Severe <2.5
Low intake
Diet, IVI
GI loss
D+V, fistula, ileus, obstruction
Urine loss
Defective proximal reabsorption
- recovery ATN
- post relief obstruction
- prox RTA
- drug tubule damage
- diuretics
- DM (osmotic diuresis)
- Conns
- RAS activation
- steroids/Cushings
- cirrhosis
- liqourice
- ↑↑ BP
K into cells
alkalosis
B agonists
insulin
Effects
ECG
T-wave flattening
Prominent U wave
ST depression
Prolonged PR
Arrhythmias, ↓ contractility
Weakness
Rx
Maximum conc for peripheral is 40mmol/L (venous necrosis)
Maximum rate is 40mmol/h
0.3 mmol ↓ equates to about 100mmol total loss from body store
Anaesthesia
Risk is of arrhythmia
Cancel elective <3 (if chronically low and un-digitalised unlikely to get problems)
Emergency – treat 1st
↑ sensitivity to neuromuscular blockade
If digitalised should be >4
Hyperkalaemia
↑ intake
Cell death
Rhabdomyolysis
Haemolysis
Internal bleeding
Tissue necrosis
Burns
Shift out of cells
Acidosis
B blockers
Dig toxicity
Impaired excretion
Low GFR (ARF/CRF)
↓ aldosterone → ↓ tubular excretion
- ACEi
- NSAIDS (block PG mediated renin release)
- adrenal disease
- heparin
- ß blockers (symp stims renin release)
- k sparing diuretics
- tubular disorders
ECG changes progressing through
Peaked T-waves, widened QRS, prolonged PR, loss of P, ST depression, VF, asystole. These potentiated by ↓ Ca, Na and acidosis
N + V + D
Rx
>6.5
If ECG changes Ca to stabilise myocardium - 10ml 10% calcium gluconate or 5 mls 10% calcium chloride
Insulin 10u in 50mls 50% dex
ß2 agonist (salbutamol)
Bicarbonate (50mmol)
Ion exchange resin – calcium resonium 15g PO or 30g PR TDS
Anaesthetic
This is the most dangerous electrolyte abnormality
Cancel elective
Emergency – treat 1st
Avoid sux