Cardiac Glycosides

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Chapter: Essential pharmacology : Cardiac Glycosides and Drugs for Heart Failure

These are glycosidic drugs having cardiac inotropic property. They increase myocardial contractility and output in a hypodynamic heart without a proportionate increase in O2 consumption.



These are glycosidic drugs having cardiac inotropic property. They increase myocardial contractility and output in a hypodynamic heart without a proportionate increase in O2 consumption. Thus, efficiency of failing heart is increased. In contrast, ‘cardiac stimulants’ (Adr, theophylline) increase O2 consumption rather disproportionately and tend to decrease myocardial efficiency, i.e. increase in O2 consumption is more than increase in contractility. Further, cardiac stimulants also increase heart rate and have a short-lived action, while cardiac glycosides do not increase heart rate and have a prolonged action.


William Withering, a Birmingham physician, learnt that a decoction containing ‘foxglove’ ( Digitalis) with other herbals, prepared by an old lady, relieved dropsy. He tried extract of foxglove alone and found it to be remarkably effective in some cases. He published his classic monograph ‘An account of the Foxglove and some of its medicinal uses: with practical remarks on dropsy and other diseases’ in 1785 and ascribed the beneficial effect to an action on the kidney. Later Digitalis was used indiscriminately, disregarding the precautions mentioned by Withering; was found to be toxic and fell into disrepute. Cushney and Mackenzie, in the beginning of 20th century, established its action on the heart and its use in congestive heart failure (CHF). Strophanthus was used as an arrow poison in Africa. Fraser discovered its digitalis like action in 1890. The use of Squill has come from Egyptian medicine, Toad skin from Chinese medicine and Thevetin from Unani medicine. Cases of poisoning with Thevetia and Convallaria are occasionally seen.



By convention, ‘Digitalis’ is applied as a collective term for the whole group and has come to mean ‘a cardiac glycoside’.




All are glycosides; consist of an aglycone (genin) to which are attached one or more sugar (glucose or digitoxose) moieties. The pharmacological activity resides in the aglycone, but attached sugars modify solubility and cell permeability. In general, aglycones have shortlived and less potent action.


The aglycone consists of a cyclopentanoperhydrophenanthrene (steroid) ring to which is attached a 5 or 6 membered unsaturated lactone ring. One or more hydroxyl and other substitutions are present on the aglycone and determine its polarity, e.g. digoxigenin has an additional OH group than digitoxigenin and is more polar.



Pharmacological Actions


All digitalis glycosides have qualitatively similar action; there are only quantitative and pharmacokinetic differences. Digoxin is described as prototype.




Digitalis has direct effects on myocardial contractility and electrophysiological properties. In addition, it has vagomimetic action, reflex effects due to alteration in haemodynamics and direct CNS effects altering sympathetic activity.


Force of contraction Digitalis causes a dose dependent increase in force of contraction of heart—a positive inotropic action. This is especially seen in the failing heart which is exquisitely sensitive. There is increased velocity of tension development and higher peak tension can be generated. Systole is shortened, diastole is prolonged. When a normal heart is subjected to increased impedance to outflow, it generates increased tension so that stroke volume is maintained upto considerably higher values of impedance (Fig. 37.1), while the failing heart is not able to do so and the stroke volume progressively decreases. The digitalized failing heart regains some of its capacity to contract more Forcefully when subjected to increased resistance to ejection. There is more complete emptying of failing and dilated ventricles—cardiac output is increased.



Digitalis increases force of contraction in normal heart as well, but this is not translated into increased output, because the normal heart empties nearly completely even otherwise and reduction of end diastolic volume is counterproductive.


Tone It is defined by the maximum length of the fibre at a given filling pressure, or the resting tension in the muscle fibre. This is not affected by therapeutic doses of digitalis. However, digitalis does decrease end diastolic size of a failing ventricle, but this is a consequence of better ventricular emptying and a reduction in filling pressure.


