onset / duration immediate / 30 mins

not known

Inorganic Sulphate

CVS:
▪ Peripheraly causes vasodilation and hypotension in high doses
▪ Slows rate of SA node impulse formation and prolongs SA conduction time.
▪ Prolonged PR interval and AV node effective refractory period.

RESP:
▪ Bronchodilation
• ↓ing cytosolic Ca2+ concentrations.
• ↓’d Mg levels → ↑ airway hyper-responsiveness
▪ Attenuates hypoxic pulmonary vasoconstriction

CNS:
▪ ↑s effect of CNS depressants and NMBs
▪ CNS depressand and exhibits anticonvulsant properties.
▪ Inhibition of catecholamine released from adrenergic nerve terminal and the adrenal medulla

OTHER
▪ Pain on IM injection
▪ Osmotic laxative
▪ Renal vasodilator and diuretic effects.
▪ ↓ed uterine tone and contractility
• Competes with Ca2+ at:
1. Membrane L-type VG Ca2+ channels → ↓ [Ca2+] entry
2. Low-affinity Ca2+ binding sites on SR membrane → ↓ [Ca2+] induced [Ca2+] release
• ↓ IC [Ca2+]

▪ ↑d placental perfusion
▪ ↑d clotting time of whole blood.
▪ ↓ed thrombin induced platelet aggregation.

Vd 8L/kg

Unclear.
Possible explanation: Antagonises Ca2+ activity in uterine muscle cells → relaxation

Antiarrhythmic –
Vaughan Williams Class V
Other

Level 1

fourth most common cation in the body (after Na+, K+ and Ca2+), and
~35-40% in cardiac and skeletal muscle

Used in arrhythmias, for termination of VF/torsades as per ALS and in
the treatment of digitalis toxicity. Other uses: pre-eclampsia, eclampsia and Mg replacement. O¬ff label use in acute severe asthma.

PO/IV
3 forms: oxide,Cl,SO4
All 3 for replacement
Only MgSO4 for eclampsia, arrhythmias
10ml vial 0.5mg/ml

MoA is unknown but may reflect an eff¬ect on the inward
current, possibly a Ca2+ current, responsible for the triggered upstroke arising from EADs. Magnesium ions are bound to cellular ATP, and act as a cofactor for
Na+/K+ ATPase, so that intracellular concentrations of Mg2+ may aff-ect Na+ and K+ transfer. It has benefit even in magnesium replete patients

Care should be taken when delivering IV: ECG monitoring, vital signs, deep tendon
re exes; magnesium concentrations if frequent or prolonged dosing required
particularly in patients with renal dysfunction, calcium, and potassium concentrations. Contraindicated in myasthenia gravis and care to be taken in renal failure.

IV/PO

30% (Alb)

bound to bone or excreted unprocessed in
urine

Urine (as magnesium)

IV/PO.
doses 1-2g IV over 15 mins for torsades de pointes

Electrolytes and Buffers

Pre-eclampsia/eclampsia
Hypomagnesemia
Premature Labour
AMI
Torsade de pointes and ventricular dysrhythmias
Asthma
Cerebral oedema

Presented as 50% magnesium IV solution (40 mmol in 100mL)

Multiple proposed mechanisms
1. Co-factor in enzyme reactions (as a metallo-coenzyme) eg Na+/K+ ATPase activity
2. Energy storage, utilisation, transfer (via role in formation/utilisation of ATP) eg BSL homeostasis
3. Protein and nucleic acid synthesis (stabilises DNA and RNA structure)
4. ↓ membrane excitability (eg. muscles/nerves)
5. ↓ NT release at cholinergic and adrenergic synapses
6. Antagonises Ca2+ activity

Toxicity:
• Somnolence, areflexia, AV and intraventricular conduction disorder
• Progressive muscular weakness
• Cardiac arrest
• Reversal of toxicity with Calcium administration

25-65% oral absorption

30% PB

Dissociates into Mg (active component) and Sulphate

> 50% excreted unchanged in urine

Route: PO, IV, IM

TOCOLYTIC

Level 3 for Tocolysis

Level 1 for Electrolytes and Buffers

Electrolyte

Premature Labour
(however no evidence that it delays delivery)
Helpful in pre-eclampsia (neuroprotection)

Based on protocol: Loading ~4gm → Infusion 2-4gm/hr

Monitoring: cardiac, clinical, serum levels

Potential hypotension when used with nifedipine.
Care with indomethacin.