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Pharmacology > Management of Congestive Heart Failure > Flashcards

Management of Congestive Heart Failure Flashcards

1
Q

What is a “complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood?”

A

Heart Failure

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2
Q

Left sided heart failure is a failure to properly _________ blood ______ of the body

A

Left sided heart failure is a failure to properly PUMP blood OUT of the body

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3
Q

What are the 2 types of left-sided heart failure?

A
  1. Systolic HF

2. Diastolic HF

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4
Q

Systolic HF is inadequate __________

  • the left ventricle loses its ability to _______ normally
  • Heart can’t pump /c enough force to _______ enough blood into _________
  • Heart failure /c reduced _____________ (HFrEF)
A

Systolic HF is inadequate PUMPING

  • the left ventricle loses its ability to CONTRACT normally
  • Heart can’t pump /c enough force to EJECT enough blood into CIRCULATION
  • Heart failure /c reduced EJECTION FRACTION (HFrEF)
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5
Q

Diastolic HF = inadequate ________

  • Left ventricle loses its ability to _______ normally (muscle has become stiff)
  • Heart cannot properly fill /c blood during ______ period between each beat
  • heart failure /c _________ ejection fracture (HFpEF)
A

Diastolic HF = inadequate FILLING

  • Left ventricle loses its ability to RELAX normally (muscle has become stiff)
  • Heart cannot properly fill /c blood during RESTING period between each beat
  • heart failure /c PRESERVED ejection fracture (HFpEF)
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6
Q

What are 6 symptoms of Left Sided Heart Failure?

A
  1. Pulmonary edema
  2. Orthopnea
  3. SOB
  4. Hypotension (if low EF)
  5. Crackles
  6. Paroxysmal nocturnal dyspnea
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7
Q

Right sided heart failure — back up in the area that collects ________ blood

A

Right sided heart failure — back up in the area that collects “USED” blood

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8
Q

Right sided HF usually occurs as a result of Left sided HF. Explain how this happens…

A

Left ventricle fails, which leads to increased fluid pressure transferred back into the lungs ultimately damaging the right side of the heart. Right side loses pumping power and blood backs up in veins.

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9
Q

What are the 2 symptoms of Right Sided Heart Failure?

A
  1. Peripheral edema (legs and ankle)

2. Abdomen (ascites)

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10
Q

What are 8 Risk Factors of Heart Failure?

A
  1. HTN
  2. Smoking
  3. Obesity
  4. Post MI – structural damage
  5. Coronary artery disease (CAD)
  6. Diabetes
  7. Valvular heart abnormalities
  8. Drugs — cocaine, alcohol, thiazolidineiones, anthracyclines
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11
Q

Heart Failure Classifications— New York Heart Association

Class 1 = no limitations /c _____________
Class 2 = SOB at ________ exertion
Class 3 = SOB at _____________ exertion
Class 4 = SOB at ______

*Patients can move between classes

A

Class 1 = no limitations /c PHYSICAL ACTIVITY
Class 2 = SOB at ORDINARY exertion
Class 3 = SOB at LESS THAN ORDINARY exertion
Class 4 = SOB at REST

*Patients can move between classes

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12
Q

Heart Failure Classifications — ACC/AHA

Stage A = Increased ______, but no ____________ or __________ damage (HTN, DM, increased cholesterol, obesity, family history, cardio toxins

Treatment = ________/ ________

A

Stage A = Increased RISK, but no SYMPTOMS or STRUCTURAL damage (HTN, DM, increased cholesterol, obesity, family history, cardio toxins

Treatment = ACE-I/ ARB

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13
Q

Heart Failure Classifications — ACC/AHA

Stage B = _________ damage, but ____________ (previous MI, LV hypertrophy, valvular disease)

Treatment = ______/ ________ + _________

A

Stage B = STRUCTURAL damage, but ASYMPTOMATIC (previous MI, LV hypertrophy, valvular disease)

Treatment = ACE-I/ ARB + BB

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14
Q

Heart Failure Classifications — ACC/AHA

Stage C = _________ or ________ symptoms of HF (known structural disease /c SOB, fatigue, decreased exercise tolerance)

