Cardiac Glycosides Cardiac Glycosides
Department of Department of Pharmacology NEIGRIHMSPharmacology NEIGRIHMS
Shillong, IndiaShillong, India
Cardiac Glycosides - IntroductionCardiac Glycosides - Introduction
Drugs having the cardiac ionotropic Drugs having the cardiac ionotropic property – increase in force of contractionproperty – increase in force of contraction– They increase the myocardial contractility and They increase the myocardial contractility and
improves cardiac output without proportionate improves cardiac output without proportionate increase in Oxygen consumptionincrease in Oxygen consumption
– Do not increase the heart rateDo not increase the heart rate Digitalis is the genus name for the family Digitalis is the genus name for the family
of the plants that provide most of the of the plants that provide most of the medically useful cardiac glycosides - medically useful cardiac glycosides - DigoxinDigoxin
Sources - Cardiac glycosidesSources - Cardiac glycosides
Cardenolides and BufadienolidesCardenolides and Bufadienolides Digitalis purpurea – Digitoxin, Gitoxin and Digitalis purpurea – Digitoxin, Gitoxin and
GitalinGitalin Digitalis lanata - Digitoxin, Gitoxin and Digitalis lanata - Digitoxin, Gitoxin and
DigoxinDigoxin Strophanthus gratus – OuabinStrophanthus gratus – Ouabin Thevetia nerifolia – ThevetinThevetia nerifolia – Thevetin Convallaria majalis – ConvallotoxinConvallaria majalis – Convallotoxin Bufo vulgris - BufotoxinBufo vulgris - Bufotoxin
Images of Cardiac GlycosidesImages of Cardiac Glycosides
Digitalis purpurea Digitalis lanata
Strophanthus gratus
Images of Cardiac GlycosidesImages of Cardiac Glycosides
Urginea maritima Thevetia nerifolia
Convallaria majalis
ChemistryChemistry All Cardiac glycosides All Cardiac glycosides
– aglycone aglycone (genin) part (genin) part (active (active pharmacologically)pharmacologically)
– sugar sugar (glucose or (glucose or digitoxose) attached at digitoxose) attached at Carbon 3 of nucleusCarbon 3 of nucleus
Aglycone – Steroid Aglycone – Steroid ring ring (cyclopentanoperhydr(cyclopentanoperhydrophenanthrene ring) ophenanthrene ring) and lactone ring and lactone ring attached at 17attached at 17thth position position
Cardiac glycosides - Cardiac glycosides - PharmacokineticsPharmacokinetics
Absorption and Distribution:Absorption and Distribution:– Cardiac glycosides vary in their absorption, distribution, metabolism Cardiac glycosides vary in their absorption, distribution, metabolism
and excretion characteristicsand excretion characteristics– Presence of food in stomach delays absorption of Digoxin and DigitoxinPresence of food in stomach delays absorption of Digoxin and Digitoxin– Digitoxin is the most lipid solubleDigitoxin is the most lipid soluble– Vd of Cardiac glycosides are very highVd of Cardiac glycosides are very high– All are concentrated in heart, skeletal muscles, liver and kidneyAll are concentrated in heart, skeletal muscles, liver and kidney
Metabolism:Metabolism:– DigitoxinDigitoxin is partly metabolized in liver and excreted in bile is partly metabolized in liver and excreted in bile– Cardioactive metabolite (digoxin) and other metabolites are Cardioactive metabolite (digoxin) and other metabolites are
reabsorbed in gut wall - reabsorbed in gut wall - enterohepatic circulation – long half lifeenterohepatic circulation – long half life– No relation with renal impairment No relation with renal impairment – DigoxinDigoxin is primarily excreted unchanged in urine and rate of excretion is primarily excreted unchanged in urine and rate of excretion
parallels creatinineparallels creatinine– So, renal impairment and elderly – long half lifeSo, renal impairment and elderly – long half life– All CGs are cumulative – steady state is attain after 4 half livesAll CGs are cumulative – steady state is attain after 4 half lives
Cardiac glycosides - Cardiac glycosides - PharmacokineticsPharmacokinetics
* Ouabain is administered parenterally and is excreted unchanged in urine
Pharmacological Actions on HeartPharmacological Actions on Heart
Acts on Failing Heart:Acts on Failing Heart: What is a failing Heart ??? What is a failing Heart ???
– Inability of the heart to pump sufficient Inability of the heart to pump sufficient blood to meet the metabolic demands of blood to meet the metabolic demands of the bodythe body
– Reduced efficiency of the heart as a Reduced efficiency of the heart as a pumppump
Contd. ---Contd. ---
•Starling`s law•Laplace`s law
Pharmacological actions on HeartPharmacological actions on Heart
Direct Effect on Myocardial contractility, and Direct Effect on Myocardial contractility, and electrophysiological properties and also has electrophysiological properties and also has vagomimetic effectvagomimetic effect
Force of contraction:Force of contraction:– Dose dependent increase in force of contraction in Dose dependent increase in force of contraction in
failing heart – positive ionotropic effectfailing heart – positive ionotropic effect– Systole is shortened and prolonged diastoleSystole is shortened and prolonged diastole– Contracts more forcefully when subjected to increased Contracts more forcefully when subjected to increased
resistanceresistance– Increase in cardiac output – complete emptying of failed Increase in cardiac output – complete emptying of failed
and dilated heartand dilated heart Tone:Tone:
– Decrease end diastolic size of failing ventricleDecrease end diastolic size of failing ventricle– Reduction in oxygen consumptionReduction in oxygen consumption
Contd. ---Contd. ---
Rate and Conduction: Rate and Conduction: 1.1. BradycardiaBradycardia2.2. Slowing of impulse generation (SAN)Slowing of impulse generation (SAN)3.3. Delay of conductivity of AVNDelay of conductivity of AVN
Direct depressant action on SA and AV Direct depressant action on SA and AV nodes (extravagal)nodes (extravagal)
Increase in vagal tone:Increase in vagal tone:– Is due to improvement in circulationIs due to improvement in circulation– Also due to direct stimulation in vagal center, Also due to direct stimulation in vagal center,
sensitization of baroreceptors and sensitization of baroreceptors and sensitization of SA node to Achsensitization of SA node to Ach
Contd. ---Contd. ---Str
oke
Volu
me
Preload
Normal
Digitalis
CHF
Contd. ----Contd. ----
Digitalis – Electrophysiological Digitalis – Electrophysiological actionsactions
Electrophysiological actions – Electrophysiological actions – contd.contd.
Mainly via 2 actions – autonomic and direct actionMainly via 2 actions – autonomic and direct action Direct action: Direct action:
– At therapeutic dosesAt therapeutic doses Early brief prolongation of action potentialEarly brief prolongation of action potential Followed by period of shortening of action potential – mainly platue Followed by period of shortening of action potential – mainly platue
phasephase Shortening of action potential contributes to shortening of Shortening of action potential contributes to shortening of
refractoriness of atria and ventricles – excitability increasesrefractoriness of atria and ventricles – excitability increases– At higher dosesAt higher doses
Reduced resting membrane potential – less negativeReduced resting membrane potential – less negative Extrasystoloes – oscillatory afterpotentials appear following normal Extrasystoloes – oscillatory afterpotentials appear following normal
action potentialsaction potentials In the event of below threshold action potentials (less negative) – In the event of below threshold action potentials (less negative) –
afterpotentials interfere with normal conductionafterpotentials interfere with normal conduction At further stage – after potentials themselves reach the threshold At further stage – after potentials themselves reach the threshold
to elicit action potential (ectopic beat) coupled with preceding to elicit action potential (ectopic beat) coupled with preceding normal onenormal one
Afterpolarization actions - ouabinAfterpolarization actions - ouabin
Digitalis – Electrophysiological Digitalis – Electrophysiological actionsactions
Autonomic actions:Autonomic actions:– Involves both Parasympathetic and Involves both Parasympathetic and
sympathetic systemssympathetic systems– At therapeutic doses – cardio selective At therapeutic doses – cardio selective
parasympathomimetic actionparasympathomimetic action– Sensitization of baroreceptors, central vagal Sensitization of baroreceptors, central vagal
stimulation and falicitation of muscarinic stimulation and falicitation of muscarinic transmission at cardiac muscle cellstransmission at cardiac muscle cells
– More prominent action in atria and AV nodal More prominent action in atria and AV nodal function than purkinje fibersfunction than purkinje fibers
– However sympathetic action is increased in However sympathetic action is increased in toxic dosestoxic doses
Digitalis – Electrophysiological Digitalis – Electrophysiological actionsactions
