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Pharm II > test 1 > Flashcards

test 1 Flashcards

1
Q

What is Heart Failure (HF)

A
  • Progressive disorder in which the heart is unable to pump sufficient blood to meet the needs of the body
  • Impaired ability of the heart to adequately fill with and/or eject blood
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2
Q

Two Major Types of Heart Failure

A
  • Systolic and Diastolic
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3
Q

Systolic Failure

A
  • Reduced pumping action (contractility)
  • Reduced ejection fraction
  • ~50% of HF patients
    * “younger”
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4
Q

Diastolic Failure

A
  • Stiffening and loss of adequate relaxation
  • Reduced filling and cardiac output
  • ~50% of HF patients
    * “older”
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5
Q

Heart failure causes edema how (2)

A
  1. Increase in venous pressure -> increased capillary filtration = edema
  2. decrease CO -> decreased blood pressure -> increased sympathetic activity and decreased renal blood flow -> increased renin, angiotensin II -> increase aldosterone -> increased sodium and water retention = edema
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6
Q

HF Treatment Goals (3)

A
  1. Reducing symptoms
  2. Slow disease progression
  3. Improve survival
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7
Q

Causes of Heart Failure (6)

A
  1. Ischemia
  2. Cardiomyopathy
  3. Myocarditis
  4. HTN
  5. Valve disease
  6. Congenital defects
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8
Q

Ischemia leading to HF

A
  • Coronary artery disease
  • Multiply MIs
  • Most common
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9
Q

Cardiomyopathy leading to HF

A
  • Damage to the heart muscle
  • Infection
  • Alcohol abuse
  • Drug abuse
  • Genetics
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10
Q

Myocarditis leading to HF

A
  • Inflammation of the heart
  • Viral
    * Common cause
  • Many viruses implicated
    * Coxsackie V viruses
    * Epstein-Barr virus (EBV)
    * Cytomegalovirus (CMV)
    * Hepatitis C
    * Herpes
    * HIV
  • May or may not fully or completely resolve
    * Might require valvular surgery
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11
Q

HTN leading to HF

A
  • Heart has to work harder to pump blood to body

* Causes heart to become thicker and stiffer

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12
Q

Valvular Disease leading to HF

A
  • Stenosis

* Insufficiency

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13
Q

Congenital Defects leading to HF

A
  • Bicuspid aortic valve
  • Renal artery stenosis
  • Coarctation of aorta
  • Cushing’s syndrome
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14
Q

HF Symptoms

A
  • Shortness of breath (dyspnea)
  • Orthopnea
    * Dyspnea lying down
  • Fatigue
  • Peripheral edema
  • Decreased exercise tolerance
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15
Q

Three Major Compensatory Mechanisms

A
  1. Increased sympathetic activity
  2. Activation of the renin-angiotensin aldosterone
    system
  3. Myocardial hypertrophy
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16
Q

Increased Sympathetic Activity as a compensatory mechanism

A
  • Baroreceptors sense a decrease in BP
    * Activates the SNS
  • Results in increased HR, contractility, and vasoconstriction
  • Enhanced venous return
    * Increases preload
  • Increased stroke volume and CO
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17
Q

Activation of the Renin-angiotensinaldosterone

System (RAAS) as a compensatory mechanism

A
  • Decrease flow to the kidney, due to low CO, causes release of renin
  • Leads to an increase angiotensin II levels
  • Leads to an increase in aldosterone
  • Leads to increase in blood volume
    * More blood is returned to the heart
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18
Q

Myocardial Hypertrophy as a compensatory mechanism

A
  • Thickening of the heart muscle
    * Decrease in size of the chambers
  • Chambers dilate
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19
Q

Cardiac Remodeling

A
  • Alteration in the structure (dimension, mass, shape) of the heart in response to hemodynamic load and/or cardiac injury
  • Cellular changes
    * Myocyte hypertrophy, necrosis, fibrosis
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20
Q

Seven Classes of Drug for Treatment of Heart Failure

A
  1. ACE inhibitors
  2. ARBs
  3. Aldosterone blockers
  4. β-blockers
  5. Diuretics
  6. Direct vaso - and venodilators
  7. Inotropic agents
21
Q

what do ACE Inhibitors do

A
  • Block the enzyme that cleaves angiotensin I to form angiotensin II
  • Reduces inactivation of bradykinin
  • Reduces secretion of aldosterone
  • Reduces afterload and preload
    * Increase CO
  • Been shown to significantly improve patient survival
  • Indicated in patients will all stages of LV failure
22
Q

ACE Inhibitors: Adverse Effects

A
  • DRY MOUTH
  • Rash
  • Fever
  • Angioedma
  • Hypotension
  • Hyperkalemia
  • Fetal malformations
23
Q

what do Angiotensin Receptor Blockers (ARBs) do

A

• Block the angiotensin II receptors
• Block angiotensin II action
• Actions are similar to ACE inhibitors
• Reduce afterload and preload which increases CO
•Used in patient who cannot tolerate ACE inhibitors
• Severe cough
• angioedema (rapid edema of the area beneath the skin)
- decreases cell proliferation (decrease in tumors or number of cells)
- decreases hypertrophy

