Cv Pharm, Test 2, Heart Failure

Front 1

Dilated arteries decrease

Back 1

Afterload

Front 2

What compensatory mechanisms are activated by reduced CO?

Back 2

RAAS
Sympathetics

Front 3

Increasing preload in someone with HF will cause?

Back 3

Pulmonary edema

Front 4

Vasoconstriction in HF causes?

Back 4

Increase in afterload (arteries)
Increase in preload (veins)

Front 5

Long term Consequences of HF

Back 5

Sympathetic -> ^ afterload, HR, & force of contraction, preload
RAAS -> ^ preload
Cardiac remodeling

Front 6

Goals of HF therapy

Back 6

Improve ejection fraction
Relieve pulmonary edema
Reduce cardiac remodeling

Front 7

Alleviate pulmonary edema by?

Back 7

Decreasing preload
Using a diuretic or venous dilator

Front 8

Reduce cardiac remodeling by?

Back 8

Blocking NE, ANG II, & Aldosterone

Front 9

First line to treat HF?

Back 9

ACE Inhibitor

Front 10

ACE inhibitors in HF cause

Back 10

Decrease ANG II
Increase bradykinin
Both cause vasodilation -> decrease afterload = ^ SV = ^ CO

Front 11

Biggest thing ACEI does in HF?

Back 11

Prevents cardiac remodeling

Front 12

When do you add a beta blocker?

Back 12

Stage B HF

Front 13

Beta blockers used in HF

Back 13

SR Metoprolol
Bisoprolol
Carvedilol

Front 14

Beta blockers improve HF by?

Back 14

Increase Ejection fraction
Decrease ventricular volume

Front 15

In HF, decrease CO causes

Back 15

Salt and water retention -> ^ preload = Pulomary edema & ^ Wall Stress

Front 16

Doing what to preload reduces pulmonary edema?

Back 16

Decrease

Front 17

What effect will diuretics have on CO in a patient with heart failure?

Back 17

Little to know effect!!

Front 18

What stage do you start a Loop in HF?

Back 18

Stage C

Front 19

Aldosterone causes what in HF?

Back 19

Vascular injury
Cardiac remodeling

Front 20

RALES

Back 20

Showed that adding spironolactone to patients with severe HF caused a decrease in mortality

Front 21

What stage do you start an aldosterone antagonist?

Back 21

Stage C
NYHA III

Front 22

Guidelines for using aldosterone antagonist

Back 22

MUST have normal creatinine & K+

Front 23

Spironolactone gives you a nice set of?

Back 23

Man boobs

Front 24

How does myocyte depolarization normally work?

Back 24

Na+ channels open -> depolarization
Depolarization activates voltage gated Ca2+ channels -> Ca2+ enters cell
This C2+ causes Ca2+ induced Ca2+ from the SR
Ca2+ release from SR increases intracellular Ca2+ and causes contraction

Front 25

How does myocyte repolarization normally work?

Back 25

Na+ leaves cell and K+ enters cell via Na+/K+ ATPase
Ca2+ is taken back up into SR via SERCA pump (sarcoplasmic/endoplasmic reticulum Ca2+ ATPase)
Ca2+ also leaves cell via Ca2+/Na+ exchanger

Front 26

What drives the Na+/Ca2+ exchanger?

Back 26

Transmembrane Na+ gradient
Increase of intracellular Na+ causes LESS Ca2+ going out

Front 27

Digoxin works by?

Back 27

Inhibiting the Na+/K+ ATPase on the myocyte
This causes an increase in Na+ staying in the cell during repolarization
This Na+ increases ensures that LESS Ca2+ goes out via the Ca2+/Na+ exchanger
More Ca2+ taken up by the SR -> greater force of contraction
It's all about the gradient!!

Front 28

Digoxin vs Hypokalemia

Back 28

Increased digoxin effect
This is because extracellular K+ inhibits digoxin -> less K+ = less digoxin inhibition

Front 29

Digoxin vs Hyperkalemia

Back 29

Decreased digoxin effect
This is because extracellular K+ inhibits digoxin -> more K+ = more digoxin inhibition

Front 30

Indirect effects of digoxin

Back 30

Increased vagal tone
Decreases SA/AV activity -> slows ventricular rate
Works most on the AV node!

Front 31

Ca2+ overload

Back 31

Spontaneous release of Ca2+ from SR

Front 32

Ca2+ can cause

Back 32

Delayed after depolarization -> if reaches threshold = Aftercontraction -> can cause arrhythmias

Front 33

When do you use digoxin?

Back 33

After using an ACEI, Beta B, & diuretic 1st
Used in conjunction with all of these drugs
ONLY STARTED IN STABLE PATIENTS!!

Front 34

Digoxin causes arrhythmias by?

Back 34

^ Vagal Tone -> Sinus brady & AV Block
Ca2+ overload & Symp. stimulation -> Atrial tachy, PVC's, V-tach/fib

Front 35

Early signs of digoxin toxicity

Back 35

Anorexia
Diarrhea
Nausea
Vomiting

Front 36

If and ACEI is contraindicated in a patient with HF, what could you use?

Back 36

Isosorbide dinitrate (venous)
Hydralazine (arterial)

Front 37

Decrease preload and you?

Back 37

Decrease edema
Decrease wall stress

Front 38

Decrease afterload and you?

Back 38

Increase ejection fraction
Decrease wall stress

Front 39

Your patient can not use an ACEI or ARB, use what?

Back 39

Isosorbate Dinitrate
Hydralazine

Front 40

What is goal in treatment of acute decompensated HF?

Back 40

Relieve pulmonary congestion
Decrease pump failure

Front 41

What can you use to reduce pulmonary edema?

Back 41

Loop
Venous dilator

Front 42

What can you use to increase CO?

Back 42

Arterial dilator
Increase myocardial contractility

Front 43

Nitroglycerin can be used _ to increase _ in _

Back 43

IV, NO, veins

Front 44

Nitroprusside is used _ to increase _ in _.

Back 44

IV
NO
Arteries and veins

Front 45

Nesiritide

Back 45

Recombinant human B-type natriuretic peptide
Activates guanylyl cyclase on vascular smooth muscle cells -> ^ cGMP -> DILATE ARTERIES AND VEINS
Also constricts efferent and dilates afferent arteriole in kidney

Front 46

Dobutamine

Back 46

Activates B1>B2>alpha
B1 -> heart = Positive Ionotrope (no HR affects)
B2 -> vasculature = vasodilator

Front 47

Dopamine

Back 47

Activates dopaminergic > Betas > Alphas

Front 48

Low dose dopamine

Back 48

Vasodilation of renal arteries
Increase perfusion of the kidney

Front 49

Medium dose dopamine

Back 49

Activates B1's -> positive ionotrope

Front 50

Highest dose dopamine

Back 50

Activates A1's -> Vasoconstriction

Front 51

Inamrinone

Back 51

Phosphodiesterase inhibitor
^ cAMP -> Positive ionotrope & vasodilation

Front 52

Milrinone

Back 52

Phosphodiesterase inhibitor
^ cAMP -> Positive ionotrope & vasodilation