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The document discusses cardiac glycosides and their use in treating congestive cardiac failure (CCF). It describes the mechanism of action of digoxin, noting that it increases myocardial contractility and reduces heart rate. Adverse effects and management of digoxin toxicity are also summarized. The document outlines the therapeutic uses of digoxin in CCF and arrhythmias like atrial fibrillation.

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Autacoids • Angiotensin • Kinins CCF 10/16/2019 1PATKI PHARMACOLOGY OF CCF
AT the end of the two sessions, students should be able to • Derive the signs and symptoms of Cardiac failure • Enumerate drugs used in CCF • Describe the mechanism of action of Digoxin in CCF. • Describe the role of vasodilators, Diuretics CCBs, ACE inhibitors in CCF, • Describe management of Chronic heart failure and Acute congestive cardiac failure. 10/16/2019 2PATKI
Heart Failure Click to open ! Heart Failure- Clinical syndrome … can result from any structural or functional cardiac disorder that impairs ability of ventricle to fill with or eject blood Impact! 5 million - have heart failure • 500,000 new cases every year • 25-50 billion dollars a year to care for people with HF • 6,500,000 hospital days / year and 300,000 deaths/year 10/16/2019 3PATKI
Definition-Heart Failure (HF) Key Concepts • CO = SV x HR-becomes insufficient to meet metabolic needs of body • SV- determined by preload, afterload and myocardial contractility • EF< 40% (need to understand) • *Classifications HF – Systolic failure- dec. contractility – Diastolic failure- dec. filling – Mixed 10/16/2019 4PATKI
90/140= 64% EF- 55-65 (75) normal Click for animated EF 10/16/2019 5PATKI
Preload • Volume of blood in ventricles at end diastole • Depends on venous return • Depends on compliance Afterload •Force needed to eject blood into circulation •Arterial B/P, pulmonary artery pressure •Valvular disease increases afterload Factors effecting heart pump effectiveness 10/16/2019 6PATKI
Cardiomegaly/ventricular remodeling occurs as heart overworked> changes in size, shape, and function of heart after injury to left ventricle. Injury due to acute myocardial infarction or due to causes that inc. pressure or volume overload as in Heart failure10/16/2019 7PATKI
Right Heart Failure • Signs and Symptoms –fatigue, weakness, lethargy –wt. gain, inc. abd. girth, anorexia, pain –elevated neck veins –Hepatomegaly –may not see signs of LVF 10/16/2019 8PATKI
What does this show? 10/16/2019 9PATKI
What is present in this extremity, common to right sided HF? 10/16/2019 10PATKI
Cardiac Glycosides 10/16/2019 11PATKI
Cardiac Glycosides Digitalis purpurea (Fox glove) aglycone Seeds of strophanthus gratus Strophanthin-G & Ouabain 10/16/2019 12PATKI
MOA of cardiac glycosides 10/16/2019 13PATKI
MOA of cardiac glycosides 10/16/2019 14PATKI RYANODINE RECEPTOR
Pharmacological actions of digitalis 1. Cardiac 2. Extra cardiac Cardiac actions – (more prominent in failing heart) Direct action on the heart (by inhibiting Na+ /K+ ATPase) and Indirect actions on the heart by stimulating Vagus (vagomimetic) Myocardial contractility → +ve Inotropic effect – “Cardiotonic” ↑ Force of contraction of the myocardium (more prominent in failing heart) Digitalized heart contracts more forcibly and completely This causes complete emptying of the ventricles during systole and ↑ CO This ↓ pulmonary congestion and systemic venous pressure Diastolic size of the heart is reduced – size of the muscle fibre length also reduced ↓ oxygen requirement of myocardium The digitalized heart, thus, can do more work for the same energy expenditure10/16/2019 15PATKI
