questions??

DETECTING

HYPO MAGNESEIMIA

THE MOST OVERLOOKED ELECTROLYTE IMBALANCE Long ignored as a cause of

potentially fatal arrhythmias, hypomagnesemia is now

receiving carefui attention. Find out what you need to

know to uncover this problem in your patients.

AVID WALLACE, A 73-YEAR-OLD RETIRED CON- struction worker, is admitted to your coronary care unit (CCU) with a di- agnosis of congestive heart failure (CHF). Although he denies having chest pain, he's pale, diaphoretic, and dyspneic. You auscultate moist crack- les in his lungs and note that he's pro- ducing frothy, pink-tinged sputum.

His vital signs are: pulse, 110; blood pressure, 100/64; respirations, 28; and temperature, 97.6° F (36.4° C). Car- diac monitoring shows sinus tachycar- dia, with four to five ventricular ec- topic beats per minute.

This is Mr. Wallace's second episode

BY REBECCA P. YARNELL, RN, MSN Nursing Instructor Fort Sanders School of Nursing Knoxville, Tennessee

MARTHA P. CRAIG, RN, MSN Director of Department of Nursing Maryville College Knoxville, Tennessee

of CHF since he suffered a myocardial infarction 4 years ago. He's remained otherwise healthy on a drug regimen of digoxin (Lanoxin), furosemide (La- six), and a potassium chloride supple- ment (K-Lyte/Cl). Other than a bor- derline low hematocrit of 39%, his lab results are within normal limits.

So what's gone wrong? The answer isn't immediately obvious because Mr. Wallace is suffering from hypomag- nesemia, an often overlooked and life- threatening- electrolyte deficiency, which affects many more patients than you might suspect. Recent research suggests doctors and nurses should be- come more aware of this potential problem.

This article will tell you what you need to know — how to identify patients at risk for hypomagnesemia, what causes to consider, what signs and symptoms to look for, and how to ad-

Nursing91, July 55

minister treatment. We'll also take you through Mr. Wallace's therapy and postdischarge planning.

Associated with hypokalemia Studies show that 42% of hypokalemic patients also have hypomagnesemia — many of them experiencing ventricular ectopy, one of Mr. Wallace's symp- toms. In these studies, ventricular ar- rhythmias persisted after hypokalemia was corrected and continued until hy- pomagnesemia was eliminated. The findings prove that magnesium is as important as potassium in the etiology and treatment of these cardiac prob- lems.

That's because a magnesium deficit can lead to intracellular potassium loss and sodium accumulation, altering membrane excitability. This creates ab- normal areas of automaticity, which contribute to inefficient conduction in the heart. Of course, any changes in the normal sequence of conduction

usually result in symptomatic arrhyth- mias.

Diagnosing Mr. Wallace In Mr. Wallace's case, as in so many others, no one recognizes his magne- sium deficit initially. Shortly after his admission, you insert an intravenous (I.V.) line and infuse furosemide (80 mg) and digoxin (0.25 mg) as ordered. Because Mr. Wallace is experiencing ventricular ectopy, the doctor also or- ders 250 ml of D,W with 40 mEq po- tassium chloride, infused at 25 ml/ hour, hoping to prevent the ventricular irritability from getting worse.

Over the next 24 hours, Mr. Wallace improves, his respirations slowing to 16 per minute, his chest sounds clear- ing. But the cardiac monitor reveals occasional premature ventricular con- tractions, so he's transferred to the te- lemetry unit for continued electrocar- diogram monitoring. On the unit, he's started on an oral regimen of digoxin.

MANAGING COMPLICATIONS OF MAGNESIUM THERAPY With the clinical significance of hy- pomagnesemia finally being recog- nized, you can expect to administer magnesium supplements more of- ten to your patients. Here are some guidelines to help you detect com- plications during magnesium re- placement therapy: • Monitor the patient's vital signs, checking for an irregular or de- creased heart rate, lowered blood pressure, and depressed respira- tions. Also watch ECG tracings closely, looking for peaked T waves and widened QRS complexes, both of which may indicate too mucti magnesium. • Magnesium infusions can be toxic for patients with renal problems, so keep in mind that decreased car- diac output could signal a problem. Also monitor intake and output carefully before, during, and after the infusion. • Assess the patient for impaired neuromuscular reactions, which may indicate an increased magne- sium level. Look for muscle weak- ness, respiratory depression, and, ultimately, flaccid paralysis. On- going evaluation of deep tendon re- flexes before and during magne- sium infusions will help you identify any problem before it gets too se- vere.