Rate Heart rate is decreased by digitalis. Bradycardia is more marked in CHF patients: improved circulation (due to positive inotropic action) restores the diminished vagal tone and abolishes sympathetic overactivity. In addition, digitalis slows the heart by vagal and extravagal actions.


Vagal tone is increased:


·      Reflexly through nodose ganglion and sensitization of baroreceptors.

·      Direct stimulation of vagal centre.

·      Sensitization of SA node to ACh


Extravagal: A direct depressant action on SA and AV nodes.


The vagal action manifests early and can be blocked by atropine, whereas the extravagal action becomes prominent later and cannot be reversed by atropine.


Electrophysiological Properties


The electrophysiological effects of digitalis on different types of cardiac fibres differ quantitatively and qualitatively. The Purkinje fibres, automatic and conducting tissues are more sensitive. In addition to direct effects, the indirect autonomic influences are important in the in situ heart.


(a) Action potential (AP ): The effects are illustrated diagrammatically in Fig. 37.2. The resting membrane potential (RMP), is progressively decreased (shifted towards isoelectric level) with increasing doses—excitability is enhanced at low doses (due to reduction of gap between RMP and threshold potential) but depressed at toxic doses (depolarization to below the level of critical potential which inactivates the fast channels).


The rate of 0 phase depolarization is reduced. This action is most marked in AV node and bundle of His.


The slope of phase4 depolarization is increased in the PFs—ectopic automaticity is enhanced—latent pacemakers become overt at high doses → extrasystoles. High doses of digitalis produce coupled beats by another mechanism: the RMP shows oscillations during phase-4; when their magnitude is sufficient enough, delayed after-depolarizations result (see Fig. 38.1). The SA and A-V node automaticity is reduced at therapeutic concentrations by vagal action which hyperpolarizes these cells and reduces their phase-4 slope. Toxic doses markedly reduce RMP of SA nodal cells by direct action and stop impulse generation.


(b) Effective Refractory Period (ERP):



Ventricle—ERP is abbreviated by direct action.


(c) Excitability: Enhanced at low doses but depressed at high doses as explained above.


(d) Conduction: AV conduction is demonstrably slowed by therapeutic doses due to a reduction in the rate of 0 phase depolarization. At high doses, intraventricular conduction in PFs is also depressed by uncoupling of gap junctions.

(e) ECG : Therapeutic doses of digitalis produce changes in the ECG. These are accentuated at high doses—may also produce arrhythmias. The changes are:


Decreased amplitude or inversion of T wave.

Increased PR interval (slowing of AV conduction), AV block at toxic doses.

Shortening of QT interval (reflecting shortening of systole).

Depression of ST segment (at high doses— due to interference with repolarization).


The abnormal QRS of Wolff-ParkinsonWhite (WPW) syndrome is widened because conduction through the normal AV bundle is slowed but not that through the aberrant pathway.


Mechanism Of Action


Digitalis increases force of cardiac contraction by a direct action independent of innervation. It selectively binds to extracellular face of the membrane associated Na+K+ ATPase of myocardial fibres and inhibitis this enzyme (Fig. 37.3). Inhibition of this cation pump results in progressive accumulation of Na+ intracellularly. This indirectly results in intracellular Ca2+ accumulation.



During depolarization Ca2+ ions enter the cell driven by the steep Ca2+ gradient (>1 mM extracellular to < 100 nM cytosolic during diastole) through voltage sensitive Ca2+ channels. This triggers release of Ca2+ stored in sarcoplasmic reticulum (SR) cytosolic Ca2+ increases transiently to about 500 nM (calcium transients) triggers contraction. Ca2+ is then actively taken up by SR and a fraction (equal to that which entered from outside during depolarization) is extruded mainly by 3Na+/1Ca2+ exchange transporter (NCXantiporter) as well as by sarcolemmal Ca2+ pump (Ca2+ ATPase). During phase 3 of AP membrane Na+K+ATPase moves 3 intracellular Na+ ions for 2 extracellular K+ ions. The slight (1–1.5 mM) increase in cytosolic Na+ over normal (8–10 mM) due to partial inhibition of Na+K+ATPase by digitalis reduces transmembrane gradient of Na+ which drives the extrusion of Ca2+. The excess Ca2+ remaining in cytosol is taken up into SR which progressively get loaded with more Ca2+ subsequent calcium transients are augmented.


