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Pharm II > Chronic Heart Failure > Flashcards

Chronic Heart Failure Flashcards

1
Q

Define Heart Failure & the compensatory mechs

A

Inability to provide enough oxygenated blood to the rest of the body – impaired LV pump –> dec. CO –> body tries to compensate –> inc rate, inc. strength, inc fluid retention

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2
Q

Define Preload; In heart failure would it be high or low?

A

Amount of blood (VOL) in the ventricle at END OF DIASTOLE (End Diastolic Vol)
In heart failure it would be high b/c blood isn’t being pumped out –> goes backwards

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3
Q

Define Afterload; in HF would it be high or low?

A

Amount of PRESSURE the heart has to pump up against for systole
In HF, high d/t inc. resistance (NE, Epi, extra vol); brain senses dec. CO so Symp NS is triggered –> a-receptors activated –> vasoconstriction

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4
Q

How would you calculate Ejection Fraction

What is it?

A

Amount of blood pumped / End Diastolic Vol

% of blood pumped

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5
Q

What is the prevalence/ incidence of CHF in the U.S.

Why is the rate increasing?

A

5 mill people in the U.S
500K new cases/ yr

Increasing d/t

  • Better treatment of M.Is
  • Better access to healthcare
  • Better medicine/ cheaper (Lisinopril, B-Blockers dec mortality)
  • Obesity/ poor diet/ sedentary lifestyle
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6
Q

After 5 years of heart failure, what is the mortality rate of CHF?

A

50%

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7
Q

What are two ways to lower the mortality rate?

A

Pharmacologic: ACEis/ ARBs/ B-Blockers (dec. mortality), Spironolactone (dec. mortality); Loops (DON’T dec. mortality); Digoxin (Doesn’t dec. mortality)

Non-pharmacologic: Implantable cardiac defibrillators, biventricular pacing

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8
Q

Which 5 classes of medication are proven to decrease MORTALITY

A 
ACEis
ARBs
B-Blockers
Spironolactone
Vasodilators (hydralazine / nitrates) in A.As
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9
Q

What is the best treatment course for an African American to treat CHF

A

Using a vasodilator (e.g. hydralazine, nitrates) will inc. the response to B-Blockers, ACEis

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10
Q

What is unique about Digoxin?

A

It does not dec. mortality
It has a narrow therapeutic window
Usually given to elderly pts

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11
Q

Which three factors should be taken into account when prescribing meds for a non-complicated case?

A

Compliance
Expense
Polypharmacy e.g. drug interactions, side effects like orthostasis

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12
Q

According to evidence based medicine, even after maximizing medication therapy, what is the mortality rate after 5 years?

A

30% if appropriate Rx is given

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13
Q

Approx. how much is spent on heart failure management per year?

A

$25 bill

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14
Q

Which QOL factors can be affected by CHF?

A

Ability to exercise
Walking
Difficulty breathing/ SOB/ edema
Frequent hospitalizations (chance of Afib)

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15
Q

Besides CAD, what other etiologies cause or inc. the risk of developing HF?

A
  • HTN (esp untreated) after 15 years LVH, dec. EF
  • Males
  • Valve DOs (fixable)
  • Pregnancy
  • Smoking
  • Rx-induced (e.g. NSAIDs esp. w/ renal insufficiency/ ACEis, steroids)
  • Alcohol/ illicit drug se (e.g. chronic cocaine)
  • Pericarditis
  • Hyperthyroidism
  • Diabetes
  • Obesity
  • Idiopathic
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16
Q

What are some possible symptoms/signs of HF?

A
  • SOB/ DOE
  • Edema – peripheral and/ or pulmonary
  • Orthopnea
  • Easily fatigued
  • Ascites
  • Hepatomegaly
  • Heart murmurs
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17
Q

Define NYHA classification of HF

A

-Based on symptoms
Class 1: ordinary activity DOESN’T cause symptoms
Class 2: ordinary activity causes symptoms
Class 3: less than ordinary activity causes symptoms
Class 4: symptoms are present at rest

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18
Q

Define ACC classification of HF

A

Class A: high risk for HF (HTN, obese) but w/o structural heart dz or symptoms of HF
Class B: structural heart dz (on echo/ imaging) but w/o sxs of HF
Class C: structural heart dz with prior or current symptoms of HF (LV hypertrophy, dec. EF)
Class D: REFRACTORY HF requiring specialized interventions (quality of care; IV drug dobutamine is used as outpt for end stage HF)

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19
Q

What are the two types of HF?

