Electrolytes Flashcards
Potassium
Intracellular or Extracellular
Hormones affecting
Intracellular
Insulin and Adrenaline (B agonists) move K intracellular
Aldosterone moves into collecting duct
Why do ACE inhibitors cause hyperkalemia
ACE converts Angiotensin I to Angiotensin II which increases the release of aldosterone from the adrenal cortex = Less K excretion
Causes of hyperkalemia (5)
Renal causes: AKI, Chronic kidney disease, Type 4 RTA eg Diabetic nephropathy
Drugs: ACEi/ARBs, Beta-blockers, NSAIDs, K+ sparing diuretics eg Spironolactone, Heparin, etc Mineralocorticoid deficiency (Addison’s disease)
Exogenous K - Supplements, bananas
Endogenous K - Tumour lysis syndrome, Rhabdomyolysis, trauma, burns.
Shift from intracellular to extracellular space - Acidosis e.g. DKA
ECG changes in hyperkalaemia
Tall tented T waves Long PR Flat P waves Broad QRS Sine waves - Late sing. Cardiac arrest imminent
Symptoms of hyperkalaemia.
Often asymptomatic Palpitations/ chest pain Bradycardia/ Heart block Tachypnoea Muscular weakness/ paralysis Generalized weakness/ fatigue Depressed tendon reflexes Cardiac arrest
Management of hyperkalaemia
For K+ 5.5 – 6.0 mmol/L: Stop K sparing drugs and
restrict dietary or IV potassium intake.
K+ 6.0 – 6.5 mmol/L with no ECG Changes: Oral Calcium Resonium 15g 3-4 times a
day in water. Prescribe lactulose 10-20 ml qds with
it. It takes around 10 hours for effect.
K+> 6.5 mmol/L or >6.0 mmol/L
with ECG Changes - 10ml 10% calcium gluconate IV over 5 minutes.
Insulin IV &; Salbutamol nebs drives K into cells+ 50ml 50% dextrose.
Use central access if available, otherwise use a large
peripheral vein.
Look for normalisation of ECG on cardiac monitor.
ECG changes in hypokalaemia
Flattened & inverted T waves;
Increased amplitude and width of the P wave
Prolongation of the PR interval
ST depression
Prominent U waves
Arrhythmias: VT, VF, Torsades de Pointes.
Hypokalaemia features
Often asymptomatic until arrest.
Weakness, fatigue, constipation, muscle cramping, palpitations.
Causes of hypokalaemia
Decreased intake: anorexia nervosa,
malnutrition, chronic alcoholism,
inappropriate IV therapy.
Transcellular shift: insulin, beta-agonists,
theophylline, re-feeding syndrome.
Renal loss: diuretic therapy, mineralocorticoid
excess/therapy, aminoglycosides, alkalosis,
renal tubular acidosis, magnesium depletion.
Extrarenal loss: Chronic D&V, laxative abuse,
fistula, villous adenoma.
Extra renal loss vs renal loss
Urine potassium < 10 indicates extra-renal loss, urine
potassium > 20 indicates renal loss.
Nb. If extra-renal K+ loss (e.g. vomiting /diarrhoea)
is associated with dehydration this can stimulate
aldosterone release which will increase renal K+ loss
Management of hypokalaemia
Treat the cause, in general oral K+ is
preferred. In severe and potential life threatening
hypokalaemia the rate of K+ infusion should not
exceed 20 mmol/h.
If secondary to low Mg then give Mg replacement –
otherwise potassium may be refractory to treatment
Management of Hypomagnesemia
≤ 0.5 mmol/L - IV infusion (peripheral or central) magnesium sulphate 20 mmol
(5g) in 500 ml 0.9% saline or 5% dextrose over 12
hours for 3-5 days.
With life threatening symptoms ( e.g seizures,
arrhythmias): IV bolus of 8mmol MgSO4 (2g) over
10-15 minutes followed by infusion as stated above.
Nb. Mg can accumulate in the kidneys so needs to be reduced and monitored in CKD
Maintenance requirements
Water
Na
K
20-25ml/kg/day
1mmol/kg/day
1mmol/kg/day
Features of hyponatraemia
Rarely occur below 120mmol/L
Result from movement of water into brain cells causing cerebral oedema
Headache, confusion, convulsions and coma
Causes of hyponatraemia
Dilutional - Heart failure, liver failure, renal failure, hypoalbuminaemia
Hypovolemia (Determine difference by Na in urine)
- Renal - Diuretics, Osmotic diuresis (hyperglycemia), adrenocortical insufficiency.
- Extra renal - Haemorrhage, vomiting, burns, diarrhoea.
