Heart failure

1. HEART FAILURE
PRESENTED BY:
Dr. Pratibha Bansal
3rd Year Junior Resident
General Medicine
Dr. S. N. Medical College
Jodhpur
GUIDED BY:
Dr. Manoj Lakhotia Sir
Senior Professor and Unit Head
General Medicine
Dr. S. N. Medical College
Jodhpur

2. DEFINITION:
It is a complex clinical syndrome secondary to:
1. Structural/ functional abnormality of heart, which impairs
2. Ventricular filling/ ejection of blood,
which leads to cardinal
1. symptoms (dyspnea, fatigue)
2. Signs (crepts; edema)
3. At rest/exertion
Congestive Heart Failure << Heart Failure : Not all patients present with
symptom/signs of volume overload.

3. EPIDEMIOLOGY
1. HF is global pandemic affecting at least 26 million people worldwide1 .
2. The estimated prevalence of HF in India is said to be approx 1% of population, i.e. 8-10
million. The estimated attributable mortality is 0.1 - 0.16 million people per year.2
3. HF prevalence follows exponential pattern ,rises with age and affects 6-10%of people
aged >65 years.
4. Relative incidence of HF is lower in women than that in men , but women constitute at
least 50%of cases of HF because of longer life expectancy.
References:
1. Savarese G, Lund LH. Global public health burden of heart failure. Cardiac failure review. 2017;3(1):7.
2. Chaturvedi V, Parakh N, Seth S, Bhargava B, Ramakrishnan S, Roy A, Saxena A et.al. Heart failure in India: the INDUS (INDia ukieri study)
study. Journal of the Practice of Cardiovascular Sciences. 2016;2(1):28-35.

4. TYPES and CLASSIFICATION
1. Low vs. High output: Based on Stroke Volume and Cardiac Output
2. Left (pulmonary edema) vs. Right (raised JVP, hepatomegaly,pedal edema)
3. Backward (increased filling pressures) vs. Forward (impaired systemic
perfusion)
4. Systolic (impaired expulsion) vs. Diastolic (impaired filling)
5. Left Ventricular Ejection Fraction (Preserved [EF > 50%] vs. Mildly reduced
[EF= 40-49%] vs. Reduced [EF <40%]. Both systolic and diastolic dysfunction
can occur regardless of EF.
6. Functional Classification (NYHA, METS)

5. NYHA and METS Classification: (SOB/ Palpitation/ Fatigue)
NYHA
CLAS
S
SYMPTOMS ON ORDINARY
PHYSICAL ACTIVITY
METS ACTIVITY
1 NO >/= 7 Walk (8 kmph)/ jog/ bicycle
one flight of stairs with bag of groceries
2 SLIGHT 5-7 Walk (6.5 kmph)
Dance
One flight of stairs without stopping
3 MARKED 2-5 Walk (4 kmph)
shower/ dressing/making bed without a break
4 UNABLE TO CARRY OUT ANY
ACTIVITY WITHOUT
DISCOMFORT + SYMPTOMS
AT REST
<2 At rest

6. ETIOLOGY
HFrEF
CAD
Myocardial Ischaemia/ Infarction
Chronic Pressure Overload
HTN/ AS/ PS
Chronic Volume Overload
MR/ TR; AR; left to right shunts, PDA
Chronic Lung Disease Cor Pulmonale, Pulmonary vascular disorders
Dilated Cardiomyopathy (Non Ischaemic) Genetic/ Infiltrative/ Toxic/ Metabolic/ Viral/ Chagas
Rate, Rhythm disorders Chronic Bradyarrythmias, Chronic Tachyarrythmias
HFpEF HYPERTROPHY HOCM/ HTN
Aging
RESTRICTIVE Amyloidosis, Sarcoidosis; Hemochromatosis
Fibrosis
High
Output
Metabolic ; Nutritional Thyrotoxicosis; Beri Beri (Thiamine deficiency)
Excessive Flow Requirement Chronic Anaemia, Pregnancy, AV fistula (CKD)

7. PATHOGENESIS
1. Index event causes initial
decline in heart’s pumping
activity.
2. Compensatory mechanisms
get activated (RAAS,
Sympathetic system, cytokine
system)
3. Restore cardiac function in
normal range, but sustained
activation of these lead to
ventricular remodeling and
subsequent cardiac
decompensation.

