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PHAR253 > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

What is heart failure?

A

abnormal heart function
-any cardiac structural or functional disorder leading to inadequate CO &/or elevated ventricular filling pressures
-impairs the ability of the ventricles to fill (diastolic) with or eject (systolic) blood
complex clinical syndrome with signs and symptoms of:
-reduced CO and/or unable to meet metabolic demands or only able to maintain CO with abnormally high cardiac pressure
-pulmonary or systemic congestion at rest or with stress

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2
Q

Briefly describe the epidemiology of heart failure.

A

100,000 Canadians diagnosed each year
700,000+ living with HF in Canada today
higher mortality rates than certain cancers
50% will die within 5yrs

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3
Q

True or false: HF prognosis is worse than many cancers

A

true

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4
Q

What is a strong predictor of mortality for heart failure?

A

number of HF hospitalizations
-with each acute event, myocardial injury may contribute to progressive LV dysfunction

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5
Q

What is the pathophysiology of heart failure?

A

cardiac output is decreased
-persistent=long term activation of compensatory responses
myocardial injury–>compensatory responses in an attempt to maintain CO

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6
Q

How is heart rate controlled?

A

by the autonomic nervous system

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7
Q

What is stroke volume?

A

the volume of blood ejected per heartbeat, which is dependent on preload, afterload, and contractility

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8
Q

Differentiate preload, contractility, and afterload.

A

preload:
-stretching of the muscle fibers in the ventricle
-stretching results from blood volume at the end of diastole
contractility:
-inherent ability of the myocardium to contract normally
-influenced by preload (greater stretch=forceful contraction)
afterload:
-pressure that the ventricular muscles must generate to overcome the higher pressure in the aorta to get blood out of the heart

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9
Q

What is the Frank-Startling Law?

A

ability of the heart to alter the force of contraction based on changes in preload
increased ventricle volume=increased contractility=increased SV
if the heart is overstretched, it loses its ability to return force
-normal: more filling, greater force
-mild-moderate LV dysfunction: more filling, no more force
-severe LV dysfunction: more filling, less force

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10
Q

In general, what does pharmacotherapy target for heart failure?

A

the neurohormonal model
-NE, ANG II, aldosterone, vasopressin, cytokines
can slow progression, and reduce risk of morbidity & mortality

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11
Q

What are the compensatory responses seen in heart failure due to decreased cardiac output?

A

increased preload (via Na and water retention)
vasoconstriction
tachycardia & increased contractility (SNS)
ventricular hypertrophy & remodeling

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12
Q

What are the beneficial and detrimental effects of increased preload as a compensatory response in HF?

A

beneficial effects:
-optimize stroke volume via Frank-Starling mechanism
detrimental effects:
-pulmonary & systemic congestion

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13
Q

What are the beneficial and detrimental effects of vasoconstriction as a compensatory response in HF?

A

beneficial effects:
-maintain BP during reduced CO
-shunt blood from nonessential organs to brain and heart
detrimental effects:
-increased myocardial oxygen demand
-increased afterload decreases SV

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14
Q

What are the beneficial and detrimental effects of tachycardia & increased contractility as a compensatory response in HF?

A

beneficial effects:
-maintain CO
detrimental effects:
-increased myocardial oxygen demand
-shortened diastolic filling time
-precipitation of ventricular arrhythmias

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15
Q

What are the beneficial and detrimental effects of increased ventricular hypertrophy & remodeling as a compensatory response in HF?

A

beneficial effects:
-maintain CO
-reduces myocardial wall stress
-decreases myocardial oxygen demand
detrimental effects:
-increased risk of myocardial cell death
-myocardial ischemia
-arrhythmia
-fibrosis
-diastolic &/or systolic dysfunction

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16
Q

What are the common etiologies for heart failure?

A

tachyarrhythmia
valve disease
known or risk factors for CAD
LVH

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17
Q

Describe the universal definition for heart failure.

A

symptoms and/or signs of HF caused by structural and/or functional cardiac abnormality
-structural heart disease: LVH, valvular heart disease
-abnormal cardiac function: reduced left/right ventricular systolic function, increase filling pressures, abnormal diastolic function
elevated natriuretic peptide levels
-NT proBNP >125pg/ml
-BNP >50pg/ml
objective evidence of cardiogenic pulmonary or systemic congestion
-diagnostic modalities or hemodynamic measurements

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18
Q

What are the typical symptoms of heart failure?

A

breathlessness
orthopnea
paroxysmal nocturnal dyspnea
reduced exercise tolerance
fatigue
ankle swelling

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19
Q

What are some of the less typical symptoms of heart failure?

A

nocturnal cough
wheezing
bloated feeling
loss of appetite
syncope

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20
Q

What are the gold standard biomarkers in heart failure?

A

B-type natriuretic peptide (BNP)
NT proBNP

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21
Q

Where and when would the natriuretic peptides be produced?