Digitalis action – Blood vesselsDigitalis action – Blood vessels
Mild vasoconstrictor in Normal individualsMild vasoconstrictor in Normal individuals In CHF – compensated by improvement of In CHF – compensated by improvement of
increased in cardiac outputincreased in cardiac output No prominent action in Systolic and No prominent action in Systolic and
diastolic BP – no contraindication in diastolic BP – no contraindication in hypertensiveshypertensives
No significant action on coronary vesels – No significant action on coronary vesels – not contraindicated in patient with not contraindicated in patient with coronary artery diseasecoronary artery disease
Digitalis – mechanism of actionDigitalis – mechanism of action
Inhibition of Na/K Inhibition of Na/K ATPaseATPase
blunting of Cablunting of Ca2+2+ extrusion extrusion
CaCa2+2+ sarcomere sarcomere
shorteningshortening
Digitalis action – other tissuesDigitalis action – other tissues Kidney: Kidney:
– Diuresis due to the improvement of circulationDiuresis due to the improvement of circulation– No diuresis in Normal personsNo diuresis in Normal persons
Other smooth muscles:Other smooth muscles:– Inhibition of Na+/K+ ATPase – increased spontaneous Inhibition of Na+/K+ ATPase – increased spontaneous
activity – anorexia, nausea, vomiting and diarrhoeaactivity – anorexia, nausea, vomiting and diarrhoea CNS:CNS:
– No major visible action in therapeutic dosesNo major visible action in therapeutic doses– High doses – stimulation of CTZ - nausea and vomitingHigh doses – stimulation of CTZ - nausea and vomiting– Toxic doses – central sympathetic stimulation, mental Toxic doses – central sympathetic stimulation, mental
confusion, disorientation and visual disturbanceconfusion, disorientation and visual disturbance
Digitalis – Adverse effectsDigitalis – Adverse effects Cardiac and Extracardiac:Cardiac and Extracardiac: Extracardiac:Extracardiac:
– GIT: nausea, vomiting and anorexia etc.GIT: nausea, vomiting and anorexia etc.– CNS: CTZ stimulation, headache, blurring of CNS: CTZ stimulation, headache, blurring of
vision (Flashing light, Altered color vision), vision (Flashing light, Altered color vision), mental confusion etc.mental confusion etc.
– Serum Electrolyte: KSerum Electrolyte: K++ : Digitalis competes for K : Digitalis competes for K binding at Na/K ATPasebinding at Na/K ATPase
Hypokalemia: increase toxicityHypokalemia: increase toxicity Hyperkalemia: decrease toxicityHyperkalemia: decrease toxicity
– MgMg2+2+ : Hypomagnesemia: increases toxicity : Hypomagnesemia: increases toxicity– CaCa2+2+ : Hypercalcemia: increases toxicity : Hypercalcemia: increases toxicity
Digitalis – Adverse effectsDigitalis – Adverse effects
Cardiac:Cardiac: PSVT: Proprnolol IV or oralPSVT: Proprnolol IV or oral AV block: Atropine - 0.6 to 1.2 mg IMAV block: Atropine - 0.6 to 1.2 mg IM Ventricular arrhythmia: Excessive Ventricular arrhythmia: Excessive
ventricular automaticity: Lidocaine IV (or ventricular automaticity: Lidocaine IV (or Phenyton)Phenyton)
Tachyarrythmias: Heart rate abnormally Tachyarrythmias: Heart rate abnormally increased due to prolong diuretic and increased due to prolong diuretic and digitalis therapy – Potassium chloride digitalis therapy – Potassium chloride 20m.mol IV20m.mol IV
Digitalis – Common Drug Digitalis – Common Drug interactionsinteractions
Diuretics: Hypokalaemia (K+ Diuretics: Hypokalaemia (K+ supplementation required)supplementation required)
Calcium: synergizes with digitalisCalcium: synergizes with digitalis Adrenergic drugs: arrhythmiaAdrenergic drugs: arrhythmia Propranolol and CaPropranolol and Ca++++ channel channel
blockers: depress AV conduction and blockers: depress AV conduction and oppose positive ionotropic effectsoppose positive ionotropic effects
Digitalis - contraindicationsDigitalis - contraindications
Hypokalemia: ToxicityHypokalemia: Toxicity WPW syndrome: VF may occurWPW syndrome: VF may occur Elderly, renal or severe hepatic Elderly, renal or severe hepatic
disease: more sensitive to digitalisdisease: more sensitive to digitalis Diastolic dysfunction of heartDiastolic dysfunction of heart Partial AV block: Complete blockPartial AV block: Complete block
Digitalis – therapeutic UsesDigitalis – therapeutic Uses
Congestive Heart FailureCongestive Heart Failure
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Cardiac ArrhythmiasCardiac Arrhythmias
DigitalisDigitalis - Congestive Heart Failure- Congestive Heart Failure
Systolic dysfunction: dilated ventricles and Systolic dysfunction: dilated ventricles and unable to develope sufficient wall tension – unable to develope sufficient wall tension – IHD, Valvular disease, Myocarditis etc.IHD, Valvular disease, Myocarditis etc.
