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IN THE NAME OF ALLAH THE MOST MERCIFUL THE MOST BENOVELANT
“Congestive Cardiac Failure”

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Tableof Contents
1.Cardiac glycosides.......................................................................................................................................3
1.1 Digitalis.................................................................................................................................................3
2.Diuretics.....................................................................................................................................................4
2.1 Loop diuretics.......................................................................................................................................4
2.2 Thiazide diuretics .................................................................................................................................5
2.3 Aldosterone antagonist ......................................................................................................................................................................6
2.4 ADH antagonist ....................................................................................................................................................................................7
3.Sympathomimetics.....................................................................................................................................8
4.Beta blockers ................................................................................................................................................................................................9
5.Vasodilators ................................................................................................................................................................................................10
5.1 ACE Inhibitors.....................................................................................................................................10
5.2 Angiotensin receptors blockers ........................................................................................................... 11
5.3 Artereodilators and venodilators.....................................................................................................................................................11
6. Others..........................................................................................................................................................................................................12
6.1 Natriuretic peptide ..................................................................................................................................................................................12
6.2 phosphodiesterase inhibitors ................................................................................................................................................................12

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Special Points
1.1 Digitalis
 In congestive cardiac failure,it causes dieresis. (T, pg 131)
 Its i.v digitalization carries more risk than oral administration. (T,131)
a.Digoxin:
 Is a prototype drug.(K,216)
 Not extensively metabolized and excreted in unchanged form by the kidney.(K,216)
 It is not a first class of drug for treating CHF patients. (K,216)
 Relatively hydrophilic. (K,216)
 Loading dose is administered in emergencies. (R,279)
 Has narrow margin nof safety.(T,131)
 Not used/imdicated in patients with diastolic or right side heart failure.(L,202)
 Less plasma protein binding.i.e 25%. (K.D,499)
 Has large volume of distribution i.e 6.3L/kg.(K.D,497)
 Food delays its absorption .(T,131)
 It is shorter acting. (R,278)
 Due to neurohumoral effect ,it is unique among ionotropic agents.(G,573)
b .Digitoxin:
 Lipophilic in nature. (K.D,499)
1.Cardiac Glycosides

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 Maximum absorption i.e 90-100%. (K.D,499)
 Extensive plasma protein binding i.e 95%. (K.D,499)
 Long half life i.e 5-7 days. (K.D 499)
 Less daily elimination only 10-15%. (K.D,499)
 Administered orally. (K.D ,499)
 Its bioavailability, V.D, clearance and biotransformation is not alter in patients with
reanal failure.(www.ncbi.nlm.nin.gq/ pubmed / 7021432
 Has small volume of distribution i.e 0.6L/kg. (www.ncbi.nlm.nin.gq/ pubmed / 7021432)
2.1Loop Diuretics
 High ceiling diuretics. (R,362))
 Short duration of action. (T,107)
 Directly or indirectly has vasodilator action. (R,362)
 Furosemide : main loop diuretic. (R,362)
 metabolized by glucuronic acid. (R,362)
 rapid onset of action but short duration of action. (T,155)
 To treat hypercalcemia it is given i.v, as it promotes excretion of calcium
In urine.( T,156)
 increases blood uric acid level.( WebMed)
2.Diuretics

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“Drug interaction: with aminoglycosides causes inhanced toxicity as both are
themselves ototoxic.”(T,157)
 Torsemide : causes less loss of potassium and sodium. (R,362)
 has longer half life and longer duration of action. (R,362)
 administered once a day.(R,362)
 given orally. (T,155)
 Three times more potent than furosemide and bumetanide.( NHS.UK)
 Ethacrynic acid : not a sulphonamide but has typcal loop activity and some urisuric
action. (K,269)
 shows greater side effects like deafness.(L,284)
 shows deeper dose response curve. (L,284)
 Bumetanide : causes dieresis very rapidly. (WebMed)
2.2.Thiazidediuretics:
 Has long duration of action. (T,107)
 Well tolerated in elderly patients. ( T,106)
 Chlorthalidone : has longer duration of action i.e 48hr. and given on alternate
days(R,363)
 Long half life due to binding to RBCs.(K,268)
 Side effect kidney stones , black stools and joint pain. (NHS.UK+WebMed)
 Chlorthiazide : only parenteral thiazide available. (K,268)

