heart failure .pptx

MANAGEMENT OF HEART
FAILURE
(PG LECTURE)
PRESENTED BY : Dr. AYUSH MEGOTIA
MODERATOR : Dr. SHIVA NARANG

DEFINITION (AHA 2017)
• Complex clinical syndrome that results from structural and functional
impairment of ventricular filling or ejection of blood, which in turn
leads to cardinal clinical symptom of dyspnoea and fatigue and signs
of heart failure (HF), namely edema and rales.

Classification of heart failure(AHA 2017)
Classification Ejection
Fraction
Description
I. Heart Failure with
Reduced Ejection
Fraction (HFrEF)
≤40% a) previously referred to as systolic HF.
b) only in these patients that efficacious therapies have
been demonstrated to date.
II. Heart Failure
with
Preserved Ejection
Fraction (HFpEF)
≥50% a) Previously referred to as diastolic HF.
b) To date, no efficacious therapies have been identified
a. HFpEF, Borderline 41% to
49%
a) These patients fall into a borderline or intermediate
group.
b) Their characteristics, treatment patterns, and
outcomes appear similar to those of patient with
HFpEF.
b. HFpEF, Improved >40% a) recognized as a subset of patients with HFpEF who
previously had HFrEF.
b) These patients with improvement or recovery in EF
may be clinically distinct from those with persistently
preserved or reduced EF.

Staging of Heart Failure
ACCF/AHA Stages of HF NYHA
Functional
Classification
A At high risk for HF but without
structural heart disease or symptoms
of HF.
Class I No limitation of physical
activity. Ordinary physical
activity does not cause
symptoms of HF.
B Structural heart disease but without
signs or symptoms of HF.
(NYHA Class I)
Class II Slight limitation of Physical activity .
Comfortable at rest. but ordinary
physcial activity results in symptoms of
HF.
C Structural heart disease with prior or
current symptoms of HF.
(NYHA Class I-IV)
class III
Marked limitation of physical activity.
Comfortable at rest. But less than
ordinary activity causes symptoms of
HF.
D Refractory HF requiring specialized
interventions.
(NYHA Class IV)
Class IV Unable to carry on any physical
activity without symptoms of HF,
symptoms at rest.

ETIOLOGY
Depressed EF
• CAD
• Chronic pressure/volume
overload- HTN, valvular
heart disease, septal defects
• Chronic lung disease
• DCMP
• Toxin/drug induced
• Viral
• Chagas’ disease
• Arrythmias
Preserved EF
• Primary hypertrophic
cardiomyopathies
• Pathologic hypertrophy
secondary to HTN
• Restrictive cardiomyopathy–
amyloidosis, sarcoidosis,
hemochromatosis etc.
• Aging
• Endomyocardial disorders

Biomarkers in heart failure
Natriuretic peptides : BNP
and NT-proBNP
Soluble ST-2
Galectin-3

Raised levels of natriuretic peptides : Not
always heart failure.
Cardiac causes
• ACS
• Myocarditis,pericarditis
• LVH
• Valvular heart disease
• Arrythmia
• Cardioversion
• Cardiac surgery
• Toxic metabolic myocardial
insults,including cancer
chemotherapy
Non cardiac causes
• Advanced age
• anemia
• Severe pneumonia
• OSA
• Pulmonary artery htn
• Renal dysfunction
• Bacterial Sepsis
• Severe burns

Factors triggering acute heart failure
Arrythmias
Acute
coronary
syndrome
Hyper
tension
Infection
Pulmonary
embolism
Drugs
Metabolic/
hormonal
derangements

Criteria for hospitalization in ICU/CCU include
any of the following:
• Evidence of severe decompensated HF,including
hypotension,worsening renal failure,altered mentation
• Dyspnea at rest a/w either tachypnea or significant
hypoxemia(Sao2<90%0
• Hemodynamically significant arrhythmia
• ACS
Hospitalisation also considered in:
• Worsened congestion even in the absence of dyspnea and reflected by
significant weight gain >4 kg
• Other s/s of pulmonary or systemic congestion
• Newly diagnosed HF
• Complications of HF therapy(electrolyte disturbance)

Phenotypic presentations of ADHF
Acute decompensation
“pulmonary edema”:
Hypoxia is an important
clinical feature.
“hypertensive AHF” :
characterized by vascular type
fluid redistribution.
Hypertension is predominant.
Volume overload is not the
usual feature.
“low output”: Signs of
hypoperfusion
“cardiogenic shock”:
Hypotension with end
organ failure is common.

Cardiopulmonary resuscitation-the very first step
• Immediately provide circulatory support
(pharmacological, mechanical) in patients with
cardiogenic shock and ventilatory support
(oxygen, NIV, mechanical ventilation) in patients
with respiratory failure.