Treatment = _______/ _________ + _____ + __________
Maximizes therapy for symptom relief = ____________, _____________, and _________

A

Stage C = CURRENT or PRIOR symptoms of HF (known structural disease /c SOB, fatigue, decreased exercise tolerance)

Treatment = ACE-I/ ARB + BB + DIURETICS
Maximizes therapy for symptom relief = DIGOXIN, ALDOSTERONE ANTAGONIST, and BiDil

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15
Q

Heart Failure Classifications — ACC/AHA

Stage D = _______ stage, very low _______, marked symptoms at _________

Treatment = ________, _____, ___________, ___________

A

Stage D = END stage, very low EF, marked symptoms at REST

Treatment = ICD, O2, TRANSPLANT, HOSPICE

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16
Q

Compensatory mechanisms — the body works to maintain circulatory ___________ for a ________ time

A

Compensatory mechanisms — the body works to maintain circulatory HOMEOSTASIS for a LIMITED time

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17
Q

What are 5 compensatory mechanisms in response to decreased cardiac output?

A
  1. Vasoconstriction
  2. Hypertrophy
  3. Salt and water retention
  4. Tachycardia
  5. Brain Natriuretic Peptide (BNP)
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18
Q
  • How does vasoconstriction compensate for a decreased cardiac output?
  • What 2 hormones mediate this?
A
  • increase BP to increase blood flow and perfusion to tissues
  • 1) angiotensin II, 2) Norepinephrine (NE)
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19
Q
  • How does Hypertrophy compensate for a decreased cardiac output?
  • What does this lead to?
  • What 3 hormones mediate this?
A
  • Heart tries to increase size of the muscle for better pumping
  • stiffening of myocytes
  • 1) angiotensin II, 2) aldosterone, 3) norepinephrine
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20
Q
  • How does salt and water retention compensate for a decreased cardiac output?
  • What 2 hormones mediate this?
A
  • increased fluid in vasculature to increase perfusion to tissues
  • 1) angiotensin II, 2) aldosterone
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21
Q
  • How does tachycardia compensate for a decrease in cardiac output?
  • What 2 hormones mediate this?
  • Tachycardia leads to an increased risk for what?
A
  • Increased rate of pumping to increase perfusion to tissues
  • 1) norepinephrine, 2) epinephrine
  • arrhythmias
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22
Q

Brain Natriuretic Peptide (BNP) — compensate for a decrease in cardiac output

  • Secreted by the _________ of the heart in response to excessive __________ of the heart muscle cells
  • Decreases systemic vascular _________ and central venous ___________, and increases ___________
  • Body’s natural mechanism to get rid of ___________
A
  • Secreted by the VENTRICLES of the heart in response to excessive STRETCHING of the heart muscle cells
  • Decreases systemic vascular RESISTANCE and central venous PRESSURE, and increases NATRIURESIS (excretion of Na+ in the urine)
  • Body’s natural mechanism to get rid of EXTRA FLUID
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23
Q

What are 5 non-pharmacological approaches?

A
  1. Remove precipitating cause (ex. drugs, excessive fluid or salt intake)
  2. Exercise (for stable pts to improve tolerance and function)
  3. Diet (Na+ and fluid restriction, alcohol cessation)
  4. Weight control
  5. Education (KEY)
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24
Q

Pharmacotherapy in CHF — Principles of Therapy

  1. Block __________ neurohormonal activation caused by decreased _____________ that promotes further cardiac _________ and ___________
  2. Prevent/minimize _________ and _______ retention
  3. Eliminate or minimize symptoms of ___________ (improve quality of life-reduce morbidity)
  4. Slow progression of _________ dysfunction
  5. Decrease _____________
  6. Decrease __________
A
  1. Block COMPENSATORY neurohormonal activation caused by decreased CARDIAC OUTPUT that promotes further cardiac DETERIORATION and DAMAGE
  2. Prevent/minimize SODIUM and WATER retention
  3. Eliminate or minimize symptoms of HF (improve quality of life-reduce morbidity)
  4. Slow progression of CARDIAC dysfunction
  5. Decrease HOSPITALIZATIONS
  6. Decrease MORTALITY
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25
Q

What 5 drug classes focus on the inhibition of compensatory mechanisms (i.e. prevention of cardiac remodeling)?

