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PHAR 253 Final > Heart Failure Drugs > Flashcards

Heart Failure Drugs Flashcards

1
Q

How can HF be classified?

A

HF Stages: Acute / Decompensated vs Chronic vs Advanced

Left Ventricular Ejection Fraction

NYHA Classification: severity of symptoms & functional status

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2
Q

Define chronic HF

A

persistent and progressive (CHF = chronic heart failure

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3
Q

Define acute/decompensated HF?

A

Acute/decompensated: gradual or rapid change in signs and symptoms, resulting in the need for urgent therapy

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4
Q

Define advanced HF

A

frequent decompensations, mechanical devices, transplantations, palliative

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5
Q

What is LVEF?

A

Left Ventricular Ejection Fraction (LVEF) – amount of blood that is in the heart that is being pumped out

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6
Q

Heart Failure definitions based on LVEF

A

o If LVEF ≥50% = HF-pEF
–> HF with preserved EF
–> Diastolic dysfunction where there are problems with heart stiffness and ventricular relaxation and filling.
–> More so in elderly, females, DM, AF, HTN
–> Slow onset

If LVEF 41-49% = HF-mEF
–> HF with mid-range or mildly reduced EF

LVEF ≤40% = HF-rEF
 HF with reduced EF
 Systolic dysfunction where there are problems with the heart pump/ventricular contractility
 Usually after an acute CAD event

HF-impEF

baseline LVEF >40%, &
≥10% increase in EF, &
a second measurement of LVEF >40%

Once had HF-REF

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7
Q

New York Heart Association Classifications

A

 Class I: no limitation of physical activity, ordinary physical activity does not cause symptoms
 Class II: slight limitation, ordinary physical activity causes symptoms
 Class III: marked limitation, less than ordinary activity causes symptoms
 Class IV: severe limitation, symptoms present even at rest

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8
Q

Diagnosis of HF

A
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9
Q

Describe the pharmacotx for HF

A

HF-ref LVEF < or = to 40%

ARNi or ACEi /ARB than substitiute ARNI
Beta Blocker
MRA
SGLT-2 Inhibitor

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10
Q

Goal of pharmacotx

A

o Benefits: Decreased risk of mortality and hospitalizations
o Improve HF symptoms
o Strive to initiate the standard therapies within 3-6 months after diagnosis, and then titrate to target or max tolerated dose

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11
Q

Describe the RAAS systems

A
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12
Q

ACEi Heart Failure Types and Dose

A

Captopril 10mg BID,
enalapril 20-35mg OD
lisinopril 4-8 mg OD,
ramipril 5mg BID
trandolapril 4mg OD

Can everyone listen, rats talk

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13
Q

Titration Acei

A

double dose every 1-3 weeks

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14
Q

C.I. ACEi

A
  • Bilateral renal artery stenosis or unilateral if only 1 kidney
  • History of angioedema
  • Pregnancy
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15
Q

Cautions of ACEi

A
  • High potassium, SCr >220umol/L, or eGFR <30mL/min
  • SBP less than 90mmHg or symptomatic hypotension
  • Moderate to severe stenosis
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16
Q

Drug Interactions Acei

A
  • increased risk of hyperkalemia with K+ supplements, K+ sparing diuretics, MRA (spironolactone), renin inhibitors, TMP, NSAIDs, low salt supplements high in K+
  • Lithium
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17
Q

ADverse effects ACEi

A
  • Hypotension
  • Angioedema – facial, lip, tongue, and upper airway swelling, develops over hours. Symptoms resolve within 48-72 hours of stopping.
  • Dry cough (dry and absent prior to initiation)
  • Hyperkalemia ( range range 3.5 to 5mmol/L
    mild hyperkalemia (i.e. K+ up to 5.5mmol/L) is often acceptable
  • Worsening of renal function (up to 30% decrease of eGFR is acceptable)
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18
Q

ARB’s used in HF and dose

A

Candesartan 32mg OD, valsartan 160mg BID

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19
Q

Indication for ARB in HF

A

ACEi intolerance (cough and angioedema) but no difference between the two, just more evidence with an ACEi.

