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PCM Exam 2 Pharm > Drugs Used in Heart Failure > Flashcards

Drugs Used in Heart Failure Flashcards

1
Q

What is heart failure and its symptoms?

A

Heart failure -When cardiac output is inadequate to provide O needed by the body

Symptoms:
Tachycardia, decreased exercise tolerance, dyspnea, peripheral & pulmonary edema, cardiomegaly

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2
Q

What are the risk factors associated with Heart Failure?

A

Hypertension • Coronary artery disease • Myocardial infarction • Diabetes mellitus • Family history of cardiomyopathy • Use of cardiotoxins • Obesity

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3
Q

HFrEFvs HFpEF?

A

HFrEF - heart failure with reduced ejection fraction = systolic heart failure. Mechanical pumping action (contractility) and the ejection fraction of the heart are reduced

HFpEF - Heart failure with preserved ejection fraction = diastolic heart failure/ Stiffening and loss of adequate relaxation leads tp abnormal ventricular filling, resulting in a reduction in cardiac output (ejection fraction may be normal)

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4
Q

what is Congestive Heart Failure (CHF)

A

Abnormal increases in blood volume & interstitial fluid. Symptoms include dyspnea from pulmonary congestion in left HF, and peripheral edema in right HF

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5
Q

what are the Physiologic Compensatory Mechanisms in HF

A

Chronic activation of SNS & renin-angiotensin- aldosterone pathway is associated with cardiac tissue remodeling. This prompts additional neurohumoral activation leads to vicious cycle which leads to death

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6
Q

What are the 4 primary factors that function to have Cardiac performance

A

(1) Preload
(2) Afterload
(3) Contractility
(4) Heart rate

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7
Q

what is preload?

A

Force stretching the ventricles
• Force of contraction of myocardial cells depends on length they are stretched (Frank-Starling phenomenon)

an increase in ventricle ‘stretching’

increase in force contraction

However, preload can be too high!
• Due to volume overload, poor myocardial
contractility etc.

congestive heart failure

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8
Q

What is Afterload?

A

Force against which ventricles must act.
• Dependent on vascular resistance (aortic BP)

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9
Q

What is Cardiac Muscle Contraction?

A

Force of cardiac muscle contraction is directly related to [Ca2+]i

Sources of [Ca2+]i
• Voltage-sensitive Ca2+ channels

  • Exchange with Na+
  • Released from sarcoplasmic reticulum

Removal of [Ca2+]i
• Na+/Ca2+ exchange

• Uptake by sarcoplasmic reticulum

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10
Q

Effects of Factors on Cardia Performace?

A
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11
Q

Drugs used to treat HFrEF (Systolic HF)

A
  • Diuretics
  • Spironolactone
  • Inhibitors of angiotensin (ACE-inhibitors / ARBs)
  • Direct vasodilators
  • b-adrenoceptor antagonists (b-blockers)
  • Inotropic agents
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12
Q

Drugs used to treat HFpEF (Diastolic HF)

A
  • Diuretics
  • ACEI /ARBs
  • b-adrenoceptor antagonists (b-blockers)
  • Calcium-channel antagonists
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13
Q

What are the recommended therpay by stage of CHF

A
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14
Q

What are diuretics?

A
  • Relieve pulmonary congestion & peripheral edema • Reduce symptoms of volume overload (eg, orthopnea)
  • decreasedplasma volume which leads to decreased venous return to the heart (preload)
  • decreased cardiac workload & O2 demand
  • Also decreased afterload (reducing plasma volume which leads to BP)
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15
Q

What are the clinical applications of diuretics

A

• Integral component of treatment for congestive symptoms
and/or intravascular volume overload

  • No evidence of a mortality benefit with thiazide or loop diuretics alone
  • Thiazide diuretics : patients with hypertensive heart disease (with congestive symptoms). Often ineffective as monotherapy due to weak diuretic effect
  • Loop diuretics : more effective diuretics than thiazides (useful if edema present)
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16
Q

What is the mechanism of the inhibitors of Angiotensin?