*Shown to improve outcomes - decrease __________

A
  1. ACE-I
  2. ARBs
  3. ARNI
  4. Beta blockers
  5. Aldosterone antagonists

*Shown to improve outcomes - decrease MORTALITY (death)

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26
Q

What 3 drug classes focus on hemodynamics (i.e. trying to increase the ability of the heart to move blood)?

*Do not decrease _______, but critical for ___________ control and management of ___________

A
  1. Diuretics
  2. Vasodilators
  3. Inotropic agents

*Do not decrease MORTALITY (death), but critical for SYMPTOM control and management of DECOMPENSATION

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27
Q

Angiotensin Converting Enzyme Inhibitors (ACE-I)

  • First line therapy from Stage ____ through ___ / Class ___ through ______
  • Should be used in ______ patients, even if _______________
  • Decreases morbidity (________) and mortality (_______)
  • Block actions of ____________ to prevent cardiac remodeling
A
  • First line therapy from Stage A through D / Class I through IV
  • Should be used in ALL patients, even if ASYMPTOMATIC
  • Decreases morbidity (DISEASE) and mortality (DEATH)
  • Block actions of ANGIOTENSIN II to prevent cardiac remodeling
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28
Q

Angiotensin Converting Enzyme Inhibitors (ACE-I)
The blocking of angiotensin II prevents cardiac remodeling resulting in
- decreased v___________
- decreased ____________ production (decreased salt/water retention)
- decreased __________ stimulation
- decreased ______________ hypertrophy
- increased ____________ prostaglandins

A

The blocking of angiotensin II prevents cardiac remodeling resulting in

  • decreased VASOCONSTRICTION
  • decreased ALDOSTERONE production (decreased salt/water retention)
  • decreased SYMPATHETIC stimulation
  • decreased LEFT VENTRICULAR hypertrophy
  • increased VASODILATORY prostaglandins
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29
Q

Angiotensin Converting Enzyme Inhibitors (ACE-I)

  • Can use any ACE-I: importance is to reach _______ doses, as tolerated
  • Caution /c ________ or __________ during aggressive diuresis (can really bottom out blood pressure)
A
  • Can use any ACE-I: importance is to reach TARGET doses, as tolerated
  • Caution /c INITIATION or UP-TITRATION during aggressive diuresis (can really bottom out blood pressure)
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30
Q

All Angiotensin Converting Enzyme Inhibitors (ACE-I) end in what?

A

“-pril”

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31
Q

What drug class do these drugs belong to?

  • Lisinopril
  • Enalapril
  • Ramipril
  • Benzaepril
  • Moexipril
  • Quinapril
  • Trandolpril
A

ACE-I

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32
Q

What are 3 adverse effects of ACE-I?

A
  1. Cough (#1 reason ppl don’t want to be on ACE-I)
  2. Hyperkalemia (can lead to arrhythmias)
  3. Angioedema (requires ER admission)
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33
Q

Angiotensin II Receptor Blockers (ARBs)

  • First line therapy from Stage ___ through ____ / Class ______ through ___
  • Block actions of ____________ (vasoconstriction, salt/water retention and hypertrophy)
  • Decreases morbidity and mortality (similar to ________)
  • Titrate to ______ doses, as tolerated
A
  • First line therapy from Stage A through D / Class I through IV
  • Block actions of ANGIOTENSIN II (vasoconstriction, salt/water retention and hypertrophy)
  • Decreases morbidity and mortality (similar to ACE-I)
  • Titrate to TARGET doses, as tolerated
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34
Q

Angiotensin II Receptor Blockers (ARBs)

- Alternative to ________. Equivalent but not shown to be ___________. Historically used less than ACE-I d/t _____

A
  • Alternative to ACE- I. Equivalent but not shown to be SUPERIOR. Historically used less than ACE-I d/t COST
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35
Q

What are the 3 ARBs indicated for CHF?

A
  1. Valsartan (Diovan)
  2. Candesartan (Atacand)
  3. Losartan (Cozaar)
36
Q

What are the 2 adverse effects of ARBS?

What is the benefit of ARBS compared to ACE-I?