The relationship of cytosolic [Na+] and [Ca2+] is such that a small percentage increase in Na+ concentration leads to a large percentage increase in Ca2+ concentration.


Moreover, raised cytosolic Ca2+ induces greater entry of Ca2+ through voltage sensitive Ca2+ channels during the plateau phase. It has been shown that 1 mM rise in cytosolic [Na+] results in 20–30% increase in the tension developed by ventricular fibres.


Binding of glycoside to Na+K+ATPase is slow. Moreover, after Na+K+ATPase inhibition, Ca2+ loading occurs gradually. As such, inotropic effect of digitalis takes hours to develop, even after i.v. administration.


Inhibition of Na+K+ ATPase is clearly involved in the toxic actions of digitalis. At high doses, there is depletion of intracellular K+; toxicity is partially reversed by infusing K+. Excessive Ca2+ loading of SR results in spontaneous cycles of Ca2+ release and uptake producing oscillatory afterdepolarizations and aftercontractions. Since both therapeutic and toxic effects of digitalis are due to myocardial Ca2+ loading, these are inseparable and therapeutic index is low.


Blood Vessels


Digitalis has mild direct vasoconstrictor action—peripheral resistance is increased in normal individuals. However, in CHF patients this is more than compensated by the indirect effect of improvement in circulation, i.e. reflex sympathetic overactivity is withdrawn and a net decrease in peripheral resistance occurs. Venous tone is improved in normal individuals as well as in CHF patients.


Digitalis has no prominent effect on BP: systolic BP may increase and diastolic may fall in CHF patients—pulse pressure increases. Hypertension is no contraindication to the use of digitalis.


Despite a weak direct coronary constrictor action, therapeutic doses of digitalis have no significant effect on coronary circulation— coronary insufficiency is no contraindication to its use. Coronary debt may even decrease if ventricles were in a dilated state.




Diuresis is seen promptly in CHF patients, secondary to improvement in circulation and renal perfusion. The retained salt and water is gradually excreted. No diuresis occurs in normal individuals or in patients with edema due to other causes.




Digitalis has little apparent CNS effect in therapeutic dose. Higher doses cause CTZ activation nausea and vomiting. Still higher doses produce hyperapnoea, central sympathetic stimulation, mental confusion, disorientation and visual disturbances.




The pharmacokinetic properties of digoxin and digitoxin are presented in Table 37.1.



Digitoxin is the most lipid soluble, digoxin is relatively polar, while ouabain has the highest polar character. Bioavailability of digoxin tablets from different manufacturers may differ. Presence of food in stomach delays absorption of digoxin as well as digitoxin.


The volume of distribution of cardiac glycosides is large, e.g. 6–8 L/Kg in case of digoxin. All are concentrated in the heart (~20 times than plasma), skeletal muscle, liver and kidney.



Digitoxin is primarily metabolized in liver, partly to digoxin, and undergoes some enterohepatic circulation. Digoxin is primarily excreted unchanged by the kidney: mainly by glomerular filtration; rate of excretion is altered parallel to creatinine clearance. Its t½ is prolonged in elderly patients and in those with renal insufficiency: dose has to be reduced. Dose of digitoxin is not greatly altered in renal failure.


Cardiac glycosides are cumulative drugs. When maintenance doses are given from the beginning, steady state levels and full therapeutic effect are attained after 4 × t½, i.e. 6–7 days for digoxin and 4 weeks for digitoxin.




