Magnesium sulfate (MgSO4) is significant in anesthesia and critical care, acting as a blocker of NMDA receptors and calcium channels, and is essential for maintaining physiological functions. It has various applications including treatment for hypomagnesemia and hypermagnesemia, cardiovascular management, and as a bronchodilator in respiratory conditions. Proper dosage and monitoring are critical due to potential side effects and interactions with other medications.

1. Uses of MGSO4 in Anaesthesia and Critical care
Presenter : Dr.Soma Srikiran(p.g)
Moderator : Dr.Chaithanya kumar (A.P)

2. Overview
• Introduction
• Proporties
• Physiological role of magnesium
• Pharmacokinetics
• Pharmacodynamics
• Magnesium in anaesthesia and critical care medicine
• Hypomagnesemia
• Hypermagnesaemia
• Magnesium Toxicity
• Summary

3. INTRODUCTION
• Ever since the study of magnesium sulfate in clinical anesthesia begins in 1996, magnesium
has drawn attention in the field of anesthesia and pain medicine.
• In humans Mg++ is the fourth most plentiful cation after Na+, K+, and Ca++, Intracellularly it
is the 2nd most common cation after K+
• Among the numerous actions of magnesium, the blockade of N - methyl - D aspartate
(NMDA) receptor and calcium channel has an important role in anesthesia
• Half of the body Mg++ lies in soft tissues, including muscles, remaining in bones and some
in RBCs. Extracellular Mg++ is both ionized and unionized, it is the ionized form which is
physiologically active.

4. Proporties
• Its Atomic number = 12
• Valency = 2
• Atomic weight 24.3 grms
• 4th
most abundant cation in the body
• 2nd
most abundant intracellular cation
• 50 – 60% - bone
• 20% - skeletal muscle
• 99% - intracellular
• Normal plasma Mg+2
conc–0.75–1.1m.mol/L
-60% - ionized
-20 – 30% - bound to protein
• Therapeutic range - 4 -6 mEq/L

5. Physiological role of magnesium
a. Mg++ inhibits mobilisation of calcium mediated by inositol tri phosphate pathway.
b. It acts as mediator for Na+/K+ ATPase system, thus essential in maintaining transmembrane
potential, by maintaining Na+/k+ gradient across the membrane.
c. Generation of cAMP via adenylcyclase is dependent on Mg++.
d. Mg++ controls the release and action of Parathyroid Harmone, thus regulates Calcium
metabolism.
e. Mg++ helps in Oxidative Phosphorylation, Glucose utilization and Protein synthesis

7. Pharmacokinetics
• Mg++ homeostasis is maintained and regulated by hormonal and metabolic effect on GI
absorption and renal excretion.
• Normal Serum Mg++ CONC are 0.7 to 1.05mmol/l (1.4 to 2.2meq/l).
• Mg++ is mainly excreted by the kidneys.
• It is reabsorbed in the ascending limb of loop of Henle, Aldosterone increases renal
excretion while Parathormone increases gut absorption, and reduces renal excretion.
• Mg++ is widely distributed in plant and animal food esp green leafy vegetables, spices, nuts,
Soyabean and shellfish

8. • Maximal supplemental dose is 350 mg/day

9. Pharmacodynamics
A. Cardiovascular system
a. Direct depressant effect on myocardial and vascular smooth muscle.
b. Inhibits the release of catecholamines from the adrenal medulla, peripheral adrenergic
terminals and directly blocks catecholamine receptors.
c. As a result, cardiac output and vascular tone are reduced resulting in hypotension and
decreased pulmonary vascular resistance.
d. Anti-arrhythmic: slows the rate of impulse formation at the SA node, prolongs SA
conduction, the PR interval and the AV node refractory period.

10. B. Nervous system
a. Reduces the release of acetylcholine at the neuromuscular junction by antagonizing
calcium ions at the pre-synaptic junction.
b. Causes reduced excitability of nerves.
c. Anticonvulsant, as it reduces cell excitability by blocking Ca++ channels.
d. Reverses cerebral vasospasm.
C. Musculoskeletal
a. It decreases release of acetyl-choline at N-M-J thru its Ca++ channel blocking effect.
b. Involved in terminating contraction, initiating relaxation in skeletal muscles, thus it
potentiates Non depolarizing neuromuscular relaxants drugs.
c. In combination with the effects above excessive plasma concentrations can cause
muscle weakness.