A

AE:

  1. Hyperkalemia
  2. Angioedema

Benefit:
- no dry cough

37
Q

What 3 conditions should ARBs be avoided in?

A
  1. Acute renal failure
  2. Pregnancy
  3. Bilateral renal artery stenosis
38
Q

Angiotensin II Receptor Blocker/ Neprilysin Inhibitor (ARNI)

  • First in class medication = Sacubitril/valsartan (_________)
  • ARB combined /c neprilysin inhibitor
  • Newest ACC/AHA/HFSA guidelines include an ANRI as an ________ effective option to ACE-I or ARBs
A
  • First in class medication = Sacubitril/valsartan (ENTRESTO)
  • ARB combined /c neprilysin inhibitor
  • Newest ACC/AHA/HFSA guidelines include an ANRI as an EQUALLY effective option to ACE-I or ARBs
39
Q

ARNI = ________ combined /c _________ inhibitor

  • Neprolysin inhibition prevents the degradation of several _________ peptides that play an important role in counter-regulating ______ (Ex. brain natriuretic peptide)
  • Increased bioavailability of natriuretic peptides resulting in ________, __________, and _________ effects.
A
  • Neprolysin inhibition prevents the degradation of several VASOACTIVE peptides that play an important role in counter-regulating HF (Ex. brain natriuretic peptide)
  • Increased bioavailability of natriuretic peptides resulting in NATRIURETIC, VASODILATORY, and ANTI-PROLIFERATIVE effects.
40
Q

ARNI’s can be used in place of an ______/________ to further reduce morbidity and mortality in symptomatic patients /c NYHA class II or III HF /c reduced ejection fraction

A

ARNI’s can be used in place of an ACE-I/ARBs to further reduce morbidity and mortality in symptomatic patients /c NYHA class II or III HF /c reduced ejection fraction

41
Q

Angiotensin II Receptor Blocker / Neprilysin Inhibitor (ARNI)

  • increased risk of ___________ (avoid in pts /c a h/o angioedema)
  • d/t increased risk, pts on an _______ require a 36-hour washout period when switching to sacubitril/valsartan
  • Not to be given in combo /c an ________ or _________ (ex. direct renin inhibitor)
A
  • increased risk of ANGIOEDEMA (avoid in pts /c a h/o angioedema)
  • d/t increased risk, pts on an ACE-I require a 36-hour washout period when switching to sacubitril/valsartan
  • Not to be given in combo /c an ACE-I or ALISKIREN (ex. direct renin inhibitor)
42
Q

What are 3 adverse effects of Angiotensin II Receptor Blocker / Neprilysin Inhibitor (ARNI)?

*recommended to start at _____ dose and titrate to _______ dose, as BP tolerates

A
  1. Hypotension
  2. Hyperkalemia
  3. Increased serum creatine (SCr)

*recommended to start at LOWER dose and titrate to TARGET dose, as BP tolerates

43
Q

Beta Blockers

  • Indicated in Stages ___, ____, and ___ / Classes ____, _____, and _____
  • Start when _______ damage is detected
  • Should be used in all ______ patients /c __________ dysfunction
A
  • Indicated in Stages B, C, and D / Classes II, III, and IV
  • Start when STRUCTURAL damage is detected
  • Should be used in all STABLE patients /c LEFT VENTRICULAR dysfunction
44
Q

Beta Blockers

  • Decrease ________ (disease) and ________ (death)
  • decrease _______ and block actions of __________ and other sympathetic neurotransmitters on the heart and vascular system
A
  • Decrease MORBIDITY (disease) and MORTALITY (death)

- decrease HR and block actions of NE and other sympathetic neurotransmitters on the heart and vascular system

45
Q

Beta Blockers result in:

  • Decreased ____________ and ________ rate (not ideal, but okay b/c of other benefits of drug)
  • Decreased ________ arrhythmias (sudden cardiac death)
  • Decreased __________ and _______ cell death
A
  • Decreased VASOCONSTRICTION and HEART rate (not ideal, but okay b/c of other benefits of drug)
  • Decreased VENTRICULAR arrhythmias (sudden cardiac death)
  • Decreased HYPERTROPHY and CARDIAC cell death
46
Q