1. Digoxin: DIGOXIN 0.25 mg tab., 0.05 mg/ml pediatric elixir, 0.5 mg/2 ml inj. LANOXIN 0.25 mg tab, CARDIOXIN, DIXIN 0.25 mg tab, 0.5 mg/2 ml inj.


2. Digitoxin: DIGITOXIN 0.1 mg tab.


All glycosides have the same safety margin; choice of preparation depends on kinetic properties. Digoxin is well absorbed orally, has reasonably quick action, intermediate t½, dose adjustments are possible in 2–3 days, can be used for routine treatment as well as emergency; in case of toxicity—discontinuation of the drug produces reasonably rapid disappearance of manifestations. Thus, it is an all purpose and most commonly used glycoside.


Digitoxin may be used for maintenance; because of its long t½, diurnal fluctuations in blood level are low. However, any dose adjustment takes weeks and toxic effects are more persistent. Therefore, most physicians prefer digoxin for maintenance therapy also.


Adverse Effects


Toxicity of digitalis is high, margin of safety is low (therapeutic index 1.5–3). Higher cardiac mortality has been reported among patients with steadystate plasma digoxin levels > 1.1 ng/ml during maintenance therapy. About 25% patients develop one or other toxic symptom. The manifestations are:


Extracardiac: Anorexia, nausea, vomiting and abdominal pain are usually reported first: are due to gastric irritation, mesenteric vasoconstriction and CTZ stimulation. Fatigue, no desire to walk or lift an arm, malaise, headache, mental confusion, restlessness, hyperapnoea, disorienta tion, psychosis and visual disturbances are the other complaints. Diarrhoea occurs occasionally. Skin rashes and gynaecomastia are rare.


Cardiac: Almost every type of arrhythmia can be produced by digitalis: pulsus bigeminus, nodal and ventricular extrasystoles, ventricular tachycardia and terminally fibrillation. Partial to complete AV block may be the sole cardiac toxicity or it may accompany other arrhythmias. Severe bradycardia, atrial extrasystoles, AF or AFl have also been noted. In about 2/3 patients showing toxicity, extracardiac symptoms precede cardiac; in the rest serious cardiac arrhythmias are the first manifestation. The central actions of digitalis appear to contribute to the development of arrhythmias by inducing fast and irregular activity in the cardiac sympathetic and vagus nerves.




Further doses of digitalis must be stopped at the earliest sign of toxicity; nothing more needs to be done in many patients, especially if the manifestations are only extracardiac.


(a) For Tachyarrhythmias: When they are caused by chronic use of digitalis and diuretics (both induce K+ depletion)—infuse KCl 20 m.mol/hour (max. 100 m. mol) i.v. or give orally in milder cases. K+ tends to antagonize digitalis induced enhanced automaticity and decreases binding of the glycosides to Na+K+ATPase by favouring a conformation of the enzyme that has lower affinity for cardiac glycosides. When toxicity is due to acute ingestion of large doses of digitalis, plasma K+ may be high; it should not be given from outside. In any case, it is desirable to measure serum K+ to guide KCl therapy. K+ is contraindicated if higher degree of AV block is present: complete AV block and ventricular asystole can be precipitated.


(b) For Ventricular Arrhythmias: Lidocaine i.v. repeated as required is the drug of choice. It suppresses the excessive automaticity, but does not accentuate AV block. Phenytoin is also effective but seldom used now, because sudden deaths have occurred when it was injected i.v. in digitalis intoxicated patients. Quinidine and procainamide are contraindicated.


(c) For Supraventricular Arrhythmias: Propranolol may be given i.v. or orally depending on the urgency.


(d) For AV Block And Bradycardia: Atropine 0.6–1.2 mg i.m. may help; otherwise cardiac pacing is recommended.


