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Digoxin Toxicity Clinical: GIT: N&V, abdo pain CVS: Hypotension Bradycardia: (vagotonic effect) 1st/2nd/3rd degree block Slow AF (rate <60) Increased Automaticity: VE’s, bigeminy SVT/PAT with AV block VT Reverse tick ST depression (lat leads) Short QT Toxicity has been associated with virtually every type of arrhythmia. The 2 general mechanisms by which toxic arrhythmias are produced are: 1. 2. Enhanced atrial automaticity from higher serum digoxin levels can promote tachyarrhythmias and increased ventricular ectopy. Ventricular premature contractions are often early signs of digoxin toxicity but may be nonspecific. Bidirectional ventricular tachycardia and nonparoxysmal junctional tachycardia are strongly suggestive but not pathognomonic. Excessive vagal activity, on the one hand, gives rise to bradyarrhythmias which comprise majority of electrocardiographic changes documented for digoxin toxicity hospitalizations. Toxic digoxin levels may directly affect the sinoatrial node and cause sinus arrest or sinus exit block. Concurrent increased automaticity and vagal tone demonstrated by atrial tachycardia with atrioventricular block is also highly characteristic of toxicity notwithstanding therapeutic drug levels. Although older literature suggest that patients with moderate to severe left ventricular dysfunction are more susceptible to digoxin’s toxic effects, results from the DIG trial failed to demonstrate any differences in the risk of toxicity between subgroups defined by LVEF, cause of Heart failure (i.e., ischemic versus nonischaemic) and New York Heart Association class. However, ventricular arrhythmias may be more common in the presence of structural heart disease owing to enhanced automaticity. Paroxysmal atrial tachycardia is the classic finding in acute digoxin toxicity – an indication of AV nodal conduction delay CNS: Lethargy, confusion/delerium, visual disturbance (yellow discoloration) INVESTIGATION ECG Digoxin Level Confirms poisoning Provides indication for Fab Check 4-6hrs post ingestion then every 2 hrs until resolving U&E: Hyperkalemia OF ANY MAGNITUDE = SEVERE POISONING Levels higher in renal failure Ca/Mg/PO4 Does level help? Not an absolute indicator of toxicity Levels >6hrs since last dose correlate with toxicity (needs time to redistribute) Ie levels in first few hours post dose not reliable Indicators of severity Potentially lethal dose: Adult > 10mg, Child > 4mg K+ > 5.5 = 100% MORTALITY without Fab NB Start usual treatment for hyper-K+, if not working Fab Hypomagnasaemia (increases severity) High level >6hrs post dose ECG changes NB: “DLIF” Digoxin like immunoreactive factor Somepeople have endogenous substance in blood that cross reacts with Digoxin assay May have levels of 0-3ng/ml Commonly seen in neonates, pregnancy, liver & renal failure Management Hyperkalaemia Aim K+ < 5 Insulin/Glucose Actrapid 10 units Glucose 50ml 50% (Children 0.1U/kg and 0.5g/kg) HCO3- (correct acidosis) 100mEq IV bolus (1mEq/kg in kids) AV BLOCK Atropine 0.6mg IV up to 1.8mg (Children 20mcg/kg per dose) EXTERNAL PACING RARELY EFFECTIVE Ventricular Arrhythmias Lignocaine 1mg/kg (max 100mg) over 2 mins Phenytoin, MgSO4 Beware DCR: may induce more unstable rhythm – relatively contraindicated CONTRAINDICATIONS: ISOPRENALINE – increases Ventricular Arrhythmias CLASS Ia drugs: May worsen AV block, potentiate ventricular arrhythmias DCR - relative Calcium for hyperkalaemia? Dunn: “role unclear” Murray “contraindicated” Digoxin blocks Na+/K+ ATPase, which increases intracellular Ca2+ Theoretical risk of giving Ca2+ will increase this iCa2+ further Recent ACEP abstract – no adverse effects Indications for Digibind: ACUTE ARRHYTHMIAS: Refractory, life threatening CARDIAC ARREST: need 20 vials Fab and continue resusc for at least 30min HAEMODYNAMIC INSTABILITY: BP or bradycardia HYPERKALAEMIA: > 6 (NOT DUE TO RENAL FAILURE), Refractory OR: K+ >5.5 AND ECG CHANGES “Steady state” Digoxin level >20 nmol/L ( > 6hrs post dose) Practically = difficult to do, and difficult to interpret Need to marry with clinical situation CHRONIC: LEVEL > 6 nmol/L ARRHYTHMIA: classic = MAT INSTABILITY: Regardless of level (ie low level may NOT reflect clinical picture) ARF or dose Level: Treatment = correct renal failure & stop Dig if no other clinical features (as above) But: K+ often normal (unless in renal failure) DON’T GIVE: Calcium for K+: theoretically bad, although 1 vial = 40mg Lowers serum Digoxin by 1nmol/L Costs $1000! Works within 30min Serum level goes up as more enters circulation from tissue binding sites Levels won’t indicate free Digoxin for 1 week Beware: Rebound hypokalaemia (usually whole body K+ deplete) If Digoxin was used for rate control, Fab may result in Tachyarrhythmias as it wears off. CHRONIC POISONING: Variable severity, still life threatening Untreated mortality 15-30% in 1 week