A

synthesized & released from the ventricle in response to pressure or volume overload

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22
Q

What occurs when plasma concentrations of natriuretic peptides are elevated?

A

increased natriuresis, diuresis & attenuate RAAS & SNS activation

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23
Q

Can the natriuretic peptides alone be used to diagnose heart failure?

A

good for ruling out HF, not to establish HF on its own
should not be used independent of signs/symptoms & other diagnostics

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24
Q

Which natriuretic peptide is used for heart failure?

A

either can be used (similar)
-dependent on local lab
absolute values & thresholds are not interchangeable

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25
Q

What is a clinically meaningful change in natriuretic peptide levels?

A

> 30%

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26
Q

What does an echocardiogram provide information on?

A

size and shape of heart
pumping capacity (ejection fraction)
location and extent of damage tissues
pressure estimates

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27
Q

What are the classifications of heart failure?

A

HF stages: acute/decompensated vs chronic vs advanced
left ventricular ejection fraction
NYHA classification: severity of symptoms & functional status

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28
Q

Differentiate chronic HF, acute/decompensated HF, and advanced HF.

A

chronic:
-persistent & progressive
acute/decompensated HF:
-gradual or rapid changes in HF signs/symptoms
-results in need for urgent therapy
advanced HF:
-frequent decompensations
-mechanical devices
-transplantation
-palliative therapies

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29
Q

What is the ejection fraction?

A

compares the amount of blood in the heart to the amount of blood pumped out

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30
Q

Differentiate between a normal EF, borderline EF, and reduced EF.

A

normal: 50-70%
borderline: 41-49%
reduced: <40%

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31
Q

Describe LVEF >50%.

A

HF-pEF: HF with preserved EF
-diastolic dysfunction
-problems with heart stiffness/ventricular relaxation & filling
-slow onset
-elderly, females, DM, AF, HTN

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32
Q

Describe LVEF 41-49%.

A

HF-mEF: HF with mid-range or mildly reduced EF

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33
Q

Describe LVEF <40%.

A

HF-rEF: HF with reduced EF
-systolic dysfunction
-problems with the heart pump/ventricular contractility
-usually after an acute CAD event

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34
Q

What is HFimpEF?

A

HF with improved EF
-had HF-rEF
-baseline LVEF >40% & >10% increase in EF
-second measurement of LVEF >40%

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35
Q

Describe the New York Heart Association Classification of HF.

A

Class I: asymptomatic
-no limitation of physical activity
-ordinary physical activity does not cause symptoms
Class II: mild
-slight limitation of physical activity
-comfortable at rest
-ordinary physical activity causes symptoms
Class III: moderate
-marked limitation of physical activity
-comfortable at rest
-less than ordinary activity causes symptoms
Class IV: severe
-severe limitation and discomfort with physical activity
-symptoms present at rest

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36
Q

What are the standard therapies for HFrEF?

A

ARNI or ACEI/ARB
beta-blocker
MRA
SGLT2 inhibitor

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37
Q

Which ACEIs and ARBs are approved for HF?

A

ACEI:
-captopril
-enalapril
-lisinopril
-ramipril
-trandolapril
ARB:
-candesartan
-valsartan
ARNI=sacubitril/valsartan

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38
Q

Which beta-blockers are approved for HF?

A

bisoprolol
carvedilol
metoprolol

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39
Q

Which MRAs are approved for HF?

A

eplerenone
spironolactone

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40
Q

Which SGLT2 inhibitors are approved for HF?

A

dapagliflozin
empagliflozin

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41
Q

What are the benefits of the standard therapies for HFrEF?

A

decreased risk of mortality
decreased risk of HF hospitalizations
improve HF symptoms

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42
Q

Describe the desired titration for the standard therapies of HFrEF.

A

strive to initiate within 3-6 months after diagnosis and titrate to target or maximally tolerated doses

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43
Q

Provide a quick summary of RAAS.

A

drop in BP or drop in fluid volume–>renin release from kidney
renin activates angiotensinogen–>ANG I
ACE acts on ANG I–>ANG II
ANG II
-acts on adrenals to release aldosterone (reabsorb H20+Na)
-causes vasoconstriction
net result=increased preload and afterload

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44
Q

What is the MOA of ACEI?

A

blocks conversion of ANG I to ANG II
increased bradykinin

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45
Q

What are the benefits of ACEIs in HFrEF?

A

decrease the risk of all-cause mortality
decrease the risk of HF hospitalizations

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46
Q

What is the difference in dosing of ramipril for hypertension compared to heart failure?

A

OD for HTN
BID for HF

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47
Q

What is the dose titration for ACEI in HF?

A

double dose q1-3wks

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48
Q

List the starting dose and target dose for each ACEI in HF.