Recommendations for O2 therapy and ventilatory
support:
• Oxygen therapy is recommended in patients with SpO2 <90% or PaO2
<60 mmHg.
• Non-invasive positive pressure ventilation (CPAP, BiPAP) should be
considered in patients with respiratory distress (respiratory rate >25
breaths/min, SpO2 <90%).
• Intubation is recommended, if respiratory failure, leading to
hypoxaemia (PaO2 <60 mmHg (8.0 kPa)), hypercapnia (PaCO2 >50
mmHg (6.65 kPa)) and acidosis (pH <7.35), cannot be managed non-
invasively.

Volume management
• Randomized clinical trials of high- versus low-dose or bolus versus
continuous infusion diuresis have not provided clear justification for
the best diuretic strategy in ADHF.
• Continuous infusion of a diuretic may be useful when large doses are
required or the effect is suboptimal.
• Thus in cases of severe congestion, consider continuous infusion (not
trial supported).
• Reduced toxicity with the use of continuous infusion.
• Continue diuresis until euvolemia has been achieved.

• Torsemide has a higher oral bioavailability, thus can be given orally in
advanced heart failure if furosemide becomes less bioavailable due
to gut congestion.
• Role of adjuvant diuretics for augmentation: Addition of a thiazide
diuretic in combination provides a synergistic effect. Metolazone in
doses of 2.5-10 mg can cause severe electrolyte imbalance.
• Dose of commonly used diuretics: Furosemide: 20-240 mg daily
(maximum dose that can be used in a day: 600 mg); Torsemide: 10-
100 mg daily.

Ultrafiltration (UF)
• There is no evidence favouring ultrafiltration over loop diuretics as
first-line therapy in patients with AHF. Role of ultrafiltration in the
management of ADHF is limited to those patients who are diuretic
unresponsive.
• Benefits over diuretics: controlled rates of fluid removal, no direct
neurohormonal activation and neutral effects on serum electrolytes.
Thus, it is also referred to as aquapheresis. It has also been shown to
restore diuretic sensitivity.

Vascular therapy
• Includes iv nitrates, nitroprusside and nesiritide.
• I.V. vasodilators should be considered for symptomatic relief in AHF
with SBP >90 mmHg (and without symptomatic hypotension).
• In patients with Hypertensive AHF, i.v. vasodilators should be
considered as initial therapy to improve symptoms and reduce
congestion.

Vasodilator Dose Main side effect/
limitation
Nitroglycerine Start with 10-20
µg/min, increase up to
200 µg/min
Hypotension,
headache, tolerance on
continuous use
Isosorbide dinitrate Start with 1 mg/h,
increase up to 10
mg/hour
Hypotension,
headache, tolerance on
continuous use
Nitroprusside Start with 0.3
µg/kg/min and increase
up to 5 µg/kg/min
Hypotension,
isocyanate toxicity
Nesiritide Bolus 2 µg/kg + infusion
0.01 µg/kg/min
Hypotension

Inotropic therapy:
• Helps to increase cardiac output, increase blood pressure, improve
peripheral perfusion ,maintain end organ function and relieves
congestion acutely.
• Mainly indicated in those patients of ADHF who have a low cardiac
output and/or hypotension.
• These agents cause an increase in intracellular concentration of
cAMP, thus increasing cytoplasmic calcium.
• Drugs in this class include sympathomimetic amines (Dobutamine)
and PDE-3 inhibitor (Milirinone).

Recommendations on using inotropic
agents/vasopressors in patients of ADHF:
• May be considered for short term in patients with hypotension and/or
signs/symptoms of hypoperfusion despite adequate filling status.
• Inotropic agents are not recommended unless the patient is
symptomatically hypotensive or hypoperfused. Long-term inotropic therapy
increases mortality whereas short-term use is associated with increased
arrhythmia.
• A vasopressor (norepinephrine preferably) may be considered in patients
who have cardiogenic shock, despite treatment with another inotrope. In
such cases, intra-arterial blood pressure measurement may be considered.
• They are currently indicated as bridge therapy (to either left ventricular assist
device support or to transplant) or as selectively applied palliation in end-
stage heart failure.

Inotropic
agent
Bolus Infusion rate
Dobutamine No 2-20 µg/kg/min
Dopamine No 3-5 µg/kg/min; inotropic (β)
>5 µg/kg/min : (β), vasopressor
(α)
Milirinone 25-75 µg/kg over 10-20
min
0.375–0.75 μg/kg/min
Doses of inotropes used to treat acute heart
failure:

Recommendations on thrombo-embolism
prophylaxis and other drugs in ADHF:
• Thrombo-embolism prophylaxis (e.g. with LMWH) is recommended
in patients not already anticoagulated and with no contra-indication
to anticoagulation, to reduce the risk of deep venous thrombosis and
pulmonary embolism.
• Digoxin can be considered as first line therapy for acute control of
ventricular rate in patients with atrial fibrillation.
• Opiates may be considered for cautious use to relieve dyspnoea and
anxiety in patients with severe dyspnoea but nausea and hypopnea
may occur.