A

Systolic & Diastolic

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20
Q

Systolic HF

  • What’s the frequency?
  • What’s the problem?
  • What’s the cause?
A
  • Most common (85%)
  • Problem with ejection of blood to the lungs/ systemc circulation (low EF <40%)
  • Result of hypertrophy and dilatation of the ventricle (thin walls)
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21
Q

Diastolic HF

  • What’s the problem?
  • What’s the cause?
  • Treatment?
A
  • Inability of the heart to fill appropriately –> arrhythmias (Afib), tachy; EF s nml or inc.
  • Usually results from stiffness of myocardium
  • More difficult to treat; treatment not well-defined (no specific drugs like ACEis/ ARBs)
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22
Q

What is a normal EF range?
What is the EF of diastolic HF? Why?
What is the EF of systolic HF? Why?

A

Nml EF: 55-75% pumping out 7/10 mL –> 70% EF

Diastolic: EF > 55% pumping out 3/5 mL –> ~60% EF d/t dec. EDV (can’t hold as much blood)

Systolic: EF 30% EF

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23
Q

What are the 4 compensatory mechanisms of HF?

A
  • Carotids, kidneys sense dec. CO & tries to compensate; the SYMPATHETIC NS produces Epi, NE to inc. CO, vasoconstrict
  • Vasoconstriction leads to VENTRICULAR HYPERTROPHY
  • The RAAS SYSTEM tries to inc. flow through the kidneys, converts Angiotensinogen –> AgI, AgII –> Na+/ H2O retention (inc. volume, inc. pressure, vent. hypertrophy)
  • FRANK STARLING MECH: inc EDV, heart dilates, vents. expand to compensate for inc. volume, delays HF for a period
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24
Q

Which drugs would affect the activation of the Sympathetic NS?

A

Beta-Blockers

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25
Q

Which drugs would affect the mechanism behind LV Hypertrophy?

A

ACEi/ ARBs
Spironolactone
B-Blockers

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26
Q

Which drugs would affect the RAAS system?

A

ACEis works on enzyme

ARBs: direct receptor blocker (otherwise inc. K+)

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27
Q

Which drugs would affect the Frank-Starling mechanism?

A

Diuretics: treating end product

ACEi/ ARB/ spironolactone: may help w/ chronic fluid overload (shuts down aldosterone & prevents end product)

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28
Q

Which 2 drugs used in HF reduce morbidity (not mortality)?

A

Digoxin

Diuretics

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29
Q

What is ACC Stage A?
What kind of pts does this describe?
What is the typical therapy?

A
  • Without structural dz or symptoms of HF
  • HTN; CAD; DM; Obesity; Metabolic syndrome
    OR Using cardiotoxins, F h/o cardiomyopathy
    -ACEi or ARB for vascular dz of DM
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30
Q

What is ACC Stage B?
What kind of pts does this describe?
What is the typical therapy?

A
  • Structural dz w/o sxs of HF: incidental findings (older pt who needs full physical)
  • Previous M.I; LV remodeling incl. LVH, EF); asymptomatic valvular dz
  • ACEi or ARB + B-Blocker (to delay/prevent progression to Stage C)
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31
Q

What is ACC Stage C?
What kind of pts does this describe?
What is the typical therapy?

A
  • Structural dz (e.g. LVH) w/ prior or current HF symptoms (e.g. peripheral edema)
  • Known structural heart dz AND SOB, fatigue, reduced exercise tolerance
    -Diuretics (i.e. Loop 80mg/day), ACEi, B-Blockers (5mg/day)
    For selected pts: aldosterone antagonist, ARBs, digitalis, hydralazine/ nitrates
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32
Q

What is ACC Stage D?
What kind of pts does this describe?
What is the typical therapy?

A
  • Refractory HF requiring specialized interventions
  • Marked symptoms at rest despite maximal Rx therapy
  • Hospice care; heart transplant; continuous IV inotropes; mechanical support; experimental surgery/ drugs (dobutamine, may inc mortality)
33
Q

What is a class of drugs that also works on the AV node and works the same was as B-Blockers?

A

Nondihydropyridines: no role in systolic HF

34
Q

Which B-Blockers can be used for HF?