Do NOT combine with ACE due to increased risk of hypotension, hyperkalemia, and renal dysfunction.

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20
Q

C.I., D.I., A.e, of ARB

A

 Contraindications, cautions, drug interactions, adverse effects, monitoring, and titration are the same as ACEi

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21
Q

What is an ARNI

A

ARNI: sacubitril/valsartan (Entresto)

Angiotensin receptor neprilysin inhibitor

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22
Q

MOA of ARNI

A
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23
Q

Paradigm Trial Findings

A

Entresto vs enalapril

  • Higher reduction in hospitalization and CV death compared to enalapril
  • Adverse effects: Entresto had more symptomatic hypotension (and SBP <90mmHg), and angioedema (not stat signficant)
  • But less SCr elevation, cough, and discontinuations
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24
Q

Indication of ARNI

A

Those who remain symptomatic despite treatment to decrease CV death, HF hospitalizations, and symptoms (strong recommendation).

Those who are admitted to hospital due to acute decompensated HF should be switched before discharge (strong recommendation).

Those who are admitted to the hospital with a new diagnosis should be treated with ARNI as first line therapy. (weak recommendation)

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25
Q

EDS Criteria ARNi

A

HF with NYHA class II or III with LEVH <40, symptoms despite more than four weeks of triple therapy, elevated BNP, under care of a HF specialist.

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26
Q

Unique of ARNI Initiation

A

Needs a 36 hour washout period if switching from an ACEi (not required for ACEi)

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27
Q

C.I. of ARNI

A

History of ACEi/ARB angioedema

Concurrent Acei

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28
Q

CAution of ARNi

A

recent symptomatic hypotension

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29
Q

Drug Interactions, A/e, and monitoring of ARNi

A

Drug interaction/adverse effects/monitoring – same as ACEi/ARB

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30
Q

Dosing of ARNi

A

Dosing: target = 200 mg BID
* >50% ACE/ARB target dose: start 100mg BID, then double in 3-6wks
* <50% ACE/ARB target dose, high risk of hypotension, or ARB naïve: start 50mg BID, then double in 6 weeks

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31
Q

Beta-blockers HF and Initiation

A

Bisoprolol 10mg OD, carvedilol 25mg/50mg (>85kg) BID, metoprolol XL 200mg OD

Double dose every 2-4wks when titrating

Avoidabrupt withdrawal. tape rover 1-2 weeks

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32
Q

MOA BB

A

Blocks norepinephrine at the beta-adrenergic receptors.

Improves myocardial function by prolonging ventricular filling time, resulting in a more productive heartbeat

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33
Q

C.I. BB

A

 2/3rd degree AV block or HR <50bpm in the absence of a pacemaker
 PR interval greater than 0.24seconds
 Severe/uncontrolled asthma
 Severe PAD

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34
Q

Caution BB

A

NYHA class IV or HF exacerbation within 4 weeks. SBP < 90 mmHg or HR <50bpm

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35
Q

A/e of BB

A

 Hypotension: 90-100mmHg without symptoms is acceptable
 Bradycardia: 50-60bpm without symptoms acceptable
 Worsening HF symptoms/fatigue: may get worse before better

initial negative inotropic effect, may cause fluid retention.

Start low and titrate up slowly

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36
Q

Efficacy of BB

A

 Metoprolol succinate (LX) showed benefit vs placebo. Not available in Canada though
 Carvedilol was superior to metoprolol tartrate (SR)

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37
Q

Safety BB

A

 Bisoprolol and metoprolol are cardio-selective.

