Download Digoxin Toxicity

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