11. D. Respiratory system
a. Magnesium is an effective bronchodilator but does not affect respiratory drive
b. Respiratory failure may occur as a result of excessive muscle weakness.
E. Genito-urinary system
a. Powerful tocolytic, decreasing uterine tone and contractility.
b. Mild diuretic properties.
F. Haematological system
a. Platelet activity is reduced resulting in prolonged bleeding time,
b. Deficiency is associated with platelet hyper-reactivity which plays significant role in MI,
Pre-eclampsia and eclampsia.
c.Also required for the utilization of Thiamine.
.

12. Magnesium in anaesthesia and critical care medicine
Cardiovascular System
• Anaesthetising hypomagnesaemic patients may precipitate arrhythmias.
• The vasodilatory and myocardial depressant effects of anaesthetic induction drugs and
volatiles can also precipitate severe hypotension in these patients.
• Magnesium sulphate therapy should be avoided in patients with A-V Block due to risk of
precipitating asystole or worsening arrhythmias.

13. • Magnesium is effective at abolishing tachyarrythmias and is recommended for the treatment
of torsade de pointes, digoxin-induced and ventricular arrhythmias unresponsive to other
treatment.
• A bolus of magnesium, 2g over 10 minutes should be given.
• In shock refractory ventricular fibrillation (VF), a 2g bolus dose IV is given.
• Interestingly, magnesium does not interfere with the inotropic action of adrenaline
(epinephrine).

14. • Magnesium can be used during surgery for phaeochromocytoma due to its calcium channel
blocking properties and suppression of catecholamine release.
• An initial bolus dose of 40-60mg/kg IV followed by 2g/hr has been a suggested regimen.
• Magnesium and Ca 2+ Channel Blocking drugs can cause an exaggerated hypotensive
effect due to their dual effect on the Ca 2+ channel.
• Combination may cause increased neuromuscular side-effects and increased magnesium
toxicity.

15. Nervous System
Eclampsia - it is defined as the occurrence of grand mal seizures during pregnancy or
during/after delivery in a woman with preeclampsia,not attributable to other cause.
Pre-eclampsia - it is a multisystem disorder of pregnancy associated with new - onset of
hypertension, usually with accompanying proteinuria, which occurs most often after 20 weeks of
gestation and frequently near term and that disappears untill 12 weeks after the labor.
• In beginning with gestational hypertension and progressing to develop severe features,
ultimately leading to its more severe manifestations, such as eclampsia and HELLP
syndrome.

16. Treatment
• The World Health Organization (WHO) recommends magnesium sulphate therapy for
prevention of eclampsia in women with severe pre-eclampsia.
• Loading dose is 4-6g IV and maintenance 1-3g/hour are generally used.
• Rapid infusion causes flushing, warmth and hypotension.
• The maintenance phase should only be commenced if the patellar reflex is present and
respirations exceed 12/minute. A therapeutic range 2-3.5mmol/L has been recommended.
• A dose of 40mg/kg is given immediately following the induction drug and 30mg/kg in women
who have already been given magnesium

17. Respiratory System
• As a result of smooth muscle relaxation, magnesium dilates both the bronchi and pulmonary
vasculature.
• Magnesium therapy appears to improve Peak Expiratory Flow Rates (PEFR) in patients with
acute severe asthma, particularly children.
• It should be considered in refractory cases with impending respiratory failure.
• At the current time, there appears to be little evidence for the role of magnesium in
bronchospasm with Chronic Obstructive Pulmonary Disease (COPD)

18. Tetanus
• Magnesium reduces spasms and autonomic instability in tetanus.
• It also causes hypotension, bradycardias, hypocalcaemia and respiratory muscle paralysis
requiring ventilation as a result of magnesium therapy.
• A proposed regimen for the management of tetanus is 5g magnesium sulphate IV over
20mins followed by 2g/hour IV.
• This can be increased by 0.5g/hour until there is relief of spasms or loss of patellar reflexes.
• If continuous infusion is not available, 2.5g IV every 2 hours

19. Hypomagnesemia
Hypomagnesaemia is defined as a serum concentration <0.7mmol/L
Causes
I. Decrease intake:
i. Deficiency in diet,
ii. Mal absorption (as in chr alcoholics, Pancreatic insufficiency pt)
II.Inappropriate IV infusions - massive haemodillution
III. Increased renal losses:
i. Drug induced especially Digoxin, Gentamycin, loop diuretics, cyclosporine, cis-platinum
ii. Batters Syndrome.
iii. Intrinsic renal dysfunction.
iv. Hyperaldosteronism

20. IV. Extra renal losses:
i. GI tract-prolonged diarrhoea or long term NG suction.
ii. Primary Hyperparathyroidism.
iii. Insulin administration.
iv. Massive citrated blood transfusions

