POTASSIUM DISORDERS of illnesses that cause potassiwn disorders, such as paralysis, tachycardia, rashes, or striations. Patients with a

 

POTASSIUM DISORDERS

of illnesses that cause potassiwn disorders, such as paralysis, tachycardia, rashes, or striations. Patients with a

hyperkalemia-induced QRS widening may appear bradycardic before degeneration into a sinusoidal rhythm (see

Diagnostic Studies).

DIAGNOSTIC STUDIES

� Laboratory

An electrolyte panel will detect abnormalities of potassiwn

(turnaround time is approximately 30-40 minutes). A

potassiwn level can be obtained using many blood gas analyzers. Advantages include a more rapid turnaround time (2

minutes). However, blood gas analyzers are unable to detect

a hemolyzed sample and therefore may overdiagnose hyperkalemia. A magnesiwn level should be obtained in patients

with hypokalemia, because of the difficulty in correcting low

potassiwn in the setting of low magnesiwn levels.

� Electrocardiogram

Symmetrical T-wave peaking, P-wave flattening, QRS widening, or a sinusoidal pattern are characteristic of hyperkalemia (Figure 67-1). Unfortunately, the electrocardiogram

(ECG) lacks sensitivity to detect elevated potassiwn levels.

Only 50-60% of patients with potassium levels >6.5

mEq/L have any of the preceding ECG findings.

Hypokalemia is manifested by U-waves, T-wave flattening,

and ST -segment depression. Dysrhythmias, including ventricular fibrillation, may occur in patients with severe

hypokalemia or in patients with moderate hypokalemia

and a history of cardiac disease.

MEDICAL DECISION MAKING

Patients with a history consistent with a potassiwn disorder ( eg, missed dialysis, profuse diarrhea) should have

immediate ECG testing performed and should be placed

on a cardiac monitor. An electrolyte panel or arterial

blood gas with electrolytes should be drawn. If an ECG is

consistent with hyperkalemia, therapy should be initiated

immediately, before confirmatory tests. Before treating

isolated hyperkalemia detected on an electrolyte panel,

pseudohyperkalemia (hemolysis) should be ruled out by

communication with the lab. Patients who are dialysis

dependent or who remain hyperkalemic despite treatment should have emergent dialysis arranged. Patients

with hypokalemia should have potassium and magnesium repleted (Figure 67-2).

TREATMENT

� Hyperkalemia

All patients with hyperkalemia should be put on a cardiac monitor, and an ECG should be performed. If QRS

widening or arrhythmias are noted on a rhythm strip or

ECG, calcium, given as calcium gluconate 10% (less irrif>1;e I of t

Figure 67-1 . ECG changes of hyperkalemia. Note the pea ked T waves and widened QRS complex.

CHAPTER 67

Suspected electrolyte disorder

Electrolyte

panel, mon itor,

ECG

and K· decreases,

admit to mon itored

setting with

nephrology consu lt

· Obta in Mg

level

· Replace K·

· Sea rch for

u nderlying cause

K· < 2.5 mEq/L,

admit to

monitored

setting

K· > 2.5 m Eq/L,

consider

discharge when

correcti ble cause

is identified

.A Figure 67-1. Potassium disorders diag nostic a lgorithm. ECG, Electroca rdiogram.

tation to peripheral veins) or calcium chloride 10% (3x

more calcium) should be administered to stabilize myocardial membranes. Calcium can be repeated every 5 minutes

until the ECG normalizes. The duration of action is 30-60

minutes. Calcium is not indicated in the stable patient

when the ECG shows only peaked T waves. Avoid giving

calcium when treating hyperkalemia with coexisting digoxin

toxicity, because intracellular calcium is already elevated in

digoxin toxicity. Further administration of calcium may

cause asystole and death.

Therapy should also be instituted to induce an intracellular shift of potassium. Insulin 0.1 Unit/kg intravenously

(IV) is administered to shift potassium into the cell via an

intracellular messenger. Within 30 minutes, insulin will

reduce the potassium level by 0.5-1.0 mEq/L. In patients

with normal glucose levels, administer 25-50 g ( 1/2-1 amp)

of dextrose rv. An alternate method in stable patients is to

add 10 Units of regular insulin in 500 mL of D10W and

administer this over a 1-hour period. Patients with chronic

renal failure given insulin should have fingerstick glucose

monitoring initiated, as hypoglycemia is not uncommon.

Nebulized albuterol also shifts potassium back into cells

and may work synergistically with insulin. Albuterol 10-20

mg in 4 mL of NS is given via nebulizer over 10 minutes.

Sodium bicarbonate (NaHC03

) also shifts potassium back

into cells and leads to increased potassium excretion by the

kidneys. One amp (SO mEq) infused over a 5-minute period

has an onset in 5-10 minutes and lasts 2 hours.

POTASSIUM DISORDERS

Finally, potassium elimination therapy should be initiated. Furosemide 20-40 mg IV in patients not already

taking the drug will reduce potassium levels. The onset is

several hours, and the amount of decrease in the potassium level is variable. Cation exchange resins like sodium

polystyrene sulfonate (Kayexalate) remove up to 1 mEq

potassium per gram. A standard dose is 30 g mixed with

50 mL of 20% sorbitol to induce diarrhea. It can be

administered rectally (50 g with 200 mL 20% sorbitol), if

necessary. Onset is delayed and may take more than 4

hours. Dialysis should be activated early for patients in

renal failure. Dialysis is also indicated in refractory cases.

Treatment for the underlying disorder (eg, steroids for

Addisonian crisis, Fab fragments for digoxin toxicity)

should be initiated as soon as possible.

� Hypokalemia

Patients with hypokalemia should be put on a cardiac

monitor. Oral K+ replacement (40 mEq/day) is safe and

generally recommended in patients with mild to moderate

hypokalemia. IV K + should be used if cardiac dysrhyth ­