POTASSIUM EXCESS (HYPERKALEMIA)

HYPERKALEMIA o Addison’s disease

• Serum potassium level greater than 5 mEq/L [5 o Hypoaldosteronism
mmo/L] • Potassium release from cells
• Seldom occurs in patients with normal renal o Burns
function. o Severe infection
• In older adults, there is an increased risk of o Trauma
hyperkalemia due to decreases in renin and o Crash injury
aldosterone as well as an increased number of o Intravascular hemolysis
comorbid cardiac conditions. o Metabolic acidosis
• Hyperkalemia is often caused by iatrogenic o Insulin deficiency
(treatment-induced) causes. • Pseudohyperkalemia (a false hyperkalemia) has
• Less common than hypokalemia. several causes:
• Usually more dangerous because cardiac arrest is o Improper collection or transport of a
more frequently associated with high serum blood sample
potassium levels. o Traumatic venipuncture
• Acute hyperkalemia is a medical emergency o Use of a tight torniquet around an
requiring prompt recognition and treatment to exercising extremity while drawing a
avoid a fatal cardiac dysrhythmia and cardiac blood sample
arrest. o Producing hemolysis of the sample
before analysis
PATHOPHYSIOLOGY o Marked leukocytosis
• Major causes of hyperkalemia are: o Thrombocytosis
o Decreased renal excretion of potassium o Drawing blood above a site where
o Rapid administration of potassium potassium is infusing
o Movement of potassium from the ICF o Familial pseudohyperkalemia, in
compartment to the ECF compartment which potassium leaks out of RBCs
• Hyperkalemia is commonly seen in patients with while the blood is awaiting analysis.
untreated kidney injury • Measurements of grossly elevated levels of
o Particularly those in whom potassium potassium in the absence of clinical manifestations
levels increase because of infection or should be verified by retesting.
excessive intake of potassium in food or
medications. CLINICAL MANIFESTATIONS
• Patients with hypoaldosteronism or Addison • Mild to moderate (5.5-6.9 mEq/L)
disease are at risk for hypokalemia because of o Nerve and muscle irritability
lack of aldosterone. § Vague muscle weakness is an
o Lack of aldosterone activity at the early sign
nephron causes inadequate sodium and o Paresthesia
water reabsorption into the bloodstream o Tachycardia
and inadequate excretion of potassium o Diarrhea
in the urine. o Intestinal colic = abdominal pain
o Deficient adrenal hormones lead to • Severe (higher than 7.0 mEq/L)
sodium loss and potassium retention. o Impaired cardiac conduction
• Medications have been identified as a probable o Cardiac arrest
contributing factor in more than 60% of o Convulsions
hyperkalemic episodes. Medications commonly o Severe neuromuscular weakness
implicated are: o Flaccid paralysis
o KCl § Ascending muscle weakness
o Heparin o ECG changes
o ACE inhibitors § Prolong PR interval
o NSAIDs § Wide QRS
o Beta-blockers § Tall, tented T wave
o Cyclosporine § ST segment depression
o Tacrolimus o Metabolic acidosis
o Potassium-sparing diuretics o Paralytic ileus
o Antibiotics
o Chemotherapeutic drugs ASSESSMENT AND DIAGNOSTIC FINDINGS
o Nonsteroidal anti-inflammatory drugs • ECG changes
o Spironolactone o Tall, tented T waves
o Potassium, in excessive amounts o Possibly flattened P waves
• Increase potassium intake o Prolonged PR intervals
o Overconsumption of dietary potassium o Widened QRS complexes
o Excessive use of salts or potassium o Depressed ST segments
supplements • Serum potassium level greater than 5 mEq/L
o High volume blood transfusion • Decreased arterial pH, indicating acidosis
o Use of certain drugs
• Decreased potassium excretion MEDICAL MANAGEMENT
o Acute or chronic renal failure • In disorders involving potassium level changes,
o Disorders that damage the kidneys ECG must be obtained immediately.

