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CV II Exam III > Drugs used in heart failure (Linger) > Flashcards

Drugs used in heart failure (Linger) Flashcards

1
Q

digoxin

A

cardiac glycoside

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2
Q

inamrinone

A

bipyridine

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3
Q

milrinone

A

bipryidine

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4
Q

beta -agonist s (2)

A

dobutamine

dopamine

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5
Q

bumetanide

A

loop diuretic

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6
Q

furosemide

A

loop diuretic

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7
Q

torsemide

A

loop

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8
Q

HCTZ

A

thiazide diuretic

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9
Q

eplerenone

A

aldosterone antagonist

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10
Q

spironolactone

A

aldosterone antagonist

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11
Q

Conivaptan

A

ADH antagonist

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12
Q

Tolvaptan

A

ADH antagonist

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13
Q

Captopril, Enalapril, Fosinopril, Lisinopril, Quinapril, Ramipril

A

ACE inhibitors

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14
Q

Candesartan, losartan, valsartan

A

ARB

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15
Q

Isosorbide dinitrate

A

venodilator

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16
Q

hydralazine

A

arteriolar vasodilator

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17
Q

nitroprusside

A

combined arteriolar and venodilator

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18
Q

bisoprolol, carvedilol, metoprolol, nebivolol

A

B- blockers

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19
Q

nesiritide

A

natriuretic peptide

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20
Q

when does HF occur?

A

when cardiac output is inadequate to provide the oxygen needed by the body, usually due to a decrease in contractility of the myocardium, which can be caused by diminished coronary blood flow

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21
Q

what type of agents (working on what) are more valuable in long-term treatment of heart failure?

A

agents that act directly on organs and systems other than the heart

(ie. ACE inhibitors, ARB’s, Beta blockers and Aldosterone receptor antagonists)

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22
Q

i) Reduced cardiac output and contractility
ii) Reduced ejection fraction ( 60%)
iii) Typical of acute failure (e.g., resulting from myocardial infarction)
iv) Responds to positive inotropic agents

what is this?

A

systolic failure

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23
Q

i) Occurs as a result of hypertrophy and stiffening of the myocardium
ii) Cardiac output is reduced
iii) Ejection fraction may be normal
iv) Does not typically respond optimally to positive inotropic agents

what is this?

A

diastolic failure

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24
Q

what are the signs and symptoms of heart failure?

A

d) Signs and symptoms of all forms of heart failure include tachycardia, decreased exercise tolerance, shortness of breath, peripheral and pulmonary edema, cardiomegaly;

*** decreased exercise tolerance is the major direct consequence of diminished cardiac output while other manifestations result from compensatory adaptations

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25
Q

what are the uses of digoxin

A

heart failure

a-fib

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26
Q

how many doses a day can you give digoxin typically

A

once a day for patients with normal renal function

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27
Q

what is the MOA of digoxin

A

at the molecular level, digoxin causes inhibition of the membrane-bound (sarcolemma) Na+/K+ ATPase, ultimately causing an increase in the contraction of the cardiac sarcomere

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28
Q

what are the 2 desired effects of digoxin

A

(1) to improve contractility of the failing heart and
(2) to prolong the refractory period of the atrioventricular node in patients with supraventricular arrhythmias (no effect on preload or afterload)

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29
Q

what is the mechanism by which digoxin has positive inotropic effects?