Beta Blockers
- Carvedilol provides _______ blockade, which further decreases ___________ (afterload) and provides greater _________ in blood pressure

A
  • Carvedilol provides ALPHA-1 blockade, which further decreases SVR (afterload) and provides greater REDUCTION in blood pressure
47
Q

Beta Blockers

  • Used to be contraindicated in _______ d/t decreased cardiac ________ / _________ inotrope, but shown to be beneficial
  • Blocks compensatory mechanisms mediated by __________, ____________, and ___________
A
  • Used to be contraindicated in HF d/t decreased cardiac OUTPUT / NEGATIVE inotrope, but shown to be beneficial
  • Blocks compensatory mechanisms mediated by NE, EPI, and ANGIOTENSIN II
48
Q

Beta Blockers — NOT recommended to initiate during acute decompensated HF

  • Do not _______ or up-titrate until euvolemic
  • Do not __________ in pts who are stable on dose prior to admission
  • Hold if hemodynamically ________
A
  • Do not INITIATE or up-titrate until euvolemic
  • Do not DISCONTINUE in pts who are stable on dose prior to admission
  • Hold if hemodynamically UNSTABLE
49
Q

Beta Blockers

- Start at _____ dose and titrate up to ______ dose, as tolerated

A
  • Start at LOW dose and titrate up to TARGET dose, as tolerated
50
Q

What are 4 adverse effects of beta blockers?

A
  1. Fatigue
  2. Bradycardia
  3. Mask signs of hypoglycemia
  4. Bronchospasm (at high doses)
51
Q

Loop Diuretics

  • Indicated in Stage _____ and ____ / Class _____ and ______ (symptomatic)
  • decreases _______ congestion, ________ edema, _____________ distention (JVD) and symptoms
  • increases _______ function and ______ tolerance
A
  • Indicated in Stage C and D / Class III and IV (symptomatic)
  • decreases PULMONARY congestion, PERIPHERAL edema, JUGULAR VENOUS distention (JVD) and symptoms
  • increases CARDIAC function and EXERCISE tolerance
52
Q

Loop Diuretics

  • Decrease _______, but NOT ______
  • Never use as the _____ therapy for HF, but ________ of symptom management
A
  • Decrease MORBIDITY, but NOT MORTALITY

- Never use as the ONLY therapy for HF, but CORNERSTONE of symptom management

53
Q

What drug class do these belong to?

  • Furosemide (Lasix)
  • Bumetanide (Bumex)
  • Torsemide (Demadex)
A

Loop Diuretics

54
Q

Mechanism of Action of Loop Diuretics

Inhibits reabsorption of __________ and _________ in the ascending loop of henle, and proximal and distal renal tubules

  • interferes /c ________-__________ cotransporter system
  • Causes increased ________ of water, sodium, chloride, magnesium, and calcium
  • monitor and replace ___________ (especially K and Mg)
  • Loop diuretics may become drugs of abuse for _________
A

Inhibits reabsorption of SODIUM and CHLORIDE in the ascending loop of henle, and proximal and distal renal tubules

  • interferes /c CHLORIDE-BINDING cotransporter system
  • Causes increased EXCRETION of water, sodium, chloride, magnesium, and calcium
  • monitor and replace ELECTROLYTES (especially K and Mg)
  • Loop diuretics may become drugs of abuse for ANOREXIA
55
Q

Aldosterone Antagonists

  • Indicated for stage _____ and ____ / Class _____ and ______
  • Should be considered in patients receiving _______ therapy /c an ACE-I/ARB/ARNI, beta-blocker, diuretic, or after a _____ /c ____________ dysfunction
A
  • Indicated for stage C and D / Class III and IV
  • Should be considered in patients receiving BACKBONE therapy /c an ACE-I/ARB/ARNI, beta-blocker, diuretic, or after a MI /c LV dysfunction
56
Q

What drug class do these belong to?