A

enalapril:
-start: 1.25-2.5mg BID
-target: 10mg BID/20mg BID in NYHA IV
lisinopril:
-start: 2.5-5mg daily
-target: 20-35mg daily
perindopril:
-start: 2-4mg daily
-target: 4-8mg daily
ramipril:
-start: 1.25-2.5mg BID
-target: 5mg BID
trandolapril:
-start: 1-2mg daily
-target: 4mg daily

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49
Q

What are the contraindications to ACEI?

A

bilateral renal artery stenosis
history of angioedema
pregnancy

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50
Q

What are some cautions for ACEIs?

A

K+ greater than 5.2mmol/L
SCr greater than 220umol/L
eGFR < 30ml/min
SBP < 90mmHg or symptomatic hypotension
moderate to severe aortic stenosis

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51
Q

What are the drug interactions for ACEI?

A

increased risk of hyperkalemia:
-K+ supps
-K+ sparing diuretics
-MRA
-renin inhibitors (aliskiren)
-TMP
-NSAIDs
-low salt substitutes high in K+
lithium: increased risk of lithium toxicity

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52
Q

What are the adverse effects of ACEI and the appropriate monitoring for those adverse effects?

A

hypotension
-monitor bp (there is no target bp in HF)
-symptomatic hypotension
angioedema
-symptoms
dry cough
-document presence/absence before initiating
hyperkalemia
-lab work at baseline & 1-2wks after starting therapy/dose change
-normal range: 3.5-5mmol/L
worsening renal function
-lab work at baseline & 1-2wks after starting therapy/dose change

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53
Q

Describe ACEI-induced angioedema.

A

ACEI are the leading cause of angioedema but its rare
common symptoms:
-facial, lip, tongue, and upper airway swelling
-develop over several hours
airway compromise is a life-threatening consequence
other sx are self-limiting & resolve within 48-72hrs

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54
Q

What is the MOA of ARBs?

A

block the angiotensin receptor to prevent ANG II effects

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55
Q

What is the place in therapy of ARBs for HF?

A

use if ACEI intolerance
-cough
-angioedema

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56
Q

Compare ACEI to ARB in HF.

A

more evidence with ACEI
no significant differences in rates of hypotension, hyperkalemia or renal dysfunction
do NOT combine eachother due to risk of hypotension, hyperkalemia & renal dysfunction

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57
Q

What is the difference in dosing of valsartan for hypertension compared to heart failure?

A

OD for HTN
BID for HF

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58
Q

List the starting dose and target dose for the ARBs in HF.

A

candesartan:
-start: 4-8mg daily
-target: 32mg daily
valsartan:
-start: 40mg BID
-target: 160mg BID

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59
Q

What are the contraindications, cautions, drug interactions, adverse events, monitoring, and titrations for ARBs?

A

similar to ACEI

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60
Q

What is the MOA of Entresto?

A

sacubitril:
-inhibits neprilysin (neprilysin breaks down BNP)
valsartan:
-ARB action

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61
Q

What were the benefits found for Entresto from the PARADIGM trial?

A

further reduced HF hospitalizations and CV death

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62
Q

True or false: Entresto has less symptomatic hypotension compared to an ACEI or ARB

A

false
Entresto has more symptomatic hypotension

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63
Q

What is the EDS criteria for Entresto?

A

HF with NYHA class II or III and:
-LVEF <40%
-NYHA class II-III sx despite >4wks of a stable dose of ACEI/ARB in combination with BB, and MRA
-BNP >150pg/ml or NT-proBNP>600pg/ml
-under care of HF specialist

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64
Q

What are the contraindications of Entresto?

A

concurrent ACEI use (36hr washout period ACEI<–>ARNI)
-washout not required for an ARB
history of ACEI/ARB angioedema

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65
Q

What is a caution for Entresto?

A

recent symptomatic hypotension

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66
Q

What are the drug interactions, adverse effects, & monitoring parameters for Entresto?

A

same as ACEI/ARB

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67
Q

What are the doses available of Entresto?

A

24/26mg=50mg
49/51mg=100mg
97/103mg=200mg
sacubitril/valsartan

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68
Q

What is the starting dose and target dose for Entresto?

A

start: 50-100mg BID
target: 200mg BID

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69
Q

Describe initiation and titration of Entresto.

A

> 50% ACEI/ARB target dose: 49/51mg po BID
-double dose in 3-6 wks
<50% ACEI/ARB target dose, risk of hypotension, or ACEI or ARB naive: 24/26mg po BID
-double dose in 6 wks

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70
Q

What is the MOA of beta-blockers in heart failure?

A

block norepinephrine at the beta-adrenergic receptor
improves myocardial function by prolonging ventricular filling time, resulting in a more productive heartbeat

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71
Q

What is the benefit of beta-blockers in HFrEF?

A

decrease the risk of all-cause mortality
decrease the risk of HF hospitalizations

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72
Q

List the starting dose and target dose for each beta-blocker in heart failure.