A
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17
Q

What are the ACE inhibitors and what is their effects?

A

Captopril / Enalapril / Lisinopril
• Agents of choice in HF
•decreases vascular resistance & BP which leads to increased cardiac output ( afterload)
•decreases salt & H20 retention (preload)
•decreases long-term remodeling of the heart

•ACE inhibitors improve symptoms in patients with HF, decrease incidence of hospitalization & MI, and prolong survival

18
Q

What are the clinical applications of ACE inhibitors in HF

A

Recommended for all patients with:
• symptomatic heart failure • asymptomatic patients with decreased LVEF or history of MI

Suggested for patients:
• at high risk of developing heart failure due to
atherosclerotic disease, obesity, diabetes
mellitus or hypertension

19
Q

What are the adverse effects of ACE inhibitors?

A
  • Hypotension,
  • Persistent dry cough
  • Hyperkalemia
  • Angioedema
  • Acute renal failure (patients with bilateral renal artery stenosis)
  • Teratogenic
20
Q

What are the ARBS and what is their effect?

A

Candesartan / Valsartan

  • Potent competitive antagonists of angiotensin type I receptor
  • DO NOT affect bradykinin levels
  • Clinical Application In HF: Substitute for patients who can’t tolerate ACE inhibitors (severe cough or angioedema)
  • Adverse Effects :Similar to ACE inhibitors (no cough) Teratogenic
21
Q

What are direct vasodilators and what is their effect?

A
22
Q

• Concurrent use of hydralazine & isosorbide dinitrate recommended for what types of patients:

A
  • who cannot tolerate ACEI or ARB or,
  • in African American patients with advanced heart failure as an adjunct to standard therapy
23
Q

What are the adverse effect of direct vasodilators?

A
  • Hydralazine & isosorbide dinitrate = Headache, dizziness
  • Hydralazine =Tachycardia, peripheral neuritis, lupus-like syndrome
  • Contraindications =Sildenafil
24
Q

What are the B-Blocksers and their mechanism of action?

A
  • Studies demonstrate reverse cardiac remodeling & reduction in mortality & hospitalization (30-40% in patients with NYHA II-IV HF)
  • decrease HR and decrease contractility & inhibition of renin release (b1 receptors)
  • Prevent deleterious effects of norepinephrine on cardiac
  • muscle fibers which leads to decreased remodeling, hypertrophy etc
  • Can get initial exacerbation of symptoms (start at low
    dose & gradually increase over several weeks)
25
Q

What are the clinical apllications of B-Blockers in Heart Failure?

A
  • Recommended in addition to an ACEI for patients with:
  • symptomatic heart failure - asymptomatic patients with a decreased LVEF or history of MI
  • N B. USE CAUTIOUSLY in decompensated HF and are
    contraindicated in cardiogenic shock
26
Q

What are the adversde effects of b-blockers?

A
  • Same as all b-blockers
  • Use cautiously in asthmatics and patients with severe bradycardia
  • Fluid retention (upon initial treatment) – an increasing dose of concurrent diuretic may help
27
Q

Sprionolactone effets?

A
  • Patients with advanced heart disease have elevated aldosterone levels due to: • angiotensin stimulation • reduced hepatic clearance
  • MOA
    Aldosterone antagonist which prevents Na+ retention, myocardial hypertrophy & hypokalemia
28
Q

What are the clinical applications and adverse effects of Spironolactone in HR?

A
    • ACE inhibitors are shown to decrease morbidity & mortality in patients with severe heart failure
  • Adverse Effects
    Hyperkalemia (esp. in patients taking ACEIs/ARBs, K+ supplements or who have renal failure) GI disturbances (gastritis, peptic ulcer)
    CNS effects (lethargy, confusion) Endocrine abnormalities (gynecomastia, decreased libido, menstrual irregularities)
29
Q

What is Digoxin?