A

(a) Inhibition of the Na+/K+ ATPase stops the cellular Na+ pump activity and reduces the rate of active Na+ extrusion out of the cell, which results in a rise in intracellular Na+ concentrations
(b) Rising intracellular Na+ concentrations reduce the transmembrane Na+ gradient that drives the extrusion of intracellular Ca2+ during myocyte repolarization by the Na+/Ca2+ exchanger (NCX)
(c) With reduced Ca2+ efflux and repeated entry of Ca2+ with each action potential, Ca2+ accumulates in the myocyte
(d) Ca2+ uptake into the sarcoplasmic reticulum (SR) is increased and more Ca2+ becomes available for release from the SR during the next action potential, which enhances myocardial contractility
(e) Therefore, cardiac glycosides increase myocardial contractility by ultimately increasing the releasable Ca2+ from the SR **
(f) The magnitude of the positive inotropic effect correlates with the degree of Na+/K+ ATPase inhibition

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30
Q

what are the electrical cardiac effects at therapeutic levels of digoxin…. (effects on action potentials and mechanism of action)

A

(a) Direct actions on the membranes of cardiac cells follow a well-defined progression: an early, brief prolongation of the action potential, followed by action potential shortening (especially the plateau phase)

(b) The decrease in action potential duration may be the result of increased potassium conductance that is caused by increased intracellular calcium
(i) Digoxin-induced elevated intracellular Ca2+ increases the activity of Ca2+-dependent K+ channels
(ii) Increased Ca2+-dependent K+ channel activity promotes K+ efflux and a more rapid repolarization (i.e., shortened cardiac action potential)

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31
Q

what are digoxins effect on the parasympathetic NS.

A

increases parasympathetic tone and reduces centrally mediated sympathetic nervous system tone

(iv) Cholinergic innervation is more concentrated in the atria, resulting in increased actions of digoxin on atrial and atrioventricular nodes compared to Purkinje or ventricular function (see table below)

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32
Q

what are the most common cardiac manifestations of digoxin toxicity ?

A

toxic levels–> (less negative resting potential, shortening of AP, Delayed after depolarizations)

(b) Most common cardiac manifestations of digoxin toxicity include changes to atrioventricular junctional rhythm, premature ventricular depolarization, bigeminal rhythm, and second-degree atrioventricular blockade (it is claimed that digoxin can cause virtually any arrhythmia)

(c) If allowed to progress, the tachycardia may deteriorate into fibrillation that could be fatal unless corrected
(d) At toxic levels, sympathetic outflow is increased by digoxin, which exaggerates toxic effects of the drug

33
Q

what are the effects of Digoxin on the EKG at therapeutic doses? at toxic doses?

A

Therapeutic –> increase PR interval, decrease QT interval

toxic–> tachy, fibrillation, arrest at very high doses

34
Q

what is the effect of digoxin on the Sinus node

A

decreases rate

35
Q

what is the effect of digoxin on atrial muscle

A

decreases refractory period

36
Q

what is the effect of digoxin on the AV node

A

decrease conduction velocity

increase refractory period

37
Q

what is the effect of digoxin on purkinje system and ventricular muscle

A

slight decrease in refractory period

38
Q

toxicity of digoxin has what effect on the GI system? CNS? other side effects of toxicity–> something that occurs in men?

A

(3) Gastrointestinal system (most common site of digoxin toxicity outside the heart)
(a) Anorexia, nausea, vomiting, and diarrhea
(b) Due to direct effects on the GI tract and CNS actions

(4) CNS: vagal and chemoreceptor trigger zone stimulation can cause GI symptoms; disorientation, hallucinations, and visual disturbances and/or changes
(5) Gynecomastia is a rare effect that can occur in men

39
Q

what are the interactions that Digoxin has with K+ and what are the results of hyper and hypokalemia

A

(1) Digoxin and potassium bind to competing sites on the Na+/K+ ATPase

(a) Hyperkalemia can reduce the effects of digoxin (especially the toxic effects)
(b) Hypokalemia can potentiate the toxic effects of digoxin

hyperkalemia –> inhibits abnormal cardiac automaticity

40
Q

what are the outcomes of having hypercalcemia and hypomagnesemia ?

A

increase the risk of a digoxin-induced arrhythmia

41
Q

what are bipyridines used for?

A

Approved for the short-term ** support of the circulation in acute decompensated heart failure

42
Q

MOA of bipyridines ?