Diastolic dysfunction: Thickened wall, Diastolic dysfunction: Thickened wall, filling is impaired and low output – filling is impaired and low output – prolonged hypertension, CHD, prolonged hypertension, CHD, hypertrophic myopathyhypertrophic myopathy
Long standing CHF patients have both the Long standing CHF patients have both the types of dysfunctionstypes of dysfunctions
Digitalis therapy improves the conditions Digitalis therapy improves the conditions in CHF, but neither arrest progression nor in CHF, but neither arrest progression nor reverse pathological changereverse pathological change
Enlarged Heart - Images
Digoxin DigitalizationDigoxin Digitalization Digoxin has low therapeutic window and margin of safety is Digoxin has low therapeutic window and margin of safety is
very lowvery low Therapeutic level of digoxin is 0.5 – 1.5 ng/mlTherapeutic level of digoxin is 0.5 – 1.5 ng/ml It is administered such a way that patient gets maximum It is administered such a way that patient gets maximum
benefits with minimal adverse effectsbenefits with minimal adverse effects Previously rapid digitalization was done but obsolete nowPreviously rapid digitalization was done but obsolete now Slow digitalization:Slow digitalization:
– Administer digoxin 0.25 mg (or even 0.125mg) daily in the Administer digoxin 0.25 mg (or even 0.125mg) daily in the evening – full response in 5-7 daysevening – full response in 5-7 days
– If no improvement administer administer 0.375 for 1 weekIf no improvement administer administer 0.375 for 1 week– If no, administer 0.5 mg in next weekIf no, administer 0.5 mg in next week– Monitor patient for blood levels, if no monitor in improvement Monitor patient for blood levels, if no monitor in improvement
of signs and symptomsof signs and symptoms– If bradycardia, stop the drugIf bradycardia, stop the drug
Digitalization – contd.Digitalization – contd.
Rapid digitalization (oral): Rapid digitalization (oral): – Administer 0.5 to 1 mg statAdminister 0.5 to 1 mg stat– 0.25 mg every 6 Hrly0.25 mg every 6 Hrly– Monitor for toxicityMonitor for toxicity– Patient is digitalized within 24 HrsPatient is digitalized within 24 Hrs
Rapid IV: Seldom used nowRapid IV: Seldom used now– As desperate measure in CHF and atrial As desperate measure in CHF and atrial
fibrillationfibrillation– 0.25 mg slow IV stat followed by 0.1 mg every 0.25 mg slow IV stat followed by 0.1 mg every
HrlyHrly
Digoxin - Cardiac ArrhythmiasDigoxin - Cardiac Arrhythmias Cardiac dysrhythmia (arrhythmia)Cardiac dysrhythmia (arrhythmia)
– Large and heterogeneous group of conditions in which there is Large and heterogeneous group of conditions in which there is abnormal electrical activity in the heartabnormal electrical activity in the heart
– The hearts too fast or too slow, and may be regular or irregularThe hearts too fast or too slow, and may be regular or irregular Atrial fibrillation is the most common type of arrhythmias Atrial fibrillation is the most common type of arrhythmias
although not life threateningalthough not life threatening– Often irregular and rapid atrial contractions originating in atrial Often irregular and rapid atrial contractions originating in atrial
musclesmuscles– Ultimately interferes with ventricular contractions (heart beat)Ultimately interferes with ventricular contractions (heart beat)– If treated, it is not life threateningIf treated, it is not life threatening– Generally occurs above 50 years of ageGenerally occurs above 50 years of age– Digitalis action:Digitalis action:
Acts by decreasing the number of impulses passing down the AV node – Acts by decreasing the number of impulses passing down the AV node – direct, vagomimetic and sympathetic actiondirect, vagomimetic and sympathetic action
Decreases average atrial ERP – increases fibrillation frequencyDecreases average atrial ERP – increases fibrillation frequency Decreases the ventricular rate and pulse deficit is abolishedDecreases the ventricular rate and pulse deficit is abolished Can bring down ventricular rate to 70-80/minCan bring down ventricular rate to 70-80/min
Digoxin - Cardiac ArrhythmiasDigoxin - Cardiac Arrhythmias