A
  • Inotropic Agent
  • • Cardiac glycoside
  • • Derived from digitalis (foxglove) plant
  • • Widely used in treatment of HF
  • • Digoxin can decrease the symptoms of heart failure, increase exercise tolerance and decrease rate of hospitalization, but DOES NOT increase survival
30
Q

What are the disadvantages of Digoxin?

A

• Narrow therapeutic margin • Unfavourable, complicated pharmacokinetics • Drug sensitivity varies between patients • Drug sensitivity may change during therapy • Severe, potentially lethal adverse effects

31
Q

What is DIgoxin Mechniams of Action?

A
  • Po sitively inotropic - Increases force of heart contraction
  • Negatively chronotropic - Decreases heart rate
32
Q

What is the mechanism of action of the Inotropic action of Digoxin?

A

• Inotropic action : increase cytoplasmic Ca2+ concentration
that enhances contractility of cardiac muscle and leads to
increases cardiac output

  • also
  • enhances vagal tone which leads to decreased HR • reduces sympathetic activity • reduces peripheral resistance which leads to myocardial O2 demand
33
Q

DIGOXIN mechanism of action for Ca2+ effects?

A
34
Q

Digoxin Summary?

A
35
Q

What are the clinical application of DIgoxin?

A

• HF with atrial fibrillation (main application)

• Can be used (in addition to ACEI & b-blocker) to
decrease symptoms, increase exercise tolerance &
decrease rate of hospitalization

36
Q

Digxon PK?

A

• Very potent (narrow safety margin)
• Widely distributed (including CSF)
• t ½ = ~36-40 h
• Accumulates in muscle which leads to a large Vd (loading dose
required)

37
Q

What are the adverse effects of DIgoxin?

A

Digoxin toxicity = one of most common ADRs
• Cardiac effects: arrhythmias, characterized by slowing of AV conduction (atrial arrhythmias)
• GI effects: anorexia, nausea & vomiting
• CNS effects: headache, fatigue, confusion, blurred vision, alteration of color perception, halos on dark objects

• Hypokalemia • Drug accumulation / relative overdose • Hypomagnesemia or hypercalcemia • Hyperthyreosis • Abnormal renal function • Respiratory disease • Acid-base imbalances • …. age above 65, low body weight, fever etc

38
Q

Digxoin Interactions:

A
39
Q

What are the PDE III inhibitors?

A
  • Inhibit myocardial cAMP PDE activity which leads to increased cAMP levels (+ve inotropic effect and increased cardiac output)
  • Possess systemic & pulmonary vasodilator effects (reduce both preload and afterload)
  • Shown to increase AV conduction slightly
  • Used for short-term therapy in patients with intractable heart failure
40
Q

Dopamine

A

Stimulates both adrenergic & dopaminergic receptors
• Lower doses = mainly dopaminergic stimulating
(produce renal and mesenteric vasodilation)

• Higher doses = both dopaminergic & b1
stimulating (produce cardiac stimulation & renal
vasodilation)

• Large doses = stimulate alpha receptors
(vasoconstriction)

• Used in the treatment of shock (eg, MI, open heart
surgery, renal failure, cardiac decompensation) which
persists after adequate fluid volume replacement.
Dopamine also promotes diuresis.

41
Q
A

Dobutamine is administered as a racemic mixture
1 1
• (-) isomer is an a
agonist • (+) isomer is an a
and a mild b
-receptor agonist and a weak b
1
1
2
-antagonist, a potent b agonist
agonist
-receptors
1
-receptors)
2
• At therapeutic levels the stimulation of b
predominate, leading to a potent inotropic effect (with
little change in heart rate). Net vascular effect is mild
vasodilation (b • Used to increase cardiac output in acute management
of heart failure (eg, MI)

PCM Exam 2 Pharm (14 decks)

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