Carvedilol is not cardio-selective and effects B1, B2, a1 receptors which lowers blood pressure more and effects the lungs

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38
Q

Drug Interactions BB

A

risk of bradycardia / AV block with verapamil, diltiazem, amiodarone, digoxin

risk of hypertensive crisis with clonidine

risk of reduced -blocker efficacy with phenobarbital

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39
Q

MRA HF

A

o Spironolactone 25-50mg OD, eplerenone 50 mg OD

Double dose ever 4-8 weeks when titrating. We are happy with lower dose spironolactone

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40
Q

MOA MRA

A

Inhibits aldosterone which prevents reabsorption of sodium and water.

Is a weak natriuretic agent and minimally impacts blood pressure unless it is elevated (pathway-2 trial for resistant hypertension)

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41
Q

Use of MRA in HF vs HTN

A

Used in HF for neurohormonal benefit whereas loop diuretics are used for congestion/fluid overload

Minimalimpact on blood pressure

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42
Q

C.I. of MRA

A

hyperkalemia (K+ greater than 6), severe hepatic impairment for eplerenone

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43
Q

Caution MRA

A

high potassium (>5+)

CrCl <30mL/min (spironolactone – beers list - hyperkalemia)

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44
Q

A/e of MRA

A

 Hyperkalemia
 Spironolactone: gynecomastia, erectile dysfunction, menstrual irregularities

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45
Q

D.I> of MRA

A

o Drug interactions: same as ACEi
 Spironolactone: increases digoxin
 Eplerenone: Caution with strong CYP 3A4 inhibitors and 25 mg daily with modertae

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46
Q

Monitoring of MRA

A

Potassium and Scr baseline and 1 wk after starting/titrating. Then every 3 months, then every 6 months

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47
Q

EDS MRA

A

Eplerenone is much way more expensive. EDS criteria if previously tried spironolactone

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48
Q

SGLT2I used in HF

A

Dapagliflozin (Forxgia)
Empagliflozin (Jardiance

49
Q

MOA of SGLT-2i

A

Unknown

increases natriuresis and diuresis in the kidney, reduces preload and afterload, decreases hypertrophy, fibrosis, and O2 demand

50
Q

Monitor A1C in HF

A

NO

51
Q

A1C SGLT2-I

A

the A1c-lowering effect of SGLT2i is diminished in the presence of CKD:
minor at eGFR 30-45mL/min
absent at an eGFR <30mL/min

52
Q

DAPA-HF trial

A

decreases CV death or worsening HF (hospitalization)

53
Q

Emperoror-reduceed trial

A

decreases HF hospitalization, but CV death was non-statistically significant

See a renal decline in 15-20%  Will see rebound and renal protection

54
Q

SGLT-2i trials findings

A

o Trials showed volume depletion as an adverse effect, but this can be a good thing in HF patients and we can back off on the furosemide.
o Trials showed that there is no effect on A1C in those without diabetes

55
Q

SGLT-2i CI

A

severe renal or hepatic dysfunction
dapagliflozin CrCl <25mL/min
empagliflozin CrCl <20mL/min

56
Q

Caution SGLT-2i

A

hypovolemia, acute illness (hold if dehydrated, i.e. SADMANS)

57
Q

What is SADMANS

A

sulfonylurea, ACE-inhibitor, diuretic, metformin, angiotensin receptor blocker, and non-steroidal anti-inflammatory,SGLT-2

58
Q

D.I. SGLT-2i

A

diuretics (monitor for hypovolemia)

59
Q

A/E SGLT-2i

A

genital mycotic infections, euglycemic diabetic ketoacidosis in T2DM

60
Q

Monitoring SGLT-2i

A

volume status
if euvolemic, consider reducing loop diuretic by 30-50% (40%)

SCr at 14 - 30 days, 60 days, the q4 months
early 15-20% reduction in eGFR is acceptable

