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CV Exam III > CIS: DRUGS USED IN HEART FAILURE > Flashcards

CIS: DRUGS USED IN HEART FAILURE Flashcards

1
Q

Inotropic Agents

A
  • Cardiac glycosides (e.g., digoxin)
  • Bipyridines
  • Inamrinone
  • Milrinone
  • Beta-adrenergic receptor agonists
  • Dobutamine
  • Dopamine
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2
Q

Agents Without Positive Inotropic Effects

A
  • Diuretics
  • Angiotensin converting enzyme (ACE) inhibitors
  • Angiotensin Receptor Blockers (ARBs)
  • Vasodilators
  • Beta-adrenergic receptor blockers
  • Natriuretic peptide
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3
Q

Heart Failure

A
  • Major contributor to morbidity and mortality worldwide
  • Five million cases of heart failure in the United States
  • Variety of causes and classifications
  • This CIS is limited to discussion of low-output failure due to systolic dysfunction
  • Heart failure occurs when cardiac output is inadequate to provide the oxygen needed by the body
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4
Q

heart failure therapies are focused on

A

heart failure due to reduced ejection fraction from systolic dysfunction

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5
Q

Compensatory Changes Associated with Heart Failure

A 
Increase sympathetic discharge
   increase force
   increase rate
   increase preload
   increase afterload

Increase ang II
remodeling
increase afterload and preload

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6
Q

Drug Therapy of Heart Failure

•Historic focus on end-point components

A
  • Volume overload (congestion) treated with diuretics
  • Myocardial dysfunction (heart failure) treated with positive inotropes
  • Stabilize hemodynamic decompensationand reduce symptoms
  • Do NOT improve survival
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7
Q

Drug Therapy of Heart Failure

•Current therapies target organs other than the heart

A
  • Renin-angiotensin-aldosterone system
  • Sympathetic nervous system
  • Goals are to reduce preload and afterload, and reduce maladaptive cardiac remodeling
  • ACE inhibitors, ARBs, aldosterone antagonists, and certain β-blockers have been shown to reduce mortality
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8
Q

A 58 y/o caucasianmale is admitted with a chief complaint of increasing shortness of breath and a recent 17 pound weight gain. Two weeks prior to admission, he noted the onset of dyspnea on exertion after one flight of stairs, orthopnea, and ankle edema. Since then, his symptoms have increased. He notes episodic bouts of paroxysmal nocturnal dyspnea and has only been able to sleep in a sitting position. He also notes a productive cough, nocturia(2-3 times/night) and mild, dependent edema.

History
•Long history of heartburn
•10-year history of osteoarthritis managed with various NSAIDs
•Depression
•Hypertension
•Strong family history of diabetes
Physical exam
•Dyspnea, cyanosis, and tachycardia
•BP –160/100 mmHg
•Pulse –90 bpm
•5’11’’, 172 lbs
•Respiratory rate –28 breaths/min
•Chest examination reveals inspiratory crackles and wheezes bilaterally
•S3 gallop is heard on cardiac examination
•Neck vein distention is noted
•3+ pitting edema of the extremities
Current medications
•Hydrochlorothiazide
•Ibuprofen –600 mg QID
•Ranitidine (Zantac)
•Citalopram (Celexa)

Which class of diuretics are the most efficacious for reducing volume overload and are an appropriate choice for this patient?

A

Loop diuretics

furosemide
torsemide
bumetanide
ethacrynic acid

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9
Q

Loop Diuretics

A
  • Prototypes: furosemideand ethacrynicacid
  • MOA: inhibit the luminal Na+/K+/2Cl-cotransporter(NKCC2) in the TAL of the loop of Henle
•Results in:
↓ intracellular Na+, K+, Cl-in TAL
↓ back diffusion of K+ and positive potential
↓ reabsorption of Ca2+and Mg2+
↑ diuresis
  • Ion transport is virtually nonexistent
  • Relieve the “congestive” aspect of CHF
  • Improve symptoms, but not mortality
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10
Q

Loop Diuretics

Indications

A
  • Edema
  • Heart failure
  • Hypertension
  • Acute renal failure
  • Hypercalcemicstates
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11
Q

Loop Diuretics

Adverse effects

A
  • Hypokalemia
  • Alkalosis
  • Hypocalcemia
  • Hypomagnesemia
  • Hyperuricemia
  • Ototoxicity
  • Sulfonamide hypersensitivity (not all)
  • May worsen renal function
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12
Q

He is prescribed furosemide and an additional agent to control his blood pressure and edema. He returns 2 weeks later with controlled blood pressure but with a swollen tongue and a nagging cough. Which agent was most likely given that resulted in these symptoms?

Which is an appropriate replacement therapy in this situation to control blood pressure and edema in combination with furosemide?