ROJAS
POTASSIUM EXCESS (HYPERKALEMIA)
• Shortened repolarization and peaked T waves are • IV administration of sodium bicarbonate
seen initially in hyperkalemia. (NaHCO3)
• To verify results, a repeat serum sodium level o May be necessary in severe metabolic
should be obtained from a vein that is not acidosis to alkalinize the plasma, shift
concomitantly infusing an IV solution containing potassium into the cells, and furnish
potassium. sodium to antagonize the cardiac
• In nonacute situations, restriction of dietary effects of potassium.
potassium and potassium-containing o Effects of this therapy begin within 30 to
medications may correct the imbalance. 60 minutes and may persist for hours;
• Administration, either orally or by retention enema, however, they are temporary.
of cation exchange resins may be necessary. o Circulatory overload and hypernatremia
o The use of cation resins requires normal can occur when large amounts of
bowel function. hypertonic sodium bicarbonate are
• If less than 5.5; given.
o Dietary restriction • Bicarbonate therapy
• Improve urine output o To antagonize the effect of potassium
o Force fluids • Actual removal of potassium from the body is
o IV saline required
o Potassium wasting diuretics o Dialysis
DIAGNOSTIC TESTS: § Hemodialysis (best treatment)
• ECG § Peritoneal dialysis
• 24 hour urinary excretion test o Cation exchange resins
o Exceeding 20 mEq/24 hour – renal • Closely monitor the patient’s cardiac status,
potassium loss including ECG tracings
• Repeat serum K level without IV infusion • Administer 10% calcium gluconate
containing K o To counteract the myocardial effects of
• SERIOUS CASE: administration of cation hyperkalemia
exchange resin • Administer regular insulin and hypertonic
o (kayexalate) either by oral or retention dextrose by IV
enema o To move potassium into the cells
o Cannot be used if there is paralytic ilius o Using therapy, monitor for hypoglycemia
because of intestinal perforation • Administer NaHCO3 to a patient with acidosis
o To shift potassium into the cells.
EMERGENCY MANAGEMENT • Closely monitor fluid I&O
• If serum potassium levels are dangerously • If the patient doesn’t respond to treatment,
elevated, it may be necessary to administer IV prepare him for dialysis
calcium gluconate
o Within minutes after administration, NURSING MANAGEMENT
calcium antagonized the action of • Thorough history taking and physical assessment
hyperkalemia on the heart but does not • Monitor every 4-8 hours:
reduce the serum potassium o VS
concentration. o Bowel function
o Calcium chloride and calcium gluconate o Urine output
are not interchangeable o Lung sounds
§ Calcium gluconate contains o Peripheral edema
4.5 mEq of calcium • Monitor ECG or apical pulse
§ Calcium chloride contains • Monitor I&O
13.6 mEq of calcium • Monitor closely for signs of hyperkalemia
o Caution is required when using calcium • Observe signs of muscle weakness and
preparations to reduce potassium levels. dysrhythmias
• Monitoring blood pressure • Presence of paresthesia is noted and GI
o Essential to detect hypotension, which symptoms
may result from the rapid IV • Prolonged use of torniquet is avoided
administration of calcium gluconate • Caution patient not to exercise the extremity
• The ECG should be continuously monitored before drawing a blood to avoid falsely elevated
during administration potassium level
o The appearance of bradycardia is an • Encourage patient to adhere to the prescribed K
indication to stop the infusion. restriction
o The myocardial protective effects of • Encourage to avoid K rich foods
calcium last about 30 minutes.
• KCl should not be added to a hanging bottle
o Extra caution is required if the patient
(produces bolus)
has received an accelerated dose of
digitalis-based cardiac glycoside to
reach a desired serum digitalis level
rapidly as parenteral administration of
calcium sensitizes the heart to digitalis
and may precipitate digitalis toxicity.

ROJAS