systemic and pulmonary vascular resistances. In addition, magnesium sulfate has been shown,to have a transient hypotensive effect on mean arterial pressure, related to bolus infusion, that is not present with continuous infusion.

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    The risk of neuromuscular blockade (reversed with calcium gluconate) with contemporaneous use of nifedipine and MgSO4 is <1% [329,330]. MgSO4 is not an antihypertensive, having the potential to lower BP transiently 30 min after a loading dose [331–334]. Infused nitrogylcerin (vs. oral nifedipine) is comparably effective without adverse effects [335–337].

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    MgSO4 should not be used as an antihypertensive per se. When MgSO4 is used for other indications (such as eclampsia prophylaxis or treatment, or for fetal neuroprotection), a loading intravenous (iv) dose of 2–5 g may be associated with a transient fall in blood pressure 30 min later,27–30 but this has not been consistently shown.31 The concomitant use of MgSO4 and nifedipine has no contraindication, as the risk of neuromuscular blockade is less than 1%,32 and blockade is reversed with 10 g of intravenous calcium gluconate.

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    Provided that respiratory failure and hypoxia are avoided, magnesium is remarkably safe from a cardiac perspective with plasma Mg2+ concentrations as high as 12.5 mol l−1 being required before cardiac arrest occurs.29 Studies in animal models26 and pregnant women30 have failed to demonstrate any myocardial depression and have reported an increase in cardiac output associated with raised plasma Mg2+ concentrations. In dogs, magnesium enhanced inotropy and lusitropy with increased cardiac output up to plasma concentrations of 6 mmol l−1, and this level was described as ‘haemodynamically safe’.27

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This study was presented in part to the Society for Obstetric Anesthesia and Perinatology, May 28, 1983, Vancouver, British Columbia, Canada.

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