Misc CHF Drug Info Flashcards

1
Q

What is the mechanism of digoxin?

A

Na/K ATPase inhibitor, vagal stimulation, AV block

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2
Q

What drug interactions with diltiazem?

A

Inhibits CYP–statins

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3
Q

Amiodarone side effects?

A
Blue/grey skin
photosensitivity
hepatotoxicity
hypo/hyperthyroidism
pulmonary fibrosis
hypotension
bradycardia
corneal microdeposits
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4
Q

Propafanone/flecainide side effects?

A

dizziness, blurred vision, HF exacerbation

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5
Q

Ibutilide/dofetilide ADEs?

A

TdP

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6
Q

Sotalol ADE?

A

TdP

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7
Q

Dronedarone ADEs?

A

Bradycardia, diarrhea, nausea, asthenia, rash

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8
Q

Dronedarone interactions?

A

Digoxin, diltiazem, verapamil

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9
Q

Dronedarone CI?

A

HF patients!

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10
Q

Adenosine mechanism?

A

Inhibits AV node, terminates re-entry pathway

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11
Q

Procainamide ADEs?

A

Hypotension, QT prolongation, TdP

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12
Q

Epinephrine class?

A

Vasopressor

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13
Q

Dofetilide dose?

A

> 60: 500 mcg BID
40-60: 250 mcg BID
20-39: 125 mcg BID
<20: None

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14
Q

Amiodarone dose:

Ventricular rate control?

A

100-200 mg PO daily

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15
Q

Amiodarone dose:

Conversion?

A

10 g loading dose in 600-800 mg increments –>200 mg daily

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16
Q

Amiodarone dose: Maintenance?

A

400-600 mg LD x 2-4 weeks

100-200 mg daily MD

17
Q

Amiodarone dose:

Ventricular tachycardia?

A

150 mg IV x 10 minutes

1mg/min IV x 6h + 0.5 mg/min x 18 hours

18
Q

Amiodarone dose:

Ventricular tachycardia prevention?

A

400 mg daily PO

19
Q

Amiodarone dose:

V fib?

A

300 mg IV

then 150 mg IV

20
Q

Drug classes that cause TdP (Wendt)?

A
Antiarrhythmics
Antibiotics
Cancer
Opiate
Antidepressants
Antipsychotics
CCBs
antiemetics
Gastric pro-motility
Antihistamines
Diuretics
21
Q

Digoxin mechanism of action?

A

Lowers Na gradient
Less Ca ejected
More Ca in SR (more Ca released during AP)
STRONGER contractility

22
Q

Mechanism of Action: Beta agonists in CHF?

A

Beta receptor –> Gs –> Increased cAMP–> PKA activiation –> Increased calcium (activates Ca channels) –> Increased contractility

23
Q

Mechanism of action: PDE3 inhibitors in CHF?

A

Blocks PDE –> less cAMP degradation –> more cAMP in the cell –> Increased Calcium –> increased contractility

24
Q

What are vasopressors used for in CHF?

A

Hyponatremia

25
Q

What does decreased CO cause?

A

decreased renal blood flow (which activates RAAS)

Increased carotid sinus firing (which activates sympathetic discharge)

26
Q

What are cardiovascular causes of ADHF?

A
MI
valvular disease
uncontrolled HTN
PE
Arrhythmias
Worsening HF
27
Q

What is the cut-off PCWP for wet?

A

> 18

28
Q

What is the cut off CI for cold?

A

<2.0

29
Q

How is CI calculated?

A

CO/BSA

30
Q

T/F: Inotropes affect preload

A

FALSE

31
Q

What should be monitored w/ADHF?

A
Weight (qAM)
HR/BP
Ins/outs
S/S of edema
Electrolytes (qd)
Renal function (BUN/SCr) (qd)
32
Q

How do you dose loop diuretics in ADHF?

A

Give Bolus of normal diuretic therapy for a day–half of the dose if furosemide

33
Q

How can you overcome diuretic resistance?

A
Add thiazide
Increase frequency of dose
Limit sodium/water intake
IV infusion
ultrafiltration
34
Q

How to monitor loops?

A

Urine output, s/s congestion regularly

35
Q

Vasopressor ADE?

A

Osmotic demyelination

36
Q

What is the MOA of adenosine in VSM?

A

Binds to A2 receptor –> Gs –> activation of AC –> increased cAMP –> Relaxation

37
Q

What is the MOA of adenosine in heart?

A

Binds to A1 receptor –> Gi –> inhibition of AC —> decreased cAMP –> Decreased activation of HCN/CCB –> decreased contractility/HR