• Keep calcium gluconate and cal- cium gluceptate on hand for rapid reversal of toxic effects. Also keep resuscitation equipment available. As you're watching for potentially toxic magnesium levels, remember that your patient's level may also re- main normal despite continuous in- fusion. That's because serum levels are a poor indicator of intracellular magnesium levels, which fluctuate independently from serum levels.

• You may also be asked to admin- ister I.M. magnesium, usually or- dered as magnesium sulfate (20 grams in 2 ml). But some experts question the effectiveness of this therapy because many patients show no change in serum levels af- ter injection. One reason may be that the injectable concentration of magnesium exceeds the renal tubu- lar threshold. You can address this problem by getting an order to ad- minister injections more frequently.

• Oral magnesium therapy poses problems too. Because of its laxa- tive effect, magnesium hydroxide can exacerbate the deficiency through gastrointestinal loss. Mag- nesium chloride avoids this problem but is unpalatable. Timed-release tablets of magnesium chloride are available, but using them for contin- uous therapy is expensive.

furosemide, and a potassium supple- ment — the same medications he'd been taking at home. He starts to feel en- ergetic and is allowed to resume a full activity level.

But his progress doesn't last long. On the morning of the fourth day, he com- plains of vague discomfort and fatigue. A nurse on the telemetry unit notes that he seems nervous and uneasy. A few hours later, he develops ventricular tachycardia, with its characteristic wide QRS complexes, missing P waves, and a heart rate of 150 to 158 beats/ minute. The nurse gives a stat order of lidocaine (50 mg I.V. bolus), followed by an infusion administered at 3 mg/ minute. Mr. Wallace is transferred back to the CCU, where you're at a loss to explain what went wrong again.

Hypomagnesemia discovered The reason isn't apparent until the car- diologist asks for stat serum magne- sium and potassium levels. The results show a potassium level of 3.9 mEq/ liter (normal is 3.8 to 5.5) and a mag- nesium level of 1.3 mEq/liter (normal is 1.5 to 2.5). He orders replacement therapy —5 grams of magnesium sul- fate and potassium chloride, 15 mEq in 250 ml of D,W, to be administered over 10 hours.

You use a controller to administer the infusion and monitor the infusion site carefully for signs of infiltration. You also check and document Mr. Wal- lace's heart rate and blood pressure hourly, aware that a drop in either vital sign could mean that excess magne- sium is slowing conduction in the myo- cardium, compromising cardiac out- put. This is possible because hyper- magnesemia, like hypomagnesemia, slows conduction in the myocardium. (See Managing Complications of Mag- nesium Therapy.)

Two hours after starting the infusion, you find Mr. Wallace's vital signs are stable. A rhythm strip reveals a normal sinus rhythm with an occasional but rare premature ventricular contraction.

Mr. Wallace returns to the telemetry unit after spending 24 hours oh the CCU. His serum magnesium and po- tassium levels are checked daily. Dis- charge is planned within a few days because his electrolyte levels return to normal and his CHF resolves.

His diuretic is changed from furose- mide to triamterene/hydrochlorothiazide (Maxzide), which spares potassium and magnesium. He'll no longer need to take potassium supplements but will

56 Nursing91, July

CAUSES OF HYPOMAGNESEMIA GASTROINTESTINAL • Alcoholism • Protein-calorie malnutrition • Prolonged I.V. therapy (without

magnesium replacement) • Gastric suction • Intestinal bypass for obesity • Diarrhea • Colonic neoplasms • Laxative abuse • Bulimarexia • Short-bowel syndrome • Malabsorption

RENAL • Diuretics • Antibiotics (ticarcillin, gentamicin,

carbenicillin) • Cispiatin • Cyclosporine • Hypercalcemic states (including

malignancies) • Postobstructive diuresis • Acute tubular necrosis (diuretic

phase) • Hereditary renal magnesium

wasting • Aldosteronism

MISCELLANEOUS • Excessive lactation • Exchange transfusion • Acute intermittent porphyria From Tlic AuiLriciiii Journal of Mvdiciiic. * |yS7 Cahners Publishing Co., Inc.. New York. N.Y. Adapted wilh pcr- missiiin of the publisher.

need monthly serum electrolyte screen- ings to detect any future abnormalities.