Atrial flutter:Atrial flutter:– Regular and synchronous contractionsRegular and synchronous contractions– Atrial rate is less than AF (200-350)Atrial rate is less than AF (200-350)– Digoxin enhances AV block and reduces ventricular rateDigoxin enhances AV block and reduces ventricular rate– Converts atrial flutter to fibrillation – reduction in atrial Converts atrial flutter to fibrillation – reduction in atrial
ERP ERP PSVT:PSVT:
– Heart rate is 150-200/minHeart rate is 150-200/min– A-V conduction is 1:1 due to reentry in SA or AV nodeA-V conduction is 1:1 due to reentry in SA or AV node– IV injection of Digoxin prevents this by increasing vagal IV injection of Digoxin prevents this by increasing vagal
tonetone
Pharmacotherapy of CHF – Pharmacotherapy of CHF – Goal Goal
Improvement of cardiac performanceImprovement of cardiac performance– Ionotropic drugs: digoxine, dopamine, Ionotropic drugs: digoxine, dopamine,
dobutamine and amrinonedobutamine and amrinone– Diuretics: frusemide and thiazidesDiuretics: frusemide and thiazides– Vasodilators: ACE inhibitors/AT1 antagonists, Vasodilators: ACE inhibitors/AT1 antagonists,
hydralazine or nitroprussidehydralazine or nitroprusside Arrest or reversal of disease progression:Arrest or reversal of disease progression:
– ACE inhibitors or AT1 antagonistsACE inhibitors or AT1 antagonists– Beta-blockersBeta-blockers– Aldosterone antagonistsAldosterone antagonists
Heart failure - classificationHeart failure - classification Class I (Mild): Class I (Mild): No limitation of physical activity. Ordinary No limitation of physical activity. Ordinary
physical activity does not cause undue fatigue, palpitation, or physical activity does not cause undue fatigue, palpitation, or dyspnea (shortness of breath).dyspnea (shortness of breath).
Class II (Mild): Class II (Mild): Slight limitation of physical activity. Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in Comfortable at rest, but ordinary physical activity results in fatigue, palpitation, or dyspnoea.fatigue, palpitation, or dyspnoea.
Class III (Moderate): Class III (Moderate): Marked limitation of physical activity. Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes Comfortable at rest, but less than ordinary activity causes fatigue, palpitation, or dyspnoea.fatigue, palpitation, or dyspnoea.
Class IV (Severe): Class IV (Severe): Unable to carry out any physical activity Unable to carry out any physical activity without discomfort. Symptoms of cardiac insufficiency at rest. without discomfort. Symptoms of cardiac insufficiency at rest. If any physical activity is undertaken, discomfort is increased.If any physical activity is undertaken, discomfort is increased.
Pharmacotherapy of CHF – Pharmacotherapy of CHF – contd.contd.
Diuretics: FurosemideDiuretics: Furosemide– Decrease in preload and improvement of ventricular functionDecrease in preload and improvement of ventricular function– Removal of peripheral oedema and pulmonary congestionRemoval of peripheral oedema and pulmonary congestion
Vasodilators:Vasodilators:– Nitrates (GTN and IDN): reduce preload by pooling of blood in Nitrates (GTN and IDN): reduce preload by pooling of blood in
capacitance vesselscapacitance vessels– Arteriolar dilators (Hydralazine, Minoxidil, CCBs etc) decrease Arteriolar dilators (Hydralazine, Minoxidil, CCBs etc) decrease
in peripheral resistance and facilitates more blood pumping by in peripheral resistance and facilitates more blood pumping by weak heartweak heart
– Pre and afterload reductionPre and afterload reduction ACEIs/ARBs effectve orally and Nitroprusside IV dilatorACEIs/ARBs effectve orally and Nitroprusside IV dilator In severe decompensated patients: IV nitroprusside (titrated) + In severe decompensated patients: IV nitroprusside (titrated) +
loop diuretic + IV ionotropic drugs loop diuretic + IV ionotropic drugs For maintenance, Hydralazine + ACEIs/ASRBs are usedFor maintenance, Hydralazine + ACEIs/ASRBs are used ACEIs and ARBs are recmmended for all grades of failureACEIs and ARBs are recmmended for all grades of failure
ACE inhibitors/ARBs
Afterload reduction Preload reduction Reduction of facilitation of
sympathetic nervous system Reduction of cardiac hypertrophy Drugs of choice in heart failure (with
diuretics) Used in all class of CHF
CHF – Beta blockers, how?CHF – Beta blockers, how?