A1c in T2DM

61
Q

Secondary Meds

A
62
Q

SHIFT TRIAL

A

IVAbradine

sinus rhythm with a resting HR ≥70bpm

No mortality benefit, just hospitilization reduction

Only benenfit if baseline hr of 77 bpm

63
Q

Dose Ivabradine

A

start with 2.5mg BID in the elderly

only available in 5mg and 7.5mg tablet strengths, but the 5mg tablets are scored

double dose every 2-4 weeks if HR >60bpm

Target dos eof 7.5 mg BID

64
Q

C.I. Ivabradine

A

3rd degree AV block, sick sinus syndrome, pacemaker dependence, prolonged QT interval, unstable CV conditions, severe renal or hepatic dysfunction

strong CYP 3A4 inhibitors

moderate CYP 3A4 inhibitors that reduce HR (e.g. verapamil, diltiazem)

65
Q

D.I. Ivabradine

A

amiodarone (risk of QT prolongation, atrial fibrillation, excessive bradycardia)

digoxin (excessive bradycardia)

Verapamil, Diltazem –> Bradycardia

simvastatin (reduces simvastatin by 50%)

66
Q

A/e Ivabradine

A

atrial fibrillation
transient flashes of light (phosphenes)

67
Q

Monitoring Iva

A

HEART RATE

increase dose (up to 7.5mg BID) if HR > 60bpm

reduce dose if HR <50bpm or symptomatic bradycardia

68
Q

Digoxin benefit

A

reduces the risk of HF hospitalizations, but not mortality

69
Q

MOA digoxin

A

positive inotropic effect (i.e. strengthens myocardial contractions – improves CO)

offsets sympathetic nervous system activation

increases parasympathetic activity (“rest & digest”) and reduces HR (negative chronotropic effect), and therefore enhances diastolic filling

70
Q

Digoxin C.I.

A

ventricular fibrillation

71
Q

Caution Digoxin

A

acute MI, AV block, bradycardia, renal or thyroid dysfunction, hypokalemia

72
Q

D.I. Digoxin

A

amiodarone (reduce digoxin by 50%), dronedarone, b-blockers, calcium channel blockers, flecainide, propafenone

clarithromycin, erythromycin

73
Q

A/e Digoxin

A

toxicity (anorexia, nausea, vomiting, dizziness, visual changes)

74
Q

Digoxin monitoring.What should be monitored?

A

HR
SCr (caution if CrCl <30mL/min)
K+ (risk of arrhythmia with hypokalemia)

75
Q

Digoxin dose

A

0.0625mg to 0.25mg po once daily

no HF target dose & no loading dose required for HF
consider lower doses
(0.0625mg or 0.125mg daily) in the elderly, females or those with renal impairment

76
Q

Iva and DIgoxin both

A

lower raised resting heart rates in HF patients

reduce the risk of HF hospitalizations, but not mortality

77
Q

Iva compared to digoxin

A

has less real-world experience, cannot be used in AF patients, is more expensive

has less drug interactions, does not require dose adjustments in renal impairment or therapeutic drug monitoring

78
Q

Vericguat Benefit

A

reduces the risk of HF hospitalizations, but not mortality

79
Q

MOA of Vericguat

A

NO reduced in HF –> NO sCG formation –> CGMP

Increases sCG increasing cGMP

80
Q

Benefits of verigcout

A

Decreased mycocardial thickening and stifeening

Decreased ventricular remodelling

Decreased fibrosis

Decreased vasoconstriction

Dcereased vascular stiffness

81
Q

C.I. Vericguat

A

concomitant use of other sGC stimulators, pregnancy

82
Q

Vericguat D.I.