Cardioversion by DC shock is contraindicated because severe conduction defects may be unmasked in the digitalis intoxicated heart. Attempts to enhance the elimination of digitalis by diuretics or haemodialysis are not very effective.


Digoxin Antibody


Developed for measuring plasma concentration of digoxin by radioimmunoassay, it has been found effective in treating toxicity as well. Digoxin specific antibody cross-reacts with digitoxin also. The Fab fragment has been marketed in Europe as DIGIBIND (38 mg vial). It is nonimmunogenic because it lacks the Fc fragment. Given by i.v. infusion it has markedly improved the survival of seriously digitalis intoxicated patients. The digoxin-Fab complex is rapidly excreted by kidney.


Precautions And Contraindications


·      Hypokalemia: enhances digitalis toxicity by increasing its binding to Na+K+ ATPase.


·      Elderly, renal or severe hepatic disease: patients are more sensitive.


·   Myocardial infarction: severe arrhythmias are more likely. Digitalis should be used after MI only when heart failure is accompanied with AF and rapid ventricular rate.


·   WolffParkinsonWhite syndrome: Digitalis is contraindicated—decreases the ERP of bypass tract in 1/3 patients. In them rapid atrial impulses may be transmitted to ventricles VF may occur. Digitalis can increase the chances of reentry by slowing conduction in the normal AV bundle and accelerating it in the aberrant pathway.




·    Diuretics: cause hypokalemia which can precipitate digitalis arrhythmias; potassium supplements may be given prophylactically.


·       Calcium: synergises with digitalis precipitates toxicity.


·      Quinidine: reduces binding of digoxin to tissue proteins as well as its renal and biliary clearance by inhibiting efflux transporter Pglycoprotein plasma concentration is doubled toxicity can occur. Verapamil, diltiazem, captopril and amiodarone: increase plasma concentration of digoxin to variable extents.


·      Adrenergic drugs: can induce arrhythmias in digitalized patients; both increase ectopic automaticity.


·     Digoxin absorption can be reduced by metoclopramide (gastrointestinal hurrying) and sucralfate which adsorbs digoxin. Antacids, neomycin, sulfasalazine also can reduce digoxin absorption; stagger their administration.




The two main indications of digitalis are CHF and control of ventricular rate in atrial fibrillation/flutter.


1. Congestive heart failure


CHF occurs when cardiac output is insufficient to meet the demands of tissue perfusion. Heart failure may primarily be due to systolic dysfunction or diastolic dysfunction.


Systolic Dysfunction The ventricles are dilated and unable to develop sufficient wall tension to eject adequate quantity of blood. This occurs in ischaemic heart disease, valvular incompetence, dilated cardiomyopathy, myocarditis, tachyarrhythmias.


Diastolic Dysfunction The ventricular wall is thickened and unable to relax properly during diastole; ventricular filling is impaired because of which output is low. It occurs in sustained hypertension, aortic stenosis, congenital heart disease, AV shunts, hypertrophic cardiomyopathy.


However, most patients, especially longstanding CHF, have both systolic and diastolic dysfunction. Cardiac glycosides primarily mitigate systolic dysfunction. Best results are obtained when myocardium is not primarily deranged, e.g. in hypertension, valvular defects or that due to rapid heart rate in atrial fibrillation. Poor response and more toxicity is likely when the myocardium has been damaged by ischaemia, inflammation or degenerative changes and in thiamine deficiency, as well as in high output failure (in anaemia).


Cardiac glycosides are incapable of reversing the pathological changes of CHF or even arresting their progress. Associated with hypertrophy, cardiac muscle undergoes remodeling which may involve shift of isoforms of various functional proteins such as myosin, creatine kinase, Na+K+ATPase, etc. Cardiac glycosides do not affect remodeling.