21. Sign and symptoms
Hyperirritability, chest pain, Palpitation, Arrhythmia, Hypertension, Angina (Coronary Artery
Spasm), Increased Digoxin toxicity in pts on digoxin, due to decrease in K+ intracellularely and
also increased Digoxin uptake by myocardium. Arrhythmias esp Torsades de pointes, Re-
entrant Arrhythmias, VT and VF. Supraventricular and ventricular tachyarrhythmias may also
occur
ECG - Prolonged PR and QT intervals, ST depression and flattening of T wave
N-M Junction - Myoclonus, Cramps Stridor, and Dysphagia, Chvostek’s sign,
Trousseau’s sign due to associated Ca++ deficiency

22. • Trousseau’s sign(carpopedal spasm after inflating a BP cuff above systolic BP for > 3min
• Chvostek’s signs (tapping over branches of the facial nerve at the point they emerge from
the parotid
Psychiatric Distur - Anxiety, Depression, Confusion, Psychosis.
Eletrolyte distur
• Usually accompanied with Ca++ & K+ Deficiency.
• There is intractable K+ deficiency which is not corrected till you correct Mg++ deficiency

23. Treatment
• Approximately 10 to 20mmols/day dietary intake is sufficient
• chronic losses 35 to 70mmols can be given in 5% dextrose.
• An amp of Mg++ contains 50%w/v (500mg/ml) solu.
• Each ml contains 2mmols, in severe deficiency 8mmols (4ml) ie 2gms in 50ml of 5% grams
dry wt. may be given over 30min.
• Chronic deficiency can be corrected with larger amounts (40-80mmol) given IV over 24
hours

24. Hypermagnesaemia
• The most common cause of hypermagnesaemia is iatrogenic as a result of intravenous
therapy, particularly if there is co-existing renal failure.
Serum Mg conc.
10-12.5mmol/L cardiac arrest
5-7.5mmol/L respiratory paralysis
4-5mmol/L muscle weakness & loss of tendon reflexes

25. Clinical Features
• Increase in frequency and severity as the serum concentration increases.
• Initial clinical presentation includes headache, nausea, vomiting and diarrhoea, hypotonia
and muscle weakness.
• Significant neuromuscular block can occur, causing respiratory muscle weakness and
ultimately respiratory arrest.
• Hypotension and bradycardia occur at high plasma concentrations
• ECG may show prolonged AV conduction and widening of the QRS complex, which can
progress to severe arrhythmias and finally cardiac arrest.

26. Management
IV calcium gluconate (2.5-5mmol) can
antagonise the actions of magnesium and
therefore is useful in the immediate
management of patients with severe
hypermagnesaemia, followed by inducing a
diuresis or dialysis.

28. Magnesium Toxicity

29. Treatment
• Administration of calcium gluconate 10% i.e 10ml in 100ml NS/IV/over 10-20 mins
• Repeat calcium gluconate admin.. if necessary.
• If respiratory arrest occurs begin CPR

30. Summary
• In humans Mg++ is the fourth most plentiful cation after Na+, K+, and Ca++, Intracellularly it
is the 2nd most common cation after K+.
• MOA- the blockade of N-methyl - D aspartate (NMDA) receptor and calcium channel has
an important meaning to anesthesia.
• It is described as a physiological antagonist of calcium. It is the second most abundant
intracellular ion and is a cofactor to many enzymes. It depresses myocardium and vascular
smooth muscle directly.
• Normal Serum Mg++ CONC are 0.7 to 1.05mmol/l (1.4 to 2.2meq/l).Onset: Two minutes
Duration: 30 minutes.
• Uses - as an antihypertensive agent -1-2 g IV bolus followed by an intravenous infusion of 1
g/h

31. • As an antiarrhythmic agent: The dose is 2 g (8 mmol) intravenously over 20 minutes followed
by 16 g (64 mmol) over 24 hours.
• As a bronchodilator: Magnesium is used in a dose of 500 mg daily.
• Hypomagnesaemia is defined as a serum concentration <0.7mmol/L
• Treatment 10 to 20mmols/day dietary intake is sufficient
• Chronic losses 35 to 70mmols can be given in 5% dextrose.
• Severe deficiency 8mmols (4ml) ie 2gms in 50ml of 5% Gdw may be given over 30min.
• Hypermagnesaemia 10-12.5mmol/L cardiac arrest
5-7.5mmol/L respiratory paralysis
4-5mmol/L muscle weakness & loss of tendon reflexes
• Treatment - IV calcium gluconate (2.5-5mmol)

32. References
Morgan & Mikhail’s Clinical anesthesiology - 6th Edition.
Thankyou