  • Spironolactone (Aldactone)
  • Eplerenone (Inspra)
A

Aldosterone Antagonists

57
Q

Aldosterone Antagonists Decrease ___________ (disease) and __________ (death)

A

Aldosterone Antagonists Decrease MORBIDITY (disease) and MORTALITY (death)

58
Q

Aldosterone Antagonists

  • Block actions of _________ in the kidneys, heart, and vasculature
  • decreased _______ retention = decreased _______ retention
  • Blocks direct _______ actions on the myocardium (prevents remodeling)
  • Decrease _____ and ______ loss = decrease ventricular _________
A
  • Block actions of ALDOSTERONE in the kidneys, heart, and vasculature
  • decreased SODIUM retention = decreased FLUID retention
  • Blocks direct FIBROTIC actions on the myocardium (prevents remodeling)
  • Decrease K and Mg loss = decrease ventricular ARRHYTHMIAS
59
Q

What are 3 adverse effects of Aldosterone Antagonists?

A
  1. Hyperkalemia
  2. Hyponatremia
  3. Gynecomastia (“man boobs”)
60
Q

Digoxin

  • Indicated in stage ____ and ____ / Class _____ and _____
  • Should be considered in patients /c __________ LV dysfunction despite optimal ACE-I/ARB/ARNI, beta blockers, diuretic and aldosterone antagonists therapy
A
  • Indicated in stage C and D / Class III and IV
  • Should be considered in patients /c SYMPTOMATIC LV dysfunction despite optimal ACE-I/ARB/ARNI, beta blockers, diuretic and aldosterone antagonists therapy
61
Q

Digoxin

  • Decreases ________, but NOT _________
  • Use is _________ and has generally declined
  • Makes people “_________”
A
  • Decreases MORBIDITY, but NOT MORTALITY
  • Use is CONTROVERSIAL and has generally declined
  • Makes people “FEEL BETTER”
62
Q

Mechanism of Action of Digoxin

inhibition of ____________ ATPase pump in myocardial cells

  • Transient increase in intracellular _________ –> promotes _______ influx –> increased __________
  • Positive inotrope: minimal increase in __________
  • Negative chronotrope: minimal decrease in ___________
A

inhibition of SODIUM/POTASSIUM ATPase pump in myocardial cells

  • Transient increase in intracellular SODIUM –> promotes CALCIUM influx –> increased CONTRACTILITY
  • Positive inotrope: minimal increase in CONTRACTILITY
  • Negative chronotrope: minimal decrease in HEART RATE
63
Q

Digoxin

  • Therapeutic range for HF = _______ ng/mL
  • No evidence that higher levels do better in HF (toxic > __ ng/mL)
  • Antidote = _______ (binds to digoxin and then excreted by the kidneys
  • Caution in ______ impairment — renal eliminated (often dosed every _____ hours)
  • Avoid discontinuation unless there is compelling reason — withdrawal has been associated /c _________ HF symptoms
A
  • Therapeutic range for HF = 0.5 - 0.9 ng/mL
  • No evidence that higher levels do better in HF (toxic > 2 ng/mL)
  • Antidote = DIGIBIND (binds to digoxin and then excreted by the kidneys
  • Caution in RENAL impairment — renal eliminated (often dosed every 48 hours)
  • Avoid discontinuation unless there is compelling reason — withdrawal has been associated /c WORSENING HF symptoms
64
Q

Isosorbide and Hydralazine (BiDil)

  • Isosorbide does ________ dilation
  • Hydralazine does ________ dilation –> enhances effects of _______
  • Reduces both ___load and ____load
A
  • Isosorbide does VENOUS dilation
  • Hydralazine does ARTERIAL dilation –> enhances effects of NITRATES
  • Reduces both PRELOAD and AFTERLOAD
65
Q

When to consider Isosorbide and Hydralzine (Bidil):

  • _______________ as adjunct to backbone therapy (ACE-I/ARB, beta blockers, diuretic)
  • Alternative to ACE-I/ARB in those _________ (ie.e angioedema)
  • Titrate up to ________ dose, which is given TID
A
  • AFRICAN AMERICANS as adjunct to backbone therapy (ACE-I/ARB, beta blockers, diuretic)
  • Alternative to ACE-I/ARB in those INTOLERANT (ie.e angioedema)
  • Titrate up to TARGET dose, which is given TID
66
Q

What are 5 adverse effects of Isosorbide and Hydralzine?