A

carvedilol: based on body weight
-start: 3.125mg BID
-target: 25mg BID/50mg BID (>85kg)
bisoprolol:
-start: 1.25mg daily
-target: 10mg daily
metoprolol: long-acting formulation preferred
-start: 12.2-25mg daily
-target: 200mg daily

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73
Q

What is the dose titration for beta-blockers in heart failure?

A

double dose every 2-4 wks

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74
Q

What are the contraindications of beta-blockers?

A

in absence of pacemaker: 2nd or 3rd degree AV block or HR <50bpm
PR interval greater than 0.24s
severe/uncontrolled asthma
severe PAD

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75
Q

What are cautions for beta-blockers?

A

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

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76
Q

What are the drug interactions for beta-blockers?

A

risk of bradycardia/AV block
-verapamil, diltiazem, amiodarone, digoxin
risk of hypertensive crisis with clonidine
risk of reduced beta-blocker efficacy with phenobarbital

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77
Q

What are the adverse effects of beta-blockers and the monitoring for these adverse effects?

A

hypotension
-monitor bp
-symptomatic hypotension
bradycardia
-monitor HR (resting of 50-60=acceptable)
-symptomatic bradycardia
worsening HF symptoms/fatigue
-may get worse before better
-initial inotropic effect
avoid abrupt withdrawal; taper over 1-2 weeks

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78
Q

Differentiate between metoprolol, bisoprolol, and carvedilol.

A

cardioselective: bisoprolol, metoprolol
non-cardioselective: carvedilol
-B1, B2 and a1–>lower bp more
-B2–>lungs

79
Q

Can a GP prescribe a beta-blocker for a patient with NYHA III to IV HF?

A

should be reserved for a HF specialist

80
Q

What is the MOA of MRAs?

A

blocks aldosterone from working

81
Q

List the starting dose and target dose of the MRAs in HF.

A

spironolactone
-start: 12.5mg daily
-target: 25-50mg daily
eplerenone
-start: 25mg daily
-target: 50mg daily

82
Q

Where does the benefit come from for MRAs in HFrEF?

A

neurohormonal activity
-weak natriuretic agent
-minimal impact on bp, unless bp is elevated

83
Q

What is the dose titration for MRAs in HF?

A

double dose every 4-8 weeks

84
Q

What are the contraindications for MRAs?

A

both: K+>6mmol/L
eplerenone: severe hepatic impairment (Child-Pugh class C)

85
Q

What are cautions for the MRAs?

A

both: K+>5mmol/L
CrCl < 30ml/min (increased risk of hyperkalemia)

86
Q

What are the drug interactions of the MRAs?

A

both: same as ACEI
spironolactone: increases digoxin serum concentrations
eplerenone:
-caution with strong CYP 3A4 inhibitors
-consider using 25mg daily with moderate 3A4 inhibitors

87
Q

What are the adverse effects of MRAs?

A

both: hyperkalemia
spironolactone:
-gynecomastia (dose-dependent), erectile dysfunction, menstrual irregularities

88
Q

Describe the monitoring for MRAs.

A

K+ and SCr baseline & 1wk after starting or titrating, then monthly x 3 months for one year and then q6months
SCr: caution when CrCl<30ml/min

89
Q

Which MRA is on the BEERS list?

A

spironolactone
-avoid if CrCl <30ml/min due to risk of hyperkalemia

90
Q

Which MRA is an EDS drug?

A

eplerenone
-chronic HF in pts who have previously tried spironolactone
-pts should be on an ACEI/ARb or an ARNI and a BB

91
Q

Do we use MRAs for congestion/fluid overload in HF? What about for blood pressure?

A

no, weak natriuretic agent
-loop diuretics are used for congestion/fluid overload
minimal impact on blood pressure
-only if bp is elevated

92
Q

What are the many possible MOAs of SGLT2 inhibitors in HF?

A

decreased preload
decreased arrhythmias
decreased afterload
decreased fibrosis
decreased hypertrophy
decrease O2 demand

93
Q

What is the benefit of SGLT2 inhibitors in HFrEF?

A

decreased HF hospitalizations,CV deaths, and poor renal outcomes
-empa: hospitalizations only

94
Q

True or false: a patient with HF who does not have diabetes does not need to be concerned about lowered blood glucose if they use an SGLT2 inhibitor

A

true
minimal impact on BG from SGLT2i in non-diabetic pts with HF

95
Q

Describe the addition of an SGLT2 inhibitor to heart failure therapy in a patient with T2DM.

A

insulin or insulin secretagogues?
-no=add SGLT2
-yes=what is the A1C?
A1C < 8.0%
-add SGLT2
-reduce insulin secretagogue by 50% or stop
-insulin: decrease by 10-20% or consult diabetes team
-counsel on hypoglycemia
A1C > 8.0%
-add SGLT2
-low risk of hypoglycemia
-no adjustment of insulin or secretagogue

96
Q

Describe the A1C lowering effect of SGLT2 inhibitors in the presence of CKD.