Because of lower inotropic state, the failing heart is able to pump much less blood at the normal filling pressure (Fig. 37.4), more blood remains in the ventricles at the end of systole. The normal venous return is added to it and Frank-Starling compensation is utilized to increase filling pressure: the heart may be able to achieve normal stroke volume, but at a filling pressure which produces congestive symptoms (venous engorgement, edema, enlargement of liver, pulmonary congestion dyspnoea, renal congestion oliguria).



Digitalis induced enhancement of contractility increases ventricular ejection and shifts the curve relating stroke output to filling pressure towards normal, so that adequate output may be obtained at a filling pressure that does not produce congestive symptoms. Improved tissue perfusion results in withdrawal of sympathetic overactivity


heart rate and central venous pressure (CVP) are reduced. Compensatory mechanisms retaining Na+ and water are inactivated diuresis edema is cleared. Liver regresses, pulmonary congestion is reduced dyspnoea abates, cyanosis disappears. Low output symptoms like decreased capacity for muscular work are mitigated.

A dilated ventricle automatically becomes inefficient according to Laplace equation.


Wall tension = Intraventricular Pressure × Ventricular Radius


i.e. to generate the same ejection pressure a dilated ventricle has to develop higher wall tension. By reducing end diastolic volume (due to better emptying), digitalis restores efficiency of translation of cardiac work into cardiac output. That is why O2 consumption does not increase proportionately.


Dosage The dosing schedule and route depend on the desired speed of action and the factors which govern individual susceptibility. Generally, higher dose is needed for more severe CHF.


There is some recent evidence that maintenance therapy with submaximal inotropic doses (producing steady stage digoxin levels < 1 ng/ml) may benefit by counteracting neurohumoral activation of CHF without risk of toxicity.


Slow Digitalization In most mild to moderate cases, maintenance dose of digoxin (0.125–0.25 mg/day) is given from the beginning. Full response takes 5–7 days to develop, but the procedure is much safer. In case adequate response is not seen after 1 week, increase the dose to 0.375 and then to 0.5 mg after another week. Evaluation of adequate response is primarily clinical. Relief of signs and symptoms of failure, reduction of heart rate and body weight to normal are the best guide. Bradycardia (HR < 60/min) is an indication for stopping further medication. ECG changes are not valuable in quantitation of doses unless arrhythmias occur.


Rapid Oral Digitalization Digoxin 0.5–1.0 mg stat followed by 0.25 mg every 6 hours with careful monitoring and watch for toxicity till response occurs—generally takes 6–24 hours (total dose 0.75–1.5 mg). This is seldom practised now.


Emergent I.V. Digitalization It is practised rarely now, only as a desperate measure in CHF or in atrial fibrillation. Digoxin 0.25 mg followed by 0.1 mg hourly is given by slow i.v. injection with close ECG, BP and CVP monitoring till response occurs (2–6 hours, total dose 0.5–1.0 mg).


Current status of digitalis Before the introduction of high ceiling diuretics and ACE inhibitors, digitalis was considered an indispensible part of anti-CHF treatment. It is not so now. Many mild-to-moderate cases can be managed without digitalis, i.e. with diuretics and vasodilators, especially an ACE inhibitor. Lately, β blockers have got added to the standard therapy. Emergency i.v. use of digoxin for CHF is practically extinct. However, digitalis is still the most effective drug capable of restoring cardiac compensation, especially in patients with dilated heart and low ejection fraction; all patients not controlled by ACE inhibitor/AT1 receptor blocker, blocker and diuretic should be treated with digitalis. Uncertainty exists in the area of maintenance therapy, i.e. after decompensation has been corrected in patients not having atrial fibrillation (AF). There has been a trend to discontinue digitalis once compensation has been restored, especially in mild-to-moderate cases.