A

enalapril

losartan (dont get the bradykinin effects so you dont get the cough)

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13
Q

Angiotensin II:

A 
•Arterial vasoconstrictor
•Increases retention of sodium and water
•Increases aldosterone secretion
•Promotes catecholamine release from the adrenal medulla
•Promotes arrhythmias
•Promotes vascular and cardiac hypertrophy
and remodeling
•Stimulates myocyte death
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14
Q

ACE inhibitors and ARBs reduce

A

mortality

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15
Q

The patient is now stable on furosemide and losartan. A third drug is prescribed that has been shown to reduce symptoms and improve survival in patients with HF. You inform your patient that his symptoms may temporarily get worse upon initiation of this drug, but that dramatic improvement should be apparent after 3-6 months of therapy. Which drug was most likely prescribed?

A

metoprolol

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16
Q

Beta Receptors in HF

A
  • Compensatory sympathetic hyperactivationin patients with HF initially increases CO
  • Chronic stimulation of causes downregulationand desensitization of beta receptors, reducing responsiveness of myocardium
  • High dose β-blocker therapy can antagonize the supportive effects of catecholaminesand worsen heart failure
  • Treatment only initiated in stable patients

always start with a stable pt and increase dose, also let them know they could get worse for a time

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17
Q

Beta Blockers Improve

A

LVEf and reduce mortality

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18
Q

Rationale for β-blocker Use in HF

A
  • Beta blockade upregulates myocardial β1 receptor density; inotropic and chronotropic responsiveness of myocardium is improved
  • Circulating levels of vasoconstrictors (e.g., NE, renin, endothelin) are reduced
  • Beneficial remodeling
  • Reduces myocardial O2requirement
  • Improve survival after myocardial infarction
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19
Q

all drugs that reduce mortality in heart faiulre have been shown to have a beneficial effect on

A

heart remodeling

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20
Q

Aldosterone antagonist (spironolactone, eplerenone

A
  • Reduces mortality and hospitalizations
  • Beneficial at a variety of LVEF reductions in various HF classes
  • May be especially useful after MI
  • Monitor for adequate renal function and normal plasma [K+]

may have benefical remodeling on heart

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21
Q

Hydralazine + oral nitrate (usually isosorbidedinitrate)

A

arteriolar vasodilator

  • Reduces mortality and improves quality of life
  • Beneficial in patients (particularly blacks) with reduced LVEF who have persistent symptoms despite therapy with ACE inhibitor and beta-blocker
22
Q

•Some drugs that reduce preload

A
  • Venodilators
  • ACE Inhibitors
  • Angiotensin Receptor Blockers
  • Diuretics
23
Q

•Some drugs that reduce afterload

A
  • Arteriodilators
  • ACE Inhibitors
  • Angiotensin Receptor Blockers
24
Q

The patient develops palpitations. In light of this presenting symptom and due to the presence of a third heart sound (S3), the patient is given a drug that may cause paroxysmal atrial tachycardia with block at toxic concentrations. Which agent was given?

A

digoxin

25
Q

Cardiac Glycosides

A

•Digoxin: only cardiac glycoside available in US
•Clinical indications: heart failure, atrial fibrillation
•Well absorbed and widely distributed
•MOA: inhibits the membrane-bound Na+/K+ ATPase and increases myocardial contractility (50-100% in patients with HF)
•Improves symptoms and reduces hospitalizations, but no net effect on mortality
•Narrow therapeutic index (2-4)
increase in sudden death

26
Q

Digoxin Mechanism of Action

A

blocks na/k ATPase you you don’t exhangege na/ca so you keep ca in and the heart contracts harder

27
Q

Strength of Cardiac Muscle Contraction Depends on

A

calcium concentration

28
Q

Effects of Digoxin: Therapeutic Levels

A
  • Brief prolongation of action potential, followed by AP shortening
  • Increases intracellular calcium
  • Increases cardiac contractility
  • Increases parasympathetic tone and reduces sympathetic tone
29
Q

Effects of Digoxin: Toxic Levels

A
  • Depolarization of the resting potential, a marked shortening of the action potential, and the appearance of oscillatory depolarizing afterpotentialsfollowing normally evoked action potentials
  • When afterpotentialsreach threshold, they elicit action potentials (premature depolarizations, ectopic beats)
  • Most common cardiac manifestations of digoxin toxicity is arrhythmia
  • If allowed to progress, the tachycardia may deteriorate into fibrillation that could be fatal unless corrected
  • At toxic levels, sympathetic outflow is increased by digoxin
30
Q

Effects of Digoxin on Electrical Properties of Cardiac Tissue

Tissue/variable
Effects at therapeutic dose
Effects at toxic dose

A

Sinus node
↓Rate
↓Rate

Atrial muscle
↓Refractory period
↓Refractory period, arrhythmias

Atrioventricular node
↓Conduction velocity
↑Refractory period
↓Refractory period, arrhythmias

Purkinje system, ventricular muscle
Slight ↓refractory period
Extrasystoles, tachycardia, fibrillation

Electrocardiogram
↑ PR interval, ↓QT interval
Tachycardia, fibrillation, arrest at extremely high dosage

31
Q

Which of the patient’s current medications might be expected to potentiate the toxic effects of digoxin?

