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2nd Semester Final > Drugs for Treatment of Heart Failure Lecture PDF > Flashcards

Drugs for Treatment of Heart Failure Lecture PDF Flashcards

8=D

1
Q

Types of heart lesions that can facilitate the vicious cycle of heart failure (5)

A
  • ischemia
  • infarction
  • myopathy
  • hypertension
  • valve disease
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2
Q

Vicious cycle of heart failure mech of action

A
  • Cardiac lesion decreases cardiac performance
  • Baroreceptor fails to be stimulated resulting in increased sympathetic response
  • vasomotor response to constrict to increase pressure to perfuse various organs of the body
  • Kidney’s juxtaglomerular cells activates RAAS system which causes vasoconstriction and fluid retention (aldosterone)
  • workload of heart is increased (afterload and preload)
  • increased workload causes myocardial cell structural damage
  • further impaired decreased cardiac performance dropping cardiac output even more
  • this stimulates causes failure to stimulate baroreceptors….
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3
Q

Drug classes for management of heart failure (4)

A
  • B blockers
  • ACE inhibitors
  • aldosterone antagonists
  • diuretics
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4
Q

2 natriuretic peptides released by heart and their function

A

1) Atral natriuretic peptide - released in response to increased stretching of atrium to promote loss of Na+ and H2O into urine
2) B natriuretic peptide - Released in response to increases stretching of ventricles and promote arterial and venous dilation and increase GFR to kidney resulting in decreased systemic resistance and loss of Na+ and H2O in urine

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5
Q

Natriuretic peptides are beneficial in ____

A

diagnosis of heart failure

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6
Q

Why are ACEI preferred to ARB’s in HF

A

ACEI increase levels of bradykinin which also help in vasodilation and reducing pressure making them HIGHLY efficacious agents, despite the side effect of cough

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7
Q

Drug treatment clinical outcomes in patients with heart failure with preserved ejection fraction

A

-little evidence it improves clinical outcomes beyond relief

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8
Q

3 routine therapies for heart failure and how they impact the condition

A
  • diuretics (decrease preload, afterload, pulmonary edema, cardiac distension)
  • RAAS inhibitors (promote dilation of artereioles and veins and decrease aldosterone release)
  • B blockers (not understood mechanism)
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9
Q

DOC for patients with severe heart failure and why

A

Loop diuretics (furosemide), promote strong diuresis and work even when GFR is low

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10
Q

Unless contraindicated, all patients with HFrEF should receive what drug class for treatment?

A

ACEI

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11
Q

3 major benefits of ARB’s

A
  • promote dilation of arterioles
  • promote dilation of veins
  • decrease release of aldosterone
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12
Q

ARB’s 4 effects in heart failure, but why are they not preferred?

A
  • improve LV ejection fraction
  • reduce heart failure symptoms
  • increase exercise tolerance
  • reduce mortality

Do not increase kinin levels having less favorable impact on cardiac remodeling than ACEI

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13
Q

sacubitril/valsartan (entresto) drug class, function, and mech of action

A
  • Angiotensin receptor neprilysin inhibitor (ARNI)
  • approved for patients with class II-IV HF to be used in place of an ACEI or ARB as it is superior than elanapril alone when looking at reduced risk of CV related death
  • functionally increases natriuretic peptide levels by inhibiting neprilysin that breaks them down
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14
Q

sacubitril/valsartan (entresto) ADR’s (4)

A
  • hypotension by volume depletion
  • cough
  • hyperkalemia
  • fetal harm
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15
Q

Aliskiren (tekturna) function

A

Can shut down RAAS by binding renin, should work as well as ACEI and ARB’s but is only approved for HTN and not for treatment of HF (doesn’t improve outcomes)

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16
Q

Aldosterone antagonists functions (2) and two examples

A
  • Block receptors for aldosterone in heart and blood vessels, can prevent myocardial remodeling and delay fibrosis (aldosterone increases fibrosis of myocardium and vascular) (as well as its original function to prevent Na+ and thus H2O retention with K+ excretion)
  • spironolactone and eplerenone
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17
Q

To avoid the endocrine effects of spironolactone, it is preferable to use the equivalent…

A

…eplerenone (inspra)

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18
Q

B-blockers indication and 3 uses in HF

A

Used in patients class II-IV HF, thru unknown mechanism -can increase LV ejection fraction

  • prevent progressive enlargement
  • decrease intracardiac and pulmonary vascular pressures over 1-3 months
19
Q

B blockers ADR’s (4)

A
  • caution in patients with asthma or severe bradycardia
  • fluid retention
  • fatigue
  • hypotension (need to start at low dose)
20
Q

