Approach to Hyperkalemia
Potassium: enters the body via oral intake
or IV infusion and is largely stored in cells, and then is excreted in the
urine. The major causes of hyperkalemia are increased K+ release from cells and
most often, reduced urinary K+ excretion
Definition: depends on the lab; K>5-5.5
History: medications, history of AKI/CKD,
excessive exercise, RTA IV
Clinical Symptoms:
· Muscular:
weakness and even paralysis of extremities; but rarely respiratory muscle
involvement
· Cardiac:
palpitations, orthostatic symptoms if bradycardic (on ECG: tall, peaked T
waves, especially in the precordial waves, widened QRS, wide and flat P wave,
VF, VT and PEA can arise!)
DDx
· “Pseudohyperkalemia” – hemolysed blood sample, leukocytosis,
thrombocytosis
o
Due
to K+ movement out of the cells during or after blood specimen has been drawn
o
Suspect
when: no apparent cause for the hyperkalemia in an asymptomatic patient with
normal ECG
o
Consider
technique of venipuncture: try w/o tourniquet or the fist clenching (K+ moves
out of cells with exercise!) or trauma to demonstrate a true serum K
o
K+
moves out of platelets after clotting has occurred
o
High
WBC (i.e. d/t CLL)à can falsely elevate K+
concentration d/t cell fragility
· Increase Intake: RARE, unless it occurs acutely
o
K+
loadà some stays in ECFà mild elevation in plasma [K]à stimulates secretion of
aldosteroneà
enhances both Na+ reabsorption & K+ excretion by the principal cells
· Trans-cellular Shift out of Cell: metabolic acidosis, insulin
deficiency (DM), Beta-blockade, digoxin intoxication, cellular necrosis (i.e.
tumour lysis, rhabdo, ischemic bowel)
o
Metabolic Acidosis: buffering excess H+ ions in the cellsàK+ movement into ECF, a
transcellular shift obligated by the need to maintain electro-neutrality
o
Insulin deficiency, hyperglycemia, hyperosmolality: insulin normally promotes K+
entry into cells; shift in DKA, despite the fact that there may be marked
deficit d/t urinary losses
o
Beta-Blockers: interfere with B2-adrenergic facilitation of K+ uptake by the cells,
especially after a K+ load; primarily with non-selective BB (i.e. labetolol,
propranolol)
· Increase Release: rhabdomyolysis, tumor lysis, strenuous exercise,
intravascular hemolysis
o
Increased tissue catabolism with increased breakdownà release of intracellular K into
extra-cellular fluid
· Decrease in Output:
o
Decrease in distal tubular flow: renal failure, decrease effective
circulating volume
o
Hypoaldosteronism: decrease renin, adrenal insufficiency, Type
IV RTA, ACEi/ARB, spironolactone, NSAIDs
Investigations:
· CBC, lytes, extended lytes, Cr,
Urea, glucose, serum osmolality, UA, urine lytes, urine osmolality, consider
VBG
· ECG: peaked T waves (pre-cordial
leads), widened QRS, flattened P waves
· Hypoaldosteronism work-up: serum
aldosterone and plasma renin activity
Measurement of 24h urinary K+
excretion: of limited utility in patients with persistent, stable hyperkalemia;
· The trans-tubular K+ gradient is NOT a reliable test for the diagnosis of
hyperkalemia
NOTE: most healthy patients can handle
large K+ loads with only a small rise in serum K+; thus, the most common cause of persistent hyperkalemia, is associated
with impaired urinary K+ excretion d/t reduced secretion of or response to
aldosterone, AKI/CKD, and/or effective arterial blood volume depletion
Management
· Indications for Acute management: ECG changes + hyperkalemia (i.e. K>6-6.5),
serum K>6.5-7 even if no ECG changes, serum K is rapidly increasing
Place patient on a cardiac monitor
Stabilize the cardiac membrane: Calcium
Gluconate 10%,
10mL (1000 mg) IV push over 2 min, with a cardiac monitor on!
o
Antagonizes
the membrane actions of hyperkalemia (Calcium is also helpful, as hypocalcemia
increases the cardiotoxicity of hyperkalemia)
o
Hyperkalemia
induced depolarization of resting membrane potential leads to deactivation of
Na channels and decreased membrane excitability
o
Effect begins within minutes; but
only lasts 30-60 minutes!
o
CaCl contains 3x the concentration
of elemental Ca then Ca Gluconate
§ CaClà500-1000 mg (5 to 10 mL of a 10%
solution), infused over 2 min
o
Concentrated
Ca infusions: irritating to veins and extravasation can cause tissue necrosis;
central/deep vein line= preferred! DO NOT GIVE IN HCO3 solution àcan cause precipitation of Calcium
Gluconate
· What about Digoxin?? Hypercalcemia potentiates the cardio-toxic
effects of digitalis;
o
Ca
should still be given for the appropriate indications…
o
In
these patients, use a dilute solution, administered slowly (i.e. 10 mL of 10%
Calcium Gluconate in 100 mL of 5% dextrose in water over 30 minutes)
Shift K+ into the cells: Insulin,
NaHCO3, short acting beta-agonist (SABA)
· Insulin & D50: given an amp of D50
(i.e. 50 mL push—25 g of glucose), followed by Regular Insulin 10 units IV
o
Drives
K into cells, via enhancing the activity of the Na-K-ATPAse pump
o
Usually
give with D50; given insulin alone if BG >14
o
Effect
of insulin: within 10-20 minutes; peak at 60 min, lasts 4-6 h
o
Create Alkalosis: NaHCO3
1 amp IV over 5 minutes; raise systemic pH, resulting in H+ ion release from
the cells as part of the buffering reaction; K+ moves into cells to maintain
electro-neutrality
§ Alternative: 150 mEq in 1L of 5%
dextrose in water over 2-4 h
o
Beta-Agonist: ventolin 2-4 puff INH
o
Monitor
HR, cardiac monitor
o
Measure
K and other lytes: 1-2 hours after initiation of therapy
o
Serial
ECGs
· Removal of K+:
o
Kayexalate
30g PO daily- QID, each dose followed by lactulose 30 mL PO
§ MOA: removes K by exchanging Na
ions for K ions in the intestine, especially in the LI before the resin is
passed from the body
§ Follow with lactulose
o
Ca
resonium
o
Diuretics
(i.e. Lasix 40 mg IV)
o
If
refractory—Dialysis
· Treat underlying cause
o
Discontinue
offending drug: K+ sparing diuretic, ARB/ACEi, K+ supplement, NSAID, TMP
ARTICLE: here is a short review (it's an older article, but there are good cases and ECGs) out of Emergency Medicine (2002), titled "Recognising signs of danger: ECG changes resulting from an abnormal serum potassium concentration"
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