This document provides an overview of heart failure management. It defines heart failure and describes its types and classifications. Symptoms include dyspnea and fatigue while signs include circulatory congestion or hypoperfusion. Treatment involves establishing a diagnosis, determining risk factors and severity, and taking a multidisciplinary approach. The main treatment goals are reducing mortality and morbidity by modifying risks, preventing disease progression, and improving quality of life. Guideline directed medical therapy includes diuretics, ACE inhibitors, beta blockers, MRAs, ARNIs, and SGLT2 inhibitors. Device therapies like ICDs and CRT can be used, and management depends on the ACC/AHA stages of heart failure.

1. Dr. Ashok Dutta
MBBS, FCPS(Med), MD( Card.), FACC
Associate Professor & Senior Consultant.
NHFH & RI. Dhaka
Heart failure management-
Overview.

2. All the cardiac diseases –lead to HF.

3. Definition & Types of HF
Heart failure is a complex pathophysiological state. Failure of the heart to
pump sufficient amount of blood to fulfill the body demand or can do so at
the cost of raised filling pressure-LVEDP ( compensated HF).
When heart fails to maintain adequate cardiac output.
Symptoms-dyspnea and fatigue
Signs of circulatory congestion or hypoperfusion.
Classification:
 Acute or Chronic Heart Failure
 Left or Right Heart failure,
 High output or Low output Failure,
 Systolic & Diastolic Failure,
 HFrEF & HFpEF.

4. Heart Failure Nomenclature
depending on Echo, RNVG, CMR.
There is up to 10% inter/intra-observer variability of EF.
EF in between 40-49% is Gray Zone.

5. HF Classification
ACC/AHA Stages of Heart Failure (HF) Compared to NYHA Functional Classification
HF Classification: Stages A-D
Disease Evolution & Progression
NYHA- Functional Classification
Class I-IV
Stage A: Patient at high risk for developing HF with
no structural disorder of the heart.
None
Stage B: Patient with structural disorder without
symptoms of HF
Class I: No symptoms with ordinary activity
Stage C: Patient with past or current symptoms of
HF associated with underlying structural heart
disease
Class II: Slight limitation of physical activity. Comfortable at rest, but
ordinary physical activity results in fatigue, palpitation, dyspnea, or
angina.
Class III: Marked limitation of physical activity. Comfortable at
rest, but less than ordinary physical activity results in
fatigue, palpitation, dyspnea, or angina.
Stage D: Patient with end-stage disease who
requires specialized treatment strategies
Class IV : Unable to carry out any physical activity without
discomfort. Symptoms of cardiac insufficiency may be
present even at rest

6. Management outline of HF r EF
• Establish a firm Diagnosis of HF, exclude the HF mimicking conditions(obesity,
Lung disease, CKD, CLD, anemia, drugs).
• Determine the risk factors/etiology, ppt factors, comorbidities and severity of HF.
• Precipitating factors- poor compliance to Rx, drugs-NSAIDs/steroid, anemia,
obesity, arrhythmias (AF), CAD, progression of pathology.
• Multidisciplinary approach( for Comorbidities)- Gen. practitioner
(GP),Internist, dietician, Diabetologist, pulmonologist, nephrologist, cardiac
rehabilitation, EPS.
• Objectives:
• Reduce Mortality (death), prolong life expectancy.
• Morbidity- symptoms, quality of life, exercise capacity, reduce HF hospitalization.
• Modification of risk factors/etiology and prevention of disease progression.