A

cause selective inhibition of phosphodiesterase isozyme 3 (PDE3), which increases cyclic adenosine monophosphate (cAMP) concentrations (phosphodiesterase enzymes degrade cellular cAMP and cGMP)

(2) Increased concentrations of cAMP in the heart result in direct stimulation of myocardial contractility and acceleration of myocardial relaxation

(a) cAMP-dependent protein kinases (PKA) in the heart phosphorylate and activate voltage-gated Ca2+ channels, increasing the amount of Ca2+ entering the cell during an action potential
(b) Increased concentrations of Ca2+ increase the force of contraction of the heart
(c) PKA also phosphorylates other targets resulting in a faster rate of relaxation

43
Q

what is the effect of increasing cAMP in the vasculature

A

balanced arterial and venous dilation with a consequent fall in systemic and pulmonary vascular resistances and left and right heart filling pressure

(a) cAMP-dependent protein kinases in smooth muscle phosphorylate and inactivate myosin-light chain kinase
(b) Inactivation of myosin-light chain kinase causes smooth muscle relaxation (vasodilation)

44
Q

what are Caffeine and theophylline classified as?

A

nonspecific PDE inhibitors and their use in HF is limited by their lack of specificity and side effects

45
Q

toxicity of inamrinone

A

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

46
Q

milrinone toxicity

A

arrhythmias (bone-marrow suppression and liver toxicity is less likely compared to inamrinone)

47
Q

what are beta agonist used for?

A

short term support of the circulation in acute decompensated heart failure

48
Q

what is the MOA of b agonists

A

act via stimulation of the cardiac myocyte dopamine D1 receptor (dopamine) and β1-adrenergic receptor (dobutamine)

(1) Receptor activation leads to stimulation of the GS-adenylyl cyclase-cAMP-protein kinase A (PKA) pathway
(2) PKA phosphorylates a number of substrates that enhance Ca2+-dependent contraction and speed relaxation

49
Q

dobutamine

A

(1) Stimulates β1-receptors with little effect on β2- or α-receptors (β1 selective)
(2) The β agonist of choice for the management of patients with systolic dysfunction and HF
(3) Principal hemodynamic effect is an increase in stroke volume due to its positive inotropic action and an increase in cardiac output
(4) The major side effects are excessive tachycardia and arrhythmias
(5) Parenteral administration

50
Q

low doses of dopamine

A

dopamine causes vasodilation by stimulating dopaminergic (D1) receptors on smooth muscle (causing cAMP-dependent relaxation) and by stimulating presynaptic D2 receptors on sympathetic nerves in the peripheral circulation (inhibiting norepinephrine release and reducing α-adrenergic stimulation of vascular smooth muscle)

51
Q

intermediate doses of dopamine

A

dopamine directly stimulates β receptors on the heart and vascular sympathetic neurons (enhancing cardiac contractility and neural norepinephrine release)

52
Q

high doses of dopamine

A

high doses, dopamine causes peripheral arterial and venous constriction via α-adrenergic receptor stimulation, which may be desirable in patients where circulatory failure is the result of vasodilation (e.g., sepsis, anaphylaxis)

53
Q

what is the roles of diuretics in HF?

A

i) Play a key role in the pharmacological management of ‘congestive’ symptoms in patients with HF
ii) Major mechanism of action in HF is to reduce extracellular fluid volume, venous pressure, and ventricular preload (highlights the central role of the kidney in the hemodynamic, hormonal, and autonomic responses to myocardial failure)
iii) Results in reduction of edema and its symptoms, and reduction of cardiac size, which leads to improved pump efficiency
iv) Reduces preload with no significant effect on afterload

loop diuretics are widely used
thiazide diuretics are used more in systemic HTN treatment

54
Q

what does increased aldosterone do to the heart and what are the systemic effects?

