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C HAP TE R 7 / Fluid and Electrolyte and Acid–Base Balance and Imbalance 163

calcium in vascular smooth muscle also causes increased vascular Diuretics (except for spironolactone, triamterene, and
resistance. In many people with essential hypertension, increased amiloride) cause increased renal excretion of magnesium and can
intracellular calcium occurs with normal plasma calcium levels. lead to hypomagnesemia. 21 Individuals with heart failure are at
Parathyroid hormone and parathyroid hormone-related factor are high risk for hypomagnesemia or total-body magnesium deple-
implicated in transepithelial calcium transport and likely play a tion. 103 In addition to diuretic therapy, people with heart failure
role in the hypertensive mechanism. often have congestion of the splanchnic vessels, which decreases
magnesium absorption. Also, the secondary hyperaldosteronism
Magnesium Balance and elevated catecholamines of heart failure increase urinary ex-
cretion of magnesium. 104 Among people with heart failure, those
Magnesium balance is the net result of magnesium intake and ab- who are hypomagnesemic have more arrhythmias than those who
sorption, distribution, excretion, and abnormal losses. These are normomagnesemic and hypomagnesemia is associated with
components are summarized in Table 7-6. Similar to calcium, shorter survival. 103,105 Individuals with acute MI often have ion-
magnesium in the plasma exists in three forms: protein-bound, ized hypomagnesemia. 106 Hypomagnesemia may be a causative
complexed, and ionized (free). Only the ionized magnesium is factor for MI as well as a result of pathophysiologic changes im-
physiologically active; however, the only widely available clinical mediately after MI.
laboratory measure for magnesium is the total serum magnesium Hypomagnesemia causes increased neuromuscular excitability.
concentration (bound, complexed, and ionized). The signs and symptoms of hypomagnesemia include hyperactive
Magnesium, like potassium, is primarily an intracellular ion. reflexes, positive Chvostek’s sign, positive Trousseau’s sign, leg and
For this reason, plasma levels of magnesium do not necessarily re- foot cramps, muscle twitching, grimacing, tremors, dysphagia,
flect the intracellular magnesium content. Total-body magnesium nystagmus, ataxia, tetany, seizures, extreme confusion, cardiac ar-
depletion may be present even when the plasma magnesium is rhythmias, and hypertension.
normal. Intracellular magnesium is a cofactor for many enzymes,

including Na –K adenosine triphosphatase (ATPase). Changes Cardiac Effects of Hypomagnesemia and Total-Body

in magnesium balance, especially hypomagnesemia, cause alter- Magnesium Depletion. Magnesium is a cofactor for Na –K
ations in ion transport across membranes. Because the function of ATPase, the enzyme that plays a major role in the regulation of in-
cardiac and smooth muscle depends on ion fluxes, magnesium tracellular potassium concentration in the myocardium. When
imbalances have myocardial and vascular effects. magnesium is deficient, the decreased intracellular magnesium
leads to decreased activity of this enzyme. As a result, the intra-
Hypomagnesemia and Total-Body cellular potassium ion concentration decreases and intracellular
Magnesium Depletion sodium concentration increases in myocardial cells. Decreased ac-
Hypomagnesemia and total-body magnesium depletion are caused tivity of Na –K ATPase interferes with the reentry of potassium

by decreased magnesium intake or absorption, decreased physio- ions into depolarized cells and promotes diastolic leak of potassium
logic availability of magnesium, increased magnesium excretion, from cells that are already depolarized. In addition, hypomagne-
loss of magnesium by an abnormal route, or any combination of semia causes increased membrane permeability to potassium, an
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these factors. Specific causative factors for hypomagnesemia are effect that also tends to decrease intracellular potassium concentra-
listed in Table 7-11. Hypomagnesemia and total-body magne- tion in the myocardium.
sium depletion are common in chronic alcoholism; therefore, In hypomagnesemia, the sinus node has an increased sponta-
people who have alcoholic cardiomyopathy need assessment for neous firing rate, and there is a rate-dependent decrease in the du-
hypomagnesemia.
ration of the cardiac action potential. The absolute refractory period
is shortened, and the relative refractory period is lengthened. Hy-
pomagnesemia thus predisposes to arrhythmias, especially tach-
Table 7-11 ■ CAUSES OF HYPOMAGNESEMIA yarrhythmias. The imbalance is associated with supraventricular
tachycardia, supraventricular ectopy, ventricular ectopic beats,
Category Clinical Examples
ventricular tachycardia, ventricular fibrillation, and torsade de
Decreased magnesium intake Prolonged IV therapy without Mg 2
pointes. 106–109 Whether these arrhythmias are caused directly by
or absorption Chronic malnutrition the hypomagnesemia itself or by hypomagnesemia-induced
Chronic diarrhea changes in potassium transport across myocardial membranes is
Steatorrhea
Pancreatitis uncertain. What is clear, however, is that both hypomagnesemia
Malabsorption syndromes and total-body magnesium depletion lead to cardiac arrhythmias
Chronic alcoholism that can be corrected only by the administration of magnesium.
Ileal resection Clinical studies demonstrate that correction of ionized hypomag-
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Increased magnesium excretion Gastrointestinal: Steatorrhea nesemia during coronary artery bypass surgery (CABG) leads to
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Renal: Diabetic ketoacidosis; diuretic 110
therapy; increased aldosterone fewer postoperative episodes of ventricular tachycardia. Ad-
(CHF, cirrhosis, hyperaldostero- ministration of magnesium reduces postoperative arrhythmias in
nism); chronic alcoholism; renal CABG patients and in children having surgery for congenital
damage from drugs (amphotericin heart defects, regardless of whether they are initially hypomag-
B, aminoglycosides) 111,112
Magnesium loss by abnormal route Emesis nesemic. In individuals who are not hypomagnesemic,
Nasogastric suctioning magnesium has been used pharmacologically to treat arrhyth-
Drainage from GI fistula mias, including atrial fibrillation, ventricular tachycardia, and
torsade de pointes, and to reduce arrhythmias in acute MI and
IV, intravenous; GI, gastrointestinal. in heart failure. 113,114