Sie sind auf Seite 1von 10

Magnesium

Magnesium

4 th most common mineral in the body


Approx. of the total body content of
2000 mEq is incorporated in bone and
is slowly exchangeable
of Mg in extracellular space is bound
to serum albumin
Plasma level of Mg: poor indicator of
total body stores in the presence of
hypoalbuminemia
Should be replaced until levels are in
the upper limit of normal

Regulation
Magnesium (Mg2+) is the fourth most abundant
cation in the body. Thus, magnesium homeostasis
needs to be tightly regulated
This is facilitated by intestinal absorption and renal
excretion.
Magnesium absorption is dependent on two
concomitant pathways found in both in the
intestine and the kidneys: passive paracellular
transport via claudins facilitates bulk magnesium
absorption, whereas active transcellular pathways
mediate the fine-tuning of magnesium absorption.

Serum Magnesium
Normal serum Mg2+ = 1.4-2.2 mEq/L
Patients serum Mg2+: 2.0mEq/L
(normal)

Hypermagnesemia
Rare but can be seen with severe renal
insufficiency and parallel changes in
potassium excretion
Mg-containing antacids and laxatives can
produce toxic levels in patients with renal
failure
Excess intake in conjunction with TPN, or
rarely massive trauma, thermal injury, and
severe acidosis, may be associated with
symptomatic hypermagnesemia

Clinical Manifestations
Symptoms
Nausea and vomiting
Neuromuscular dysfunction with weakness,
lethargy, and hyporeflexia
Impaired cardiac conduction leading to
hypotension and arrest
ECG changes: similar to hyperkalemia
PR interval
widened QRS complex
elevated T waves

Treatment
Eliminate exogenous sources of
magnesium
Correct concurrent volume deficits
Correct acidosis if present
To manage acute symptoms: calcium
chloride (5 to 10 mL) is given to
immediately antagonize the
cardiovascular effect
If elevated levels or symptoms
persist: hemodialysis

Hypomagnesemia
Common problem in hospitalized patients,
particularly in the critically ill
Kidney: primarily responsible for Mg homeostasis
o Regulation by Ca/Mg receptors on the renal
tubular cells that respond to serum Mg
concentrations
May result from alterations of intake, renal
excretion, and pathologic losses
Poor intake: starvation, alcoholism, prolonged IV
fluid therapy, and TPN with inadequate
supplementation of magnesium.

Clinical Manifestations

Hyperactive reflexes
Muscle tremors o Tetany
(+) Chvosteks and Trousseaus signs
Severe deficiencies can lead to delirium and
seizures
ECG changes
Prolonged QT and PR intervals

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes (irregular ventricular rhythm)

Arrhythmias

Treatment
If asymptomatic and mild: Oral
For those with severe deficits (<1.0 mEq/L) or those
who are symptomatic: 1 to 2 g of Mg2SO4 IV over
15 minutes
Under ECG monitoring, it may be given over 2
minutes to correct torsades de pointes
Caution should be taken when giving large amounts
of Mg toxicity may develop
The simultaneous administration of calcium
gluconate will counteract the adverse side effects of
a rapidly rising magnesium level and correct
hypocalcemia, which is frequently associated with
hypomagnesemia.

Das könnte Ihnen auch gefallen