A

PDE5 inhibitors (e.g. sildenafil), long-acting nitrates
contraindicated with other sGC stimulators (i.e. riociguat)

Can use nitro spray

83
Q

Vericguat A/e

A

anemia, symptomatic hypotension, syncope

84
Q

Vericguat dose and titration

A

initial: 2.5mg po daily x 2 weeks

titration: increase to 5mg po daily x 2 weeks, then to 10mg po daily based on BP & clinical HF symptoms:

SBP ≥100mmHg: increase dose or maintain if on 10mg po daily
SBP 90-99mmHg: maintain dose
SBP <90mmHg & asymptomatic: reduce dose
SBP <90mmHg & symptomatic: hold dose

85
Q

Monitoring vericguat

A

Hgb, BP

86
Q

Hydralazine NItrate MOA

A

Hydralazine is a direct acting arterial vasodilator, which reduces afterload on the left ventricle and enhances the hearts ability to pump (i.e. enhances stroke volume & cardiac output)

Nitrates are venous dilators which reduce preload (SV and CO) and pulmonary / systemic edema formation

87
Q

Hydralazine Benefit

A

Decreased all caus emortality and HF hospitilizations

88
Q

C.I. Hydralqazine

A

acute dissecting aortic aneurysm, mitral valve rheumatic heart disease

89
Q

D.I. Hydralazine

A

can reduce digoxin levels, & increase metoprolol levels

90
Q

A/e Hydralazine

A

Hypotension, edema, tachycardia

91
Q

Monitoring hydralazine

A

BP and HR

92
Q

D.I. Isorbide dinitrate

A

Contraindicated within 24 to 48 hours of PDE5 inhibitors (increase hypotensive effect & HR)

avoid within 24hours of sildenafil and vardenafil, & 48 hours of tadalafil

sGC stimulators

93
Q

A/e Isorbide dinitrate

A

hypotension, headache, lightheaded

94
Q

Monitoring Isorbide dinitrate

A

BP and HR

95
Q

Hydralazine/Isorbide dinitrate Target Dose

A

75-100 mg TID or QID/ 40 mg TID

96
Q

Important counselling HYdralazine/Isorbide Dinitrate

A

Ensure 12-hour nitrate free interval to prevent tolerance, regardless of formulation

97
Q

HfPef Meds

A

o Identify and treat underlying causes
o Identify and treat comorbid conditions that might exacerbate HF (HTN, DM, AF)
o Control symptoms – loop diuretics to control congestion and peripheral edema
o Consider spironolactone to reduce HF hospitalizations
o Candesartan may reduce HF hospitalizations
o Entresto did not reduce CV deaths or HF hospitalizations in HFpEF group
o Recommend empagliflozin to reduce hospitalizations for HF, however not clinically significant for CV death/renal outcome
o No treatment available to reduce mortality

98
Q

Hf-mef TX

A

o Diuretics as needed
o SGLT2i
o Particularly for those with LVEF on the lower end of the spectrum:
 ACEi/ARB/ARNI - particularly for those with LVEF on the lower end of the spectrum
 MRA
 Beta-blockers for HFrEF

99
Q

Diuretics Use

A

o Used to reduce pulmonary and peripheral edema by decreasing preload and decreasing Na and water retention

100
Q

Diuretics Benefit/ Drawback

A

o Benefit: most rapid symptomatic relief, improves exercise tolerance and QOL, reduce HF hospitalizations
o Does not alter survival or alter disease progression, irks delaying initiation/titration of medications that do

101
Q

Goal of Diuretics

A

o Goal – Euvolemia
 Dry weight (no extra fluid accumulation) with no or mild HF symptoms

o Volume deplete - Hypovolemia
 Weight is below dry weight. Risk of worsening renal function and decreasing cardiac output. Identify and address causes, reduce diuretics

o Volume overload – Hypervolemia
 Increase in weight and new or worsening HF symptoms. Identify and address causes, increase diuretics.