A

diminished effect in the presence of CKD
-minor at eGFR 30-45ml/min
-absent at an eGFR < 30ml/min

97
Q

What are the contraindications of SGLT2 inhibitors?

A

severe renal or hepatic dysfunction
-dapagliflozin: CrCl < 25ml/min
-empagliflozin: CrCl < 20ml/min

98
Q

What are cautions for SGLT2 inhibitors?

A

hypovolemia
acute illness (SADMANS, hold if dehydrated)

99
Q

What are the drug interactions of SGLT2 inhibitors?

A

diuretics
-monitor for hypovolemia

100
Q

What are the adverse effects of SGLT2 inhibitors?

A

genital mycotic infections
euglycemic diabetic ketoacidosis in T2DM

101
Q

Describe monitoring for SGLT2 inhibitors.

A

volume status
-if euvolemic consider reducing loop diuretic by 30-50%
SCr at 14-30 days, 60 days, then q4months
-early 15-20% reduction in eGFR is acceptable
A1C in T2DM

102
Q

What are the indications for each SGLT2 inhibitor in regards to HF?

A

dapagliflozin: HFrEF
empagliflozin: HF in general

103
Q

What are the additional interventions for HFrEF?

A

HR > 70bpm and sinus rhythm
-ivabradine
recent HF hospitalization
-vericiguat
black patient on optimal GDMT or patients unable to tolerate ACEI/ARB/ARNI
-consider combination hydralazine-nitrate
suboptimal rate control for AF or persistent symptoms despite optimized GDMT
-consider digoxin

104
Q

What is the MOA of ivabradine?

A

slows diastolic depolarization
-lowers HR

105
Q

What is the place in therapy for ivabradine?

A

symptomatic HF-rEF despite guideline directed therapy in sinus rhythm and a raised resting HR, & hospitalization within 12 months
-Canadian Cardiovascular Society: >70bpm
-Health Canada: >77bpm

106
Q

What is the benefit of ivabradine in HF?

A

reduces the risk of HF hospitalization
-not mortality

107
Q

What is the starting dose and target dose of ivabradine in HF?

A

start: 2.5-5mg BID
target: 7.5mg BID

108
Q

What is the dose titration of ivabradine?

A

double dose q2-4 wks if HR>60bpm

109
Q

What are the contraindications of ivabradine?

A

3rd degree AV block
sinus syndrome
pacemaker dependence
prolonged QT interval
unstable CV conditions
severe renal or hepatic dysfunction
strong 3A4 inhibitors
-ketoconazole, clarithromycin, ritonavir
moderate 3A4 inhibitors that reduce HR
-verapamil, diltiazem

110
Q

What are the drug interactions of ivabradine?

A

see contraindications
amiodarone (risk QT prolongation, afib, bradycardia)
digoxin (bradycardia)
simvastatin (reduces simvastatin by 50%)

111
Q

What are the adverse effects of ivabradine?

A

atrial fibrillation
transient flashes of light (phosphenes)

112
Q

Describe the monitoring for ivabradine.

A

heart rate
-increase dose (up to 7.5mg BID) if HR>60bpm
-reduce dose if HR<50bpm or symptomatic bradycardia

113
Q

What is the indication for ivabradine?

A

treatment of stable chronic HF with reduced LVEF (<35%) in adult patients with NYHA II-III or who are in sinus rhythm with a resting heart rate >77bpm if the following are met:
-see slide 129

114
Q

What is the place in therapy for digoxin?

A

pts with HFrEF in sinus rhythm who continue to have mod-severe symptoms, despite appropriate doses of guideline directed therapy to relive symptoms & reduce hospitalization
additional use of digoxin in pts with HFrEF and chronic AF and poor control of ventricular rate and/or persistent symptoms despite optimally tolerated BB or BB cannot be used

115
Q

What is the benefit of digoxin in HF?

A

reduces the risk of HF hospitalizations
-not mortality

116
Q

What is the MOA of digoxin?

A

positive inotropic effect
-strengthens myocardial contractions
offsets SNS activation
-increases parasympathetic activity and reduces HR and therefore enhances diastolic filling

117
Q

What is a contraindication of digoxin?

A

ventricular fibrillation

118
Q

What are some precautions for digoxin?

A

acute MI
AV block
bradycardia
renal or thyroid dysfunction
hypokalemia

119
Q

What are the drug interactions for digoxin?

A

amiodarone
dronedarone
beta-blockers
calcium channel blockers
flecainide
propafenone
clarithromycin
erythromycin

120
Q

What are the adverse effects of digoxin?

A

toxicity
-anorexia, nausea, vomiting, dizziness, visual changes

121
Q

Describe monitoring for digoxin.

A

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

122
Q

What is the dosing for digoxin?