Mechanical Assist Devices
• In patients of severe persistent systolic heart failure who fail to
respond adequately to optimal medical therapy, mechanical assist
devices may be required.
• These include Intra-aortic balloon pump (IABP) and Mechanical
cardiac support devices.
• They either be used for short-term as a bridge to recovery or to
cardiac transplantation (bridge to transplantation) or for long-term
as permanent support for lifetime therapy (destination therapy).
• Available as a therapeutic option in both acute as well as end-stage
chronic heart failure.

Parameters associated with worse
outcomes:
• Increased BUN >43mg/dl
• Increased serum creatinine>2.75
• Sbp<115mmhg
• Elevated troponin I level

MANAGEMENT OF CHRONIC
HEART FAILURE

Management of heart failure with
preserved ejection fraction (HFpEF):
• Identification and correction of risk factors like hypertension, ageing,
atherosclerosis and diabetes.
• Following should be the general therapeutic principles while treating
a patient of HFpEF:
Control of congestion
Stabilization of heart rate and blood pressure.
Treat and prevent myocardial ischemia
Detect and treat sleep apnea
Improvement of exercise tolerance

Management of HFpEF
• No treatment has yet been shown, convincingly, to reduce morbidity or mortality in patients with HFpEF or
HFmrEF.
Class I
1. Systolic and diastolic blood pressure should be controlled in accordance with
published clinical practice guidelines to prevent morbidity. (LOE: B)
2. Diuretics should be used for relief of symptoms due to volume overload . (LOE: C)
Class IIa
1. Coronary revascularization is reasonable in patients with CAD in whom symptoms
(angina) or demonstrable myocardial ischemia is judged to be having an adverse effect
on symptomatic HFpEF despite optimal medical therapy. (LOE: C)
2. Management of AF according to published clinical practice guidelines in patients with
HFpEF is reasonable to improve symptomatic HF . (LOE: C)
3. The use of beta-blocking agents, ACE inhibitors, and ARBs in patients with
hypertension is reasonable to control blood pressure in patients with HFpEF. (LOE: C)
Class IIb
1. The use of ARBs might be considered to decrease hospitalizations for patients with
HFpEF.(LOE: B)

SUMMARY OF THE TREATMENT IN
HFpEF
• Excessive use of vasodilators or diuretics may lead to hypotension and
syncope due to excessive decrease in preload.
• Targeted therapy like RAAS directed therapy, digoxin, beta-blockers,
PDE-5 inhibitors or nitrates is ineffective.
• ARNIs show early promise.
• Evaluation for and correction of underlying ischemia is beneficial.
• Appropriate identification and treatment of sleep-disordered
breathing should be strongly considered.

Impact of Interatrial shunt device (IASD) on
survival in HFpEF
• Impaired left ventricular diastolic function leading to elevated left
atrial pressure, particularly during exertion is a key driver of
symptoms and outcomes in HFpEF.
• Kaye DM et al .ESC heart Fail. 2019- The current study suggests IASD
implantation may be associated with a reduction in mortality in
HFpEF. Large‐scale ongoing randomized studies are required to
confirm the potential benefit of this therapy.

Management of Heart Failure
with Reduced Ejection Fraction
(HFrEF)

NEUROHORMONAL ANTAGONISM
• Neurohormonal antagonism with RAAS blockers and beta-
blockers form the cornerstone of disease modifying therapy
in the patients with HFrEF.
• These drugs reduce symptoms, improve QOL, decrease
rehospitalization and reduce mortality (due to pump failure
or arrhythmia).
• These drugs lead to attenuation of decline and
improvement in cardiac structure and function.

 ACEIs cause a 23% reduction in mortality and a 35%
reduction the combined endpoint of mortality and
hospitalizations.
 Patients treated with beta-blockers provide a further 35%
reduction in mortality on top of the benefit provided by
ACEI alone.
 ACEIs and beta-blockers are also recommended in patients
with asymptomatic LV systolic dysfunction to reduce the
risk of HF development.
 Use of ACEI is generally safe in patients with mild renal
insufficiency and use of beta-blockers is usually tolerable in
patients with moderately controlled diabetes, asthma and
obstructive lung disease.

 ARBs are non-inferior to ACEIs in terms of reducing
mortality and hospitalizations.
 The most important factor in determining the extent of
reduction in mortality and thus the prognosis is the possibility
of achieving optimal doses of these agents.
 A number of patients with advanced heart failure may not be
able to achieve optimal doses of neurohormonal inhibitors due
to either intolerance or clinical instability. Such individuals
represent a high-risk cohort with poor prognosis.
 Neurohormonal escape: Circulating levels of angiotensin II
return to pre-treatment levels in some patients on long-term
ACEI therapy. ARBs blunt this phenomenon by binding
competitively to the AT1 receptor.

