Download digoxin - Cardiology

DIGOXIN DYSRHYTHMIAS

NO MORTALITY BENEFIT ( DIGITALIS INVESTIGATION GROUP),1997
DIGOXIN

Inhibition of Na+k+-ATPase pump

Parasympathetic activation

Sympathetic inhibition

Inhibition of renin release from the kidney
MORTALITY- undiagnosed digitalis
toxicity

Study DREFIUS AND COLLEAGUES

Atrial tachycardia with block – 100% mortality when digoxin is continued
16% when digoxin is discontinued

Junctional tachycardia- 81% mortality when digoxin continued
16% when digoxin dicontinued
Therapeutic levels

Previous levels : 1 to 2 ng/ml

Current level : 0.5 to 1.5 ng/ml

0.125mg has the similar haemodynamic and autonomic effects like 0.25

Turnaround level : 1ng/ml (modest 6% mortality reduction in levels 0.5 to 0.8
ng/ml, no benefit 0.9 to 1.1 ng/ml, more than 1.2 ng/ml mortality
increased by 12%)
EFFECTS OF DIGOXIN ON ECGTHERAPEUTIC

Prolongation of P-R interval

Slowing of ventricular response in atrial flutter and atrial fibrillation

Isolated A-V junctional escape impulses

Conversion of atrial arrythymias to sinus rhythm
EXCESSIVE OR TOXIC EFFECTS

ATRIAL TACHYCARDIA WITH BLOCK

Non paroxysomal junctional tachycardia

A-V dissociation

Second or third degree A-V Block

SA block

AV junctional rhythm
UNEQUIVOCAL SIGNS

Isolated VPC

Ventricular bigeminy

Multifocal VPC

Ventricular tachycardia

Bidirectional VT

Ventricular fibrillation
THERAPEUTIC
1) ST-T CONFIGURATION
2) P-R PROLONGATION (200 TO
300 MS)
3) AF- VENTRICULAR SLOWING
NODAL ESCAPE( AVERAGE
VENTRICULAR RATE 50 TO 70)
EXCESSIVE
1) SINUU RHYTHM ------ AF or AT
with irregular ventricular
response
2) NODAL TACHYCARDIA WITH
AV DISSOCIATION
3) S-A BLOCK----NODAL
RHYTHM
WITH
RETROGRADE CONDUCTION
TOXIC
1) BIGEMINY
2) MULTI FOCAL VPC OR VPC IN
RUNS
3) BIDIRECTIONAL VT
4) VENTRICULAR FIBRILLATION
4) SECOND DEGREE OR
COMPLETE AV BLOCK
CONTINUE
REDUCE
STOP
Digoxin –sinus node

No change in Automaticity

High doses depression in the automaticity of sinus node(it can also
increase with toxic doses)

Therapeutic doses can impair sinoatrial conduction

Sick sinus syndrome –lengthening of sinus node recovery time and sino
atrial conduction time

If digoxin therapy is indicated in heart failure sss –EPS

Corrected SNRT MORE THAN 1000 IS predictive of further lengthening of
pauses
Digoxin -Atrium

Atrium more sensitive than the sinus node for direct effect on digoxin

Decreased effective refractory period

Increased conduction velocity
Toxic doses – conduction velocity can be decreased
Decreased membrane responsiveness
Digoxin –AV node

Effective refractory period of digoxin is prolonged (combination of vagal
and direct effect)

Conduction velocity is decreased

Decreased amplitude and upstroke velocity of action potential

Therapeutic slowing of ventricular respone is due to decremental
conduction within the node

Second or third degree AV block –digitalis intoxication is due to failure of
propogation within the node
DIGOXIN –His Purkenje system

Increased automaticity –enchanced phase 4 depolarization

Increased excitability

Decreased conduction velocity

Increased effective refractory period
TOXIC DOSES – decreased membrane responsiveness
decreased effective refractory period
DIGOXIN - VENTRICLES

Decreased membrane responsiveness

Increased conduction velocity

Decreased effective refractory period
Low concentration

Resting membrane potential unchanged

Action potential amplitude unchanged

Time of course of depolarization and repolarization remains unchanged
High concentrations

Progressive loss of resting potential

Decreased upstroke of action potential

Shortening of plateau phase

Increased rate of spontaneous diastolic depolarization
SA BLOCK

Even in therapeutic doses

Recognised by
sinus rhythm
group beating
shortened PP interval
pause less than twice the shortest PP cycle
ATRIAL TACHYCARDIA WITH BLOCK

Block secondary to lengthening AV node refractory period and rapid atrial
rate

When digoxin is discontinued conduction improves before converting to
sinus rhythm – brief period of 1:1 conduction

Ventriculo phasic behavior of P’ P’ interval

P’P’ interval containing R wave is shorter than P’P’ interval without the R
wave
JUNCTIONAL TACHYCARDIA

Underlying rhythm can be sinus, atrial fibrillation, atrial flutter, atrial
tachycardia

Retrograde conduction is usually absent due to AV block created by
digitalis

V1 – QRS morphology helps to differentiate between junctional
tachycardia from fascicular VT
FASCICULAR VENTRICULAR
TACHYCARDIA
QRS width narrower than usual
Rsr’ pattern in V1
ANTEROSUPERIOR FASICLE-right axis deviation
POSTERO INFERIOR FASCICLE-left axis deviation
Bidirectional ventricular tachycardia

Beat to beat alteration of normal QRS AXIS IN LIMB LEADS

QRS width narrower than usual

Ventricular rate 140 to 180/m

QRS ALTERNANS in V1

Mortality 100%

Triggered activity due to DAD is the predominant cause
Ventricular bigeminy

Mc manifestations of digoxin overdosage – ventricular extrasystoles

They are not diagnostic of digoxin toxicity
Concealed ventricular bigeminy
Concealed ventricular bigeminy
Digitalis effect

Prolonged PR interval

ST segment depression

Decreased amplitude of T waves

Shortened QT

Increased U wave amplitude
Digitalis effect and toxicity

Digoxin effect

Digoxin toxicity

Inverse check mark sign of ST manifest
in leads which have dominant upright
QRS ONLY

Inverse check mark sign of ST manifest
in leads which have dominant upright
QRS ONLY as well as leads with
dominant negative QRS

Downward slope of ST begins from
isoelectric base

If the beginning of the ST is already
depressed it denotes toxicity or
primary ST depression such as
ischaemia

T wave raises above the baseline
before becoming isoelectric

T wave does not raises above the
baseline
Increased sr digoxin levels

Lean body mass

Decreased renal excretion
hypokalemia ,beta blockers ,congestive heart failure ,renal disease
,elderly patients

Decreased non renal clearance
quinidine,verapamil,amiodarone,propafenone

Decreased conversion in the gut
erythromycin,tetracycline