24
Q

ARBs: Adverse Effects

A
  • Similar to ACE inhibitors
    * Less risk of cough
  • Should not be combined with ACE inhibitors
    * Similar mechanism and adverse effects
  • Teratogenic
25
Q

what do Aldosterone Antagonists do

A
  • Block aldosterone
  • Prevents salt and water retention
  • Prevents myocardial hypertrophy
26
Q

what do β-blockers do

A
  • Prevent changes that occur because of chronic activation of the SNS
  • Decrease HR
  • Inhibit renin release
  • Decrease remodeling, hypertrophy, and cell death
  • Recommended for all patients with chronic, stable HF
  • Metoprolol, Bisoprolol, and carvedilol reduce morbidity and mortality
27
Q

β-blockers: Adverse Effects

A
  • Bradycardia
  • Hypotension
  • Fatigue
  • Insomnia
  • Sexual dysfunction
  • Alter lipid panel
    * Decrease HDL
    * Increase triglycerides
28
Q

what do Diuretics do

A
  • Relieve pulmonary congestion and peripheral edema
  • Decrease plasma volume
    * decrease preload/afterload
  • Loop diuretics commonly used
29
Q

what does Isosorbide dinitrate do

A
  • Causes vascular smooth muscle relaxation
  • Converts nitrite ions to nitric oxide which causes an increase in cGMP leading to dephosphorylation of myosin light chain
  • Causes dilation of large veins
    * Reduces preload
30
Q

what does Hydralazine do

A
  • Relaxes vascular smooth muscle mainly in arteries and arterioles
  • Decreases SVR and CO by releasing nitric oxide from the endothelium
31
Q

what does Hydralazine and isosorbide dinitrate do

A
  • Fixed dose combo (Bidil)

* Been shown to improve survival in the African/American community

32
Q

Vaso – and Venodilators: Adverse Effects

A
  • Headache
  • Hypotension
  • Reflex tachycardia
33
Q

what do Inotropes do

A
  • Increase intracellular Ca2+ concentration
    * Enhance cardiac contractility
    * Increase CO
  • Associated with reduced survival
    * Except digoxin
    * Only used for short period
    * Hospital setting
34
Q

Inotropes: Cardiac Glycosides/Digitalis

A
  • Come from the digitalis (foxglove) plant
  • Low therapeutic index
  • Digoxin
35
Q

how does Digoxin work

A
  • Inhibits the Na+ /K+ - adenosine triphosphatase (ATPase)
  • Reduces ability of myocyte to actively pump Na+ out of cell
    * Increases intracellular Na+
  • Increases intracellular Ca2+
  • Increases cardiac contractility
36
Q

when is digoxin used

A
  • Indicated in patients with severe HF
    * After initiation with ACE inhibitors, β-blockers, and diuretic therapy
  • Reduced HF admissions and improved survival
    * Low doses
  • Long half-life
    * 30-40 hours
  • Tolerated at low doses
    * (0.5-0.8 ng/ml)
37
Q

Digoxin: Adverse Effects

A
  • Digoxin toxicity
    * Arrhythmias
    * Anorexia
    * Nausea
    * Vomiting
    * Blurred vision
  • Severe Toxicity
    * V-Tach
  • Administration of digoxin antibody
    * Digibind
38
Q

what does Dobutamine do

A
  • β-agonist: positive inotropic effect
  • Increases cAMP which activates protein kinase
    * Protein kinase phosphorylates slow Ca2+ channels
    * Increases Ca2+ entry into myocardial cell enhancing contraction
  • Given by IV infusion
  • Used in short-term treatment of HF
    * Hospital setting
39
Q

what does Milrinone do

A
  • Phosphodiesterase inhibitor
  • Increases cAMP which activates protein kinase
    * Protein kinase phosphorylates slow Ca2+ channels
    * Increases Ca2+ entry into myocardial cell enhancing contraction
  • Short-term IV therapy
40
Q

how do inotropes work

A
  1. binding of a β-agonist, such as dopamine or dobutamine, activates adenylyl cyclase, which produces cAMP
  2. cAMP activates protein kinase, which in turn phosphorylates Ca2+ channels
  3. Phosphorylation of Ca2+ channels increases Ca2+ flow into the cell, causing increased force of contraction of the heart
  4. Phosphodiesterases inhibitors prevents hydrolysis of cAMP and, thus, prolonging the action of protein kinase
41
Q

Stage A of Heart Failure

A
  • High risk, no symptoms
  • HTN
  • DM
  • Family history
  • High sodium and alcohol intake
  • Poor diet and exercise
  • Loop diuretics prescribed
42
Q

Stage B of Heart Failure

A
  • Structural heart disease, no symptoms
  • Diagnosed with HF
  • ACE inhibitor or ARBs prescribed
43
Q

Stage C of Heart Failure

A
  • Cardiac dysfunction present
  • Symptomatic
  • β-blockers added
44
Q

Stage D of Heart Failure

A 
•Remain symptomatic despite optimal drug
therapy and treatment
•Surgical options necessary
        •Heart transplant
        •LVAD or BiVAD
        •Pacemaker placement
45
Q

what is stage A

A
  • at high risk for HF but without structural heart disease or symptoms of HF
46
Q

what is stage B

A
  • structural heart disease but without signs or symptoms of HF
47
Q

what is stage C

A
  • structural heart disease with prior or current symptoms
48
Q

what is stage D

A

advanced HF

Pharm II (37 decks)

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