Ivabradine (Corlanor) drug class and indications

A
  • SA node inhibitor (selective for funny channels slowing firing of SA node and reducing HR)
  • indicated for patients with resting HR of at least 70bpm and are on max doses of B blockers or have contraindications of it, and have and LVEF equal or less than 35%
21
Q

Ivabradine (Corlanor) mech of action

A

-causes dose dependent reduction in HR by blocking channels responsible for cardiac pacemaker current, does not affect BP

22
Q

Ivabradine (Corlanor) ADR’s (3) and contraindications (3)

A
  • Bradycardia
  • hypertension
  • afib
  • Low BP
  • sick sinus syndrome
  • 3rd degree heart block
23
Q

Sympathomimetic and PDE inhibitors function

A

IV drugs for treatment of acute heart failure when vasodilator drugs are not effective in restoring hemodynamics

24
Q

Dopamine (inocor) function at diff doses

A

Low - stimulate kidneys
Intermediate - increase inotropy and thus SV/CO
Large - stimulates a1 receptors on vascular smooth muscle producing vasoconstriction

25
Q

Dobutamine function

A

Catecholamine with selective activation of B1 adrenergic receptors not acting on a1 receptors and thus does not increase vascular resistance, preferred for short term treatment of acute HF by IV

26
Q

Amrinone (Inocor) drug class and function

A
  • Phosphodiesterase inhibitor
  • Short term treatment of HF by increasing cAMP activity creating a pos inotropic effect refractory to digoxin, diuretics, and vasodilators
27
Q

Isosorbide dinitrate plus hydralazine (ISDN) drug class and function

A
  • Vasodilator
  • Used for treatment of HF, used to dilate veins, release nitric oxide, and cause relaxation of vascular smooth muscle in severe refractory HF to reduce congestion
28
Q

Isosorbide dinitrate plus hydralazine (ISDN) drug interaction

A

-should not be taken with phosphodiesterase inhibitors such as sildenafil

29
Q

Hydralazine function

A

Adjunct treatment for CHF in combo with ISDN allowing for vasodilation improving CO and renal blood flow

30
Q

BiDil (Nitromed) function

A

Fixed dose combo of ISDN that is approved for adjunctive use in treatment of heart failure in black patients

31
Q

Nitroglycerin function

A

Potent venodilator causing a dramatic decrease in preload on the heart, in HF used to reduce acute severe pulmonary edema but should not be taken with PDE5 inhibitors such as sildenafil

32
Q

Sodium nitroprusside (nitropress) function

A

Agent to rapidly dilate arterioles and veins for short term therapy of severe HF

33
Q

Nesiritide (natrecor) function

A

Synthetic form of BNP used in short term IV treatment, dilates both veins and arterioles reducing pre and afterload

34
Q

Digoxin (lanoxin, loxicaps) drug class and function

A
  • Old school family of drugs known as cardiac glycosides
  • indicated for HF and control of arrhythmias derived from purple foxglove plant, does NOT prolong life despite reducing symptoms by increasing contractility and exercise tolerance
35
Q

Digoxin (lanoxin, loxicaps) mech of action

A
  • accelerates entry of Ca2+ into cardiac muscle cells
  • during AP, Na+ and Ca2+ enter cardiac muscle cells and K+ exits
  • Then Na/K ATPase pumps things back and Ca2+ leaves via Na/Ca transporter
  • Inhibits adenosine triphophate (ATPase which energizes Na+/K+ pump
  • buildup stimulates exchane of Na for Ca2+, increasing levels in cell
  • greater contraction
  • too much K+ will inhibit effect of digoxin
36
Q

What must be monitored and kept in normal range when on digoxin?

A

K+

37
Q

Beneficial effects of digoxin (3)

A
  • decrease sympathetic tone (more complete ventricular filling)
  • increased urine output
  • decreased renin release
  • electrical effects on heart
38
Q

Efficacy of digoxin in HF depends on…

A

…cardiac reserve, if heart is too sick there will be minimal effects

39
Q

Digoxin electric effects

A
  • inhibit Na+/K ATPase
  • enhance vagal influences on heart
  • increase automaticity potentially generating ectopic foci resulting in ventricular arrhythmias
  • AV block with escape beats***
40
Q

Most common cause of arrhythmias

A

Hypokalemia secondary to diuretic use

41
Q

Diagnosis of cardiotoxicity in digoxin administration

A

-very complex, unknown if arrhythmia caused by digoxin or disease process, resolution upon withdrawal confirms diagnosis

42
Q

Drug for patients with bradycardia or AV block due to digoxin toxicity and why

A

Atropine - it is an anticholinergic that inhibits parasympathetic action on the heart, therefore reversing some of the effect of digoxin toxicity via a separate mechanism

43
Q

Digoxin dosing

A

Use ng/ml opposed to mg

2nd Semester Final (207 decks)

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