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CVS Pharmacology > Drug Therapy Of Heart Failure > Flashcards

Drug Therapy Of Heart Failure Flashcards

1
Q

Treatment of diastolic heart failure

A

BB, verapamil, diuretics (in volume overload), ACEI (to prevent remodeling)

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2
Q

Compare compensated & decompensated heart failure

A
  • Inability of heart to pump blood results in dec blood pressure whicha ativates renin-angiotensin system & adrenergic, leading to VC & inc Aldisterone w salt & water retention, inc HR & ventricular hypertrophy, thus compensated heart failure.
  • Persistent activation of adrenergic & renin-angiotensin systems causing inc after & preload on diseased heart , leading ventricular dilation & inc O2 consumption with constant supply, damage of cardiac myocytes. Inc EDV & EDP with dec COP, thus it is decompensated HF.
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3
Q

Mention drugs used to dec preload in AHF & CHF

A

CHF, ACEI, ARBs, nitrates, loop diuretics

AHF, nitroprusside, nitrates, loop diuretics

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4
Q

Mention drugs used to dec afterload in AHF & CHF

A

CHF, hydralazine, ACEI, ARBs

AHF, nitroprusside

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5
Q

Mention drugs which inc contractility in AHF

A

Dopamine
Dobutamine
Inamrinone

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6
Q

Mention drugs which protect heart & dec mortality in CHF

A 
Beta bloccker (MBC)
Spironolactone/eplerenone
(ACEI/ARBs/ARNI)
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7
Q

Compare hydralazine & nitrates

A

H: causes arteriodilatation, dec afterload, inc COP, improved symptoms of low COP.
N: cause venodilation, dec preload & venous return, dec psystemuc, pulmonary conhpgestion, improve congestive symptoms.

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8
Q

Describe mechanism of action of ACEI

A

Inhibit ACE which converst ang I to ang II and breaks down bradykinin
Leading to dec ang II & inc bradykinin w inc in vasodilator PG & NO

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9
Q

Mention advantages if ACEI

A
  1. Vasodilatation in both arteries (inc COP) and veins (dec venous congestion)
  2. Inhibition of aldosterone secretion ( Na & water loss, K retention)
  3. Prevent ventricular hypertrophy & cardiac remodelling after myocardial infarction
  4. Dec central & peripheral NE thus it blunts sympathetic reflexes, dec BP with no reflex tachycardia
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10
Q

Mention drug acting on tissue ACE & having dual elimination

A

Fosinopril

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11
Q

Advantages of ACEI

A
  1. Improve exercise tolerance & congestive symptoms
  2. Renoprotective esp in diabetics
  3. Dec CVS mortality
  4. Does no induce tachycardia/salt & water retention
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12
Q

Mention indications of ACEI

A
  1. Hypertension
  2. Heart failure (all cases of LV dysfunction)
  3. Myocardial infarction
  4. Nephropathy
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13
Q

GR: ACEI is used in AMI

A
  1. Dec aldosterone-induced remodelling & prevent heart failure
  2. Dec sudden death (dec arrhythmia 2ry to hypokalemia & symp overactivity
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14
Q

Mention members of ACEI which are NOT prodrugs

A

Captopril

Lisinopril

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15
Q

Lisinopril can be used in ….

A

Liver disease

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16
Q

Only ACE used in emergeny

A

Enalaprilat (given IV)

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17
Q

ACEI need dose adjustment in ……

A

Renal disease

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18
Q

Most common side effect of ACEI & most serious one.

Why?

A

Chronic dry cough (common)
Angioedema (rare but fatal)
Both due to accumulation of bradykinin

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19
Q

Mention less common adverse effects of ACEI

A
  1. 1st dose hypotension
  2. Hyperkalemia
  3. Hypersensitivty
  4. GIT
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20
Q

Mention serious side effects of ACEI

A

Renal impairment in high renin states (parients on diuretics, bilateral renal stenosis)
Fetotoxic & teratogenic
Bone marrow depression

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21
Q

Describe mechansim of action of ARBs

A

Block AT1 receptor which mediates most of the pathological CVS effects of Ang II
Spare AT2 receptor, VD & anti-proliferative effects

22
Q

Advantages if ARBs over ACE

A
  1. No dry cough, no BK production (angioedema still occurs)
  2. Antagonize Ang II produced by ACE & non ACE pathways
  3. Avoid hormonal escape (inc renin) with prolonged ACEI use
  4. Inc AgII activity on AT2, VD & antiproliferative effects
23
Q

Mention mechanism of action & disadvantages of hydralazine

A

K channel opener, hyperpolarization, prevent Ca influx causing arteriodilatation
Dis: rapid tolerance due to sympathetic & renin-angiotensin systems activation leading to salt & wtaer retention & inc HR

24
Q

Mention inidcations of hydralazine

A
  1. Heart failure with nitrates (alternative to ACEI)

2. HYPERTENSION (IV in eclampsia)

25
Q

Describe mechanism of action of nitroprusside & its indication

A

NO donor, in cGMP, VD by inhibiting Ca influx in wall of bv
Ind: most hypertensive emergencies (hypertensive encephalopathy), acute severe HF esp if associated with severe rise in BP

26
Q

Describe toxicity of nitroprusside

A
  1. Severe hypotension & myocardial infarction (due to reflex tachycardia)
  2. Cyanide & thocyanate toxicity
  3. Thiocyanate toxicity: CNS side effects & delayed hypo-thyroidism
27
Q

GR: Diuretics are used in HF

A

Dec plasma volume and venous return (preload), dec pulmonary congestion (improve orthopnea & nocturnal dyspnea), dec peripheral (ankle) edema.