Heart rate – causes bradycardia (more marked in CHF patients) Reduces HR (-ve chronotropic effect) by direct and indirect action (small dose) Extravagal – direct depressant action on SA and AV nodes Electrophysiological properties – differs with the cardiac fibres Action Potential – RMP progressively ↓  Excitability ↑ at low doses (↓ gap between RMP & TP) but depressed at toxic dose  The slope of phase 4 depolzn ↑ in PFs & ventricular muscle – ectopic automcity. Results in ventricular extra systoles, Coupled beats (due to delayed after d)  ERP – ↑ at AV node & bundle of His 10/16/2019 16PATKI
Conduction velocity Conduction through AV node depressed (by both action) ECG ↑ 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 Ĉ repolarzn) 10/16/2019 17PATKI
Blood vessels – digitalis has mild direct vasoconstrictor action – not significant Extra cardiac actions Kidney – digitalis causes diuresis in CHF secondary to improvement in circulation and renal perfusion (no diuresis in patients with edema due to other causes) CNS- in high doses – CTZ activation – vomiting, central sympathetic stimulation, confusion, disorientation, blurring of vision GIT – Anorexia, nausea, vomiting (CTZ stimulation and direct action on the gut) 10/16/2019 18PATKI
Pharmacokinetics Digoxin / Digitoxin commonly used glycoside – administered by oral route food delays the absorption, widely distributed, concentrated in heart, liver, kidney and skeletal muscle crosses BBB mainly excreted unchanged in urine (digoxin- filtered at the glomeruli) (dose adjust-renal fail) Cardiac glycosides are cumulative drugs Steady state levels and full therapeutic effect with daily maintenance from the beginning are attained after 6-7 days for digoxin and 4 weeks for digitoxin (after 4xt1/2 ) Preparations Digoxin – 0.25mg tab, 0.5mg/2ml inj 0.05mg/ml paediatric elixir Used for routine and in emergency Digitoxin – 0.1mg tab Used for maintenance (long t1/2) 10/16/2019 19PATKI
Adverse effects Toxicity of digitalis is high – margin of safety is low (Therapeutic Index is 1.5 - 3) Extra cardiac A/E Anorexia, nausea, vomiting, fatigue, mental confusion, restlessness, psychosis, visual disturbances, diarrhoea, skin rashes, gynecomastia(rare) Cardiac A/E Bradycardia, partial/complete heart block, coupled beats (bigeminy), ventricular extrasystoles/tachycardia/fibrillation, atrial extrasystoles, AF Factors affecting digitalis toxicity Age, IV digitalization, hypokalemia, hypercalcaemia, hypomagnesaemia, Hyper/hypothyroidism, renal failure, myocarditis (predisposing factors) 10/16/2019 20PATKI
Management of digitalis toxicity  Potassium supplementation – mild toxicity KCl 5gm daily oral tid More serious arrhythmias - IV infusion KCl 20m.mol/hr Stop digoxin and K depleting diuretics  Supraventricular arrhythmias – treated with oral/IV propranolal  Ventricular arrhythmias – Lignocaine IV (suppresses excessive automaticity and doesn't accentuate AV block)  AV block and bradycardia – Atropine 0.6 – 1.2mg im /cardiac pacing 10/16/2019 21PATKI
Digoxin antibodies (Digibind) Used in serious digitalis toxicity It neutralizes circulating digitalis - given IV - rapidly reverses the toxicity (40mg neutralises 0.6mg of digoxin stored in the body) But very expensive 10/16/2019 22PATKI
Contraindications a. Hypokalemia b. Elderly, associated disease like renal/hepatic disease c. MI except when HF with AF and rapid ventricular rate d. Hyper / hypothyroidism (slow elimination) e. Partial AV block f. Myocarditis (more prone to arrhythmias) g. Wolff-Parkinson-White syndrome – Digitalis may enhance transmission through bypass tract and ↑ transmission of rapid atrial impulses to ventricles - VF 10/16/2019 23PATKI