8. Heart Failure Treatment Algorithm1
as per AHA/ACC stage of HF .
Stage D has
a 30-78%
mortality/year2
1 Jessup M and Brozena S. N Engl J Med 2003; 348: 2007-2018
2 Davis, et al. Am J Hospice and Palliative Medicine. 2005; 22 (3): 211-22
Stage D
Refractory symptoms
requiring special
intervention
Stage A
High risk
with no
symptoms.
HTN, DM,
DL, Smoker,
f/H.
Stage B
Structural
heart
disease-
LVH, CAD,
VHD,
CHD,
no
symptoms
Stage C
Structural disease, previous or
current symptoms- 4 cornerstones-
Diuretics, ACE-I, BB, MRA, SGLT2
Inhibitors.
Hospice
VAD, transplantation
Ionotropes.
Revascularization, mitral-valve surgery
CRT-P/D, His or LB pacing
Consider multidisciplinary team-DM, COAD, CKD, lungs diseases.
Dietary sodium restriction, life style.
ACE-I /ARB in all cases, BB in selected patients-MI/arrhythmia.
Rx HTN, DM, DL; ACE-I/ARB in some cases.
Risk-factor modification, patient and family education

10. Diuretics and MRA.
(Furosemide,Bumetanide,Torasemide, HTZ, Spironolactone, Eplerenone)
• Loop diuretics choice of drug for all HFrEF and congestion, should be
started first . S/E- E.I.
• ACE-I reduces the aldosterone secretion but it’s transient and with chronic
therapy with ACE-I, aldosterone level rapidly return to normal.
• MRA is indicated in HFrEF < 35%, NYHA- II-IV and patient is on other
standard Rx ( Diuretic, ACE-I & BB).
• MRA is C/I in CKD with S. Creatinine >2.5 mg/dl, CCR < 30 ml/mint.
• Check S. K+ after 3 days.
• Painful gynecomastia- 10-15%, Eplerenone is an option.
• MRA- diuretic , K sparer, ↓myocardial fibrosis.

11. ACE-I & ARB
• Overwhelming evidences of benefits of ACE-I in reducing mortality ,
increase the longevity, improve symptoms, HF hospitalization.
• Indicated in all patients with symptoms and asymptomatic patients with LVEF <40%.
• ACE-I inhibits Kininase , thereby reduce breakdown of bradykinin, that has
addition benefits in vasodilatation, over ARB.
• Should be started with low dose, preferable after with diuretics because if
diuretics are not used, fluid retentions from kidneys will attenuates the
effects of ACE-I and ARB.
• Dose should be increased gradually every 24-48 hrly ( c.f. to BB- 5-7 days
interval) till higher/recommended dose is not achieved.
• However before giving the highest dose of ACE-I, better to start BB, so that
BB can be used in adequate dose to reduce the HR without producing
hypotension.
• Higher the dose of ACE-I (BB), better the benefit. But it’s better to treat
with low/modest dose of both ACE-I & BB, than highest dose of any one of
these.

12. ACE-I and ARB.
• Abrupt withdrawal may deteriorate the symptoms, so should be avoided
except in life-threatening condition e.g. angioedema and hyperkaelemia.
• Blood pressure, renal function and S. K+ -monitoring after 1-2 wks.
specially if there in preexisting CKD.
• ARB are indicated only when ACE-I are not tolerated due to cough,
angioedema, skin rash.
• Losartan, valsartan(widely studied) and candesartan.
• Aliskiren-direct renin inhibitor- major trials fails to prove it’s benefit and
there not recommended as an alternative to ACE-I or ARB.
• Hydralazine and NO3- alternative if ACE-I & ARB both are not tolerated,
specially in African American black people.

14. ARNI( ARB+ Neprilysin inhibitors)
Valsartan & Sacubitril.
Neurohumoral system modulation.
• RAAS inhibitors- so reduce vasoconstriction, H2O retention,
myocardial hypertrophy, fibrosis.
• Neprilysin Inhibitors- Slows degradation of natriuretic peptides,
bradykinin& adrenomedulin- thereby enhance diuresis, natriuresis, &
myocardial relaxation.
• Reverse ventricular remodeling (recovery/normalization or remission).
• ARNI- is included in GDMT.
• It should not be started within 36 hrs. of stopping ACE-I because of
angioedema.

