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CVM DF > Drugs For Heart Failure > Flashcards

Drugs For Heart Failure Flashcards

1
Q

what is an inotropic agent

A

agent that modifies the force or speed of contraction of myocardium

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2
Q

what are some positive inotropic agents and what are they used for

A

cardiac glycosides like digoxin
used to directly treat myocardial dysfunction
-increase contractility

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3
Q

systolic heart failure effects

A

reduced CO and contractility
reduced ejection fraction below 45%
respond to positive inotropic agents

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4
Q

diastolic failure effects

A

from hypertrophy
CO reduced
ejection fraction may be normal
does not rewspond to postive intotropic agents

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5
Q

cardiac glycosides

example and clinical use

A

digoxin

used to treat heart failure and a fib

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6
Q

half life of digoxin for pts with normal fenal function

A

36-48 hours

in pts with renal insufficiency (or older pts) half life increases to 3.5-5 days

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7
Q

pt taking what may increase renal digoxin clearnace

A

pts with HF taking vasodilators or sympathomimetic agents

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8
Q

Digoxin MOA

-2 desired effects

A

inhibition of membrnae bound sarcolemma Na+/K+ ATPase
-casues increase in contraction of cardiac sarcomere

  • improves contractility
  • prolongs refractory period of AV node in pts with SVT arrhythmias (no affect on preload or afterload)
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9
Q

how do cardiac glycosides ultimately increase myocardial contractility

A

by increaseing the releasable Ca2+ from the SR

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10
Q

length of AP and cardiac glycosides

A

may be shortened bc increased Ca2+ dependent K+ channel activity elevated

-promotes K+ efflux and more rapid repolarization

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11
Q

parasympathomimetic effects are inhibtied by

A

atropine

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12
Q

digoxin and electrical cardiac effects at therapeutic levels

A

parasympathomimetic effects
-cholinergic innervation is more concentrated in the atria, resulting in increased actions of digoxin on atrial and AV nodes compared to purkinje or ventricular fnct

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13
Q

electrical cardiac effects at toxic levels

A

depol of resting potential
marked shortening of AP
appearance of oscilatory depolarizing afterpotentials

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14
Q

most common cardiac manifesations of digoxin toxicity include

A

changes to AV junctional rhythm
premature ventricular depol
bigeminal rhythm
2md degree av block

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15
Q

toxicity of digoxin

A

heart: arrhythmias

GI: anorexia, nausea, vomiting, diarrhea

CNS: vagal and chemoreceptor trigger zone stimulation can cause GI symptoms, disorientation, hallucinations, visual distrubance and or changes

Gynecomastia: rare and can affect men

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16
Q

digoxin and hyper/hypokalemia

A

hyper can reduce effects of digoxin toxicity

hypokalemia enhances effect

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17
Q

____calcemia and ___magnesemia increase risk of digoxin incued arrhtyhmia

A

hypercalcemia

hypomagnesia

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18
Q

what are the bipyridines

A

inamrinone and milrinone

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19
Q

bipyridine administration

A

only parenteral, short term therapy

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20
Q

bipyridine MOA

  • inhibits what enzyme
  • effect on heart
  • effect on calcium
  • effect on vasculature
  • effect on CO and afterload
A

inhibits PDE3 which usually degrades cAMP and cGMP so there is an increase in each

  • increased cAMP in heart result in direct stimulation of myocardial contractility and acceleration of myocardial relaxation
  • cAMP dependent PKs in heart phosphorylate and activate voltage gated Ca2+ channels and increase the amt of Ca2+ entering cell during AP
  • increased concentration of cAMP in vasculature
    • vasodilation by inactivating myosin LCK

-PDE3 inhibitors increase CO and decrease LV afterload

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21
Q

inamrinone toxicity

A

nausea, vomiting, arrhythmias, thrombocytopenia, and liver enzyme changes

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22
Q

milrinone toxicity

A

arrhythmias

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23
Q

B adreneergic agonist in HF

A

dobutamine

24
Q

MOA of dobutamine and dopamine

A

increase cAMP–>PKA–>phosphorylation of substrates that enhance Ca2+ dependent contraction and speed relaxation

