Once J.P.’s potassium levels are replenished and she can take medicine by mouth,
oral potassium chloride can be started (see Chapter 9, Essential Hypertension, and
follow-up. Her BP is 170/90 mm Hg with a pulse of 80 beats/minute, and her physical examination is
remarkable for 2+ pedal edema. Laboratory tests show the following:
Before conducting any extensive evaluation to identify the etiology of
hyperkalemia, the serum potassium concentration ought to be repeated to confirm the
presence of hyperkalemia. Also to be ruled out are the different causes of spurious
hyperkalemia, which can result from severe leukocytosis (>500,000/μL),
137 or hemolysis within the blood collection tube.
Pseudohyperkalemia is a test-tube phenomenon that occurs when potassium is
released from leukocytes, platelets, or erythrocytes during blood coagulation. These
disorders can be confirmed easily by comparing serum (clotted) and plasma
(unclotted) potassium concentrations from the same blood sample. The two values
should agree within 0.2 to 0.3 mEq/L. Improper tourniquet technique, causing
strangulation of the patient’s arm before blood sampling, may also result in spurious
Identifying the etiology of hyperkalemia can be approached systematically by
considering possible disturbances in internal and external potassium balance. The
former involves transcellular flux of potassium from the intracellular to the
extracellular space, whereas the latter involves either increased intake, including
increased endogenous potassium load (e.g., rhabdomyolysis,
), or decreased elimination. A thorough medication history is important to
identify drugs associated with hyperkalemia.
Kidney Diseases, for additional information on hyperkalemia.)
A dietary history should ascertain whether A.B.’s consumption of potassium-rich
foods, salt substitutes, or potassium supplements has increased. Dietary intake alone
will not induce hyperkalemia unless renal excretion is impaired. Usually, the GFR
must be less than 10 to 15 mL/minute, unless there is concurrent hypoaldosteronism
or distal tubular potassium secretory defects.
1 A.B.’s renal insufficiency is mild, with
an estimated CrCl of 40 mL/minute.
Conditions associated with low renin and aldosterone, which usually present as
hyperkalemia and hyperchloremic metabolic acidosis, decrease potassium excretion
by the kidneys. These include diabetes,
145 obstructive uropathy, sickle cell disease,
lupus nephritis, and various tubulointerstitial diseases (e.g., gouty nephropathy,
analgesic nephropathy). Adrenal insufficiency presents commonly with hyperkalemia
because of mineralocorticoid deficiency.
146 A.B.’s hyperglycemia because of poorly
controlled diabetes may cause movement of potassium-rich fluid from the
intracellular space to the extracellular space because of the increased tonicity.
Elevating the plasma tonicity by 15 to 20 mOsm/kg will increase the plasma
potassium concentration by 0.8 mEq/L.
147 Patients with diabetes, mineralocorticoid
deficiency, or end-stage renal failure, which commonly results in hyporeninemic
hypoaldosteronism, are particularly susceptible.
A.B. is also taking several medications that may impair her ability to excrete
potassium. Captopril indirectly decreases aldosterone secretion by decreasing the
Ibuprofen inhibits prostaglandin production as well as renin and
149 Other drugs that cause hyperkalemia by impairing renin and
aldosterone production include AT2
155 Triamterene, a component of her
diuretic, inhibits tubular potassium secretion, as do amiloride, spironolactone, high-
159 and digitalis preparations.
/K+ ATPase, digitalis decreases tubular potassium secretion and
reduces cellular potassium uptake. Arginine,
blockers, α-adrenergic agonists, and hypertonic solutions also cause hyperkalemia by
impairing transcellular potassium distribution into the intracellular space.
beats/minute; RR, 20 breaths/minute; and temperature, 98°F. Laboratory data are as follows:
The ECG reveals an increased PR interval and a widened QRS complex. What clinical manifestations of
hyperkalemia are evident in V.C.?
Hyperkalemia decreases the intracellular/extracellular potassium ratio. Hence, the
resting membrane potential becomes less negative and moves closer to the threshold
excitation potential. Muscle weakness and flaccid paralysis result when the resting
membrane potential approaches the threshold potential, rendering the excitable cells
unable to sustain an action potential.
The cardiac toxicity of hyperkalemia is a major cause of morbidity and mortality,
with ECG findings paralleling the degree of hyperkalemia. When plasma potassium
is greater than 5.5 to 6.0 mEq/L, narrow, peaked T waves and a shortened QT
interval are seen. As the plasma potassium concentration increases further, the QRS
complex widens and the P-wave amplitude decreases. As the level reaches 8 mEq/L,
the P wave disappears and the QRS complex continues to widen and merge with the
T wave to form a sine wave pattern. If these ECG changes are not recognized and no
treatment is initiated, ventricular fibrillation and asystole will ensue. Hyponatremia,
hypocalcemia, and hypomagnesemia all reduce the threshold potential, thereby
increasing the patient’s susceptibility to the cardiac effects of hyperkalemia.
muscle weakness, ECG, chronic renal failure, and serum potassium concentration all
are consistent with severe hyperkalemia.
CASE 27-10, QUESTION 2: How should V.C.’s hyperkalemia be treated?
Hyperkalemia with ECG changes requires urgent treatment. Three therapeutic
modalities are available: (a) agents that antagonize the cardiac effects of
hyperkalemia, (b) agents that shift potassium from the extracellular into the
intracellular space, and (c) agents that enhance potassium elimination. Considering
V.C.’s severe ECG changes, 10% calcium gluconate IV should be administered at a
dose of 10 to 20 mL over the course of 1 to 3 minutes. Calcium counteracts the
depolarizing effect of hyperkalemia by increasing the threshold potential, thus making
it less negative and moving it away from the resting potential. The onset of action
occurs in a few minutes, but the effect is short-lived, lasting approximately 15 to 60
minutes. The dose can be repeated in 5 minutes if ECG changes do not resolve and as
needed afterward for recurrence. With no response after the second dose, additional
attempts, however, are not beneficial. When the hyperkalemia presents with a
digitalis overdose, calcium should be used cautiously because it can worsen the
cardiotoxic effects of digoxin.
Because the serum potassium concentration is not affected by calcium
administration, maneuvers should be used to shift potassium from plasma into the
cells. Three modalities are available: insulin and glucose, β2
Insulin rapidly shifts potassium into the cell in a dose-dependent fashion. The
maximal effect occurs at insulin concentrations greater than 20 to 40 times the basal
levels. Therefore, endogenous insulin secreted in response to dextrose administration
is insufficient, and exogenous insulin must be administered.
concentrations of dextrose may worsen hyperkalemia, particularly in diabetic
patients because intracellular potassium may be shifted to the extracellular space
owing to the elevated plasma tonicity,
it is always administered with insulin to
prevent hypoglycemia. Regular insulin (5–10 units) can be given with 50 mL of 50%
dextrose as IV boluses, followed by a continuous infusion of 10% dextrose at 50
mL/hour to prevent late hypoglycemia.
In dialysis patients susceptible to
experiencing fasting hyperkalemia, 20 units of insulin can be added to 1 L of 10%
dextrose and administered at a rate of 50 mL/hour to prevent the hyperkalemia.
insulin–dextrose combination lowers serum potassium by direct stimulation of
cellular potassium uptake and potentiates the potassium-lowering effect of βadrenergic stimuation.
165 The reduction in potassium is apparent 15 to 30 minutes
after the start of the therapy and persists for 4 to 6 hours.
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