Sequence of administration:
• Either agent can be started first. In the CIBIS III trial
comparing bisoprolol vs enalapril, outcomes did not vary
when either agent was initiated first.
• What does matter is that optimally titrated doses of both
ACEIs and beta blockers can be established in a timely
manner.
• ARBs can be added if patients in intolerant to ACEIs or beta-
blockers, but simultaneous administration of ACEI, ARBs and
beta-blockers have shown worse outcomes. (Val-HeFT trial).

Class effect Dose Uptitration:
– ACEIs exert their
beneficial effects as a
class; however, the
beneficial effects of beta-
blockers are limited to
specific drugs only, which
are carvedilol, bisoprolol,
and metoprolol
succinate.
– More the dose is taken
towards the target dose;
more is the reduction in
mortality and
hospitalization. Up
titration should be done
at every 2 weeks if well
tolerated.

Drug class Generic drug Initiation (mg) Target dose
(mg)
ACEI Lisinopril 2.5-5 qd 20-35 qd
Enalapril 2.5 bid 10-20 bid
Captopril 6.25 tid 50 tid
Ramipril 2.5 qd 10 qd
ARBs Losartan 50 qd 150 qd
Valsartan 40 bid 160 bid
Candesartan 4-8 qd 32 qd
Beta blockers Metoprolol
succinate CR/XL
12.5-25 qd 200 qd
Carvedilol 3.125 bid 25-50 bid
Bisoprolol 1.25 qd 10 qd

Angiotensin receptor-neprilysin Inhibitor
(ARNI):LCZ696
• combination of neprilysin inhibitor plus angiotensin II receptor
blocker (ARB)
• recommended as an alternative to ACE inhibitor (or ARB) therapy.
• MOA : combines of ARB with augmentation of beneficial counter-
regulatory systems such as natriuretic peptides by the inhibition of
neprilysin.

Neprilysin inhibition- counter the effects of neurohormonal overactivation
like vasoconstriction, sodium retention, and maladaptive remodeling

Recommendation : ( 2017 ACC/AHA Guideline for the Management of
Heart Failure)
For patients with NYHA class II or III HFrEF who have tolerated an ACE
inhibitor or ARB in doses equivalent to at least enalapril 10 mg twice
daily for ≥4 weeks with adequate BP with:
•Current or prior elevated BNP level ≥150 pg/mL or NT-proBNP
≥600 pg/mL;
( or, h/o of hospitlization with HF within the previous 12 months,
BNP≥100 pg/mL or NT-proBNP ≥400 pg/mL);
and No history of angioedema , hypersenstivity to any
component
Sacubitril-Valsartan has been recommend to replace the ACE inhibitor
or ARB
( only after 36 hr interval of last dose of ACEI)

But
The 2016 European Society of Cardiology HF guidelines recommended ARNI in
place of ACE inhibitor for ambulatory patients with HFrEF who remain
symptomatic despite optimal treatment with an ACE inhibitor, a beta blocker,
and a mineralocorticoid receptor antagonist.

• ARNI should not be administered concomitantly with ACE
inhibitors or within 36 hours of the last dose of an ACE
inhibitor.
• ARNI should not be administered to patients with a history
of angioedema.
• Dose: 100 mg bid initially upto 200 mg bid.
• Ratio of sacubitril: valsartan = 97:103
• Cost in INDIA: Rs 35 per tablet of 100 mg.

Mineralocorticoid Receptor Antagonist
(MRA):
• Increased aldosterone production in patients of HFrEF is associated
with higher mortality due to sodium retention, electrolyte imbalance,
endothelial dysfunction and myocardial fibrosis.
• Use of MRA is thus, associated with reduction in mortality and
hospitalizations in all stages of symptomatic class II to IV HFrEF.
• Significant reduction in sudden cardiac death.
• Eplerenone is selective and Spironolactone is non-selective
mineralocorticoid receptor antagonist.

• Main concerns are hyperkalemia and worsening renal function, thus
KFT and serum K+ levels must be closely monitored.
• Spironolactone or eplerenone are recommended in all symptomatic
patients(NYHA II- IV) (despite treatment with an ACEI and a beta-
blocker) and LVEF ≤35%.,crcl>30ml/min and ‘K’ levels <5meq/l
Drug Initial dose Target dose
Eplerenone 25 qd 50 qd
spironolactone 12.5-25 qd 25-50 qd

IVABRADINE:
• Ivabradine is a selective inhibitor of the sinoatrial
pacemaker modulating "f-current" (If), thus, slows
the sinus rate by prolonging the slow
depolarization phase
• It does not have a negative ionotropic effect like
beta-blockers.
• It has shown beneficial effects on mortality and
hospitalizations in patients of HFrEF with a heart
rate > 70 beats/min. (SHIFT trial).

