A 60 year old male presents to ED with a 1 week history nausea, decreased oral intake and occasional vomiting. He has a background of poorly controlled hypertension on Perindopril.
Metabolic acidosis – pH 7.26 and HCO3 16mmol/l
Compensation- Expected CO2 = 1.5x HCO3 +8 = 32mmHg
AG = Na – (Cl+HCO3) = 19
Delta gap = AG-12/24-HCO3 = 0.87
The above VBG shows a metabolic acidosis with a raised AG and a delta gap that confirms a isolated HAGMA. There is a moderately raised potassium, more than expected for the degree of acidosis and a moderately increased creatinine. There is a mildly elevated lactate and a normal BSL. The common causes of a HAGMA are toxins, lactic acidosis, renal failure and ketones. In this clinical context the most likely cause is the renal failure, as the patients BSL is normal, lactate only mildly raised and there is no history of toxin ingestion. The renal failure is most likely secondary to the underlying uncontrolled hypertension and exacerbated by the use of an ACE inhibitor. The raised potassium is due to the renal failure and the use of ACE inihibitors.
Agents used in management of hyperkalaemia
|Agent||MOA||Dose||Onset of Action||Duration of Action|
|Stabilisation of myocardium||10ml 10% IV||<5min||30-60min|
|Sodium HCO3||Redistribution||1mEq/kg IV||15min||1-2 hours|
|Salbutamol||Redistribution||10-20mg neb||15min||1 hour|
|Glucose and insulin||Redistribution||50g 25-50ml and 10 units actrapid||20-30min||2-4 hours|
|Calcium Resonium||Elimination||30g oral or rectal||2 hours||4-6 hours|
|Frusemide (fluid overloaded patients)||Elimination||40mg IVI/Oral||1 hour||6 hours|