Drug interactions 10/16/2019 24PATKI
Therapeutic Uses 1. Congestive Heart Failure 2. To control ventricular rate in AF/AFl Low output failure especially when associated with AF. It is ineffective in high output failure – severe anaemia, thyrotoxicosis and A-V shunt Subsides pulmonary congestion – provides relief from dyspnoea ↑ Urinary output- ↓ edematous fluid by ↑ing renal perfusion Engorged tender liver regresses and engorgement of neck veins disappear because of diminished systemic venous pressure Mild to moderate cases – slow digitalization Digoxin 0.125-0.25mg/day from the beginning (maintenance dose) Relief of signs and symptoms like ↓HR, bradycardia(HR<60 stop drug) 10/16/2019 25PATKI
Therapeutic Uses Rapid oral digitalization – Digoxin 0.5mg – 1mg stat, followed by 0.25mg every 6 hrs till response occurs (6-24 hrs) – seldom practised Emergent IV digitalization – Digoxin 0.25mg followed by 1mg hrly slow IV injection with close monitoring till response occurs(2-6hrs) (total dose 0.5mg-1mg) – rarely practised Digitalis still most effective drug, especially in patients with dilated heart and low ejection fraction (systolic dysfunction) Mild to moderate cases can be managed without digitalis – with diuretics , vasodilators (like ACE inhibitor) and β blockers. 10/16/2019 26PATKI
Therapeutic Uses Cardiac arrhythmias Atrial Fibrillation (500 beats/min) To control ventricular rate – protects the ventricles from the too rapid atrial impulses by depressing AV conduction Ventricular rate of 70-80 not achieved – verapamil /β blockers may be added Atrial flutter (AFl) (200-300 beats/min) regular and homogenous AFl is often converted to AF and withdrawal of digoxin at this stage may restore normal rhythm (since the cause of atrial inhomogeneity is gone) PSVT (150 – 200/min and 1:1 AV conduction) PSVT with HF - ↑ vagal tone and terminates arrhythmia. Verapamil, adenosine –more effective, act faster and less toxic. 10/16/2019 27PATKI
Ventricular function curves in the normal heart, in CHF, and in CHF treated with digitalis10/16/2019 28PATKI
Management of acute LVF with pulmonary edema Semi-upright posture Oxygen 6-8litres/min Furosemide 40-80mg IV– Repeated every 30 min Morphine IV 2-5mg IV Aminophylline IV slowly 250-500mg Sublingual 0.4mg rpt every 15 min if required /IV Nitroglycerine Digoxin IV 0.5mg – associated with AF/SVT 10/16/2019 29PATKI
Goals of Treatment-ADHF/Pulmonary Edema) • MAD DOG • Improve gas exchange – Start O2/elevate HOB/intubate – Morphine –dec anxiety/afterload – A- (airway/head up/legs down) AMINOPHYLLINE – D- (Drugs) Dig not first now- but drugs as • IV nitroglycerin; IV – D- Diuretics – O- oxygen /measure sats; • Hemodynamics, careful observation – G- blood gases 10/16/2019 30PATKI
Newer agents used in heart failure Newer agent Mode of action Uses Dopexamine Agonist at D1, D2 dopamine and β2 adrenergic R Vasodilator action, ↓after load, improves renal blood flow Heart failure Levosimendan Pimosendan PDE inhibitor, sensitizes the troponin system to calcium - +ve inotropic effect, vasodilator IV loading dose 6-24 μg/kg followed by 0.05-0.2 6-24 μg/kg Acute decompensated HF Istaroxime Inhibits Na+ K+ ATPase, facilitates the sequestration of Calcium in the SR HF Less arrhythmogenic than Digoxin Conivapton Tolvapton Vasopressin receptor antagonists HF 10/16/2019 31PATKI
TERIMA KASIH 10/16/2019 32PATKI kegagalan jantung Your comments- drpatki@gmail.com