Treatment of CHF Flashcards

1
Q

Class I CHF is defined by what?

A

Low ejection fraction

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2
Q

Class I is treated by>

A

ACEi or ARBs

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3
Q

Why are ACEi and ARBs good CHF treatments>

A
THey prevent and reverse the myogenic effects of ANgiotensin II such as:
hypertrophy of cardiac myocytes
hypertrophy of vascular smooth muscle
cardiac and ventricular fibrosis
atherosclerosis
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4
Q

What effect do ACEi and ARBs have on Bradykinin

A

They increase its concentration, It is a vasodilator and also an antifibrotic mediator

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5
Q

What are the harmful drug interactions with ACEi?

A

Diuretic therapies EXCEPT spironolactone

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6
Q

Contraindications for ACEi and ARBs

A

angioedema (mostly just ACEi), pregnancy, renal insufficiency, hepatic insufficiency

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7
Q

Keep in mind the pregnancy issue

A

ok

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8
Q

Why were beta blockers previously contraindicated in CHF?

A

Because Beta receptors are the delivery site for sympathetic action on the heart so it makes sense that you wouldn’t want to block this if the pump is failing

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9
Q

How are Beta blockers helpful in management of CHF

A
They attenuate the not so great effects of chronic high epinephrine and norepinephrine such as:
increased myocardial oxygen consumption
beta receptor downregulation 
arrhythmias
fibrosis and myocyte apoptosis
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10
Q

Short term hemodynamic effects of beta blockers

A

reduced cardiac output and reduced blood pressure

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11
Q

Long term effects of beta blockers in CHF?

A

increased CO, decreased LVEDP…it may get worse before it gets better

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12
Q

Beta blockers in summary

A

Reverse desensitization, increase receptor number, restore fast signaling modes (contractility) over slow signaling modes (gene expression).

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13
Q

What beta blockers are used in CHF

A

Metoprolol

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14
Q

What drug do you add when pts become class II

A

diuretics

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15
Q

What diuretics are most commonly used

A

High ceiling Diuretics like Furosemide or Bumetanide

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16
Q

Explain teh diuretic effects of ACEi’s and ARBs

A

They reduce sodium retention by preventing aldosterone release, their effect is not always sufficient tp prevent edema, the dose of the diuretic should be lowered

17
Q

How to spironolactone and epelerone have benefits beyond their diuretic effect

A

Aldosterone can have mitogenic and fibrogenic effects on the myocardium that stimulate fibrosis- spironolactone blocks this

18
Q

Digoxin mechanism

A

inhibits the Na/K ATPase transporter which leads to increased intracellular calcium levels and increased ionotrophy (contractility)

19
Q

Digoxin toxicity

A

Very narrow therapeutic window and a great deal of variability b/w patients.
Arrhythmias, blurred vision, yellow halo, headache, fatigue, dizziness, seizures. Use Digi bind to reomve it in life threatening situations

20
Q

Digoxin drug interactions

A

tons of them. ANything that changes its metabolism may move it out of the therapeutic wondow.
Quinidine decreases levels, Amiodarone, VERAPAMIL

21
Q

Greatest benefit of digoxin sen in what pts

A

those with ejection fraction of 25% and less and with cardiac enlargement

22
Q

Add what to therapy for class III

A

Digoxin

23
Q

Add what to Therapy for class IV

A

Strong vasodilators transplants and deveices

24
Q

Hydralazine

A

vasodilator

25
Q

Dobutamine

A

Beta 1 and 2 agonist (1 more than 2) increased ionotropy and a vasodilator

26
Q

Milrinone

A

Phosphodiesterase inhibitor…enhances Cyclic AMP signaling

27
Q

Talk about ANP and BNP in general

A

Natriuretic peptides that are released from atria and ventricles in the heart when pressure and volume are high. They are elevated in CHF and they promote vasodilation..
They reduce preload, prevent renin release, inhibit sodium reabsorption, and cause afferent arteriolar vasodilation in the kidneys

28
Q

What is the synthetic B-type Natriuretic peptide

A

Nesirtide..used in class IV CHF