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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