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Pharmacology Unit 4 > Inotropic Agents I and II > Flashcards

Inotropic Agents I and II Flashcards

1
Q

How is CHF defined?

A

inability of the heart to pump blood at a rate commensurate with the requirements of the tissues

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2
Q

How is heart failure defined?

A

any structural or functional disorder that impairs the ability of the ventricle to fill with or eject blood

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3
Q

What are the clinical manifestations of heart failure?

A

dyspnea
fatigue
fluid retention (CONGESTIVE)

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4
Q

Does the ventricle size and function have to be abnormal?

A

no

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5
Q

According to the New York Heart Associations Functional Classifications, how is the following patient classified:
Patient is diagnosed with cardiac disease but it has no impairment in their life.

A

Class I

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6
Q

According to the New York Heart Associations Functional Classifications, how is the following patient classified:
A patient with cardiac disease who has been running 5 miles a day for 20 years can now only run 3-4 miles at the most before becoming exhausted and short of breath, but they have no symptoms at rest.

A

Class II

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7
Q

According to the New York Heart Associations Functional Classifications, how is the following patient classified:
A patient with cardiac disease who has been running 5 miles a day for 20 years and is now fatigued and out of breath walking to his mailbox and back, but they have no symptoms at rest.

A

Class III

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8
Q

According to the New York Heart Associations Functional Classifications, how is the following patient classified:
A patient with cardiac disease who is constantly fatigued and short of breath by walking around their house and has similar symptoms even while he is resting.

A

Class IV

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9
Q

There is a poor correlation between cardiac function and….

A

symptoms

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10
Q

Name some noncardiac factors that affect exercise tolerance.

A
  • peripheral vascular fxn
  • skeletal muscle physiology
  • pulmonary dynamics
  • neurohormonal and reflex autonomics
  • renal Na handling
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11
Q

How does LV dysfunction usually begin?

A

with injury to myocardium (usually progresses by change in geometry and structure)

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12
Q

Which hormones and neurotransmitters are elevated in patients with heart failure?

A 
Norepi
Angiotensin II
Aldosterone
Endothelin
Vasopressin
Cytokines
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13
Q

What are the compensatory mechanisms of the heart in heart failure?

A

increased HR, contractile stimulation and rate of relaxation

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14
Q

What are the compensatory mechanisms of the peripheral circulation in heart failure?

A 
arterial vasoconstriction (increased afterload)
venous vasoconstriction (increased preload)
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15
Q

What are the compensatory mechanisms of the kidney in heart failure?

A

arterial vasoconstriction
venous vasoconstriction
Na and water retention
increased myocardial contractile stimulation

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16
Q

What are the compensatory mechanisms of oxygen delivery in heart failure?

A
  • redistribution of cardiac output
  • altered O2 Hgb dissociation
  • increased O2 extraction by tissues
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17
Q

Which two stages are at risk for heart failure and how are they differentiated?

A
  • Stage A and B

- B has structural heart disease, A does not

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18
Q

Which two stages are in heart failure and how are they differentiated?

A
  • Stage C and D

- D has refractory symptoms of HF at rest

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19
Q

How are patients in Stage A treated?

A
  • reduce risk factors

- ACEI or ARD

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20
Q

How are patients in Stage B treated?

A

Stage A + ACEI, ARB or Beta blockers

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21
Q

How are patients in Stage C treated?

A

Stage B+

  • Diuretics
  • ACEI
  • Beta Blockers
  • Aldo Antagonist
  • ARB
  • digitalis
  • nitrates
  • pacemaker
  • defibrillators
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22
Q

How are patients in Stage D treated?

A

Stage C+

  • end of life care
  • transplant
  • chronic inotropes
  • mechanical support
  • experimental surgery or drugs
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23
Q

What is the first line therapy for heart failure?

A

ACEI’s

-alleviate symptoms, improve clinical status and reduce risk of death and hospitalization

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24
Q

What are the physiological effects of ACEI’s?

A
  • arteriovenous vasodilation (decrease SVR, BP, PCWP, and LVEDP, increases CO and exercise tolerance)
  • no change in HR or contractility
  • decreased O2 requirements
  • Increased renal, coronary and cerebral blood flow
  • diuresis and naturesis
25
Q

What are the advantages of ACEI’s?

A
  • Inhibit LV remodeling after MI
  • modify the progression of chronic CHF
  • No neurohormonal activation or reflex tachy
  • no tolerance
26
Q

what is one benefit of the ARB’s over the ACEI’s?

A

no side effect of cough

27
Q

How do ARB’s work?

A

block type 1 angiotensin II:

  • dilate arteries and veins
  • inhib angiotensin II effect on sympathetic tone
  • promotes renal excretion of Na and water
  • inhibits cardiac and vascular remodeling
28
Q

When would using an ACEI and an ARB be indicated?

A

in patients with resistant hypertension

29
Q

When there is a side effect of ____________ with and ACEI, adding an ARB is contraindicated.

A

angioedema-crossover effect

30
Q

Name the 6 ARB drugs.