Indication:
Indicated for patients with symptomatic chronic heart failure (HF)
with LVEF≤35 %, in sinus rhythm with a resting heart rate ≥70
beats/min , and who are either on a maximum tolerated dose of a beta
blocker or have a contraindication to beta blocker use with concurrent
treatment of ACEI or ARB and a Mineralocorticoid receptor blocker.
Contraindications —
●Acute decompensated HF.
●Blood pressure less than 90/50.
●Sick sinus syndrome, sinoatrial block or 3rd AV block, unless a functioning
pacemaker is present.
●Pacemaker dependence (heart rate maintained exclusively by pacemaker).
●Severe hepatic impairment.
 Dosing : started at low doses, 2.5mg BD, titrated upwards till 7.5 mg
bd till the resting heart rate falls between 50-60 beats/min.

Role of arteriovenous vasodilators in
HFrEF:
• A-Heft trial done in self identified African Americans studied a fixed
dose of isosorbide dinitrate with hydralazine in patients with
advanced symptoms of HFrEF who were receiving standard
background therapy. The study demonstrated reduction in mortality
and hospitalizations rates in the treatment group, although less
than that caused by ACEIs or ARBs.
• Hydralazine and isosorbide dinitrate should be considered in self-
identified black patients with Class III–IV despite treatment with
optimal ACE-I, a beta-blocker(COR I) or in current/prior symptomatic
HFrEF who cant be given ACEI or ARB d/t drug intolerance
/hypotenstion/renal failure(COR-IIA)

• Hydralazine and isosorbide dinitrate may be considered in
symptomatic patients with HFrEF in which RAAS based therapy is
either intolerable or contraindicated.
• Initial dose of Hydralazine Isosorbide dinitrate: 37.5/20 mg tid , target
dose : 75/40 mg tid
• Limitation : thrice daily dosing

Digoxin:
• It exerts mild inotropic effect and is sympatho-inhibitory. (It
decreases serum norepinephrine levels, plasma renin levels, possibly
aldosterone levels.)
• May be considered in symptomatic patients in sinus rhythm despite
treatment with an ACE-I, a beta-blocker and an MRA, to reduce the
risk of hospitalization.
• No reduction in mortality or improvement in QOL is seen with the
use of this drug (DIG trial). Rather, increased mortality and
hospitalizations was seen in women.

• Caution should be exerted in females, in the elderly and in patients
with reduced renal function.
• Low doses are sufficient to achieve any potentially beneficial
outcomes.

CARDIAC RESYNCHRONIZATION THERAPY (CRT)

IMPLANTABLE
CARDIOVERTER-
DEFIBRILLATOR
(ICD)

Recommendations for implantable
cardioverter-defibrillator (ICD):
1. Secondary prevention
An ICD is recommended to reduce the risk of sudden death and all-cause
mortality in patients who have recovered from a ventricular arrhythmia
causing haemodynamic instability, and who are expected to survive for >1
year with good functional status.
2. Primary prevention
An ICD is recommended to reduce the risk of sudden death and all-cause
mortality in patients with symptomatic HF (NYHA Class II–III), and an
LVEF ≤35% despite ≥3 months of OMT, provided they are expected to
survive substantially longer than one year with good functional status

• ICD implantation is not recommended within 40 days of an MI, as
implantation at this time does not improve prognosis.
• ICD therapy is not recommended in patients in NYHA Class IV with
severe symptoms refractory to pharmacological therapy.
• A wearable ICD may be considered for patients with HF who are at
risk of sudden cardiac death for a limited period or as a bridge to an
implanted device.

Other potentially effective therapies in HFrEF:
• Fish oil (PUFA) - GISSI-HF trial
• Iron supplementation(i.v.)
• Thiamine and Selenium supplementation (in those with deficiency)
• ECCP (Enhanced external counter pulsation)
• Exercise training

Treatments not recommended (unproven benefit)
in symptomatic patients of HFrEF
• Statins
• Oral anticoagulants and antiplatelet therapy
• Renin inhibitors (ASTRONAUT trial)
• EPO for anaemia
• SSRI for depression

Treatments (or combinations of treatments) that
may cause harm in patients with HFrEF
• Non-dihydropyridine calcium-channel blockers e.g. Diltiazem and
verapamil. (There is only evidence on safety for amlodipine and
felodipine in patients with HFrEF, and they can be used only if there
is a compelling indication in patients with HFrEF.)
• NSAIDs or COX-2 inhibitors
• Thiazolidinediones (glitazones).

Treatment of Stages A to D
in patients of HFrEF

Stage A
Class I
1. Hypertension and lipid disorders should be controlled in
accordance with contemporary guidelines to lower the risk of
HF. (LOE: A)
2. Other conditions that may lead to or contribute to HF, such as
obesity, diabetes mellitus, tobacco use, and known cardiotoxic
agents, should be controlled or avoided. (LOE: C).