25
Q

dobutamine is B agonist of choice for management of pts with

A

systolic dysfunction and HF

26
Q

dobutamine hemodynamic effect

A

increase in stroke volume due to its positive inotropic action and increase in CO

27
Q

major side effect of dobutamine

A

tachy and arrhythmias

28
Q

DOPAMINE AND HF low dose

A

-may be useful in pts if there is a need to raise BP

  • at low doses, causes vasodilation
    • cAMP dependent relax and stimulating presynaptic D2 receptors inhibiting norepinephrine release and action on a-adrenergic stimulation of vascular SM)
29
Q

dopamine at intermediate dose

A

directly stimulates B receptors on heart and vascular sympathetic neurons

enhances cardiac contractility and neural norepinephrine release

30
Q

high dose dopamine

A

causes peripheral arterial and venous constriction via a-adrenergic receptor stimulation

-good for pts where circulatory failure is result of vasodilation like sepsis and anaphylaxis

31
Q

thiazide diuretics are most freq used in treatment of

A

systemic hypertension and have more restricted role in treatment of HF

32
Q

loop diuretics are widely used in

A

the treatment of heart failure

33
Q

potassium sparing diuretics

A

shown to improve survival in pts with advanced heart failure via a mechanism independent of diuresis

34
Q

vasopressin (ADH) antagonist name, MOA, toxicity

A

conivaptan
blocks ADH receptors (V1a and V2)
can cause hypernatremia, nephrogenic diabetes insipidus

35
Q

selective ADH antagonist

A

tolvaptan blocks V2 ADH receptors

36
Q

inhibtior of actions of angiotensin II will reduce what

A

preload (intravascular volume reduced by blocking aldosterone secretion)

afterload (via vasodilation)

37
Q

what causes reductino in mortality and morbidity of HF pts when taking ACEI

A

kinins no longer degraded so stimulate NO, cGMP, vasoactive eicosanoids
-these prevent angiotensin II from cardiac and remodeling

38
Q

ARBS block what receptor

A

AT1

39
Q

venodilator

A

isosorbinde dinitrate

40
Q

MOA of isosorbide dinitrate

A

release NO and activates guanylyl cyclase

-venodilation and reduces preload and ventricular stretch

41
Q

AE isosorbide dinitrate

A

postural hypotension, tachy, headache

42
Q

isosorbide dinitrate useq

A

in actute and chronic HF as well as angina

43
Q

arteriolar dilators

A

hydralazine

  • direct vasodilation of arterioles, little effect on veins
  • reduces BP and afterload, increased CO
44
Q

AE hydralzine

A

tachy, fluid retention, lupus like syndrome

45
Q

combined arteriolar and venodilator

A

nitroprusside

46
Q

MOA nitroprusside

A

release NO and activates guanylyl cylase

47
Q

use nitroprusside

A

acute cardiac decompensation and HTN emergencies

48
Q

Nesiritide use

A

actuely decompensated HF with dyspnea at rest or with minimal activity

49
Q

Nesiritide MOA

A

binds guanylate cyclase receptor on vascular SM and endothelial cells–>increase cGMP–>SM relaxation

50
Q

AE nesiritide

A

excessive hypotension

reports of significant renal damage and death

51
Q

B adrenergic receptor blockers used to treat HF

  • how long required until improvement noted
  • dose to administer
A

bisoprolol (B1 selective antagonist)

carvedilol (non selective B antag, a1 antag)

metoprolol (B1 selective antag, mild to mod HF)

  • several months
  • also administrer at low doses to prevent worsening of HF due to antagonism of catecholamine effects
52
Q

sodium removal danger

A

thiazide or loop diuretic induced sodium loss causes secondary loss of potassium

-dangerous if pt is taking digoxin–>increase its action and cause arrhythmnias

53
Q

first line therpay for chronic heart failure

A

ACEI with diuretics

54
Q

vasodilators: in pts with high filling pressures, in whom principal symtom is dyspnea ___ dilators most helpful in reducing filling pressures and sympoms of pulmonary congestion

A

venous

55
Q

vasodilators: in pts with fatigue due to low left ventricular output, ___ may help increase CO

A

atrial dilators

56
Q

when is digoxin given

A

if diuretics and ACEI fail to control symptoms

-small therapeutic window

CVM DF (15 decks)

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