A

0.0625mg to 0.25mg po OD
-no target HF dose & no LD required for HF
-consider lower doses (0.0625-0.125mg daily in elderly, females or renal impairment)

123
Q

Are routine levels required for digoxin?

A

not required
-may consider when initiating therapy (t1/2=1.5-2d)
-avoid serum concentrations >1.2ng/ml in HF due to increases risk of harm

124
Q

What are some key takeaway points for digoxin and ivabradine?

A

both will:
-lower raised HR in HF patients
-reduce the risk of HF hospitalizations but not mortality

125
Q

What are some differences between ivabradine and digoxin?

A

compared to digoxin, ivabradine:
-has less real world experience
-cannot be used in AF patients
-more expensive
-requires EDS/NIHB approval
-less drug interactions
-dose not require dose adjustments in renal impairment or therapeutic drug monitoring

126
Q

What is the MOA of vericiguat?

A

increases sGC activity=increased cGMP production

127
Q

What is the place in therapy of vericiguat?

A

considered in addition to optimal HF therapies for HFrEF patients with worsening symptoms & HF hospitalizations in the past 6 months, to reduce the risk of subsequent hospitalizations

128
Q

What is the benefit of vericiguat?

A

reduces the risk of HF hospitalizations but not mortality

129
Q

What are the contraindications of vericiguat?

A

concomitant use of other sGC stimulators
pregnancy

130
Q

What are the drug interactions of vericiguat?

A

PDE5 inhibitors
long acting nitrates
CI: other sGC stimulators

131
Q

What are the adverse effects of vericiguat?

A

anemia
symptomatic hypotension
syncope

132
Q

What is the dose titration of vericiguat?

A

2.5mg po daily x 2 wks
titration: increase to 5mg po daily x 2wks, then to 10mg po daily based on bp & clinical HF symptoms

133
Q

What parameters should be monitored for vericiguat?

A

Hgb
BP

134
Q

What are the complimentary hemodynamic actions of hydralazine & nitrates (H-ISDN)?

A

hydralazine:
-direct acting arterial vasodilator which reduces afterload on LV and enhances the hearts ability to pump
nitrates:
-venous dilators which reduce preload and pulmonary/systemic edema formation

135
Q

What is the impact of heart failure on the bioavailability of nitric oxide?

A

impaired bioavailability of nitric oxide
-ISDN is a nitric oxide donor
-hydralazine may inhibit generation of nitric oxide-inactivating reactive oxygen species thereby prolonging the vasodilatory effects of ISDN

136
Q

What are the Canadian Cardiovascular Society HF Guidelines for H-ISDN in HFrEF?

A

recommend H-ISDN be considered in addition to standard GDMT at appropriate doses for black patients with HFrEF and advanced symptoms
recommend that H-ISDN be considered in patients with HFrEF who are unable to tolerate ACEI, ARB, or ARNI because of hyperkalemia or renal dysfunction

137
Q

What are the contraindications, drug interactions, adverse effects, and monitoring parameters for hydralazine?

A

contraindications:
-acute dissecting aortic aneurysm, mitral valve rheumatic heart disease
drug interactions:
-can reduce digoxin levels, increase metoprolol levels
adverse effects:
-hypotension, edema, tachycardia
monitoring:
-BP, HR

138
Q

What are the contraindications, drug interactions, adverse effects, and monitoring parameters for ISDN?

A

contraindications:
-cerebral hemorrhage, severe anemia, severe hypotension, bradycardia, hypertrophic obstructive cardiomyopathy
drug interactions:
-CI within 24-48hrs of PDE5 inhibitors
-sGC stimulators
adverse effects:
-hypotension, headache, lightheaded
monitoring:
-BP, HR

139
Q

What symptoms might nitrates help relieve in HFrEF?

A

orthopnea
paroxysmal nocturnal dyspnea
exercise-induced dyspnea or angina

140
Q

Which nitrate formulation was used in HFrEF trials?

A

isosorbide dinitrate
-mononitrate and transdermal sometimes used to aid adherence (limited evidence)
need 12 hr nitrate free interval, regardless of formulation

141
Q

What are the CCS HF Guidelines for HFpEF?

A

identify & treat underlying cause(s)
identify & treat comorbid conditions that might exacerbate HF
-HTN, DM, AF
control symptoms
-loop diuretics for congestion & peripheral edema
treat hypertension as per Hypertension Canada
-candesartan may reduce HF hospitalizations in HFpEF
consider spironolactone if K+ <5mmol/L, eGFR >30ml/min
-reduce HF hospitalizations

142
Q

True or false: CCS HF guidelines support the evidence for the recommendation for the use of Entresto in HFpEF

A

false

143
Q

What is the benefit of SGLT2i in HFpEF?

A

reduces HF hospitalizations
empa is approved for HF regardless of LVEF

144
Q

What is the benefit of standard HF therapy on HFmrEF?