Stage B
Recommendations COR LOE
In patients with a history of MI and reduced EF, ACE inhibitors or
ARBs and beta blocker should be used to prevent HF
I A
In patients with MI, statins should be used to prevent HF. I A
Blood pressure should be controlled to prevent symptomatic HF. I A
An ICD is reasonable in patients with asymptomatic ischemic
cardiomyopathy ( NYHA class I) who are at least 40 d post-MI, have an LVEF
≤30%, and on GDMT.
IIA B
Nondihydropyridine calcium channel blockers may be harmful in
patients with low LVEF.
III : Harm C

Stage C
1) Non pharmacological Interventions
1.1 Education and Social support
Patients with HF should receive specific education to facilitate HF self-care.
(Class I, LOE: B)
1.2 Sodium restriction:
Sodium restriction is reasonable for patients with symptomatic HF to reduce
congestive symptoms. (Class IIa, Level of Evidence: C)
• Because of the association between sodium intake and hypertension, LV
hypertrophy, and cardiovascular disease, the AHA recommendation for restriction
of sodium to 1500 mg/d appears to be appropriate for most patients with stage A
and B HF.
• For patients with stage C and D HF, some degree (eg, <3 g/d) of sodium
restriction in patients with stage C and D HF for symptom improvement is
advised.

1.3 Weight loss:
• A U-shaped distribution curve → mortality is greatest in cachectic patients with
HF; lower in normal, overweight, and mildly obese patient (30-35kg/m2) and
higher again in more severely obese patients.
• No large-scale clinical trials on the role of weight loss in patients with HF with
obesity have been performed.
1.5 Activity, Exercise Prescription, and Cardiac Rehabilitation: Recommendations
Class I
Exercise training (or regular physical activity) is recommended as safe and effective
for patients with HF who are able to participate to improve functional status.
(LOE: A)
Class IIa
Cardiac rehabilitation can be useful in clinically stable patients with HF to improve
functional capacity, exercise duration, HRQOL, and mortality. (LOE: B)

Stage C : Pharmacological Treatment
GOALS OF THERAPY :
●Improvement in symptoms → diuretics, beta
blockers, ACE inhibitors, ARBs, Angiotensin receptor
neprilysin inhibitor (ARNI), Hydralazine plus
nitrate, digoxin and aldosterone antagonists.
●Prolongation of patient survival →beta blockers, ACE inhibitors or ARB, Angiotensin
receptor neprilysin inhibitor (ARNI), Hydralazine plus nitrate, and aldosterone
antagonists.

Assess volume status and BP
Is volume overload present?
Initiate diuretic therapy
Add ACEI if no C/I present
Generally started soon after diuresis
Titrate ACEI to low or moderate dose(COR I)
Symptomatic hypotension and severe
asymptomatic hypotension(SBP<90mmhg)
Evaluate symptoms and BP
Evaluate and treat causes for
hypotension
yes
no
yes no
Evaluate volume status
Greater than minimal fluid retention
yes
Additional
diuresis no
Stepwise approach
for
pharmacological
management of
HFrEF

•Add B-blocker if no contraindiction present
•Titrate ACEI and B Blocker to Target dose
Is patient is black and still having NYHA III-IV symptoms and is
LVEF<40% on optimal regimen including above agents?
Add and titrate
Hydral + ISDN
(COR I)
Does patient still have NYHA class II-IV symptoms with LVEF≤35% and
serum K+< 5meq/l and eGFR>30ml/min and serum k+ and renal function
can be carefully monitored?
Any indication for Device therapy present?
Refer for ICD or CRT( CRT-D)
implantation
(COR I)
Add and titrate MRA
(COR I)
Evaluate for indications for therapy
for advanced heart failure
No signs of
Fluid retention
no
NYHA class II-III adequate
BP on ACEI or ARB, No C/I
to ARB or sacubatril
REPLACE ACEI OR ARB
with ARNI
(COR I)
no
NYHA II-III, NSR,
HR≥70bpm on
max b blocker
dose, add
IVABRADINE
(COR IIA)

Other recommendations
• Omega 3 Fatty Acids – Class IIa , LOE-B)
• reasonable to use as adjunctive therapy in patients with NYHA class II–IV
symptoms and HFrEF or HFpEF, unless contraindicated, to reduce
mortality and cardiovascular hospitalizations.
• CCB – Class III ( no benefit )
• Renin inhibitors →Aliskiren (direct renin inhibitor) failed to improve
outcomes for patients hospitalized for HF at 6 months or 12 months in one
study and is not presently recommended as an alternative to an ACEI orARB.

Device Therapy for Stage C HFrEF
Devices recommended in selected patients with HF include the
following:
● Implantable cardioverter-defibrillator (ICD)
●Cardiac resynchronization therapy (CRT)
Most patients who satisfy criteria for CRT implantation are
also candidates for an ICD and receive a combined device
(CRT-D).