A

furosemide bc you get hypokalemia

32
Q

Digoxin: Interactions with K+, Ca2+, and Mg2+

A

•Hyperkalemia can reduce the effects of digoxin, especially the toxic effects

 1) Digoxin and potassium compete for binding to the Na+/K+ATPase
 2) Hyperkalemia inhibits abnormal cardiac automaticity (i.e., hyperkalemia decreases pacemaker arrhythmogenesis)
  • Hypokalemia can potentiate the toxic effects of digoxin
  • Hypercalcemiaand hypomagnesemiaincrease the risk of a digoxin-induced arrhythmia
  • Hypercalcemiaaccelerates overloading of intracellular Ca2+ stores
33
Q

The patient’s condition declines rapidly and he is admitted to the hospital for circulatory support. Which class of agents is appropriate in this situation that increases both the force of heart contraction and produces vasodilation?

A

bipyridines

34
Q

Bipyridines (Inamrinone and Milrinone)

MOA

A

MOA: cause selective inhibition of the PDE3 phosphodiesteraseenzyme (PDE3 degrades cAMP)
•Increased concentrations of cAMPin the heart result in direct stimulation of myocardial contractility and acceleration of myocardial relaxation
•Increased concentrations of cAMPin the vasculature cause balanced arterial and venous dilation

35
Q

Bipyridines (Inamrinone and Milrinone)

Inotropic agents approved for the SHORT-TERM support of circulation in advanced HF

A
  • Chronic therapy does not show any improvement in quality or length of life
  • Chronic therapy may increase mortality
36
Q

Other agents that inhibit PDE

A
  • Sildenafil (Viagra), tadalafil(Cialis), and vardenafil(Levitra) inhibit PDE5
  • Caffeine and theophylline are nonspecific PDE inhibitors
37
Q

Distinct Effects of cAMPin Cardiac and Smooth Muscle Cells Explained by Divergent Signaling Pathways

A

in cardiac cells increased camp enhances contraction

38
Q

Treatment of Chronic vs. Acute HF

Chronic HF

A
  • Diuretics
  • ACE Inhibitors
  • ARBs
  • β-blockers
  • Aldosterone antagonists
  • Hydralazine + nitrate
  • Digoxin
39
Q

Treatment of Chronic vs. Acute HF

Acute HF

A
  • Diuretics
  • IV vasodilators
    • Nitroglycerin
    • Nitroprusside
    • Nesitiride
  • β-agonists
  • Bipyridines
40
Q

diuretic

A

decreases stroke volume

41
Q

vasodilator and inotropic agents

A

decrease congestive symptoms

42
Q

β-Adrenergic and Dopaminergic Agonists

A
  • Dobutamine(β1-selective agonist) and dopamine (dopaminergic agonist with adrenergic effects at high doses)
  • Stimulation of the sympathetic nervous system leads to positive inotropic action
  • MOA: stimulation of the cardiac myocyte via β1-receptor through the cAMP-protein kinase A pathway
43
Q

Dobutamine

A
  • Selective for β1with little effect on β2receptors
  • Positive inotropic action increases stroke volume and cardiac output
  • Major side effects are excessive tachycardia and arrhythmias (used only short-term)
  • βagonist of choice in the treatment of systolic dysfunction and HF
44
Q

Dopamine overview

A
  • Limited utility in patients with HF; useful if need to raise blood pressure (e.g., circulatory failure due to sepsis, anaphylaxis)
  • Tachycardia may provoke ischemia in patients with CAD
45
Q

Dopamine low dose

A

Vasodilation
•DA receptors on smooth muscle leads to cAMP-dependent relaxation (mesenteric and renal vasculature)
•presynaptic D2-receptor stimulation inhibits further NE release

46
Q

Dopamine intermediate dose

A

Increased cardiac contractility

•direct stimulation of heart β1-receptors

47
Q

Dopamine high dose

A

Vasoconstriction

•activation of α-receptors

48
Q

Diuretics

A

Help to manage the ‘congestive’ symptoms in patients with HF
•Major MOA: reduce extracellular fluid volume, venous pressure, and ventricular preload
•Reduces edema and its symptoms and reduces cardiac size
•Three main classes used in HF
1)Loop diuretics (effective in volume reduction)
2)Thiazide diuretics (not often used)
3)Potassium-sparing diuretics (ENaCinhibitors not used)
Aldosterone antagonists (shown to reduce mortality via action on the heart)

49
Q

Aldosterone Antagonists

A
  • Some patients in heart failure have aldosterone levels up to 20 times normal
  • Aldosterone
    • Increases sodium and water retention
    • May cause myocardial and vascular remodeling and baroreceptor dysfunction
  • Prototypes: spironolactone and eplerenone
  • These drugs have been shown to reduce mortality
50
Q

Vasodilators

A
  • Effective in acute heart failure
  • Reduce preload (venodilation) or afterload (arterial dilation); or both
  • Mechanism –cause smooth muscle relaxation by supplying nitric oxide (NO)
  • Examples: nitroglycerin, nitroprusside, hydralazine, nesiritide

CV Exam III (17 decks)

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