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
What are the advantages of ACEI's?
- Inhibit LV remodeling after MI - modify the progression of chronic CHF - No neurohormonal activation or reflex tachy - no tolerance
26
what is one benefit of the ARB's over the ACEI's?
no side effect of cough
27
How do ARB's work?
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
When would using an ACEI and an ARB be indicated?
in patients with resistant hypertension
29
When there is a side effect of ____________ with and ACEI, adding an ARB is contraindicated.
angioedema-crossover effect
30
Name the 6 ARB drugs.
- Losartan - Irbesartan - Valsartan - Candesartan - Olmesartan - Telmisartan
31
What are some side effects of the ARB's?
- decreases GFR - Increases K+ - Hypotension
32
What are the effects of the diuretics?
- decrease in volume and preload - improves arterial distensibility - neurohormonal activation (increases NE and angiotensin II)
33
Do diuretics have a direct effect on CO?
NO-but excessive preload reduction can cause decreased CO
34
What is a contraindication for use of diuretics?
hypovolemia
35
What are some side effects of diuretics?
- volume contraction | - electrolyte depletion
36
Name the two aldosterone antagonists for treatment of heart failure
spironolactone and eplerenone
37
What are some side effects of the aldosterone antagonists? (spironolactone and eplerenone)
- hyperkalemia - metabolic acidosis - gynecomastia - gastric disturbances
38
How do Beta blockers work in the setting of Heart Failure?
inhibit the adverse effects of the SNS
39
Which 3 beta blockers have demonstrated a reduction in the risk of death and hospitalization?
- Bisoprolol - Metoprolol - Carvediol
40
How should beta blockers be dosed in heart failure?
- start at very low dose | - gradually increase dose
41
What class of drugs is digoxin and what was it initially prescribed for?
- cardiac glycosides | - lower extremity edema
42
What is the mechanism of action of the cardiac glycosides (digoxin)?
inhibits Na/K ATPase-->increase in intracellular Na-->increase in Ca concentration through the Na/Ca exchanger-->increased contractility
43
What is the mechanism of the decreased sinoatrial firing rate and reduced conduction velocity through the AV node with digoxin treatment?
-increase in vagal efferent activity to the heart
44
How does Digoxin affect: - Cardiac Output - LVEF - LVEDP - Exercise Tolerance - Natriuresis - Neurohormonal activation
- Cardiac Output- increased - LVEF- increased - LVEDP- decreased - Exercise Tolerance- increased - Natriuresis- increased - Neurohormonal activation- decreased
45
What are the specific neurohormonal effects that are decreased with digoxin?
- Plasma NE - Peripheral NS activity - RAAS activity
46
What is the major drug management issue with digoxin?
-narrow therapeutic window
47
What does digoxin toxicity cause?
cardiac arrhythmias-atrial tachycardia and AV block | **Also eliminated by the kidneys**
48
List the 7 medications/classes of medications that are used to treat heart failure.
- Diuretics - Digoxin - Inotropes - Nitrates - ACE-I (ARB's) - B-Blockers - Aldosterone antagonists
49
Which of the following produces decreased mortality in HF patients? - Diuretics - Digoxin - Inotropes - Nitrates - ACE-I (ARB's) - B-Blockers - Aldosterone antagonists
- Nitrates - ACE-I (ARB's) - B-Blockers - Aldosterone antagonists
50
What is mechanism of action of Dobutamine and what is its result?
- stimulates B-1 receptors on heart | - increased contractility and heart rate
51
What is the effect of Dobutamine on the blood vessels at low doses? high doses?
- low doses- stim. B-2 receptors causing vasodilation | - high doses- stim alpha receptors causing vasoconstriction
52

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

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

53
What is the mechanism of action of Milrinone?
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
What is milrinone usually used for?
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
What is Dobutamine usually used for?
Acutely decompensated patients (about half will die after 6 months)
56
What is Nesiritide?
recombinant human B-natriuretic peptide which causes natriuresis and diuresis by decreasing: - Aldosterone - Cortisol - Na appetite * *and increases GFR**
57
What have studies recently shown regarding the efficacy of nesiritide?
- no difference in rates of death of hospitalization | - no significant improvement of symptoms
58
Which of the following exhibits neurohormonal control? - Diuretics - Digoxin - Inotropes - Nitrates - ACE-I (ARB's) - B-Blockers - Aldosterone antagonists
- Digoxin - ACE-I (ARB's) - B-Blockers - Aldosterone antagonists