8. Role of Various Drugs
(kidney)
(liver)
(lung)
1. ACE i
2. ARB
3. ARNi
4. Beta Blocker
5. MRA (DCT)
1. Natriuresis
2. Diuresis

9. SYMPTOMS - SIGNS
SYMPTOMS SIGNS
Dyspnea
Nocturnal cough
Wheezing
PND
Orthopnea
Exercise Intolerance
Peripheral Edema
Weight Gain (>2kg/wk)
Weight Loss (Advanced)
Loss of
apettite(congestion/inflam)
RUQ pain
Palpitation
Syncope
GPE:
Cachexia, peripheral edema, JVD (JVP>10-12 cm H2O = PCWP>22 mm Hg),
hepatojuglar reflux (>3cm for >15s, 40mmHg, frank starling), cold extremities
VITALS:
BP- hypotension, orthostatic hypotention(>20/10 mm Hg in 3 min)
PULSE- tachycardia, narrow PP (Prop. PP= PP/SBP <25% = CI <2.2L/min/m2
bsa), pulsus alternans
RESPIRATION: tachypnoea, cheyne-stokes (apnea= incr pCO2= sensitive respi
centres= wax= washout= waning)
CVS:
Lateralized apex(>10cm from mid-sternal), left parasternal heave, soft S1, S3
(volume overload)/S4 (atrial contr) gallop, fxnl murmurs (MR,AR- annular
dilate), loud P2
RESPI:
wheeze, crepts,reduced air entry at lung bases (pleural effusion)
PA:
Hepatomegaly, ascites

10. Chest X-RAY
1. Cardiomegaly (cardio-thoracic ratio >55%)
2. Cephalization of pulmonary markings
3. Kerley B lines (perpendicular to pleura,
subpleural interlobular septa, 1-2 cm long,
<1mm in diameter);
C (modified/ antero-posterior B lines);
D (C lines in lateral chest X-ray)
1. Pulmonary Edema
2. Pleural Effusion / Fissural effusion

11. ECG
1. CAD
2. LVH/ LAE
3. Heart Blocks
4. Low Voltage

12. USG (high NPV, PPV)
1. B lines (at least 3 lines, 2 different zones , per lung)
2. Pleural Effusion
A line (Horizontal) B line (vertical, complete)

13. NT Pro BNP
1. It is currently considered to be Trop-I of Heart Failure.
2. High sensitivity (>95%), high NPV (>94%). It helps excluding heart failure.
3. Falsely elevated levels: (less specificity)
a. Cardiac- ACS, Muscle disease (Cardiomyopathy/ LVH/ myocarditis), Valvular/ Congenital HD,
Pericardial disease, Atrial Fibrillation, Cardioversion, Trauma to Heart, Cardiac Surgery, Chemotherapy.
b. Non- Cardiac- Age, anaemia, bacterial sepsis, burns, critical illness, COPD, pulmonary embolism, PAH,
OSA, severe pneumonia, Subarachnoid hemorrhage,Stroke, Liver failure
4. Falsely decreased levels: Obesity
5. BNP levels are affected by ARNi, but not NT-PRO BNP.
6. Prognostic if BNP >1000 or doesn’t decrease by >30% in patients with ADHF at time of
discharge. (high mortality/ re-hospitalization)

14. 2D-ECHO
1. Systolic dysfxn:
a. Increase chamber size
b. Decrease EF
i. Qualitative method : E point septal separation (PLAX view)
● (E wave- anterior MV motion during rapid filling phase)
● (A wave- anterior MV motion during atrial systole)
EPSS : Distance of E point from IVS >10mm (n<7mm)
ii. Fractional Endocardial Shortening: (PLAX view, just below mitral valve). LV cavity is viewed in end of diastole and
systole. (Female= 27-45%; Male= 25-43%), poor estimation.
iii. Simson’s Biplane method: Reasonably Accurate, apical 4 chamber view (Normal EF: Female= 54-74%, Male= 52-
72%)
EF = EDV- ESV X 100
EDV
EDV= End diastolic volume
ESV= End systolic volume

15. 1. Diastolic Dysfunction:
a. Hypertrophy : PLAX view
FEMALE MALE
LV internal volume (Diastole) 38-52mm 42-58mm
LV internal volume (Systole) 22-35mm 25-40mm
IVS/ Posterior Wall 6-9mm 6-10mm
B. Altered E/A ratio (abnormal mitral inflow):
Apical 4 chamber view
Doppler waves are send in pulses across mitral
valve, to check the inflow of blood.