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 Indapamide : has little effect on potassium,uric acid and glucose excretion. (R,363)
 at subdiuretic doses lower B.P with less metabolic disturvbance.(R,363)
 Side effect causes trouble in sleeping.
 Bendroflumethiazide : main thiazide . (R,363)
 Metolazone : popular for use with loop diuretics, for synergistic effect. (K,268)
2.3 Aldosteroneantagonist
 Has limited diuretic action. (R,264)
 Spironolactone : competitive antagonist to aldosterone. (K,262
 Its inactivation occurs in liver. (K,262)
 Decreases proton(+H0 secretin and uric acid excretion. (R,264)
 Short half life i.e 10 min. (R,264)
 Slowest onset of action may take several days. (R,264)
 No diuretic effect occurs in patients with Addison’s disease. (L,286)
 Prevents remodeling, that occurs as compensation for progressive
 Failure of heart. (L,286)
 Use to treat primary and secondry hyperaldosteronism (R, 264-L,286)
 Side effects gynaecomastia , menstrual disorders , testicular atrophy and peptic
Ulceration. (R,264)
 Diuretic of choice in patients with hepatic cirrhosis. (L,286)
 Eplerenone : greater selectivity for mineralocorticoid receptors. (K,262)

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 Analogue to spironolactone. (K,262)
 Has fewer adverse effects. (K,262)
 Reduces myocardial perfusion defects after myocardial infarction. (K,262)
 Amiloride : poorly absorbed by GIT. (R,264)
 Most of the drug excreted in urine in unchanged form. (R,264)
 Longer duration of action. (R,264)
 Triamterene : it is extensively metabolized. (K,262)
 Shorter half life. (L,287)
 “Drug interaction : with indomethacin causes acute renal failure. (T)”
 Side effects : leg cramps , increases blood urea nitrogen and uric acid level. (L, 287)
 Kidney stones. (K,263)
2.4 Vasopressin / Antidiuretic Hormone(ADH)
 Causes vasodilation.
 Conivapton : non-selective V1a and V2 antagonist. (K,677)
 Given i.v. (K,677)
 Not suitable for chronic use in out patients. (K,265)
 Uses to treat hyponatremia in hospitalized patients. (K,677)
 Tolvapton : selective antagonist for V2 receptor. (K,677)
 Oral administration. (K,677)
 Long half life i.e 12-24hrs. (K,264)
 Side effect ; hypotension. (K,265)

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Beta-adrenergicantagonist:
 Drug of choice to treat effort induce angina. (L,222)
 Drugs with partial agonist activity increase heart rate at rest. (L)
 Propranolol : prototype drug of this group. (T,95)
 Has highest lipid solubility. (T,99)
 Produces central side effects. (T,99)
 Undergoes extensive first pass effect.(T,99)
 contraindicated in asthma and COPD. (T,99)
 Has high volume of distribution 4L/Kg. (L,92)
 Carvedilol : has cardioprotective effect. (T,100)
 To treat mild to severe CHF, approved by FDA. (G,569)
 Practolol : 1st selective Beta 1 antagonist, no more in use due to its toxicity. (R,174)
 Timolol : use to treat narrow angle glaucoma. (T,95)
 Reduces production of aqueous humorin eye. (L,93)
 Esmolol : available as i.v. (T,99)
 Has short half life. (L,94)
 Useful in hypotensive emergencies. (T,98)
 Nodolol : excreted unchanged in urine and has longest half life. (K,157)
 Nebivolol : most highly selective beta 1-adrenergic receptor blocker.(K,161)
 Metoprolol : to treat mild to moderate heart failure. (G,565)
3.Beta Blockers