Two large randomized trials—Randomized assessment of digoxin on inhibition of angiotensin converting enzyme (RADIANCE, 1993) and Prospective randomized study of ventricular failure and efficacy of digoxin (PROVED, 1993) on CHF patients in sinus rhythm showed that discontinuation of digitalis resulted in reduced exercise capacity and haemodynamic deterioration in a significant number of cases despite continued use of diuretic with or without ACE inhibitor. A trend has emerged in favour of maintenance ACE inhibitor and digitalis therapy with intermittent symptom based use of diuretics. However, the trials referred above also showed that digitalis can be withdrawn without haemodynamic deterioration in 60% (not receiving ACE inhibitor) and in 72% (receiving ACE inhibitor) patients.


If stable clinical state has been maintained for 2–3 months, withdrawal of digitalis may be attempted. Early reinstitution of digitalis is recommended if cardiac status declines. Continued digitalis therapy is the best course in CHF patients with atrial fibrillation.


Large studies including those by Digoxin Investigation Group (DIG) have found no evidence that digitalis decreases overall mortality in CHF patients, though episodes of decompensation and heart failure deaths are reduced. The two major limitations in the use of cardiac glycosides are low margin of safety and inability to reverse/retard the processes which cause the heart to fail.

2. Cardiac Arrhythmias


Atrial Fibrillation (AF) Digitalis is the drug of choice for controlling ventricular rate in AF, whether associated with CHF or not. However, it is incapable of curing AF, i.e. does not revert it to sinus rhythm, even perpetuates it.


Digitalis reduces ventricular rate in AF by decreasing the number of impulses that are able to pass down the AV node and bundle of His.


It increases ERP of AV node by direct, vagomimetic and antiadrenergic actions: the minimum interval between consecutive impulses that can successfully traverse the conducting tissue is increased.


A degree of AV block is naturally established in AF. Because of the relatively long ERP of AV node, many of the atrial impulses (~500/min) impinge on it while it is still refractory; others falling early in the relative refractory period get extinguished by decremental conduction. These concealed impulses, nevertheless, leave the upper margin of AV node refractory for a further period. Thus, any influence which increases rate of AF, by itself reduces ventricular rate. Digitalis decreases average atrial ERP and temporally disperses it (vagal action), thereby increasing fibrillation frequency and indirectly prolonging the interval between any two impulses that are successfully conducted to the ventricle.


When digitalis is given in AF, average ventricular rate decreases in a dose-dependent manner and pulse deficit is abolished because ventricle does not receive an impulse very early in diastole before it has had time to fill up reasonably. The therapeutic endpoint can be clearly defined: the dose should be adjusted to a ventricular rate of 70–80/min at rest. If this is not possible with digitalis alone, a β blocker or verapamil may be added.


Atrial Flutter (AFI) The atrial rate is 200–350/ min (less than that in AF), but atrial contractions are regular and synchronous. A variable degree of AV block, depending on the mean ERP of AV node, is naturally established. Digitalis enhances this AV block, reduces ventricular rate and prevents sudden shift of AV block to a lower degree (as may occur during exercise or sympathetic stimulation). Digitalis may convert AFl to AF by reducing atrial ERP and making it inhomogeneous. This is a welcome response because control of ventricular rate is easier in AF (graded response occurs) than in AFl (AV block shifts in steps). In nearly ½ of the patients when digitalis is stopped, this induced AF reverts to sinus rhythm since the cause of atrial inhomogeneity is gone. Alternatively, AFl may be terminated by cardioversion/radiofrequency ablation and its recurrence prevented by subsequent digitalis treatment.


Paroxysmal Supraventricular Tachycardia (PSVT) It is a common arrhythmia with a rate 150–200/ min and 1 : 1 AV conduction. It is mostly due to reentry involving the SA or AV node. Rigidly circumscribed magnitudes of ERP and conduction velocity are required for its persistence. A parenteral glycoside may be injected i.v.— increases vagal tone and depresses the path through the SA/AV node, or the ectopic focus, and terminates the arrhythmia (success in 1/3 cases). Verapamil/adenosine are more effective, less toxic and act faster. Digitalis is now reserved for preventing recurrences in selected cases.


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