A

decreased HF hospitalizations
-no impact on mortality

145
Q

What are the medications that may reduce risk of HF hospitalizations in HFmrEF and HFpEF?

A

HFmrEF:
-empa, dapa, candesartan, spironolactone
-Entresto similar to enalapril & valsartan
HFpEF:
-empa, dapa, spironolactone
-Entresto similar to enalapril & valsartan

146
Q

What is the therapy for HFimpEF?

A

continue quadruple therapy with improved HF, unless patient unable to tolerate therapy

147
Q

What are the key take home points regarding HFpEF, HFmEF, and HFimpHF?

A

HFpEF:
-manage risk factors (DM, HTN, AF)
-recommend a SGLT2i
-consider spironolactone, candesartan
-use diuretics for fluid retention
HFmEF:
-as above
-benefit appears to decrease as LVEF increases
-use diuretics for fluid retention
improved HF:
-continue therapy due to risk of relapse, providing the patient can tolerate it

148
Q

What is the MOA of loop diuretics?

A

inhibit Na-K-Cl transporter in ascending limb of loop of Henle
-20-25% of filtered Na+ is reabsorbed here
increase renal blood flow–>contribute to natriuresis

149
Q

What is the benefit of loop diuretics in HF?

A

most rapid in producing symptomatic relief due to fluid retention
improve exercise tolerance and quality of life
reduce HF hospitalizations
does not prolong survival or alter disease progression and can limit initiation/titration of medications that do

150
Q

What is the use of diuretics in HF?

A

relieve congestion
-maintain euvolemia

151
Q

Differentiate hypovolemia, euvolemia, and hypervolemia.

A

hypovolemia: volume deplete
-weight is below dry weight
-risk of worsening renal function
-limit optimizing HFrEF therapy
-identify & address cause(s)
-reduce diuretics
euvolemia: GOAL
-dry weight with no or mild HF symptoms (NYHA I-II)
-dry weight=ideal weight
-diuretic amount required to maintain euvolemia can change
hypervolemia: volume overload
-new or worsening HF symptoms
-increase in weight
-identify & address cause(s)
-increase diuretics

152
Q

What can reduce the efficacy of loop diuretics?

A

excessive dietary Na+ intake
NSAIDs

153
Q

Which type of diuretics maintain efficacy in impaired renal function?

A

loops
-thiazides=no

154
Q

What is the initial and maximum dose of furosemide?

A

initial: 20-40mg OD-BID
maximum: 200mg/d

155
Q

What is the initial and maximum dose of bumetanide?

A

initial: 0.5-1mg OD
maximum: 10mg daily

156
Q

What is the initial and maximum dose of ethacrynic acid?

A

initial: 25-50mg OD
maximum: 200mg BID

157
Q

What are the available loop diuretics?

A

furosemide
bumetanide
ethacrynic acid

158
Q

How should loop diuretics be started and adjusted?

A

start low & adjust based on symptoms and weight
-change in weight=marker of fluid retention or loss
wake–>void bladder–>weigh daily
if weight increases 2lbs in 1-2 days or 5lbs over 1wk–>call HCP for assessment

159
Q

When do we combine diuretics?

A

severe edema
-oral loop diuretics may not be adequately absorbed
loop + thiazide/thiazide-like

160
Q

What is diuretic resistance?

A

rebound Na+ retention
-chronic loop diuretic use can lead to increased distal nephron Na+ reabsorption

161
Q

What is metolazone?

A

thiazide-like diuretic

162
Q

What is the dosing of metolazone?

A

start with 2.5mg 2-3x/wk
-5-10mg (inpatient)

163
Q

What is the onset and duration of action of metolazone?

A

onset: 60min
duration: 12-24hr
-up to 48hr in renal impairment or chronic dosing

164
Q

What is the onset of action for furosemide?

A

30-60min

165
Q

What is something to be cautious about regarding diuretics?

A

over-diuresis
-decreased CO, renal perfusion, sx of volume depletion
-hypotension and other AE

166
Q

When should we consider reducing the dose of diuretics?

A

weight loss beyond dry weight
volume depletion: hypotension or worsening renal function

167
Q

What are the contraindications of diuretics?

A

anuria
hepatic coma or pre-coma

168
Q

What are cautions for diuretics?

A

hypokalemia
hyponatremia
eGFR < 30ml/min
SBP < 90mmHg

169
Q

What are the drug interactions for diuretics?

A

risk of digoxin toxicity if diuretic leads to hypokalemia
risk of lithium toxicity due to reduced lithium clearance

170
Q

What are the adverse effects of diuretics?

A

hypotension
volume depletion
hyperuricemia
electrolyte disturbances
ototoxicity with high doses

171
Q

What are the monitoring parameters for diuretics?

A

HF symptoms/daily morning weight
K+, Na+, SCr and urea at baseline & 5-7d after diuretic adjustment
NTproBNP or BNP
BP

172
Q

What is the recommended dietary salt intake for HF?