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 half (40-50%) bioavailability.(K.D,140)
 Less protein binding 12% (K.D,140)
 First pass metabolism is less, but 90% or more metabolized before
 excretion.
 Bisoprolol : lipid insoluble. (G,569)
Has high bioavailability>80%. (K.D,140)
 Dobutamine : its +ve isomer is a potent beta1 agonist.(K,141)
 Has greater ionotropic effect than chronotropic effect. (K,141)
 Injections are used as pharmacological cardiac stress test. (K,141)
 Development of tolerance. (T,133)
 Provides short term relief of heart failure symptoms in patients of
Ventricular dysfunction. (K,144)
 Administered i.v for short term treatment of acute heart failure. (T,86)
 USED for ionotropic supply after heart surgery.(L,80)
 Not significantly elevates oxygen demand. (L,80)
 Should be used with caution in atrial fibrillation.(L,80)
 Plasma half life short i.e 2min s given i.v .(R,179)
 Contraindicated in pheochromocytoma. (S.S)
 Dopamine : has limited utility in patients who are not in shock. (K.D,507)
4.Sympathomimetic amines

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 has dose dependent haemodynamic effect. (T,133)
 Drug of choice to treat septic and cardiogenic shock. (L,80)
 Produces less tachycardia. (R,279)
 At higher doses beneficial effects of low-moderate dose is lost.(T,133)
5.1ACE inhibitors
 Long term treatment causes diabetic and hypertensive nephropathy.(K.D,452)
 Captopril : pretreatment inhibits the pressor action of angiotensin 1 and angiotensin 2.
 (K.D,449)
 Has rapid action. (K.D,450)
 It is taken 1hr before meal. (T,104)
 Food reduces its absorption. (T104)
 Reduces mortality of patients with heart failure. (L,198)
 It is not a prodrug. (L199)
 Enalapril : is an oral prodrug. (K,184)
 available only for i.v use to treat primary hypertensive emergencies. (K.184)
 Reduces mortality in patients with arrhythmias and M.I .(L,198)
 Undergoes extensive 1st pass effect. (T,104)
 It is dose to dose more potent and has longer duration of action. (K.D,450)
 Fosinopril : is not eliminated as an active metabolite. (L,199)
5.Vasodilator

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 Perindopril : poorly absorbed from GIT. (T,104)
5.2AngiotensinReceptor blocker :
 Considered in patients who are intolerant to ACE inhibitors because of cough. (K219)
 Losartan : undergoes extensive 1st pass hepatic metabolism and converted to active
 Metabolites.(L,199)
 It is a prototype drug. (L,199)
 AT1 receptors has high affinity for it, whereas AT2 have less affinity.(K,299)
 Does not cause dry cough.(R,298)
 Saralasin : peptide analogue of angiotensin 2.(R,297)
 Candesartan : has low volumes of distribution. (L,199)
5.3Artereo and Venodilators:
 Artereodilators;
 Hydralazine : has less bioavailability. (K,181)
 Causes reflex tachycardia. (K,181)
 Causes fluid retension. (K)
 Increases cardiac output in patients with heart failure. (T,128)
 Venodilators :
 Isosorbide dinitrate: first pass effect and has less bioavailability.(T,117)
 Causes postural hypotension. (K)
 Isosorbide mononitrate : has high oral bioavailability. (T,117)

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 Has longer duration of action. (T,117)
6.1 Natriuretic Peptide:
 It causes sodium excretion in distal nephron. (R,359)
 Nesirtidine : administered i.v. (T,133)
 USE to treat acute decompensated failure. (K,224)
 SIDE EFFECTS : damages kidney and increase mortality.
6.2 Phosphodiesterases :
 Milrinone : is a potent drug. (T,133)
 Does not causes thrombocytopenia. (T,133)
6.Others

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Key to reference
(R) Rang Dales 5th edition.
(G) Goodman and Gillman’s Mannual of pharmacology.
(K) Basic and Clinical Pharmacology By Bertram G. Katzung. 12th edition.
K.D) Essentials of Medical Pharmacology By K.D Tripathi 6th edition.
(L) Lippincott’s Illustrated Reviews 5th edition.
(T) Prep Mannual For Undergraduates By Tara V Shanbhag ,Smita Senoy 2nd
edition

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