Beta Blockers: metoprolol & bisoprololBeta Blockers: metoprolol & bisoprolol1.1. Initially reduce cardiac contraction and stroke volume i.e., Initially reduce cardiac contraction and stroke volume i.e.,
ejection fraction - but slowly Ef increasesejection fraction - but slowly Ef increases
2.2. Prevention of ventricular wall stretching – prevent Prevention of ventricular wall stretching – prevent remodelingremodeling
3.3. Prevention of Renin-angiotensin systemPrevention of Renin-angiotensin system Used in mild and moderate cases of heart failure with Used in mild and moderate cases of heart failure with
dilated cardiomyopathy and systolic dysfunctiondilated cardiomyopathy and systolic dysfunction No use in severe decompensate heart, other drugs should No use in severe decompensate heart, other drugs should
be continuedbe continued Useful in class II and Class III failuresUseful in class II and Class III failures Dose: start as low dose, carvedilol – 3.125 mg/day, Dose: start as low dose, carvedilol – 3.125 mg/day,
metoprolol – 200 mg/daymetoprolol – 200 mg/day
CHF –CHF –Aldosterone antagonist (Spironolactone)
Rise in plasma aldosterone level in CHF leads to– Increase in preload due to ECF rise– Risk of arrhythmia due to hypokalaemia – sudden death– Pathological remodeling of myocardium– Enhancement of sympathomimetic activity
Spironolactone antagonizes all the above effects – mobilization of edema fluid, prevents hypokalaemia
Dose: low dose of 12.5 to 25 per day (to avoid hyperkalaemia)
Used as add on therapy to ACEI/ARBs in moderate to severe CHF
Prevents hypokalaemia induced by diuretics Serum K+ monitoring required – risk of hyperkalaemia
CHF – Phosphodiesterase III inhibitors
Amrinone: (amicor/inocor/iarditone)– Selective PDE III inhibitor– MOA: Prevents intracellular breakdown of cAMP by PDE
III – increases cAMP conc. And Ca++ influx– Clinically, positive ionotropy and vasodilatation– Dose: IV Bolus 0.5 mg/kg followed by 5-10 mcg/kg/min– Adverse Effects: Thrombocytopenia, hepatotoxicity,
arrhythmia, nausea, & vomiting– Uses: Only for short term therapy of CHF and not used
for maintenance although effective orally
CHF – Sympathomimetics (ionotropic)
Dobutamine:(2-8 mcg/kg/min)– Beta-1 agonist and acts via cAMP and increase
in Ca++ conc.– Relatively do not increase heart rate– Further Beta-2 effects – muscle vasodilatation– Less change in heart rate and BP– Cardiac workload decreases – low oxygen
demand– Uses: acute heart failure with MI, cardiac
surgery and advanced decompensate CHF– Adverse effects: Tachycardia (reflex action due
to beta-2 action), tolerance (down regulation of beta receptors after 72 Hrs)
CHF - Dopamine 3 – 10 mcg/kg/min IV Acts on pre-junctional D2 and post-
junctional D1 receptors Actions: Splanchnic and Renal
vasodilatation (D1) and suppression of NA release (D2 effect) – increase renal perfusion and increase g.f.r
Uses: Patient in shock, adjunct to frusemide in refractory cases (short term only)
Adverse effects : tachycardia, arrhythmias and peripheral vasoconstriction
Remember
Sources and names of Cardiac Glycosides Digoxin – Pharmacological actions in
failing heart, process of digitalization Digoxin – Drug interactions Role of Diuretics, Beta-blockers, ACE
inhibitors, Vasodilators, Aldosterone antagonists and PDE III inhibitors in Heart failure
Pharmacotherapy of Heart failure
Thank You
Big Hearted ?
Digitalis – mechanism of actionDigitalis – mechanism of action