Phamacologic aspects of heart failure

Question 1

Goals?

Answer 1

improve ejection fraction
symptomatic relief of pulmonary edema
reduce cardiac remodeling

Question 2

Ejection fraction=

Answer 2

SV/ EDV

increase it by increase preload, decrease afterload, increase contractility

Question 3

main way to alleviate pulmonary edema?

Answer 3

decrease preload

Question 4

Treat Stage A?

Answer 4

ACEI / ARB

Question 5

Treat Stage B?

Answer 5

ACEI

Beta blocker

Question 6

Treat Stage C?

Answer 6

ACEI
Beta blocker
Loop diuretic
rare (thiazide, K sparing)
Digoxin

Question 7

IV drugs for acutely decompensated heart failure?

Answer 7

Loop diuretics
Nitroglycerin
Nitroprusside
Nesiritide

Question 8

Does ACEI relieve pulmonary edema?

Answer 8

No it doesn’t, Na and water loss is not sufficient to alleviate the edema associated with heart failure and after several months aldosterone levels return

Question 9

ACE inhibitor MOA?

Answer 9

Increase bradykinin, decrease Ang II– arteriolar dilation, decrease afterload, increase stroke volume, increase CO

Question 10

high levels of Ang II leads to?

Answer 10

cardiac hypertrophy and remodeling

Question 11

ACEI end result?

Answer 11

prolong exercise tolerance
increase quality of life
decrease hospital readmissions for heart failure
decrease morbidity and mortality

Question 12

How much start with ACEI?

Answer 12

start at low does and titrate up every 3-7 days to dose achieved in clinical trials

Question 13

Advantages of ARB over ACEI?

Answer 13

no/less cough or angioedema

Question 14

Beta blockers used for heart failure?

Answer 14

sustained release Metoprolol
Bisoprolol
Carbedilol

Question 15

Carvedilol?

Answer 15

blocks beta 1, beta 2, alpha 1 receptors

antioxidant effects

Question 16

MOA of beta blockers?

Answer 16

prevent or reverse cardiac hypertrophy and remodeling

prevent atrial/ ventricular arrhythmias

Question 17

result beta blockers?

Answer 17

increase left ventricular ejection fraction
decrease ventricular volume
lessens symptoms of heart failure
decrease hospitalization for worsening HF
decrease mortality

Question 18

major direct benefits of beta blocker?

Answer 18

reduce cardiac output

decrease mortality

Question 19

Use beta blockers in all stage IV?

Answer 19

no, if symptoms at rest may not be able to tolerate a beta blocker

Question 20

Clinical use of beta blocker?

Answer 20

Start at low does and titrate up every few weeks
benefit is not immediate
can exacerbate HF if too much is given

used in conjunction with ACEI, may have benefit in diabetics
Carvedilol and metoprolol are FDA approved

Question 21

Initial and targe doeses for Metorpolol?

Answer 21

Initial dose for class II 25 mg
12.5 mg for more severe

target dose 200 mg or highest tolerated dose

Question 22

Adverse effects beta blocker as pertain to Heart Failure?

Answer 22

fluid retention and worsening heart failure
fatigue
bradycardia and heart block
hypotension
abrupt withdrawl can cause deterioration of cardiac function

Question 23

Contraindications for beta blocker?

Answer 23

Acute decomponsated heart failure
-wait until patient is stable before starting
Dont give if already taking beta blocker for asthma
fixed airway disease is not necessarily a contraindication

Question 24

When to take someone off a beta blocker with heart failure?

Answer 24

Leave on if taking chronic and symptoms appear, if recent initiation/ titration up then stop beta blocker

Question 25

Effect of Furosemide on Preload? CO?

Answer 25

decrease preload by increasing Na excretion, reduce pulmonary and peripheral edema little to no effect on heart failure this decrease in wall may also improve systolic function

Question 26

Diuretic effect on heart failure frank starling?

Answer 26

move down the decomponsated curve without much of change to SV

Question 27

Clin use of diuretic for heart failure?

Answer 27

loop is the best for Stage C and D (Edema) only drugs that can adequately control fluid retention no known effect on morbidity and mortality

Question 28

Adverse effects of Loop/ thaizide?

Answer 28

volume depletion (weigh themselves) hypotension worsening renal function hypokalemia (can predispose patient to cardiac arrhythmia)

Question 29

K sparing diuretics use in heart failure pharm?

Answer 29

prevent hypokalemia associated with loop or thiazide diuretics

Question 30

Aldosterone and heart failure?

Answer 30

Aldosterone levels increase dramatically in heart failure to compensate by saving h20 and Na ACEI only produce transient decrease excessive aldosterone over time will cause vascular injury (hypertension) and cardiac remodeling (heart failure)

Question 31

Clin use of aldosterone antagonists?

Answer 31

patients with LVEF of 35% or less, already on ACEI and beta blocker and Stage C, Class II-IV must monitor renal function and potassium concentrations minimize risk of life threatening hyperkalemia serum creatinine < 2.0 (female) 2.5 (male) serum K < 5.0

Question 32

Big problem with aldosterone antagonists?