A
  1. Rebound tachycardia
  2. Flushing
  3. Rash
  4. Headache
  5. Drug-induced lupus (Hydralzine)
67
Q

Ivabradine (Corlanor)

  • First in class agent for use in _____ failure /c reduced ______
  • Trial against placebo showed a decrease in rate of _________, but failed to show difference in all-cause mortality
A
  • First in class agent for use in HEART failure /c reduced EF
  • Trial against placebo showed a decrease in rate of HOSPITALIZATION, but failed to show difference in all-cause mortality
68
Q

Mechanism of Action for Ivabradine (Corlanor):

Slows down firing at the _____ node, thereby reducing __________, w/o decreasing myocardial __________

A

Slows down firing at the SA node, thereby reducing HEART RATE, w/o decreasing myocardial CONTRACTILITY

69
Q 
Indications for Ivabradine (Corlanor)
- add on to maximally tolerated guideline directed therapy (ACE-I/ARB, beta-blocker, diuretics, +/- aldosterone antagonists) in patient /c NYHA class \_\_\_\_ or \_\_\_\_\_ HF
  • patients must have a LVEF < ____%, a resting HR of > _____ bpm and be in _____ rhythm
A
  • add on to maximally tolerated guideline directed therapy (ACE-I/ARB, beta-blocker, diuretics, +/- aldosterone antagonists) in patient /c NYHA class II or III HF
  • patients must have a LVEF < 35%, a resting HR of > 70 bpm and be in SINUS rhythm
70
Q

What are 4 adverse effects of Ivabradine (Corlanor)?

A
  1. Bradycardia
  2. Atrial fibrillation
  3. HTN
  4. Heart block
71
Q

What 3 drug classes should be avoided in Heart Failure?

A
  1. NSAIDs
  2. Non-DHP calcium channel blockers (Verapamil & Diltiazem)
  3. Class I and III antiarrhythmics (except amiodarone and dofetilide)
72
Q

Why should NSAIDs be avoided in heart failure?

A

b/c they promote sodium and water retention, which blunts the diuretic response

73
Q

Non-DHP Calcium Channel Blockers (Verapamil & Diltiazem) — Avoid in Heart Failure

  • Negative inotrope –> decrease ___________ (not good when EF is low)
  • Preferred CCB if needed when EF is low = ___________ (need to watch for peripheral edema)
A
  • Negative inotrope –> decrease CARDIAC OUTPUT (not good when EF is low)
  • Preferred CCB if needed when EF is low = AMLODIPINE (need to watch for peripheral edema)
74
Q

Class I and III antiarrhythmics (except amiodarone & dofetilide) — Avoid in Heart Failure

  • Negative ________
  • _________ effects
  • Avoid ___________ in CHF /c recent symptoms/decompensation
A
  • Negative INOTROPE
  • PROARRHYTHMIC effects
  • Avoid DRONEDARONE in CHF /c recent symptoms/decompensation
75
Q

Treatment goals of diastolic dysfunction

  1. Control ____ according to guidelines
  2. Control __________
  3. Reduce ______ /c diuretics
  4. Aggressively investigate, repair, and treat myocardial _______
A
  1. Control HTN according to guidelines
  2. Control TACHYCARDIA
  3. Reduce PRELOAD /c diuretics (but not too much)
  4. Aggressively investigate, repair, and treat myocardial ISCHEMIA
76
Q

Treatment goal: Controlling HTN

- HTN impairs myocardial _________ and promotes cardiac _______

A
  • HTN impairs myocardial RELAXATION and promotes cardiac HYPERTROPHY
77
Q

Treatment goal: Control Tachycardia

  • Tachycardia decreases time for ___________ and coronary ________ to fill /c blood
  • Control of __________ improves symptoms of HF
  • Can use beta blockers, non-DHP, CCB and/or Digoxin
A
  • Tachycardia decreases time for VENTRICLES and coronary ARTERIES to fill /c blood
  • Control of HEART RATE improves symptoms of HF
  • Can use beta blockers, non-DHP, CCB and/or Digoxin
78
Q

Treatment goal: Reduce preload /c diuretics

  • Ventricular filling pressure is primarily determined by ________ blood volume
  • patients /c diastolic dysfunction are more _______ dependent for ventricular filling - if decrease too much, may cause ________
A
  • Ventricular filling pressure is primarily determined by CENTRAL blood volume
  • patients /c diastolic dysfunction are more PRELOAD dependent for ventricular filling - if decrease too much, may cause HYPOTENSION
79
Q

Treatment goal: Aggressively investigate, repair, and treat myocardial ischemia
- impairs ventricular __________

A
  • impairs ventricular RELAXATION
80
Q

What are 5 Pharmacological treatments for Diastolic Dysfunction?