A
  • Metoprolol succinate (Toprol) long-acting, QD
  • Bisoprolol: start @ dec. dose
  • Carvedilol: b.i.d, may dec. compliance; mixed a/B = vasodilation
35
Q

What is the MOA of B-Blockers?

A

Blocks B-receptors leading to dec. heart rate, dec. BP, inc. coronary artery blood flow ; dec. CO

36
Q

With an inc heart rate, how is coronary supply affected?

A

Inc stress on heart = inc systole = dec. coronary supplyf

37
Q

What is the dosing strategy for B-Blockers?

A

Can be used in stage A or B; should be used in stage C; goal dosing is essential to maximize mortality/ morbidity benefit

38
Q

What is the dose & frequency of Metoprolol succinate? Goal?

A

6.25 - 12.5 mg/day (long titration, more effective to go slow); goal 200 mg/day (still need to maximize effect on morbidity/mortality)

39
Q

What is the dose & frequency of Bisoprolol? Goal?

A

1.25 mg/day; goal 10 mg/day

40
Q

What is the dose & frequency of Carvedilol? Goal?

A

3.125 mg/day b.i.d.; goal 25 mg b.i.d

41
Q

What are 3 major ADRs of B-Blockers?

A
  • Bradycardia
  • Worsening of HF if dose is started to high or up-titrated too quickly (acute HF, cardiogenic shock)
  • Respiratory issues
42
Q

Why don’t we use metoprolol tartrate in managing HF?

A

HF clinical trial showed succinate is superior to tartrate

43
Q

What is the MOA of ACEi/ ARBs?

A

Interferes with RAAS ending with disrupting angiotensin II

  • Dec BP, Na+/H2O retention
  • Afterload reducer (dec peripheral resistance)
44
Q

What is a key PK note in prescribing ACEi/ ARBs?

A

Highly excreted via kidneys; dose reduction is often necessary as long as K+ is WNL
-NOT FOR acute renal failure d/t unstable SCr

45
Q

What is the dosing strategy of ACEi/ ARBs?

What about with B-Blocker treatment simultaneously?

A
  • Used in all stages of HF; all ACEi/ ARBs have been used in HF
  • Start/ titrate B-Blocker at some point, either BEFORE or AFTER ACEi titration; could start with B-Blocker 1st if tachycardic/ start ACEi first if HTN
46
Q

What is the dose & frequency of Lisinopril? Goal?

A
  • Start at 5 mg/day, double the dose Q2weeks until: goal dose of 20-40 mg/ day ; usually ~6 mos to reach goal
  • Goal doses are essential maximizing mortality/ morbidity benefit
47
Q

Which drug class is preferred in HF, ACEi or ARB?

A
  • Cough can be a limiting factor, won’t go away; switch to another ACEi before d/c to ARB
  • Cost benefit over ARB
48
Q

What are 3 major ADRs of ACEi/ ARBs?

A
  • Hyperkalemia
  • Cough (ACEi)
  • Hypotension
49
Q

What are 4 absolute contraindications to prescribing ACEi/ARBs?

A
  • Pregnancy
  • Hyperkalemia (K > 5.0 meq/L)
  • B/L renal artery stenosis
  • Angioedema (life-threatening)
50
Q

What is the MOA of Aldosterone Blockers?

A
  • Competes with aldosterone for intracellular mineralcorticoid receptors –> Na+/ H2O excretion (increases K+ in the blood)
  • Decreases preload
51
Q

Give two examples of Aldosterone Blockers?

A

Spironolactone

Eplerenone

52
Q

What are two PK notes for aldosterone blockers?

A
  • Highly protein bound

- Primarily renally excreted

53
Q

What are the indications for aldosterone blockers?

A
  • Specifically for STAGE C/D HF

- Not 1st line for HF; use if MAXING OUT on ACEi/ B-Blocker and still symptomatic or are admitted for exacerbation

54
Q

What is the dose & frequency of spironolactone?

For eplerenone?

A

12.5 - 25 mg/day (spiron)

25 mg/day (eplerenone)

55
Q

What are 2 major ADRs of Aldosterone Blockers?

A
  • Hyperkalemia (could push them over limit if using with ACEis)
  • Gynecomastia (spiron. only)
56
Q

What is an absolute contraindication to prescribing aldosterone blockers?

