Page 188 - Cardiac Nursing

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164 PA R T II / Physiologic and Pathologic Responses

A classic study demonstrated that heart muscle magnesium con-
tent decreases after acute MI. 115 This post-MI magnesium decrease Table 7-12 ■ CAUSES OF HYPERMAGNESEMIA
may be caused by leakage of magnesium from necrotic cells and in-
Category Clinical Examples
terference with ion transport in hypoxic cells. Another mechanism
for the cardiac muscle magnesium decrease after MI may be the ac- Increased magnesium intake Excessive use of Mg 2
-containing
tion of catecholamines. It is likely that localized decreases of my- or absorption laxatives, antacids, or urologic
ocardial magnesium after acute MI predispose to the development irrigation solutions
Excessive IV infusion of Mg 2
of cardiac arrhythmias. Animal studies show decreased tolerance to Aspiration of sea water
ischemic stress with chronic magnesium deficiency. 116 Decreased magnesium excretion Oliguric renal failure
Hypomagnesemia potentiates digitalis toxicity. Hypomagne- Adrenal insufficiency
semia-related digitalis toxicity arises in part from the intracellular
potassium deficiency caused by the magnesium imbalance. Digitalis IV, intravenous.
toxicity arrhythmias have been observed in individuals with thera-
peutic digitalis levels and either decreased serum magnesium levels
or normal serum levels with total-body magnesium depletion. magnesium deficiency can cause changes that are part of the ath-
The ECG changes in hypomagnesemia are not easily charac- erosclerotic process.
terized; rather, they are somewhat nonspecific. Prolongation of the In summary, the vascular effects of hypomagnesemia include
QT interval is frequently observed in hypomagnesemia. 109 This vasoconstriction, increased peripheral resistance, hypertension,
ECG change probably occurs because of altered potassium trans- impaired vasodilation, and a tendency to vasospasm. Current evi-
port caused by hypomagnesemia. Other ECG changes that have dence relates total-body magnesium depletion, with or without
been seen with hypomagnesemia, such as ST segment depression, hypomagnesemia, to congestive heart failure, ischemic heart dis-
prolonged PR interval, wide QRS complex, and T-wave abnor- ease, and essential hypertension.
malities, may be caused by multiple electrolyte imbalances that
occur in conjunction with hypomagnesemia, or by the hypomag- Hypermagnesemia
nesemia itself. Hypermagnesemia is caused by increased magnesium intake or
absorption, increased physiologic availability of magnesium, de-
Vascular Effects of Hypomagnesemia and Total-Body creased magnesium excretion, or any combination of these fac-
1
Magnesium Depletion. Hypomagnesemia has important ef- tors. Specific causative factors for hypermagnesemia are listed in
fects on vascular smooth muscle. A decrease in the extracellular Table 7-12. Older adults who use magnesium-containing antacids
magnesium concentration causes arteriolar vasoconstriction, in and laxatives are at especially high risk for development of hyper-
part by increasing the intracellular calcium concentration in vas- magnesemia, in part because they may have unrecognized renal
cular smooth muscle and by reducing endothelial production of insufficiency. 126,127
the vasodilators nitric oxide and prostacyclin. 117,118 The resulting The cardiac effects (bradycardia, arrhythmias, cardiac arrest)
increased peripheral vascular resistance causes the hypertension and vascular effects (flushing, hypotension) of hypermagnesemia
that often accompanies acute or chronic hypomagnesemia. In ad- are discussed next. In addition to these effects, hypermagnesemia
dition to this direct vasoconstrictive effect, hypomagnesemia also may cause a subjective sensation of warmth, diaphoresis, drowsi-
decreases the vasodilation response to acetylcholine. 119 Low levels ness, lethargy, coma, diminished deep tendon reflexes, flaccid
of dietary magnesium and low serum magnesium are associated skeletal muscle paralysis, and respiratory depression.
with increased prevalence of hypertension. 120 Meta-analysis of Cardiac Effects of Hypermagnesemia. A plasma excess of
clinical trials shows that magnesium supplementation has a small magnesium interferes with cardiac conduction throughout the
blood pressure lowering effect in hypertension. 121 heart. Atrioventricular block or complete heart block may occur
The vascular actions of hypomagnesemia promote the occur- at high plasma levels of magnesium. 127 Hypermagnesemia in-
rence of vasospasm. 122 The coronary arteries are extremely sensi- hibits myocardial contraction and depresses membrane excitabil-
tive to the effects of hypomagnesemia. Coronary artery spasm ity, although intracellular contractile mechanisms remain intact.
may cause acute myocardial ischemia in clinical hypomagne- Hypermagnesemia suppresses the sinoatrial node and causes
semia. 123 Sudden-death, associated with a reduced dietary intake sympathetic nervous system blockade. 126 Both of these factors
of magnesium, may be the result of coronary vasospasm. Plasma contribute to clinically significant supraventricular bradycardia.
free fatty acids bind ionized magnesium, rendering it physiologi- Cardiac arrest in asystole may be fatal in severe hypermagnesemia.
cally inactive. An increase in plasma free fatty acids thus causes a ECG changes associated with hypermagnesemia include prolonged
decrease in the amount of ionized magnesium. In individuals PR interval and increased duration of the QRS complex. 127,128
who have total-body magnesium depletion, it is possible that ep- These changes are somewhat variable and do not present a classic,
inephrine-induced increases in plasma free fatty acids are a trig- easily recognizable picture.
gering factor for coronary vasospasm (and subsequent sudden
death). Vascular Effects of Hypermagnesemia. Hypermagnesemia
Total-body magnesium depletion (with or without hypomag- reduces peripheral vascular resistance by inhibiting calcium move-
nesemia) appears to play an important role in the development of ment into vascular smooth muscle cells, inhibiting calcium release
atherosclerosis and ischemic heart disease. 124 Animal studies show from intracellular storage, and depressing contractile responses to
hypertension, endothelial dysfunction, and vascular remodeling vasoactive substances such as epinephrine and angiotensin II. The
with chronic magnesium deficiency. 119 Animal studies also peripheral vasodilation caused by these mechanisms leads to hy-
demonstrate plasma elevation of proinflammatory cytokines and potension. 128 Vasodilation of cutaneous vessels in hypermagnesemia
neuropeptides that stimulate free radical formation. 116,125 Thus, causes flushing.