Implantable cardioverter-defibrillator (ICD)
ICD therapy is recommended for primary prevention of SCD to reduce total
mortality in selected patients with
• non-ischemic DCM or
• ischemic heart disease, atleast 40 days post-MI with LVEF ≤35%
and NYHA class II or III symptoms on optimal medical therapy
I A
An ICD is of uncertain benefit to prolong meaningful survival in patients with
a high risk of nonsudden death such as frequent hospitalizations, frailty, or
severe comorbidities , NYHA IV
IIB B
•Use of ICDs is considered only after 3 to 6 months of minimum optimal medical therapy
and only in patients with a reasonable expectation of survival with good functional status
beyond 1 year.
•ICD therapy resulted in a 29% reduction in overall mortality compared with standard
medical therapy.( based on meta-analysis of 6 RCT ((MADIT, MADIT II, DEFINITE, SCD HeFT,
AMIOVIRT, and CAT)

Cardiac Resynchronization Therapy
RATIONALE :
 involves pacing of the left and right ventricle to restore ventricular
synchrony, thus improving LV systolic function in patients with ECG evidence
of electrical dys-synchrony ( QRS prolongation).
 Approximately 1/3 rd patients with HFrEF have a "wide" QRS complex,
defined as >120 ms and mortality increases with increasing QRS complex
duration . (LBBB, But not RBBB).
MECHANISMS :
 therapy induces immediate hemodynamic benefits by improving LV systolic
function, and promoting LV reverse remodeling, resulting in decrease in LV
size.
increases systolic blood pressure, cardiac output, and contractility.

Indicated in patients who have LVEF ≤35%, sinus rhythm, LBBB with a QRS
≥150 ms, and NYHA class II, III, or ambulatory IV symptoms and on Optimal
medical therapy(OMT)
I A(NYHA
III/IV)
B (NYHA II)
For patients with LVEF ≤35%, sinus rhythm, and NYHA class II,III, or
ambulatory IV symptoms on OMT
 LBBB with a QRS 120 to149 ms
 Non-LBBB pattern with QRS ≥150 m
IIA B
may be considered for patients who have LVEF ≤35%, sinus rhythm, a non-
LBBB pattern with a QRS duration of 120 to 149 ms, and NYHA class
III/ambulatory class IV on GDMT.
IIB B
not recommended for patients with NYHA class I or II symptoms and non-
LBBB pattern with QRS <150 ms
III:N/B B
not indicated for patients whose comorbidities and/or frailty limit survival to
<1 y.
III:N/B C

• Stage D
(= “advanced HF,” “end-stage HF,”
“refractory HF.”)

Definition of Advanced HF
ESC Definition of Advanced HF:
1. Severe symptoms of HF with dyspnea and/or fatigue at rest or with minimal exertion
(NYHA class III or IV)
2. Episodes of fluid retention (pulmonary and/or systemic congestion, peripheral edema)
and/or reduced cardiac output at rest (peripheral hypoperfusion)
3. Objective evidence of severe cardiac dysfunction shown by at least 1 of the following:
a. LVEF <30%.
b. Pseudonormal or restrictive mitral inflow pattern.
c. Mean PCWP >16 mm Hg and/or RAP >12 mm Hg.
d. High BNP or NT-proBNP plasma levels in the absence of noncardiac causes.
4. Severe impairment of functional capacity shown by 1 of the following:
a. Inability to exercise
b. 6-Minute walk distance ≤300 m
c. Peak Vo2 <12 to 14 mL/kg/min on CPET.
5. History of ≥1 HF hospitalization in past 6 mo
6. Presence of all the above features despite optimal medical or device therapy,
(unless these are poorly tolerated or contraindicated) and ruling out conditions

•Goals of therapy in Advanced HF
• Control symptoms
• Improve QOL
• Reduce hospital readmissions
• Establish patient’s end -of-life goals.
•Options
• Inotropes( dobutamine, dopamine or milrinone)
• Temporary or permanent Mechanical circulatory support
device.
• Heart transplant( gold standard)
• Palliative care.