A

(1) One of the principle features of HF is marked activation of the renin-angiotensin-aldosterone system (some patients with HF have plasma aldosterone concentrations as high as 20 times the normal level)
(2) Aldosterone not only is involved in increased sodium and water retention but may also cause myocardial and vascular fibrosis (remodeling) and baroreceptor dysfunction
(3) Antagonism of the effects of aldosterone has been shown to improve survival in patients with advanced HF (mechanism unknown)

55
Q

conivaptan MOA and toxicity

A

antagonist at ADH receptors (V1a and V2) in the cortical collecting tubule

(5) Toxicity: conivaptan can cause hypernatremia, nephrogenic diabetes insipidus

56
Q

what does inhibition of ang II do

A

reduces preload (blocks aldosterone secretion) AND afterload (via vasodilation)

(1) ACE inhibitors suppress angiotensin II production (by inhibiting ACE) and, as a result, decrease aldosterone production, reduce salt and water retention, and reduce preload
(2) ACE inhibitors reduce afterload by reducing total peripheral resistance (arterial vasodilation)
(3) ACE inhibitors decrease sympathetic nervous system activity, most likely through attenuation of presynaptic angiotensin effects on norepinephrine release
(4) ACE inhibitors reduce the long-term remodeling of the heart and vessels
(5) ACE inhibitors potentiate the effects of diuretics in heart failure

57
Q

what is the mechanism by which ACE inhibitors reduce long term remodeling of the heart and vessels ?

A

(a) Mechanism: ACE is the same enzyme as kininase II, which degrades bradykinin and other kinins
(b) Kinins stimulate the production of nitric oxide (NO), cyclic GMP, and vasoactive eicosanoids, substances which seem to oppose the effects of angiotensin II on the growth of vascular smooth muscle and cardiac fibroblasts and on production of extracellular matrix
(c) Increased levels of bradykinin that result from ACE inhibition may play a role in the hemodynamic and anti-remodeling effects of ACE inhibitors
(d) This mechanism may be responsible for the observed reduction in mortality and morbidity of HF patients

58
Q

what are the adverse effects of ACE inhibitors

A

cough
angioedema
mild hyperkalemia

59
Q

ARB’s

A

selectively block AT 1 receptor (ANG II receptor)

arbs do not alter bradykinin metabolism

60
Q

how are vasodilators used in HF?

A

i) Vasodilators are effective in acute heart failure because they provide a reduction in preload (through venodilation), or reduction in afterload (through arteriolar dilation), or both
ii) Vasodilators relax vascular smooth muscle by supplying nitric oxide (NO) and thereby activating soluble guanylyl cyclase, which increases cGMP concentrations and ultimately results in relaxation
iii) Examples include nitrovasodilators (isosorbide dinitrate, isosorbide mononitrate, nitroglycerin, sodium nitroprusside), hydralazine, and nesiritide

61
Q

What re the venodilators

A

isosorbide dinitrate

nitroglycerin

62
Q

what is the MOA of isosorbide dinitrate

uses?

adverse effects

A

(a) MOA: NO released when drug is metabolized; NO activates guanylyl cyclase
(b) Causes venodilation and reduces preload and ventricular stretch

(c) Used in acute and chronic HF as well as angina and hypertensive emergencies

(d) Long-term effectiveness limited by nitrate tolerance, which may be reduced by co-treatment with hydralazine
(e) Adverse effects include postural hypotension, tachycardia, headache

63
Q

nitroglycerin uses

A

venodilator used for acute decompensated heart failure

64
Q

what are the arteriolar dilators

A

hydralazine

65
Q

MOA of hydralazine
uses
toxicities

A

(a) Stimulates release of NO from endothelium
(b) Causes direct vasodilation of arterioles with little effect on veins
(c) Reduces blood pressure and afterload; results in increased cardiac output
(d) Used in combination with nitrates to reduce mortality in patients with HF, possibly by reducing damaging remodeling; also used in hypertensive emergencies
(e) Toxicities include tachycardia, fluid retention, lupus-like syndrome