A
  1. ACE-I
  2. Digoxin
  3. Beta Blockers
  4. Verapamil
  5. Diltiazem
81
Q

Pharmacological treatments for Diastolic Dysfunction — ACE-I

- Decreases ____________, improvement in heart failure ______ and ________ tolerance

A
  • Decreases HOSPITALIZATIONS, improvement in heart failure CLASS and EXERCISE tolerance
82
Q

Pharmacological treatments for Diastolic Dysfunction — DIGOXIN

  • no effect on all-cause ______ or on all-cause __________ hospitalizations
  • possible increase in _______ angina admissions
A
  • no effect on all-cause MORTALITY or on all-cause CARDIOVASCULAR hospitalizations
  • possible increase in UNSTABLE angina admissions
83
Q

Pharmacological treatments for Diastolic Dysfunction — Beta blockers, Verapamil, and Diltiazem
- benefits are targets at _________ relief

A
  • benefits are targets at SYMPTOMATIC relief
84
Q

Summary

  • Heart failure consists of _____ sided and _______ sided failure
  • Left sided HF includes ______ and _______ HF, which are treated differently
  • ________ has more tx options /c evidence to improve outcomes
  • __________ tx includes controlling BP and HR
  • Systolic HF should be treated /c drugs proven to decreased ________ and _________
  • ACE-I/ARBs, ARNI, beta blockers, aldosterone antagonists –> important to titrate to _____ doses, as tolerated
  • Symptomatic management = __________, ___________, and __________
  • Do not forget to avoid ________ and _________ in HF
A
  • Heart failure consists of LEFT sided and RIGHT sided failure
  • Left sided HF includes SYSTOLIC and DIASTOLIC HF, which are treated differently
  • SYSTOLIC has more tx options /c evidence to improve outcomes
  • DIASTOLIC tx includes controlling BP and HR
  • Systolic HF should be treated /c drugs proven to decreased MORBIDITY and MORTALITY
  • ACE-I/ARBs, ARNI, beta blockers, aldosterone antagonists –> important to titrate to TARGET doses, as tolerated
  • Symptomatic management = LOOP DIURETICS, DIGOXIN, and VASODILATORS
  • Do not forget to avoid NSAID and CORTICOSTEROIDS in HF
85
Q

All of the following agents have been shown to decrease mortality in patients /c systolic HF except:

A) ACE inhibitors
B) Angiotensin receptor blocker + neprolysin inhibitor (ARNI)
C) Loop Diuretics
D) Beta blockers

A

C) Loop Diuretics

86
Q

Which of the following statements is false?

A) the purpose of the pharmacologic agents used for HF is to block the compensatory neurohormonal activation caused by decreased cardiac output
B) All patients /c HF should be on ACE-I, regardless of symptoms (unless contraindicated)
C) Loop diuretics are 1st line agents in HF and should be started at Stage A/Class I
D) The use of digoxin in HF is controversial and use has declined

A

C) Loop diuretics are 1st line agents in HF and should be started at Stage A/Class I

87
Q

Which of the following statements is true regarding sacubitril/valsartan?

A) It is a combination of neprolysin inhibitor and an ACE-I
B) It was shown to decrease mortality and has been added to the guidelines as an alternative to ACE-I or ARBs
C) It is recommended to be added to patients on guideline directed therapy, including ACE-I/ARBs, beta blockers, diuretics, +- aldosterone antagonsits
D) It can be used safely in patients /c a h/o angioedema
E) it is recommended to start at the target dose, as hypotension is uncommon

A

B) It was shown to decrease mortality and has been added to the guidelines as an alternative to ACE-I or ARBs

Pharmacology (10 decks)

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