A

Hyperkalemia

57
Q

What is the MOA of the vasodilator Hydralazine? Target?

A
  • Direct arterial vasodilator (dec. BP)

- Predominately vasodilates in coronary, cerebral, and renal arteries

58
Q

What is the MOA of isosorbide nitrate?

A
  • Direct venodilator; converts into NO (vasodilator)
59
Q

What are 2 key PK notes about direct vasodilators?

A
  • Used in place of ACEi d/t complications e.g. angioedema, hyperkalemia, B/L renal artery stenosis (doesn’t have to be A.A)
  • Not renally excreted
60
Q

Why would a drug combination of a vasodilator and an ACEi or a B-Blocker be more beneficial to an A.A than to a Caucasian?

A

??

61
Q

What is the dosing strategy for vasodilators?

A
  • Used in stage C in A.As

- Used in B/C/D if a contraindication to ACEi exists, regardless of race

62
Q

What are 2 major ADRs with vasodilators?

A
  • Tolerance to nitrates

- Hypotension esp. when combined with carvedilol

63
Q

Which drug class is most effective in HF??

A
  • Loop Diuretics esp. Furosemide: excretes Na+ / H2O, can be used with dec SCr/ renal failure
  • BP can be managed w/ B-Blockers, ACEis
  • Thiazides ARE NOT effective in HF
64
Q

What is the MOA of Loop Diuretics?

A
  • Exerts action at the loop of Henle, increases Na+/ H2O excretion
65
Q

If all diuretics reduce pre-load and edema why are loop diuretics preferred over other agents such as thiazide diuretics?

A

???

66
Q

What are key PK notes regarding loop diuretics?

A
  • May require higher than usual doses to induce diuresis in pts with renal failure
  • Pts should weigh themselves every day for tailored dosing: “basal” based on wt gain/ loss
67
Q

What is the dosing strategy of loop diuretics? What are the dose ranges and frequency for Furosemide (Lasix)? Bumetanide? Torsemide?

A
  • Should only be used for symptomatic HF (C or D)
  • Furosemide: 10-40 mg/day
  • Bumetanide: 0.5 - 1 mg/day
  • Torsemide: 10- 20 mg/day
68
Q

What is the goal of Loop Diuretic therapy?

A

After initial diuresis and reduction of fluid, try to get the LOWEST DOSE POSSIBLE or even consider D/C

69
Q

How can diuretics interfere with maximizing mortality-reducing medication?

A

Affects BP which interferes with B-Blockers, ACEis

70
Q

What are the MC electrolyte imblances seen with Loop diuretics?

A
  • Hyperglycemia
  • Hyperuricemia
  • Hypokalemia
  • Hypomagnesemia
71
Q

What is the MOA of digoxin?

A
  • Positive inotropic activity & negative chronotropic activity
  • Increases the intracellular Na+ and Ca++ to inc to force of contraction
72
Q

What is the driving force behind digoxin producing negative chronotropic activity?

A

Dec. intracellular K+

Inc. intracellular Ca++

73
Q

What are some key PK notes for digoxin?

Who is most likely to have unintended toxicity when taking digoxin?

A
  • Large VD, esp larger in obese/ smaller in elderly; primarily renally excreted
  • The elderly; w/ a smaller VD, [digoxin] inc. in the blood & worse for renal failure
74
Q

What is the normal dosing strategy for digoxin? In the elderly?

A
  • Low dose for normal renal function (0.125 mg/day), should ONLY be used in symptomatic HF (C/D)
  • Elderly or renal insufficiency: 0.125 mg QOD
75
Q

What are some monitoring points for digoxin?

A

Monitor for toxicity not efficacy (>2 ng/dL); worse outcomes with higher normal levels when compared to lower normal levels (0.5-1 ng/dL vs. 1.5-2 ng/dL)

76
Q

What are 4 major ADRs associated with digoxin?

A
  • High potential for toxicity
  • Electrolyte disturbances: hypomagnesemia, hypokalemia
  • Bradycardia (esp w/ toxicity)
  • G.I. disturbances ( MC SIDE EFFECT)
77
Q

Explain: hypokalemia INCREASES the effects of digoxin; hyperkalemia DECREASES the effects of digoxin

A

???

78
Q

How can digoxin interfere with maximizing mortality-reducing medications?

A

????

Pharm II (5 decks)

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