Chapter 13: Drugs Used in Heart Failure Flashcards

1
Q

What is the fundamental physiologic defect in heart failure?

A

Decrease in cardiac output

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2
Q

The graph that relates cardiac output, stroke volume, etc, to filling pressure or end-diastolic fiber length; also known as the Frank-Starling curve

A

Ventricular function curve

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3
Q

A drug that inhibits one or more enzymes that degrade cAMP (and other cyclic nucleotides)

A

PDE inhibitor

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4
Q

An arrhythmia consisting entirely or largely of beats originating below the AV node

A

Ventricular tachycardia

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5
Q

Electrical effects (early responses) of cardiac glycosides:

A
  1. Increased PR interval, caused by the decrease in atrioventricular (AV) conduction velocity
  2. Flattening of the T wave
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6
Q

What is the most important manifestation of digitalis toxicity?

A

Increased automaticity, caused by intracellular calcium overload

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7
Q

Effects of digitalis

A
  1. Slow ventricular rate.
  2. Shortened QT interval
  3. Inversion of the T wave
  4. ST segment depression
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8
Q

Digitalis toxicity, especially arrhythmogenesis, is increased by:

A
  1. Hypokalemia
  2. Hypomagnesemia
  3. Hypercalcemia
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9
Q

The major signs of digitalis toxicity

A
  1. Arrhythmias
  2. Nausea
  3. Vomiting
  4. Diarrhea.

Rarely, confusion or hallucinations and visual or endocrine aberrations may occur.

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10
Q

Treatment of digitalis toxicity

A
  1. Correction of potassium or magnesium deficiency
  2. Antiarrhythmic drugs
  3. Digoxin antibodies
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11
Q

What is the first-line therapy for both systolic and diastolic failure and are used in heart failure?

A

Diuretics are used before digitalis and other drugs are considered.

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12
Q

Often useful in acute failure in which systolic function is markedly depressed, but they are NOT appropriate for chronic failure because of tolerance, lack of oral efficacy, and significant arrhythmogenic effects.

A

Beta1- Adrenoceptor Agonists

- Dobutamine and dopamine

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13
Q

The use of these drugs is based on the reduction in cardiac size and improved efficiency that can be achieved with proper adjustment of venous return (preload) and reduction of impedance to ventricular ejection (afterload)

A

Vasodilators

- nitroprusside or nitroglycerin

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14
Q

Reduces preload, edema by powerful diuretic action on thick ascending limb in nephron, and vasodilating effect on pulmonary vessels

A

Loop diuretics (e.g. Furosemide)

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15
Q

Antagonist of aldosterone in kidney plus poorly understood reduction in mortality.

Side effects include hyperkalemia and gynecomastia

A

Spironolactone

Eplerenone: similar to spironolactone but lacks gynecomastia effect

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16
Q

Blocks angiotensin-converting enzyme, reduces Ang II levels, decreases vascular tone and aldosterone secretion, and shown to reduce mortality

A

Angiotensin-converting enzyme (ACE) inhibitors

- Captopril

17
Q

Positive inotropic drug inhibiting Na /K ATPase sodium pump and increases intracellular Na , decreasing Ca2+ expulsion and increasing cardiac contractility

A

Cardiac glycosides: digoxin

18
Q

Beta1-selective sympathomimetic, increases cAMP and force of contraction

A

Sympathomimetics: dobutamine

19
Q

Poorly understood reduction of mortality, possibly by decreasing remodeling

A

Beta blockers

20
Q

Atrial peptide vasodilator, diuretic used in acute severe decompensated failure

Toxicity:
Renal damage, hypotension

A

Nesiritide