102
Q

Loop Diuretics MOA

A

inhibit Na-K-Cl2 transporter in the thick ascending limb of the loop of Henle

20-25% of filtered Na+ is reabsorbed here
increase renal blood flow  contributes to natriuresis

via prostaglandins (blocked by NSAIDS, which ↓ diuretic efficacy)

103
Q

Reduced Efficacy of Loop Diuretics

A

excessive dietary Na+ intake can also reduce efficacy

104
Q

Thiazide vs Loop

A

Unlike thiazides, loop diuretics maintain efficacy in impaired renal function

105
Q

Loop Diuretics and Dose

A

Furosemide (Lasix):
Initial dose: 20mg to 40mg po once daily to BID
Maximum dose: 200mg / day

Bumetanide (Bumex):
Initial dose: 0.5mg to 1mg po once daily
Maximum dose: 10mg daily

Ethacrynic acid (Edecrin):
Initial dose: 25mg to 50mg po once daily
Maximum dose: 200mg BID
No sulfa group (alternative for patients allergic to furosemide)

106
Q

Loop Diuretics Dosing

A

Start with low doses (e.g. furosemide 20mg to 40mg po daily), & adjust based on symptom assessment and daily body weights

Change in body weight is a sensitive marker of fluid retention or loss

Wake  void bladder  weigh daily while nude or same amount of clothes on

107
Q

When to call HCP

A

If weight ↑ 2lbs in one-two days or 5lbs over a week  call healthcare provider for assessment

assess fluid intake, salt intake, inter-current illness, new medications, medication adherence

temporary ↑ in diuretic therapy

can prevent HF decompensation leading to hospital admission

108
Q

Combining Diuretics. Benefits/Risk

A

Oral loop diuretics may not be adequately absorbed severe edema

Loop diuretics + thiazide or thiazide-like diuretic
less side effects than higher dose loop diuretics

Diuretic resistance
rebound Na+ retention: chronic loop diuretic use can lead to ↑ distal nephron Na+ reabsorption

109
Q

Metolazone MOA, Dose, Onset and Duration

A

Thiazide-like diuretic

Dose: start with 2.5mg 2 to 3 times/week (outpatient), 5-10mg (inpatient)

Onset of action: 60 minutes

Duration of action: 12-24hr
Up to 48hrs in renal impairment or chronic dosing

110
Q

Metolazone Admin with Furosemide

A

Onset of action: 60 minutes

Onset of action for oral furosemide: 30-60 minutes

Take 30 min sbefore Furosemide

111
Q

Caution of Diuretics

A

Caution with over-diuresis

↓ cardiac output, renal perfusion, and symptoms of volume depletion
when initiating or titrating other HF medications can lead to hypotension and other adverse effects

112
Q

Reduce Dose of Diuretic When:

A

weight loss beyond dry weight

volume depletion: hypotension or worsening renal function (e.g. ↑ in serum creatinine)

Decrease in 20 mg increments

113
Q

Diuretic C.I.

A

anuria, hepatic coma or pre-coma

114
Q

Cautoion Diuretics

A

hypokalemia, hyponatremia, eGFR <30mL/min (risk of worsening renal function if becomes hypovolemic), SBP <90mmHg

115
Q

Diuretic D.I.

A

risk of digoxin toxicity if diuretic leads to hypokalemia

risk of lithium toxicity due to reduced lithium clearance

116
Q

Diuretic A/e

A

hypotension, volume depletion, hyperuricemia, electrolyte disturbances (hyponatremia, hypokalemia, hypomagnesemia), ototoxicity with high doses (more so IV) (e.g. greater than 240mg furosemide / day)

117
Q

Monitoring Diuretics

A

HF symptoms / daily morning weight

K+, Na+, SCr and urea at baseline & 5-7 days after diuretic adjustment
–> hold or reduce diuretic if SCr increase more than 30% from baseline

NTproBNP or BNP

BP  Make sure were not too aggressive

118
Q

Dietary Guides HF

A

We suggest that patients with heart failure should restrict their dietary salt intake to between 2 g/day and 3 g/day (Weak Recommendation, Low Quality Evidence).

We suggest that restriction of daily fluid intake to approximately 2 L/day should be considered for patients with fluid retention or congestion that is not easily controlled with diuretics

PHAR 253 Final (8 decks)

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