A
  • Losartan
  • Irbesartan
  • Valsartan
  • Candesartan
  • Olmesartan
  • Telmisartan
31
Q

What are some side effects of the ARB’s?

A
  • decreases GFR
  • Increases K+
  • Hypotension
32
Q

What are the effects of the diuretics?

A
  • decrease in volume and preload
  • improves arterial distensibility
  • neurohormonal activation (increases NE and angiotensin II)
33
Q

Do diuretics have a direct effect on CO?

A

NO-but excessive preload reduction can cause decreased CO

34
Q

What is a contraindication for use of diuretics?

A

hypovolemia

35
Q

What are some side effects of diuretics?

A
  • volume contraction

- electrolyte depletion

36
Q

Name the two aldosterone antagonists for treatment of heart failure

A

spironolactone and eplerenone

37
Q

What are some side effects of the aldosterone antagonists? (spironolactone and eplerenone)

A
  • hyperkalemia
  • metabolic acidosis
  • gynecomastia
  • gastric disturbances
38
Q

How do Beta blockers work in the setting of Heart Failure?

A

inhibit the adverse effects of the SNS

39
Q

Which 3 beta blockers have demonstrated a reduction in the risk of death and hospitalization?

A
  • Bisoprolol
  • Metoprolol
  • Carvediol
40
Q

How should beta blockers be dosed in heart failure?

A
  • start at very low dose

- gradually increase dose

41
Q

What class of drugs is digoxin and what was it initially prescribed for?

A
  • cardiac glycosides

- lower extremity edema

42
Q

What is the mechanism of action of the cardiac glycosides (digoxin)?

A

inhibits Na/K ATPase–>increase in intracellular Na–>increase in Ca concentration through the Na/Ca exchanger–>increased contractility

43
Q

What is the mechanism of the decreased sinoatrial firing rate and reduced conduction velocity through the AV node with digoxin treatment?

A

-increase in vagal efferent activity to the heart

44
Q

How does Digoxin affect:

  • Cardiac Output
  • LVEF
  • LVEDP
  • Exercise Tolerance
  • Natriuresis
  • Neurohormonal activation
A
  • Cardiac Output- increased
  • LVEF- increased
  • LVEDP- decreased
  • Exercise Tolerance- increased
  • Natriuresis- increased
  • Neurohormonal activation- decreased
45
Q

What are the specific neurohormonal effects that are decreased with digoxin?

A
  • Plasma NE
  • Peripheral NS activity
  • RAAS activity
46
Q

What is the major drug management issue with digoxin?

A

-narrow therapeutic window

47
Q

What does digoxin toxicity cause?

A

cardiac arrhythmias-atrial tachycardia and AV block

Also eliminated by the kidneys

48
Q

List the 7 medications/classes of medications that are used to treat heart failure.

A
  • Diuretics
  • Digoxin
  • Inotropes
  • Nitrates
  • ACE-I (ARB’s)
  • B-Blockers
  • Aldosterone antagonists
49
Q

Which of the following produces decreased mortality in HF patients?

  • Diuretics
  • Digoxin
  • Inotropes
  • Nitrates
  • ACE-I (ARB’s)
  • B-Blockers
  • Aldosterone antagonists
A
  • Nitrates
  • ACE-I (ARB’s)
  • B-Blockers
  • Aldosterone antagonists
50
Q

What is mechanism of action of Dobutamine and what is its result?

A
  • stimulates B-1 receptors on heart

- increased contractility and heart rate

51
Q

What is the effect of Dobutamine on the blood vessels at low doses? high doses?

A
  • low doses- stim. B-2 receptors causing vasodilation

- high doses- stim alpha receptors causing vasoconstriction

52
Q

<p>

| What is the half life of Dobutamine and when can tolerance begin to develop?</p>

A

<p>

| -half life is 2 minutes-->given as continuous infusion -tolerance after 24-48 hours at same dose</p>

53
Q

What is the mechanism of action of Milrinone?

A

phosphodiesterase IIIa inhibitor-normally breaks down cAMP so this causes an increase in cAMP–>increased contractility, heart rate, and relaxation of vascular smooth muscle

54
Q

What is milrinone usually used for?

A

As a last resort for short term infusions because there is increased hypotensive and atrial arrhythmia events acutely and 2 month mortality is 50% higher than placebo

55
Q

What is Dobutamine usually used for?

A

Acutely decompensated patients (about half will die after 6 months)

56
Q

What is Nesiritide?

A

recombinant human B-natriuretic peptide which causes natriuresis and diuresis by decreasing:

  • Aldosterone
  • Cortisol
  • Na appetite
  • *and increases GFR**
57
Q

What have studies recently shown regarding the efficacy of nesiritide?

A
  • no difference in rates of death of hospitalization

- no significant improvement of symptoms

58
Q

Which of the following exhibits neurohormonal control?

  • Diuretics
  • Digoxin
  • Inotropes
  • Nitrates
  • ACE-I (ARB’s)
  • B-Blockers
  • Aldosterone antagonists
A
  • Digoxin
  • ACE-I (ARB’s)
  • B-Blockers
  • Aldosterone antagonists

Pharmacology Unit 4 (9 decks)

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