16. 1. E> A (rapid filling > filling by atrial contraction)
1. E<A (imapired; increase LV filling pressure
causing impaired filling during Rapid filling phase.
Hence, atria has to contract forcefully)
2. E>A (pseudonormal; decreased LV filling causes
more blood in atria, thus in rapid filling phase,
even more blood gushes to LV)
3. E>>A (restrictive)

17. TDI: Tissue Doppler Imaging (to d/d between cases of E>A)
1. e’ > a’ (e’ speed >8 cm/s)
1. e’ < a’ (e’ is variable)
1. e’ << a’ (e’ <8 cm/s)
4. e’ <<< a’ (as the LV filling pressure rise, atrial pressure
rise. Filling of ventricles may fail but leaflets get pushed
progressively forcefully)
Mitral valve leaflet moves up, toward LV base (i.e. away from doppler probe, hence,
negative deflections)

18. E/e’ (Mitral inflow - TDI)
Diastolic Function E/e’
Normal <9
Impaired <9
Pseudo-Normal 9-15
Restrictive >15

19. OTHERS
1. PCWP (Gold std for PAH)
● Mean Pul artery pressure >25mm Hg = PAH;
● If PCWP (pulm. capillary wedge pressure) >18mm Hg = LVF is cause)
1. Cardiac MRI (d/d ischaemic vs. non-ischaemic cause)
1. Coronary Angiography (ischaemic causes)

20. DIAGNOSIS
SUSPECTED HF
● Risk Factor
● Symptom - Signs
● Abnormal ECG
● Abnormal CXR
NT-PRO BNP > 125pg/ml
BNP > 35 pg/ml
2D- ECHO
May Not be Available
HF less likely
● Renal Failure
● Non Cardiac
Pulmonary
Edema
● Chronic Lung
Disease
● Obesity
HF confirmed
HFpEF
* LVEF>/= 50%
* Evidence of
Spontaneous/
provokable increased
LV filling pressures
HFmrEF
* LVEF = 40-49%
* Evidence of
Spontaneous/
provokable increased
LV filling pressures
HFrEF [EF < 40%]
HFimEF
Previous HFrEF, now
with EF>40%

21. OBJECTIVE EVIDENCE:
1. LV mass index:
● Female >/= 95 g per m2 BSA,
● Male >/= 115 per m2 BSA
1. Relative wall thickness >/= 0.42
RWT = IVS + PW
LV iD
1. LA volume index >34 ml per m2 BSA
2. E/ e’ > 9
3. PASP > 35 mm Hg
4. BNP/ NT PRO BNP levels:
BNP (pg/ml) NT-PRO BNP (pg/ml)
Sinus Rhythm > 35 >125
AF >105 > 365

22. STAGES OF HEART FAILURE
A (AT RISK) B (PRE- HF) C (SYMPTOMATIC) D (ADVANCED)
● HTN
● Diabetes
● Obesity
● CVD
● Genetic Variant/
Family History of
Cardiomyopathy
No previous/ current
symptom/ sign of HF, but
evidence of:
● Structural heart
disease
● Raised LV filling
pressures
● Persistently
elevated Trop-I/ NT
Pro-BNP level.
Structural heart disease
Previous/ New
Symptom / sign of heart
failure
Marked Symptoms of HF, which
despite of optimizing guideline directed
medical therapy (GDMT), interferes with
daily life activity and cause recurrent
hospitalizations.
New Onset/ De Novo Newly diagnosed
Persistent Ongoing signs/symptoms/ limiting functional capacity
Worsening Worsening sign/symptom/ functional capacity
Resolution Previous HF, now with lesser LV dysfxn / full resolution of
sign/symptom/functional capacity (REMISSION)

23. GOALS OF THERAPY IN HF
● Decrease Symptoms
● Decreasd HF related Hospital admissions
● Decreased HF related Mortality
Out of available treatment strategies, mortality can only be reduced in patients with HFrEF.

24. MANAGEMENT OF STAGES OF HEART FAILURE

25. STAGE THERAPY RECOMMENDED COMMENTS
A AT RISK 1. Manage Risk Factors (HTN/DM/Dyslipidemia)
2. Stop Smoking, Exercise, Reduce weight, Alcohol
moderation
3. BNP Screening
4. Genetic screening
5. Risk assessment Score for risk of developing HF
1. For HTN:
● AHA/ACC target: 130/80 mmHg
● ESC/ ESH target: <65 yr (130/80 mm Hg),
>65yr (140/90 mm Hg)
● Use of ACEI/ BB/ MRA is better as 1st line
as benefit in HFrEF too.
2. For DM:
● Prefer SGLT-2i as benefit as follows:
- Empa = reduce MACE (HFH+CV >> HFH >
CV mortality) [EMPEROR PRESERVED]
- Dapa = reduce mortality if HFrEF happens
- IV Liraglutide reduce MACE
3. Framingham HF risk Score (1998), Pool Cohort
Equations to prevent HF (PCP-HF) (2019)
B PRE 1. AS PER STAGE A
2. ACEI /ARB
3. BETA BLOCKER (IF EF <40% +/- MI/ACS)
4. STATINS (if MI/ ACS)
5. ICD (if after 40 day of MI, patient is still asymptomatic
with EF less than 30%)
1. Beta Blocker reduce mortality and improve
symptoms both.
2. Pioglitazone, Verapamil (non-DHP CCB)
are contraindicated if EF<50%
3. ICD to reduce SCD and overall mortality