66
Q

nitroprusside

uses

A

combined arteriolar and venodilator

(a) MOA: spontaneously converted to NO, which activates guanylyl cyclase
(b) Causes marked vasodilation and profound reduction in preload and afterload
(c) Used for acute cardiac decompensation and hypertensive emergencies

67
Q

nesiritide

MOA
adverse effects

A

(1) Recombinant form of human brain natriuretic peptide (BNP) that has been approved for treatment of acutely decompensated HF with dyspnea at rest or with minimal activity
(2) MOA: binds to natriuretic peptide receptor (NPR) on vascular smooth muscle and endothelial cells, increasing intracellular cyclic GMP, resulting in smooth muscle cell relaxation and reduced endothelin production
(3) The vasodilation, natriuresis, and diuresis produced by nesiritide counteract the effects of angiotensin and norepinephrine
(4) Given intravenously
(5) Most common adverse effects include excessive hypotension; IV administration of nitroglycerin or nitroprusside is usually preferred vasodilator therapy in acute decompensated heart failure

68
Q

bisoprolol

A

β1-selective antagonist; off-label use for HF in USA

69
Q

Metoprolol

A

β1-selective antagonist; mild-to-moderate heart failure

70
Q

carvedilol

A

nonselective α and β receptor antagonist with vasodilating activity; mild-to-severe heart failure

71
Q

nebivolol

A

β1-selective antagonist; off-label use for HF in USA

72
Q

what is the mechanism of beta antagonist is HF

A

(1) Improve contractile function (inotropic and chronotropic) by upregulating beta receptors
(2) Attenuation or prevention of the maladaptive catecholamine-induced cardiomyocyte toxicity (including apoptosis)
(3) Favorable effects on remodeling (improving LV geometry to increase ejection fraction)
(4) Reduce myocardial oxygen consumption
(5) Decrease the frequency of unstable tachyarrhythmias

73
Q

if you use thiazide and/or loop diuretics with digoxin, what can happen?

A

i) Thiazide or loop diuretic-induced sodium loss causes secondary loss of potassium, which is hazardous if the patient is to be given digoxin (hypokalemia can cause prolonged action potential duration, increased pacemaker rate, and increased pacemaker arrhythmogenesis, which enhances some of the toxic effects associated with digoxin)
ii) Hypokalemia can be treated with supplements, through the addition of an ACE inhibitor, or addition of a potassium-sparing diuretic such as spironolactone or eplerenone

74
Q

what is first line therapy for chronic heart failure

A

ACE inhibitor and along with diuretic

75
Q

use of hydralazine and isosorbide dinitrate are beneficial in what type of patients

A

ii) Concurrent use of hydralazine and isosorbide dinitrate may be beneficial in patients, particularly African-Americans, who cannot tolerate or continue to have symptoms with standard therapy

76
Q

in patients with high filling pressures in whom the principal symptom is dyspnea, what is the most useful therapy

A

venous dilators will be most helpful in reducing filling pressures and the symptoms of pulmonary congestion

77
Q

in patients with fatigue due to low left ventricular output what is the most useful

A

arteriolar dilators (hydralazine) to help increase CO (by decreasing afterload)

78
Q

at what dose should you start a beta blocker

A

i) Initiate at low doses to prevent worsening of heart failure due to antagonism of catecholamine effects
ii) Several months of therapy may be required before improvement is seen

79
Q

how should you administer digoxin…

A

i) Often given if diuretics and ACE inhibitors fail to control symptoms
ii) Slow loading is advantageous due to the small therapeutic window (mortality rate is reduced in patients with serum concentrations of less than 0.9 ng/mL but increased with levels greater than 1.5 ng/mL)
iii) Although digoxin has no net effect on mortality, it reduces hospitalization and deaths from progressive heart failure at the expense of an increase in sudden death

CV II Exam III (14 decks)

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