Answer 32

hyperkalemia

Question 33

Digoxin MOA?

Answer 33

Its a digitalis glycoside cause a positive inotropic effect block the ability of K to enter the cardiomyocyte in the Na/K ATPase which helps maintain Na concentration for the Na/Ca exchanger which is used in contraction of muscle

Question 34

Digoxin and postassium levels?

Answer 34

Works better with hypokalemia, hyperkalemia reduces the action Digoxin thiazides and loops can cause hypokalemia

Question 35

Digoxin indirect effects?

Answer 35

increase vagal activity | sensitize baroreceptors and decrease sympathetic activity, decrease activity of SA and AV node

Question 36

Toxic effects Digoxin?

Answer 36

lower dose- sinus bradycardia, AV block | higher dose- increase sympathetic tone, Ca overload

Question 37

Calcium overload?

Answer 37

With digoxin, large build up of Ca in the cell, spontaneous release from SR, cause Delayed after Depolarization DAD, if large enough can reach threshold and cause an irregular contraction cardiac arrhythmia can result

Question 38

Pharmacokinetics of DIgoxin?

Answer 38

Low therapeutic index, can easily overdose short half life, 36-48 hours might decrease hospitalizations improve symptoms, quality of life, functional capacity and exercise tolerance no effect on mortality

Question 39

Use digoxin for acute decomponsated HF?

Answer 39

not for acute

Question 40

Adverse effects of Digoxin?

Answer 40

``` Cardiac arrythmias GI tract upset CNS Visual disturbance Gynecomastia ```

Question 41

What is Digoxin immune Fab? Use Digoxin immune Fab?

Answer 41

digoxin 'antidote', Fab fragment of digoxin-specific antibody Life threatening cases of digoxin toxicity

Question 42

Vasodilators?

Answer 42

Isosorbite dinitrate Hydralazine given together orally

Question 43

Hydralazine help someone with HF?

Answer 43

mainly dilates arteries | decrease afterload which increases ejection fraction

Question 44

Isosorbite dinitrate help someone with HF?

Answer 44

mainly dilates veins | decrease preload which decreases edema

Question 45

Isosorbite dinitrate and Hydralazine clin use?

Answer 45

African Americans already on diuretic, ACEI, beta blocker (Stage C Class III-IV) In patients who cannont use and ACEI or ARB (C) decrease mortality, not as good as ACEI

Question 46

Goal in treatment of acute decomponsated HF?

Answer 46

Relieve pulmonary congestion (reduce preload) | decrease pump failure (reduce afterload, increase contractility)

Question 47

Drugs for acute decomponsated?

Answer 47

Loop, Nitroglycerin, Nitroprusside, Nesiritide

Question 48

Loop treat acute decomponsated HF?

Answer 48

vasodilate, increase systemic venous capacitance, decrease left ventricular filling pressure in addition to diuresis, decrease filling pressure reduce pulmonary edema

Question 49

Concerned with loop?

Answer 49

excessive diuresis, hypotension, worse renal failure, electrolyte disturbance

Question 50

Clin use loop acute decompoinsated HF?

Answer 50

IV for volume overload

Question 51

Nitroglycerin?

Answer 51

increases NO mainly in veins | decrease preload, not much affect on afterload

Question 52

Nitroprusside?

Answer 52

increase NO in both arteries and veins decrease preload decrease afterload

Question 53

Nesiritde?

Answer 53

recombinant human Btype natriuretic peptide

Question 54

BNP?

Answer 54

hormone released from the ventricles, tries to counteract the vasoconstriction and Na retaining effects of NE, Ang II, and aldosterone

Question 55

Nestiride MOA?

Answer 55

activates guanyly cyclase on vascular smooth muscle cells, increase cGMP, dilate arteries, dilate veins kidney, natriuresis

Question 56

Clin use Nestiride?

Answer 56

IV for acute decomponsated HF added to diuretics for patients with evidence of severly symptomatic fluid overload in the absence of systemic hypotension, relief on angina, control of hypertension complicating HF

Question 57

Nestiride adverse effects?

Answer 57

Hypotension Headache not approved for intermittent IV infuison

Question 58

Treat stage D?

Answer 58

Dobutamine, Dopamine, Phosphodiesterase inhibitors (Inamrinone, Milrinone)

Question 59

Dobutamine?

Answer 59

activates beta 1 more than beta 2 or alpha receptors Heart- Positive inotropic effect Vasculature- Vasodilation End result: increase force of contraction without significantly increase HR

Question 60

Dopamine MOA?

Answer 60

activates domaminergic, Beta, alpha receptors low dose- vasodilate of renal, splanchnic, cerebrospinal, and coronary blood vessels (increase renal blood flow, treat refractory edema) high dose- positive inotropic higher dose- vasoconstrict of arteries

Question 61

Phosphodiesterase Inhibitors?

Answer 61

increase cAMP, increase force of contraction, increase velocity of relaxation, vasodilation

Question 62

Problems with Phosphodiesterase inhibitors?

Answer 62

``` intolerable side effects minimal long term efficacy increase mortality with long term use IV infusion, once stabilize wean off drug short term, not long term ```