28
Q

Mention advantages of spironolactone in HF

A

Dec mortality by 30%, dec Na retention and worsening of edema
Minimize diuretic induced hypokalemia, dec arrhythmia & sudden death
Dec myocardial hypertrophy & fibrosis induced by local aldosterone

29
Q

Mention orecautions of using spironolactone in HF

A

Use cautiously to avoid hyoerkalemia esp if combined w ACEI or in patients with renal impairment

30
Q

Mention drawbacks of chronic sympathetic stimulation

A
  1. Induce tachycardia & inc O2 demand
  2. Inc infarct size and propensity of cardiac remodelling MI
  3. Increase effect of RAAS on heart
  4. Persistent stimulation: myocyte hypertrophy, apoptosis, cardiac dilatation & ven thinning
  5. Inc cytokines as TNF & Interleukins, hypertrophy & apoptosis & fibrosis with ven wall stiffness
31
Q

Mention effects of carvedilol on HF

A

Inc EF
Improve symptoms
Slow disease progression
Dec hospitalization & mortality

32
Q

Mention the beneficial effects of BB in HF

A

Dec HR, improve coronary filling
Dec afterload, inc COP
Cardioprotection against adrenergic & Ag II-induced arrhythmia, myocardial damage & apoptosis
Improve LV remodeling
Resensitize downregulated B1 receptors in long standing cases, thus improve cardiac contractility

33
Q

Mention mechanism of action of bipyrimidine

A

Inodioator
Inhibit PDE-3, inc cAMP:
Inc cardiac contractility & COP
VD, dec afterload (PR) & preload (pulmonary congestion)

34
Q

Mention adverse effects of inodilators

A

Thrombocytopenia

Arrhythmia

35
Q

Describe mechansim of action of digoxin

A
  1. Inhibit Na/K/ATPase pump, thus Na conc increases IC, dec Ca outflux, so Ca IC conc increases Ca release from SR, +ve inotropic effect.
  2. Indirect vagal stimulation, -ve chrono & dromotrpoic effects. Also reduce sympathetic tone 2ry to inc COP.
36
Q

Describe mechanical effects of digoxin

A
  1. Inc COP
  2. Dec EDV & ESV
  3. Reduce cardiac size
  4. Reduce sympathetic tone, dec pre & afterload
  5. Diuretic effect due to inc COP & aldosterone antagonism
  6. Mobilize edema fluid
37
Q

Describe direct electrical effects of digoxin

A

Inc Ca IC, spontaneous delayed afterdepolarization, risk of extrasystole & vent tachycardia (dec ERP in cardiomyocytes)

38
Q

Mention effect of vagal stimulation of digoxin

A
  1. Dec HR in AF
  2. Overdose may lead to bradycardia & AV block
  3. Trun Af to AF by dec APR & ERP
39
Q

Mention indications of digoxin

A
  1. Systolic HF
  2. HF + AF
  3. Chronic AF
  4. PSVT
40
Q

Mention drugs combines w digoxin in chronic AF

A
  1. BB & verapamil to control ventricular rate

2. Before procainamide to control to countract atropine like action

41
Q

Describe pharmacokinetics of dugoxin

A

2/3 absorbed rest is broken down by intestinal flora
2/3 is bound to plasma protein
2/3 is excreted in urine rest in stool
T1/2 is 36 hrs

42
Q

Describe pharmacokinetic interactions of digoxin

A

Erythromycin , inc absorption

Antiarrhythmics, dec renal excretion & displace it from tissue & plasma proteins

43
Q

Describe pharmacodynamic interactions of digoxin

A

Diuretics, hypercalcemia, sympathomimetics (tachyarrhythmias)
BB & CCB, comlete heart block

44
Q

Mention CIs of digoxin

A
  1. Acute MI & rheumatic carditis
  2. AF+WPW
  3. Ventricular tachycardia (precipitates AF)
  4. Sick sinus syndrome
  5. HOCM
  6. Incomplete hert block
45
Q

Describe manifestations of digitalis toxicity

A
  1. GIT upset
  2. Cardaic arrhythmias (tachyarrhythmias or sinus bradycardia/heart block)
  3. CNS manifestations
  4. Gynecomastia
46
Q

Steps of treatment of treatment of digitalis toxicity

A
  1. Stop digitalis & K losing diuretics
  2. KCl ,CI in heart block
  3. Lidocaine/phenytoin
  4. Stropine in bradycardia/heart block
  5. Digibind in fatal toxicity
47
Q

Mention effect of digoxin of ECG

A
  1. Prolonged PR interval
  2. Shortened QRS & QT interval, dec APD & ERP
  3. Depressed ST, flat or inverted T wave
48
Q

Mention mechansim & side effect of nestiritide

A

Increase cGMP with VD of arteries & veins

Side effects: hypotension

49
Q

Mention class of drugs of sacubitril

A

Neprilysin inhibitor

50
Q

…… is an alternative if BB are CI

A

Ivabradine

51
Q

Mention benefits of natruitic peptide

A

VD, inc GFR, reduced renin from kidneys

52
Q

Mention role of tolvaptan in HF

A

ADH antagonist, excretion of electrolyte-free water, correct dilutional hyponatremia secondary to ADH inc in HF.

CVS Pharmacology (6 decks)

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