Heart Failure Flashcards

1
Q

When does heart failure occur?

A

when the CO is inadequate to provide the oxygen needed by the body

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2
Q

Name the positive ionotropics

A
  • Digoxin
  • Bipyridines (Inamrinone, Milrinone)
  • Beta-Adrenoceptor Agonists (Dobutamine)
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3
Q

What effects does Digoxin have?

A

decrease the symptoms of heart failure, increase exercise tolerance, and decrease the rate of hospitalization, but does not increase survival

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4
Q

What is the MOA of Digoxin?

A

 Digoxin binds to and inhibits the phosphorylated -subunit of the sarcolemmal Na+/K+ ATPase, the membrane-bound transporter protein also known as the ‘sodium pump’, leading to a decrease in Na+ extrusion and an increase in cytosolic Na+ levels

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5
Q

What are the mechanical cardiac effects of Digoxin?

A

Increases the intensity of the actin and myosin filaments by increasing the free calcium concentration in the vicinity of the contractile proteins during systole

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6
Q

What is the increase in calcium due to in the mechanical cardiac effects of Digoxin?

A
  1. Increase in intracellular sodium concentration
  2. Reduction in calcium expulsion from the cell by the sodium-calcium exchanger

Leading to an overal net result of increasing contractility

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7
Q

What are the electrical cardiac effects of Digoxin?

A

Therapeutic concentrations cause a decrease in duration of cardiac action potential which decreases the atrial and ventricle refractory period (toxic concentrations reduce the RMP due to inhibition of the sodium, pump and reduced intracellular potassium along with calcium overload will lead to ectopic heartbeats/premature depolarization

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8
Q

What can happen if premature depolarization is continued?

A

will lead to self-sustaining tachycardia which may deteriorate into fibrillation which can be fatal

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9
Q

What effects does Digoxin have on other tissues?

A

All excitable tissues are affected by Digoxin including smooth muscle and the CNS
Inhibition of the sodium pump results in depolarization and increased spontaneous activity

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10
Q

What toxicities does Digoxin have on the GIT?

A
  • Anorexia

- N/V/D

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11
Q

The _____ is the most common site of Digoxin toxicity outside the heart

A

GIT

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12
Q

Name the CNS toxicities of Digoxin

A
  • Disorientation
  • Hallucinations
  • Visual disturbances
  • Convulsions
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13
Q

What is a rare toxicity of Digoxin that is reported in men?

A

Gynecomastia

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14
Q

What effects will hyperkalemia have with Digoxin?

A

interfere with Digoxin binding and will reduce its effects

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15
Q

What effects will hypokalemia have with Digoxin?

A

stimulates Digoxin binding

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16
Q

What effects will hypercalcemia have with Digoxin?

A

increases the risk of a Digoxin-induced arrhythmia

17
Q

What effects will hypomagnesemia have with Digoxin?

A

increases the risk of a Digoxin-induced arrhythmia

18
Q

Name the Bipyridines

A

Inamrinone

Milrinone

19
Q

What form are the bypyridines given in?

A

only IV

20
Q

What is the MOA of the bypyridines?

A

Selective PDE-3 inhibitors (found in the cardiac and smooth muscle) causing an increase in cAMP which leads to vasodilation and an increase in myocardial contractility due to calcium influx in the heart

21
Q

Name the toxicities of the bypyridines

A
  • Arrhythmias
  • Bone marrow toxicity (thrombocytopenia)
  • Liver enzyme changes
22
Q

Which bypridine is less likely to cause bone marrow and liver toxicities?

A

Milrinone

23
Q

What is the Beta-adrenoceptor agonist?

A

Dobutamine

24
Q

Dobutamine is used in patients with ______ and ________

A

heart failure

chronic heart failure

25
Q

What is the MOA of dobutamine?

A

Selective beta-1 agonist which will increase cAMP levels causing an increase in CO and a decrease in ventricular filling pressure

26
Q

Name the toxicites of dobutamine

A
  • Tachycardia

- Increase in myocardial oxygen consumption which can lead to angina or arrythmias

27
Q

Name the negative ionotropics

A
  • Diuretics
  • ACE Inhibitors
  • ARBs
  • Vasodilators
  • Beta-blockers
28
Q

What effects do diuretics have?

A

Reduce venous pressure and ventricular preload causing a reduction in edema and cardiac size which will improve pump efficiency

29
Q

What effect do aldosterone antagonists have on diuretics?

A

decrease morbidity and mortality due to aldosterone causing myocardial and vascular fibrosis and baroreceptor dysfunction

30
Q

What effects do ACEs and ARBs have?

A
  • Reduce PVR thus reducing afterload
  • Reduction in salt and water retention by reducing aldosterone secretion thus reducing preload
  • Reduction in angiotensin levels decreases sympathetic activity by decreasing NE release
  • Reduction in the long-term remodeling of the heart and vessels
31
Q

What effect do vasodilators have?

A

Effective in acute HF due to reduction in preload via venodilation or a reduction in afterload via arteriolar dilation or both

32
Q

Long-term use of vasodilators may __________ remodeling of the heart

A

reduce

33
Q

What effects do beta-blockers have?

A
  • Reduce mortality especially with Bisoprolol, Carvedilol, and Metoprolol in patients with severe HF
  • Cause reduced adverse effects of the catecholamines, up-regulation or beta receptors, decreased heart rate, and reduced remodeling