hyperkalaemia

Question 1

3 pathways of increased potassium

Answer 1

potassium excess due to altered metabolism or intake
extracellular shift due to acidosis, insulin deficiency or drugs
extracellular release due to pathological cell lysis

Question 2

When K+ shifts out of the cell, it’s a BAD LOSS!

Answer 2

Beta blockers, Acidosis, Digoxin, Lysis, hyperOsmolality, high Sugar, Succinylcholine

Question 3

causes of accumulating potassium excess

Answer 3

reduced excretion eg. CKD
endocrine causes eg. hypocorticolism, hypoaldosteronism
drugs eg. potassium sparing diuretics, ACE inhibitors, ARBs, NSAIDs
increased intake
K+ containing IV fluids

Question 4

causes of extracellular shift of potassium

Answer 4

acidosis
hyperosmolality
insulin deficiency
drugs: beta blockers, succinylcholine, digoxin

Question 5

causes of extracellular release of potassium

Answer 5

pathological cell lysis eg. rhabdomyolysis, TLS, haemolysis
high blood cell turnover eg. thrombocytosis, erythrocytosis, leukocytosis
pseudohyperkalaemia

Question 6

what is pseudohyperkalaemia

Answer 6

iatrogenic blood cell lysis
eg.
blood drawn from the side of IV infusion or a central line without previous flushing
prolonged use of a tourniquet
fist clenching during blood withdrawal
delayed sample analysis

Question 7

clinical features of hyperkalaemia

Answer 7

Cardiac arrhythmias (e.g., atrioventricular block, ventricular fibrillation)
Muscle weakness, paralysis, paresthesia
↓ Deep tendon reflexes
Nausea, vomiting, diarrhoea

Question 8

why does hyperkalaemia cause ↓ Deep tendon reflexes

Answer 8

While a reduced resting potential initially increases membrane excitability, persistent depolarization eventually inactivates sodium channels and leads to reduced total membrane excitability.

Question 9

what effect does high potassium have on resting membrane potentials

Answer 9

An increased extracellular potassium concentration decreases the resting potential gradient, leading to a reduced voltage. This brings the membrane potential closer to the threshold that triggers an action potential. Persistent depolarization eventually inactivates sodium channels, which ultimately reduces the net membrane excitability.

Question 10

approach to hyperkalaemic emergency

Answer 10

continuous cardiac monitoring

1. stabilise the cardiac membrane:
   Iv calcium gluconate 10ml of 0.22mol/ml IV over 2-3 minutes into a large vein
2. shift potassium intracellularly:
   - short acting insulin with glucose
   - consider the addition of inhaled SABA’s
3. correct metabolic acidosis:
   sodium bicarbonate 50ml of 1mmol/ml over 5-10 minutes
4. enhance excretion:
   oral potassium binders eg. sodium zirconium cyclisilicate (SCZ) or patiromer (these bind K in the Gi tract)

nephrology and critical care consults
admit to hospital for ongoing monitoring and treatment
repeat serum K at 1, 2, 4, 6 and 24 hours after treatment, patients whose potassium remains high will require for frequent monitoring

Question 11

what kind of insulin/glucose to administer

Answer 11

rule out hypoglycaemia first
short-acting insulin 10 units IV bolus

PLUS EITHER

glucose 50% 50 mL IV over 5 minutes (can cause vascular irritation when administered peripherally)

OR

glucose 10% 250 mL IV over 15 minutes.

Question 12

what is the reasoning for administering calcium gluconate

Answer 12

calcium gluconate 0.22 mmol/mL 2.2 mmol (10 mL) IV over 2 to 3 minutes into a large vein. Monitor response by ECG if possible
for life threatening cardiac arrhythmias or severe ECg changes.
the effect of this infusion is short lived. the dose may need to be repeated in 30-60 minutes, while undertaking specific measures to reduce potassium

Question 13

what are some oral potassium binders

Answer 13

Calcium polystyrene sulfonate.
Patiromer (Veltassa®).
Sodium polystyrene sulfonate (Kionex®).
Sodium zirconium cyclosilicate (Lokelma®).

Question 14

To remember K+-lowering treatments, think C BIG K Die (if you see a big serum K+, your patient may die!):

Answer 14

Calcium salts, Beta-agonists/Bicarbonate, Insulin + Glucose, Kation exchange medication, Dialysis/Diuretics.

Question 15

calcium salts reduce

Answer 15

cardiac irritability
Calcium reduces the threshold potential of cardiac cells and restores the normal gradient with the resting membrane potential.

Calcium salts should result in normalization of the ECG appearance within 5 minutes; observe the cardiac monitor following initial treatment and repeat the dose if the ECG tracing still appears abnormal.

Question 16

when hyperkalaemia is due to adrenal insufficiency, how should this change the management

Answer 16

When hyperkalaemia is due to adrenal insufficiency, corticosteroid replacement is the main treatment. Insulin should be avoided.