HEART FAILURE DRUGS

Question 1

What is congestive heart failure ?

Answer 1

it is a pathophysiological state in which the heart fails to pump blood at a rate equal to requirements by metabolising tissue

Question 2

What does CHF cause

Answer 2

inadequate circulation ,fluid build up in lungs , reduced oxygenation of tissues

Question 3

What is the systolic failure pathophysiolgy in chf?

Answer 3

reduced myocardial contractility , reduced Sv ,
Increased Ventricular pressure and residual blood volume
dilated ventricles

Question 4

What is the diastolic failure pathophysiology ?

Answer 4

ventricular relaxation reduces and ventricular filling decreases

Question 5

Drug for increased Preload caused by Na+ and H20 retention?

Answer 5

Diuretics

Question 6

Drugs for increased preload caused by vasoconstriction

Answer 6

Venodilators

Question 7

increased afterload drugs caused by arterial vasoconstriction ?

Answer 7

Arterial vasodilators

Question 8

What is the pathophysiology response by kidney in chf

Answer 8

retains water and na
maintains sv
allows the heart to function at high end diastolic volumes because of extra cellular fluid volume

Question 9

Pathophyiology of CHF

Answer 9

edema
increased wall stress
increased pulmonary congestion causing fluid build up
end diastolic volume leads to higher end diastolic filling
increased ventricular size

Question 10

What cycle follows after heart damage / ventricular overload / decreased ventricular contraction ?

Answer 10

1. tachycardia ,ventricular dilation , myocardial hypertrophy
2. reduced CO
3. reduced renal perfusion
4. increased sodium retention and h20
   5 .increased osmotic pressure
   6 increased AdH
   7 .increased h20 absorption
   8 .fluid overload causimg edema

Question 11

Class I ambulatory treatment

Answer 11

diuretics

Question 12

Class II ambulatory treatment

Answer 12

aceis/arbs

Question 13

class III ambulatory treatment

Answer 13

diuretics + aceis/arbs

Question 14

class IV ambulatory

Answer 14

diurectics + aceis/arbs +digoxin

Question 15

what do we use instead of aceis for pts intolerable

Answer 15

hydralazine/nitrates

Question 16

For hospitalised chf what drugs do we use with their classes in order ?

Answer 16

1. Diuretics , pref loop diuretics
2. Vasodilators , sodium nitroprusside
   3.sympathomimetics = dobutamine or dopamine
3. phosphodiesterase inhibitors amrinone

Question 17

MOA for vasodilators eg sodium nitroprusside

Answer 17

reduce preload and afterload
both veno and arterial dilators

Question 18

inotropes moa

Answer 18

increase CO

Question 19

ACEIs MOA

Answer 19

reduce vasoconstriction and and sodium and water retention

Question 20

diurectics moa

Answer 20

Reduce sodium & water retention
reduce preload
does not reduce mortality
use minimal dose to maintain euvolemia
control congestive symptoms

Question 21

Loop Diurectics examples and bio availabilty

Answer 21

furosemide 40-70%
.bumetanide 80%
torsemide 80%
ethacrynic acid for people allerrgic to sulfonamides

Question 22

Loop diuretics moa

Answer 22

inhibit the Na+K+CL- symporter in the ascending loop of henle

Question 23

thiazide diuretics moa

Answer 23

inhibit the Na +Cl - transport in distal convuluted tubule
loss of k+
great synergism with loop diuretics

Question 24

K+ sparing diuretics moa

Answer 24

amiloride acts as a Na + inhibitor absorption
Spironolactone / canrenone acts as aldosterone antagonists

Question 25

What doe aldosterone antagonists do in heart failure

Answer 25

increase survival independent of diuresis reverse pathologic remodelling that occurs in heart failure

Question 26

what are the Angiotensin II uses or actions ?

Answer 26

potent vasoconstrictor increases Na+ and H20 retention arrythmogenic stimulate release of catecholamines

Question 27

What does RAAS inhibiotrs do e.g arbs and acies

Answer 27

myocytes death promote vascular hyperplasia pathological myocardial hypertrophy

Question 28

Aceis reduce proload and afterload why ?

Answer 28

because is it both a venodilator and arterial dilators

Question 29

what are the adverse effects of ACEIs ?

Answer 29

Cough angioedema Loss of taste Proteinuria renal impairment rise in K+

Question 30

Examples of ARBs and uses

Answer 30

losartan , candesartan , telmesartan has similar mortality benefit as aceis prevent adverse ventricular remodelling

Question 31

What is the MOA of nitrates and their duration of action

Answer 31

Nitroglycerin ...transdermal , iv , ointment and raipd acting tablets isosorbide mononitrate orally are short acting isosorbide dinitrate orally act long lasting MOA = provide NO by binding to smooth muscle cells and releases NO which binds to nitrogen receptors which cause guanylate cyclase stimulation and cause cGMP increase which causes dephosphorylation of mysoin light chain kinase leading to relaxation of muscles causing vasodilation

Question 32

What is the mechanism of action for vasodilator hydralazine?

Answer 32

arterial vasodilators which reduce the afterload , of right and left ventricles by reducing pulmonary and systematic and pulmonary vascular resistance

Question 33

Write shorts notes on hydralazine except moa

Answer 33

increases renal blood flow redices renal vascular resistance effective with organic nitrates e.g isosorbide Positive inotropic effect

Question 34

Examples of B blockers and its MOA

Answer 34

metoprolol carvedilol bisoprolol MOA= improvement of ventricular structure and function , reduces chambers size while ejection fraction increases .Also it reverses the cellular events that underlie the pathological remodelling

Question 35

Write short notes on Bblockers

Answer 35

approach heart problem pts carefully initiate at low dose reduce oxidative stress in myocardium by improving myocardial energetics

Question 36

Short notes on Sodium nitroprusside ?

Answer 36

reduces ventricular and systematic resistance reduces PVR becauses preload & afterload reduces reducing wall stress increases the venous capacitance rapidly metabolised to NO and cyanide increase CO and increased renal blood flow

Question 37

what are the side effects of sodium nitroprusside ?

Answer 37

hypotension cyanide toxicity in hepatic and renal failure methemoglobinemia due to oxidation of Hb BY NO

Question 38

Nitroglycerin short notes ?

Answer 38

short acting with tablets used for lvf in MI adverse effects : headache , nitrate tolerance , increases blood alcohol because administered in ethanol

Question 39

Nesiritide short notes

Answer 39

recombinant dna Brain natriuretic peptide form increases cGMP in soomth muscles and reduce after/pre load vasodilation occurs in arterial and venous dilation nesiritide deactivated by NEP BNP deactivated by clearance receptors facilitating internalisation and enzymatic degradation

Question 40

What are cardiac glycosides (digitalis) and give examples ?

Answer 40

these are drugs that contain a steroid nucleus combined with unsaturated lactone ring and series of sugars e.g Digoxin and digotoxin

Question 41

what is the molecular mode of action of digitalis?

Answer 41

inhibit the sodium potassiu m pump whic causes an increase in intracellura Na + whic initiates Na+ and Ca2+ exchange mechanism which causes a rise in Ca2+ .CA2+ influx too through voltage gated calcium channels this increase in calcium ions causes an trigger in sarcoplasmic reticulum to release Ca2+ whic initiates a excitation contraction coupling

Question 42

What is the main action of Digoxin ?

Answer 42

increased contraction of the heart Inhibit the sympathetic activation and raas decreased HR increased Cardiac output decreased salt and water rentention reducing edema decreased preload which reducing pulmonary congestion decreased afterload which increases tissue perfusion

Question 43

What are the electrophysiological effects of digoxin ?

Answer 43

decreases sympathetic activity and increases vagal tone 1. decreases hr 2. decreases afterload and preload 3. decreased refractory period in atrial & ventricular tissues

Question 44

What are the effects of digoxin at higher doses ?

Answer 44

increases K+ serum increases automaticity and sympathetic activation causes arrhythmia

Question 45

What are the toxic effects of digoxin ?

Answer 45

overloading of intracellular Ca2+ which increases systoles which may lead to pulsus bigeminy then trigeminy which leads to tachycardia and ventricular fibrillation

Question 46

What is the pharmacokinetics of digoxin ?

Answer 46

lipophilic 70% bioavailability ,plasma protein binding is 30% t1/2 is 36-48hrs excreted unchanged however renal impairment increases half life

Question 47

What are the therapeutic uses of cardiac glycosides ( digoxin ) ?

Answer 47

1.heart failure patient who are asymptomatic or are on therapy with aceis or are in atrial fibrillation 2. atrial fibrillation with rapid ventricular response. Blocks AV node thereby protects ventricle from rapid atrial rate 3. atrial flutter , turns atrial flutter to atrial fibrillation which in turn goes back to normal rhythm after digoxin withdrawal

Question 48

What are the contraindications of Digoxin ?

Answer 48

1.partial heart block 2. rheumatic fever 3. acute myocardial infarction 4.hypertrophic obstructive cardiomyopathy

Question 49

What are the drug interactions of digoxin ?

Answer 49

1.cholestyramine , neomycin and antacaids decrease and plasma level by decreasing the absorption , while thyroxin increases renal clearance and increased volume of distribution 2.erythromycin , tetracycline and omeprazole increases plasma level by increasing absorption while quinidine , verampil , diltiazem , captopril and amiodarone reduces clearance

Question 50

Phamacodynamic interaction of digoxin | with other drugs

Answer 50

1.k+ diurectics reduce k+ which increases automaticity and (-) na+/k+ which causes toxicity 2. sympathometics increases automaticity 3.b blockers block avn and san leading to bradycardia and heart block .Also decrease myocardial conduction therefore antagonising positive inotropic effects

Question 51

What are the adverse effects of digoxin / digitalis toxicity ?

Answer 51

arrhythmias blurred vision dizziness anorexia ,nausea , vomiting abdominal pain abnormal dreams , malaise

Question 52

What is the treatment of digitalis toxicity

Answer 52

stop taking digoxin and K+ diuretics atropine treats bradycardia & 2/3 degree hear block lidocaine for ventricluar arrhythmia administer k+ in tachyarrhythmia k+ admin contraindicated in Av block

Question 53

What are the parenteral drugs used in hospitalized heart failure ?

Answer 53

1. diuretics by Iv 2.sodium nitroprusside reduces both afterload and preload 3. nitroglycerine decreases preload because its a venodilator so reduced venous congestion , edema reduced and pulmonary congestion 4. Dopamine increase myocardial contractility and renal venodilator used in acute heart failure 5. (In)amrinone milrinone prefferd reduces thrombocytopenia ,liver toxicity REDUCED PRE AND AFTER stimulate myocardial contractility used IV for short term

Question 54

.What is the MOA of dopamine or dobutamine ?

Answer 54

stimulation of cardiac myocyte dopamine D1 receptor & and B adrenergic receptor by stimulating D1 receptor muscles on smooth muscles and d2 receptors on sympathetic nerves

Question 55

where does dopamine act

Answer 55

splanchnic and renal arterail beds and increase renal blood flow therefore maintaing GFR INCREASES Cardiac output

Question 56

Explain the different effects of the dose of dobutamine or dopamine

Answer 56

low dose causes vasodilation less than 2 intermediate increase the b receptor stimulation on the heart and vascular sympathetic neurons high doses causes vasoconstriction which is used in circulatory failuure