15. Beta Blocker
• HF  activation of autonomic nervous system, adrenergic activities (alfa ἀ
1, ß 1 & ß 2)
• ß ßlockers - Metoprolol>>antiarrhythmia,Carvidilol ( alfa : Beta blocking=
1:2)>>Antifailure, bisoprolol B1>B2=100,>>BA,COAD.
• Should be started at low dose and titrated very slowly 1-2 weekly, because
initiation and increase in dosing may produce fluid retention due to abrupt
withdrawal of adrenergic support from heart and circulation. So better to
start and optimize the diuretic before starting BB and ACE-I.
• Combination of BB and ACE-I at lower tolerated dose is better than
individual drug at higher dose.
• Even after BB if HR remain >70 bpm or if BB is contraindicated, Ivabradin is
indicated. >>low BP, BA.

16. SGLT 2 Inhibitors
Cana-, Dapa-, Empagliflozin, ertugliflozin
• Diabetic patients are at higher risk of HF compared with healthy persons.
• Sodium Glucose Co-transportert 2 (SGLT2)- is not included in GDMT. It’s an
beneficial adjunctive to GDMT in HFrEF.
• Anti-diabetic effect, Cardio protection, anti-failure, reno-protection.
• Reduce HbA1C, Diuresis, weight reduction.
• It promotes hepatic ketones synthesis ( Beta OH buterate), that is utilized
by myocardium and kidney and preferentially Oxidized with more energy
production by less O2 consumption ( FFA oxidation needs more O2
utilization).
• Na+/H exchanger 1 (NHE-1) produce cardiomyocyte injury and decreases
mitrochondrial Ca+decrease ATP production. DM and HF patients have
higher NHE-1 level. SGLT2 inhibitor inhibits the NHE-1 .

18. Na/H+ Exchanger in myocyte
(HF & DM-express this system)-
myocyte injury, decrease mitochondrial ca+less ATP/energy.

19. Device therapy for CHF
• ICD- to prevent SCD.
• CRT-D/P.
• His bundle pacing & LB Pacing .
• Make QRS narrow and synchronize ventricular contraction.
• Slime- great looking. Wide QRS- worse prognosis-all cases.

20. NYHA II
Other
24%
CHF
12%
Sudden
death
64%
NYHA III
Sudden
death
59%
CHF
26%
Other
15%
NYHA IV
Sudden
death
33%
CHF
56%
Other
11%
N=103 N=232 N=27
N = number of deaths
MERIT-HF Study Group. Effect of Metoprolol CR/XL in chronic heart failure:
Metoprolol CR/XL randomized intervention trial in congestive heart failure (MERIT-HF). LANCET. 1999;353:2001-
07.
ICD in HFrEF
Mode of Death of Heart Failure patients.

21. Wide QRS Duration (LBBB/IVCD)
• Approximately 30-50% of patients
with HF have abnormal ventricular
contraction and mechanical
dyssynchrony. Many of them are
LBBB.
• VEST Study reported QRS duration is
an independent predictor of
mortality in patients with Class II-IV
HF
• Relative risk associated with the
widest QRS (>220ms) was 5
times greater than narrowest
(<90ms)

22. Effect of Ventricular Dyssynchrony
• Dyssynchrony produces:
 Ineffective ventricular Systole and reduced SVO => CO.
Impaired diastolic Filling/Diastolic dysfunction.
MR and TR.
In case of LBBB last segment of LV that is depolarized and contract is Lateral wall of LV
and anterolateral papillary muscle. So not only the synchronized contraction is lost but
also due to papillary muscle dysfunction variable degree of MR occurs , that further
decrease the effective SVO/CO.
Significant systolic improvement may be achieved by electrically stimulating the site of
late activation and improving the ventricular activation sequence.
Increase in LVEF from 25% to 30%, apparently seems to be 5%. But actually/absolutely it
is 20% improvement of cardiac contraction/SVO. Moreover with early lateral wall &
lateral papillary muscle contraction and LV synchronization MR also reduced , thereby
forward output increases.
•

24. Thank You