Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharm 2 > CHF > Flashcards

CHF Flashcards

1
Q

What are most deaths in CHF due to?

A

Arrhythmias caused by increased sympathetic stimulation to help respond to decreased O2 delivery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the 4 classes of drugs that have been proven to improve mortality in pts with CHF?

A

ACE INHIBITORS, ARBs, aldosterone antagonists, and Beta blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are venodilatory effects of ACE-I and ARBS used to reduce?

A

PRELOAD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the mechanism by which renin release increases?

A

Increased O2 demand=increased sympathetic activity=increased renin secretion, which leads to an increase in preload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the arteriolar dilating effect of drugs used to combat?

A

AFTERLOAD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What does increased afterload cause the heart to do? What effect does that have on contractility?

A

dilate, decreases contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What causes contractility to increase? Decrease?

A

Inotropic agents; B-blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the overall effect of CHF on heart rate? What will alter this effect?

A

Reflex tachycardia occurs:
• ↓ Cardiac output leads to ↑ baroreflex activation leads to ↑ sympathetic stimulation of heart
• B‐blockers will reduce cardiac work by slowing the heart rate (and decreasing contractility)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the goal of B Blockers in treatment of CHF?

A

To reduce energy expenditure and decrease HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the effect of Digoxin on the normal heart?

A

vagal stimulation sensitizes arterial baroreceptors and stimulates central vagal nuclei, which increases SA node sensitivity to acetylcholine, DECREASING CARDIAC OUTPUT. DECREASING HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the effect of Digoxin on the failing heart?

A

Sympathetic tone is already high so as digalis increases contractility and CO, this causes TPR to decrease due to baroreceptor reflex, which leads to an INCREASE IN CARDIAC OUTPUT. DECREASING HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the earliest signs of digitalis toxicity that you need to watch out for? (THEY WILL HAVE THESE)

A

GI upset, N/V/D (due to an overtake of PNS tone), they disappear after discontinuation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the most common and dangerous side effect of digoxin?

A

Arrhythmias (sinus bradycardia, ectopic ventricular beats, bigeminy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the most common cause of death by digoxin therapy?

A

Ventricular fib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How do you monitor digoxin toxicity? What is the mechanism for this?

A

Regular EKGs, measure K+ and digitalis levels (K+ and digoxin compete on Na/K pump, so if K+ gets low, digitalis tox increases significantly!)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How do you treat a digoxin toxifity?

A

1) D/C digoxin
2) oral or IV K+ (NEVER CALCIUM! MAKES THINGS WORSE)
3) give lidocaine, phenytoin, or propranolol (Mg?)
4) in serious overdoes, use digitalis immune fab
5) DO NOT CARDIOVERT for any digitalis induced arrhythmia (except V fib)

17
Q

What two things lead to an even increased toxicity of digitalis?

A

1) hypokalemia (thiazide or loop diuretics or diarrhea)

2) further decrease of SA or AV node activity (B-blockers)

18
Q

What drugs are contraindicated with digitalis use?

A

Beta blockers

19
Q

What is a new class of positive inotropic drugs called? What two drugs are in that category? What stages of CHF are they used for?

A

Bipyridines; inamrinone, milrinone; END STAGES

20
Q

What is the MOA for bipyridines?

A

inhibit cAMP phosphodiesterase to increase cAMP levels, calcium influx, and cause a significant VD effect (acts as a B1 agonist to increase CO)

21
Q

What is the downside to using bipyridines for CHF, hence why it is only used in the end stages?

A

Increase in Ca2+ influx causes an increase in SNS stimulation which predisposes a person to arrhythmias

22
Q

What is the long term effect of bipyridines compared with placebo?

A

decreased survival due to arrhythmias

23
Q

When should dopamine be deployed as a positive inotropic agent?

A

IN SEVERE REFRACTORY CASES OF CHF

24
Q

What is the low dose response to dopamine?

A

causes increased renal vasodilation due to stim of D1 receptors in the kidney

25
Q

What is the moderate dose response to dopamine?

A

B1 receptors in the heart respond to increase inotropic effect

26
Q

What is the high does response to dopamine?

A

Alpha receptors in vessels cause vasoconstriction

27
Q

What is the MOA of dobutamine? What are its effects?

A

Selective B1 agonist; postitive inotropic effect with less tachycardia, this decreases filling pressure and increases O2 consumption (end stage CHF only)

28
Q

What are the drug classes that have no positive inotropic effects and are used in CHF?

A

Diuretics, spiro and eplerenone

29
Q

What single drug class is considered the backbone of CHF treatment today?

A

ACE-Inhibitorsl decrease afterload via decreased angiotensin II vasoconstriction, decrease preload via decreased aldosterone release

30
Q

What should you move patients with trouble with a dry cough to after ACE-I therapy?

A

ARBs (-sartans)

31
Q

What are the effects of B-blockers on CHF treatment?

A

Decrease renin secretion, attenuate the effects of high NE and epi release, causes an increased upregulation of B receptors which leads to a further decrease in HR and cardiac remodeling

32
Q

What stage of CHF do we use B Blockers in? What will we switch out after they stop compensating?

A

Early stage, replace with dobutamine or inamrione, etc (B1 agonist)

33
Q

Which B-blocker is an alpha and beta blocker? Which one is just a beta blocker?

A

Carvedilol, prevents tachycardia due to inhibition of alpha 1 vasoconstriction; metoprolol

34
Q

What is the digitalis antibody called?

A

dioxin immune fab (digibind)

35
Q

What are three ACE inhibitors used for CHF?

A

Captorpril, Enalapril, Fosinopril, etc

36
Q

What are the ang II receptor blockers?

A

Losartan, valsartan, and candesartan

37
Q

What are thiazides and related compounds used to treat CHF?

A

Hydrochlorothiazide, metolazone, indapamide

38
Q

Which vasodilators are used to treat CHF? What do effect do they have on CHF?

A

Sodium nitroprusside, isosorbide, hydralazine (HIP); reduce preload, afterload, or both and decrease damaging remodeling of the heart

Pharm 2 (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions