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Pharmacology II Exam 2 (Lauren) > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

What causes sudden death in heart heart failure?

A

Arrhythmias

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2
Q

What are the main determinants of cardiac workload?

A

Preload

Afterload

Contractility

HR

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3
Q

What kinds of drugs decrease preload?

A

Venodilators

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4
Q

What kind of drugs reduce afterload?

A

Arteriodilators

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5
Q

What effect do B-blockers have on contractility

A

Decrease conractility

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6
Q

How do B blockers reduce cardiac work?

A

Slowing HR

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7
Q

When your heart is failing, what happens to preload

A

Increases due to increased blood volume and increased venous tone

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8
Q

What 2 classes of drugs will reduce preload in HF

A

Diuretic

Venodilators

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9
Q

What effect does HF have on afterload

A

Increased afterload due to increased aortic impedance and increased arterial constriction

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10
Q

What class of drugs will reduce afterload in HF

A

Arteriodilator

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11
Q

What effect does HF have on HR

A

HR is increased due to reflex tachycardia caused by sympathetic hyperactivity

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12
Q

How do B-blockers help in HF

A

They reduce energy expenditure by slowing the HR

Does not help in end stage HF

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13
Q

What is the MOA of digoxin?

A

Inhibits the Na+,K+ ATPase pump on the cell membrane. Leads to:

⬆️Intracellular Na+

⬇️Expulsion of intracellular Ca++

⬆️Intracellular Ca++ leads to increased Ca++ stores

⬆️Actin-myosin interaction by intracellular Ca++

⬆️Contractility (positive inotropy)

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14
Q

What is the #1 drug to increase inotropy

A

Digitalis

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15
Q

What effect does Digoxin have on normal healthy hearts

A

Decreases HR

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16
Q

Who can use Digoxin as an antiarrhythmic?

A

Patients NOT in heart failure!

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17
Q

How does Digoxin slow HR in normal hearts?

A

Vagal stimulation due to:

Sensitization of arterial baroreceptors

Stimulation of central vagal nuclei

Increased SA node sensitivity to ACh

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18
Q

How does Digoxin slow HR in FAILING hearts?

A

In HF, sympathetic tone will already be high, but Digitalis will reduce sympathetic tone by increasing myocardial contractility

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19
Q

Does Digitalis increase Cardiac output for everyone?

A

No, only in failing hearts.

Because peripheral vasoconstriction will increase in normal people

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20
Q

What is one of the earliest sign of digitalis toxicity?

A

GI side effects***

Will disappear after discontinuation

21
Q

Is the margin of safety wide or narrow in digoxin

A

Narrow, you can have toxicity even at therapeutic doses

22
Q

Is Digoxin a glycoside?

A

Yes, and all glycosides are toxic

23
Q

What is the most dangerous adverse effect of digoxin?

A

Cardiac arrhythmias!!!**

Includes: BIGEMINY**, sinus bradycardia, AV block, ectopic ventricular beats

24
Q

How do you treat a ~moderate~ digoxin intoxication

A

Stop drug and give potassium

25
Q

How do you treat SEVERE digoxin intoxication (life-threatening arrhythmias)

A

Stop drug, give potassium, and give Digitalis Immune Fab (Digibind)****

Do NOT cardiovert digitalis-induced arrhythmias unless Vfib

26
Q

If digitalis has caused an arrhythmia, can you cardoivert them?

A

No

Not unless it is Vfib

27
Q

What drugs will increase the toxicity of digoxin?

A

Thiazide and Loop diuretics!!**

Quinidine- displaces digoxin from tissue binding sites

28
Q

Why do thiazides and loop diuretics increase the toxicity of digoxin?

A

They cause hypokalemia!!!***

Hypomagnesemia** and Diarrhea could also increase toxicity since they reduce K+

29
Q

What effect will hypomagnesemia have on digoxin toxicity

A

Increased

30
Q

What drug class will decrease the effectiveness of digoxin

A

Calcium channel blockers lol they will literally DECREASE contractility and are CONTRAINDICATED in HF

31
Q

What kind of drug is Milrinone

A

An “inodilator”

Increase inotropy AND causes vasodilation

32
Q

What is the MOA of milrinone

A

Inhibits cAMP phosphodiesterase

Leads to increased cAMP, increased Ca influx and a significant vasodilating effect

33
Q

what is the the route of administration of milrinone

A

IV only

34
Q

What do we use Milrinone for?

A

Palliative treatment for acute HF or severe exacerbation of chronic HF (IV only, SHORT TERM use)

35
Q

How long can a patient be on milrinone?

A

SHORT TERM

Long term will kill them via an arrhythmia

36
Q

What is the adverse effect of milrinone

A

Arrhythmia

37
Q

What drug would be pointless to give at the same time you gave dobutamine or dopamine

A

B Blocker

38
Q

What is the MOA of dobutamine and dopamine

A

B1 agonists- causes an inotropic effect

39
Q

What are the 2 benefits of spironlactone and eplerenone

A

Reduce mortality rate

Correct hypokalemia caused by loop/thiazide

40
Q

How do ACEs and ARBs treat Heart failure

A

Diminish cardiac workload by:

Reduce edema and preload (inhibit aldosterone)

Decrease afterload via Vasodilation (inhibit Angiotensin II)

41
Q

Why do ACEs cause a cough

A

They reduce the bradykinin metabolism

42
Q

Are ACEs/ARBs OK in pregnancy?

A

NO

Category X in 2nd and 3rd trimester!

43
Q

What does Sacubitril/Valsartan (Entresto) do?

A

Valsartan: ARB

Sacubitril: neprilysin inhibitor (results in more vasodilation)

44
Q

Which is better at reducing mortality in HF: Sacubitril/Valsartan (Entresto) or Enalapril alone

A

Entresto

45
Q

What effect do B-blockers have on life expectancy in HR

A

Increase life expectancy ONLY in early stages of HF

Dangerous in endstage due to negative inotropic effect

46
Q

What drug is the “sweetheart” of cardiologists and why

A

Carvedilol. It is a nonspecific B blocker AND an a1 blocker so it will decrease peripheral resistance in addition to the B blocker effects

47
Q

What effect does Sodium nitroprusside (Nitropress) have

A

Dilates VEINS more than arteries. (Same thing as nitro)

48
Q

What does Isosorbide dinitrate and Nitroglycerin do?

A

Dilates veins more than arteries

Reduces preload more than afterload

49
Q

What does Hydralazine do?

A

Peripheral vasodilation via the production of NO

Pharmacology II Exam 2 (Lauren) (9 decks)

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