COR Recommendations
Class I Until definitive therapy ( MCS, heart transplantation) or resolution of the acute
precipitating problem, patients with cardiogenic shock should receive temporary
intravenous inotropic support to maintain systemic perfusion and preserve end-organ
performance. (LOE: C)
Class IIA 1.Continuous intravenous inotropic support is reasonable as “bridge therapy” In
patients with stage D HF refractory to OMT and device therapy who are eligible for
and awaiting MCS or cardiac transplantation
2. Mechanical circulatory support (MCS) ( ventricular assist devices ,VADs)
• is beneficial in carefully selected* patients with stage D HFrEF as a bridge
therapy in whom definitive management (eg, cardiac transplantation) or cardiac
recovery is anticipated or planned. (LOE: B)
* (patients with LVEF <25% and NYHA class III–IV , despite OMT, and CRT(when
indicated), with high predicted 1- to 2-year mortality or dependence on continuous
parenteral inotropic support).
USE OF IONOTROPES

Class IIB 1. Long-term, continuous intravenous inotropic support may be
considered as palliative therapy for symptom control in select patients
with stage D HF despite optimal medical and device therapy who are not
eligible for either MCS or cardiac transplantation.(LOE: B)
Class III
( Harm)
1. Long-term use of either continuous or intermittent, intravenous
parenteral positive inotropic agents (for reasons other than palliative
care) is potentially harmful in the patient with HF.(LOE: B)

HEART TRANSPLANT=GOLD STANDARD

MANAGEMENT OF CO
MORBIDITIES ASSOCIATED WITH
HEART FAILURE:-

Sleep disordered breathing :
• Includes obstructive sleep apnea, central sleep apnea and extreme
form Cheyne-Stokes breathing.
• Central sleep apnoea (CSA) has been identified as an independent
predictor of increased morbidity and mortality in patients with heart
failure.
• Mechanism: Frequent hypoxic episodes and arousals ► Adrenergic
surge ►Worsening of hypertension ► Impairment of systolic and
diastolic function ► Worsening of heart failure.

• Suspect sleep disordered breathing in those patients of HF who
present with
• Difficult to control hypertension
• Predominant symptoms of fatigue despite reverse remodelling in response to
optimal medical therapy.
• Worsening of right heart function with improvement in left ventricular
function. (pulmonary hypertension and occult pulmonary embolism should
be ruled out).

• Treatment : Nocturnal positive airway pressure
• No mortality benefit seen with Adaptive servo ventilation (SERVE-HF
trial). It is a positive airway pressure ventilatory support that is
adjusted based on the detection of apnea, or pauses in breathing,
during sleep.

Anemia
• Common comorbidity in heart failure, accountable for worsening in
functional status, more common in elderly, in presence of renal
insufficiency, and in women.
• In patients with NYHA class II and III HF and S. ferritin <100 ng/ml or
100-300 ng/ml if transferrin saturation is <20%), IV Iron
supplementation using either iron sucrose or carboxymaltose is the
recommended therapy which improves functional status.(FAIR-HF
and CONFIRM-HF trials)
• Oral Iron or Erythropoiesis stimulating agents: Not useful.

Atrial fibrillation:
• Urgent electrical cardioversion for hemodynamically unstable cases if
AF is thought to be contributing to the patient’s haemodynamic
compromise.
• For patients in NYHA Class I–III, a beta-blocker, usually given orally, is
safe and therefore is recommended as a first line treatment to
control ventricular rate, provided the patient is euvolaemic. If the
rate does not improve on beta blockers or beta-blocker is
contraindicated /intolerated, then the next drug in line is digoxin.

• For patients in NYHA Class IV, in addition to treatment for HF, an
intravenous bolus of amiodarone or, in digoxin-naïve patients, an
intravenous bolus of digoxin should be considered to reduce the
ventricular rate.
• Rhythm control may be considered in patients with persisting
symptoms and/or signs of HF, despite OMT and adequate control of
ventricular rate, to improve clinical/symptomatic status.
• Amiodarone and Dofetilide are found to be safe and effective in this
regard.

Diabetes mellitus:
• SGLT-2 inhibitors like Empagliflozin have shown significant reduction
in cardiovascular mortality as well as hospitalizations for heart
failure.
• Metformin, sulfonylureas(2nd gen.), insulin, GLP-1 analogues :
Neutral
• DPP-4 inhibitors like saxagliptin , alogliptin : potential risk
• Thiazolidinedoines : Harm

Role of SGLT-2 inhibitors in prevention of heart
failure
• Sodium-glucose co-transporter 2 (SGLT2) inhibitors promote the renal excretion of
glucose and thereby modestly lower elevated blood glucose levels in patients with type 2
diabetes.
• Indicated as add on therapy in Type 2 DM, especially in those with risk of cardiovascular
disease.
• 4 agents → canagliflozin, dapagliflozin, empagliflozin, and ertugliflozin but only
empagliflozin and canagliflozin have beneficiary CVS outcomes.
• empagliflozin preferred agent.(because of increase in the risk of lower limb amputations
and fractures in canagliflozin-treated patients).
• Also, a/w weight loss, reductions in BP without increases in heart rate and has
favorable effects on markers of arterial stiffness and vascular resistance
• Empagliflozin:
10mg or 25 mg OD in the morning with or without meals.
 Avoid in patients with eGFR <45 mL/min.
 Safe in patients with hepatic impairment.
(TAB JARDIANCE 10/25 MG ( RS 470/STRIP) )

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