A

2-3g/day

173
Q

What is the recommended daily fluid intake for HF?

A

2L/day for patients with fluid retention or congestion that is not easily controlled with diuretics

174
Q

What are examples of some drugs that can precipitate or exacerbate HF?

A

meds that cause fluid retention:
-NSAIDs, gabapentinoids, corticosteroids
meds that decrease CO:
-antiarrhythmics, non-DHP CCB
meds with high sodium content
meds with mechanism of cardiotoxicity:
-clozapine, lithium, sympathomimetic
oncology drugs

175
Q

What is class of drugs that can be bought OTC that should never be used in HF?

A

NSAIDs
-dose dependent NOT duration dependent

176
Q

True or false: HF medications are often properly dosed and optimized in Canada

A

false
underdosed and underutilized

177
Q

What is a non-pharm intervention that has been shown to reduced all-cause & HF hospitalizations by ~30%?

A

pharmacist care of patients with HF
-no safety concerns
-no cost to patient

178
Q

What are some considerations for assessing HF signs & symptoms?

A

identify recent baseline
-compared to baseline, are signs/symptoms new, worse, better or same?
ask what usual signs/symptoms are

179
Q

True or false: symptom severity equals degree of left ventricular dysfunction

A

false

180
Q

Describe the assessment of dyspnea.

A

with activity/exertion versus at rest:
-how much activity before SOB
-do they need to stop activity due to SOB
medication profile:
-meds that cause fluid retention
-non adherence (including diuretics)
-uncontrolled comorbidities that cause SOB
-multiple courses of resp ABX and/or inhalers

181
Q

What is orthopnea?

A

difficulties breathing when lying down

182
Q

How can you assess for orthopnea?

A

number of pillows
head of the bed elevated
sleeping in a recliner
how does individual wake up in morning?

183
Q

What is paroxysmal nocturnal dyspnea?

A

waking up short of breath

184
Q

Differentiate a cough that is caused by congestion/fluid retention or drug-induced.

A

congestion/fluid
-productive cough
-nocturnal cough only, particularly with orthopnea and/or PND
-diuretics, optimize HF therapy
drug induced
-dry persistent cough
-incidence: ACEI>ARNI>ARB
-document presence or absence of cough
-if cough is bothersome and not associated with HF symptoms–>hold/re-challenge, switch

185
Q

Describe the assessment of peripheral edema.

A

swelling in feet, ankles, legs, abdomen, sacral, scrotal, hands
identify location and severity
bilateral
ankle edema:
-mild at the end of the day=normal
-elevate legs x30-60min prior to bed if pt experiences nighttime SOB
abdominal edema: bloating, firm, poor appetite

186
Q

What is a sensitive marker of fluid retention or loss in HF?

A

change in body weight
->2lbs in a few days or >5lbs in a week=likely fluid retention

187
Q

What are considerations for assessing hypovolemia?

A

signs/symptoms of hypovolemia w/o signs/symptoms of HF?
-postural hypotension, below dry weight, weak, tired
does bloodwork suggest “dry”/no congestion?
-decline in renal function, SCr, increased K, BNP stable/reduced
is the patient taking more diuretic than prescribed?
-address reasons for overuse
is the patient drinking less than 1.5L/day?
-consider all fluids, including soup
does the patient have an acute illness with fluid loss?
-fever, diarrhea, vomiting, hold SADMANS

188
Q

What are considerations for assessing hypervolemia?

A

is patient experiencing signs/symptoms of congestion?
-increased weight, edema, SOB, orthopnea
does bloodwork suggest congestion?
-increased BNP, afib, anemia, COPD
is the patient taking less diuretic than prescribed?
-address reasons
-if concerned about urgency: take when at home
-if concerned about nocturia: take AM
is the patient drinking more than 2L/d?
-consider all fluids, decrease to 2L/d, salt <2g/d
is the patient taking meds that exacerbate HF?
-NaCl, NSAIDs, steroids, androgens, estrogen

189
Q

What is the preferred method for starting and titrating the standard HFrEF therapy?

A

no proven superior approach

190
Q

What should we consider when starting and titrating the standard HFrEF therapy?

A

blood pressure
heart rate
presence of: afib, CKD, hyperkalemia

191
Q

What is the target BP in HFrEF?

A

there is no target bp
-asymptomatic bp 90-100mmHg requires no change
-reassess if symptomatic hypotension

192
Q

What is a reasonable resting HR in HF?

A

50-60npm
-reassess if symptomatic bradycardia

193
Q

True or false: potassium as high as 5.5mmol/L is often acceptable in HF

A

true
-severe: >5.9mmol/L

194
Q

Which HF medications should be held in acute illness?

A

ACEI, ARB, ARNI
MRA
diuretics
SGLT2i

PHAR253 (16 decks)

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