Background
- Combined hyperkalaemia and AV nodal (Β)blocking meds
- Usually hypovolaemia combined with meds promoting ↑K+ ± renal injury
Pathophysiology
- AV node blockers (Β-blockers, Ca++ antagonists, digoxin, amiodarone and ↑K+) all cause bradycardia
- Combined effect synergistic
- ↓HR → ↓renal perfusion and ↑K+ → ↓HR cycle etc
Clinical
- Symptoms vary from asymptomatic bradycardia to multiorgan failure
- Frequently triggered (elderly especially) with dehydration
- Dehydration → AKI → reduced renal excretion of (AVN blocking) meds
- Bradycardia and shock trigger worsening renal perfusion → vicious cycle
Management
Management of: ↑K+, fluids, and bradycardia.
- Hyperkalaemia (more here): IV calcium, inhaled β agonists, insulin & dextrose
- Check volume state (clinical / US IVC status) and decide if dehydrated or overloaded
- If dehydrated consider Hartmann's (ringers lactate) or isotonic bicarb
- If overloaded, consider early peripheral inotropes (to ↑ renal perfusion) with "dirty adrenaline" prior to inotrope infusion
- Pacing may be ineffective as there is a metabolic cause for the bradycardia
- Involve renal team early ±ITU (± dialysis)