Who's at risk? Now that you're aware of the dangers of hypomagnesemia, what can you do to avoid it? Start by identifying patients at risk. First off, you should be sus- picious whenever you see a case of hy- pokalemia or multiple electrolyte de- ficiencies (such as hyponatremia and hypocalcemia). Also be on guard when you administer diuretic therapy, a com- mon cause of magnesium deficiencies. (Keep in mind, though, that a change of diuretics is not always advisable.)

Loop and thiazide diuretics are usu- ally responsible. With the growth of the elderly population and a rise in asso- ciated cases of hypertension and cor- onary disease, more people take these diuretics. In addition to furosemide, other magnesium-depleting diuretics include ethacrynic acid (Edecrin), hy- drochlorothiazide (Hydro-Diuril and Esidrix), and bumetanide (Bumex).

What to look for You may be surprised to learn that neu- romuscular irritability, the hallmark of calcium and potassium deficiencies, is also a sign of hypomagnesemia. Check for leg cramps, muscle spasms, twitch- ing, and tetany. Also watch for central nervous system symptoms such as con- fusion and disorientation.

But the most life-threatening effects of a magnesium deficit are slowed car- diac rhythms and conduction time. Ventricular and atrial premature con- tractions may develop and progress to fatal arrhythmias. The electrocardio- gram changes are similar to those seen in hypokalemia. A deficit can also lead to prolonged complexes and prolonged PR intervals. You might also see ST depressions and flattened T waves.

Dietary evaluation You should evaluate the diets of pa- tients who are at risk. What a patient eats can play a large role in preventing a deficiency. Recommend inexpensive and easily prepared meals that contain a lot of magnesium and potassium, in- cluding beans, corn, bananas, whole- grain breads, cereals, and green, leafy vegetables. Also suggest the use of herbs and other low-salt seasonings.

Recommended daily allowance stan- dards call for consumption of 350 mg of magnesium for adult males and 280 mg for adult females. Keep in mind that only one-third of dietary magnesium is

absorbed by the gastrointestinal tract. You can't depend on diet alone to

replenish magnesium when a patient has a malabsorption problem, the lead- ing cause of hypomagnesemia. (There are other causes to consider too. For a complete overview, refer to Causes of Hypomagnesemia.)

In Mr. Wallace's case, you also need to teach him about his new diuretic. He was placed on triamterene/ hydrochlorothiazide because it spares potassium and magnesium. You may see patients in similar circumstances receive such alternatives as Dyazide, which combines different concentra- tions of triamterene and hydrochloro- thiazide, and Moduretic, a mixture of amiloride and hydrochlorothiazide.

You explain the reason for the change in diuretics to Mr. Wallace, emphasizing that he should take the new pill once a day. You also make sure he understands that this medication will replace — not supplement — his old reg- imen of furosemide and potassium.

Ongoing assessment needed Once a patient has experienced this electrolyte imbalance, ongoing assess- ment is important. Frequent monitor- ing of serum magnesium and potassium levels should be done to ensure that they remain stable. With this in mind, you arrange a follow-up doctor's ap- pointment for Mr. Wallace, scheduling it for 1 month after discharge so his magnesium and potassium levels can be checked. You also set up transpor- tation for him and make sure he realizes the importance of the appointment.

Mr. Wallace is doing well, and his magnesium levels remain steady at 1.5 to 2.5 mg/dl. But if his deficiency hadn't been discovered and treated, it could have been fatal. You'll no doubt hear about other patients like him as hypomagnesemia attracts more atten- tion. Routine testing for the condition will become widespread as more doc- tors and nurses recognize the need for it. Now you'll be prepared. El

SELECTED REFERENCES Borris, M., and Papa, L.: "Magnesium: A Dis- cussion of Ils Role in ihe Treatment of Ventricular Dysrhythmia,"Cn((cfl/Cfln.'M<?rficme. 16(3);292- 293, March 1988.

M a n i n , B., and Milligan, K.: "Diurelic- A.ssociated Hypomagnesemia in the Elderly," Ar- chiws of Internal Medicine. 147(IO):I768-1771, October 1987.

Ryzen, E., et al.: "Magnesium Deficiency in a Medical ICU Populalion," Critical Care Medi- cine. 13(1): 19-21, January 1985.

Whang, R.: "Magnesium Deficiency: Pathogen- esis. Prevalence, and Clinical Implications," American Journal of Medicine. 82(3A):24-29, March 20, 1987.

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