Hyperkalaemia + hypokalaemia

Question 1

what happens to most dietary potassium

Answer 1

excreted in the urine

Question 2

is most of the body’s K intracellular or extracellular?

Answer 2

intracellular

Question 3

serum levels of K are controlled by…

Answer 3

• uptake of K+ into cells
• renal excretion (controlled by aldosterone)
• extra renal losses e.g GI

Question 4

how does aldosterone influence potassium?

Answer 4

increases K secretion + decreases Na excretion in the collecting tubule

Question 5

what is hypokalaemia defined as?

Answer 5

serum K <3.5mmol/L

Question 6

Cause hypokalemia

Answer 6

1. • hypertension:
     Cushing’s
     Conn’s syndrome: Hyperaldosteronism
2. • hypertension:
     Diuretics
     GI loss

Blood taken from a drip arm may –> spurious result

Question 7

Clinical features hypokalaemia

Answer 7

usually asymptomatic

muscle weakness may occur if severe

Question 8

What does hypoK increase the risk of?

Answer 8

arrhythmias

also predisposes to digoxin toxicity

Question 9

General Mx for hypoK

Answer 9

Identify + treat underlying cause

Withdrawal of purgatives
Assessment of diuretic Tx
Replacement with oral KCl supplements (liquid or effervescence preparations)

Question 10

Why would you give an IV infusion of potassium chloride to a hypoK patient?

Answer 10

if hypoK DKA + severe hypoK associated with cardiac arrhythmias or muscle weakness

Question 11

for hypoK, what should ampoules of potassium be mixed with?

Answer 11

NaCl 0.9%

Question 12

Why should glucose solutions be avoided?

Answer 12

They make hypoK worse

As glucose closes K+ ion channels on cell membrane that are normally open- meaning K+ can’t get out of the cell

Question 13

hyperkalaemia

Answer 13

serum K conc > 5.0 mol/L

Question 14

What is artifactual hyperK a result of?

Answer 14

red cell haemolysis

• vigorous phlebotomy
• leukemia

Question 15

cause hyperK

Answer 15

Decreased excretion: **renal impairment, **drug interference with K excretion, Addison’s disease

Redistribution (IC –> ECF): DKA, metabolic acidosis

Massive blood transfusion

Rhabdomyolysis

Drugs: K+ sparing diuretics e.g. spironolactone, ACEi, Angiotensin 2 receptor blockers (ARBs), heparin (~due to inhibition of aldosterone secretion)

Question 16

what does cortisol stimulate

Answer 16

Na retention + K loss

Question 17

Clinical features of hyperK are usually asymptomatic until….?

Answer 17

K is high enough to cause cardiac arrest

K+ induced spasm vasoconstriction

Question 18

What are symptoms of hyperK related to?

Answer 18

impaired neuromuscular transmission: muscle weakness + paralysis

there may be metabolic acidosis - Kussmaul’s resp

Question 19

Progressive abnormalities on ECG of hyperK

Answer 19

tented T wave
reduced P wave with widened QRS complex
‘sine wave’ pattern/TdP (pre cardiac arrest)

Question 20

Mx if no underlying cause of hyperK

Answer 20

recheck serum K to rule out a spurious hyperkalaemia unless ECG changes are present

Question 21

Mx of hyperK mild-moderate

Answer 21

dietary K restriction
restriction of drugs causing hyperK
loop diuretic (if appropriate) to increased urinary K excretion

Question 22

what is defined as a medical emergency in hyperK

Answer 22

severe hyperK

OR

hyper K >6.5

Question 23

Mx severe hyperK

Answer 23

• protect myocardium from hyperK: IV calcium gluconate bolus. 10% in 10mls
• drive K+ into cells: soluble insulin (10 or 12 units of actrapid) + 250mls of 10% dextrose IV. Over 15-20mins. nebulised salbutamol
  (insulin/actrapid puts K back into cells, dextrose stops hypo)
  This only shifts into the IC space, and sodium bicarb would have same effect. Can get rebound hyperkal
• deplete body K+ (after emergency Tx): calcium resonium, furosemide, dialyse

Question 24

how does crush injury cause hyperK?

Answer 24

When pt is trapped under crushing weight

Excess potassium leaking from the cells disrupts the heart conductivity –> arrhythmias or even cardiac arrest