26. C
SYMPTOMATIC
1. Low Sodium Diet
2. Fluid Restriction
3. Diuretics (Loop +/- Thiazide)
IF HFrEF: GDMT
IF HFmrEF : Largely unknown. Diuretics
recommended.Similar to HFrEF
IF HFpEF : Largely unknown. For decrease
hospitalization:
1. SGLT-2 inhibitors
2. Spironolactone if EF < 55% [TOPCAT]
3. ARNi if EF < 57% [PARAGON HF]
4. Diuretics
1. <2g/day sodium;
2. <2L/ day esp. If hyponatremia/ congestion.
3. Exercise if ambulatory
4. Vaccination (Influenza, Pneumococcal)
5. Avoid in HFrEF:
● NSAIDs salt-water retention in asc. LOH,
poor response to diuretics,
● Pioglitazone (possible ccb action, salt
water retension);
● Non-DHP CCB, Dronedarone (negative
inotrope);
● Anti arrhythmics( sotalol, flecainide,
disopyramide) as pro arrhyhtmics;
● A- blockers (unopposed beta -1 causes
increased RAAS),
● Saxagliptin,Alogliptin
D
ADVANCED
1. As in stage A-C
2. IV ionotrops
3. Ventricle Assisting Devices
4. End of life care

28. ARNi (angiotensin receptor/neprilysin inhibitor)
Recommendation:
1. Use in place of ACEi at initiation
2. Shift from ACEi to ARNi if patient is affordable
3. Sacubitril/valsartan is the first agent to be approved.
4.Higher doses are more efficacious to reduce mortality. So, start from low dose —--> maximum
tolerable doses.
PARADIGM (2014,
SacuValsa vs. Enalapril)
Monitoring/ SE:
1. Hypotension
2. Incessant cough/ angioedema (High Bradykinnin level)
3. Rise in Creatinine
4. Hyperkalemia

29. Doses for ARNi

30. BETA BLOCKERS
RECOMMENDATION
1.Initiation: if patient is dry.
2. Continuation in acute decompensation, unless hemodynamic stability or need for inotropes.
As, if removed suddenly, unopposed sympathetic activity can lead to tachycardia and arrhythmias.
3. Reduce Hospitalization and Mortality both.
CIBIS - BISOPROLOL
MERT HF - METOPROLOL
COPERNICUS - CARVEDILOL
COMET - CARVEDILOL > METOPROLOL
(non selective; alpha+ beta (1+2). So,not in COPD
SE:
1. BRADYCARDIA
2. BRONCHOCONSTRICTION (in non- selective for beta-2)

31. BETA BLOCKERS

32. MRA (Mineralocorticoid Receptor
Antagonist)
RECOMMENDATION
1. Initiation needs : Serum Creatinine <2.5 mg/dl ; K+ < 5.
2. Both equally efficacious.
3. Less side effects by Eplerenone (no anti androgenic action. So, no gynaecomastia/ loss of
libido) as in Spironolatone (anti androgenic action). But spironolactone is cheap.
4. Reduce Hospitalization and Mortality both.
5. For mortality benefits, K+ sparer diuretics > K+ depletors (SOLVD)
RALES - SPIRONOLACTONE
EMPHASIS HF - EPLERENONE
SE:
1. Hyperkalemia (K+ check = 3rd , 7th, monthly for at least 3 months, every 3 months); new monitoring
cycle if high dose/ new ARNi/ ACE-I/ ARB/ MRA used.
2. Gynanaecomastia
3. Loss of libido

33. MRA (Mineralocorticoid Receptor Antagonist)

34. SGLT - 2 INHIBITORS
RECOMMENDATION
1. Creatinine clearance >30 ml/min
(Dapagliflozin), >20ml/min
(Empagliflozin)
2. Beneficial in patients even without
diabetes.
3. Reduce Hospitalization and
Mortality both.
EMPEROR - EMPAGLIFLOZIN (even without DM)
DAPA HF - DAPAGLIFLOZIN
SE:
1. Euglycemic Ketosis (as mild dehydration and glucosuria)
2. UTI/ Genital tract infections (as glucosuria)
MOA: Reduce glucose REABSORPTION from PCT.

35. SGLT - 2 INHIBITORS

36. DIURETICS (all other than MRA)
RECOMMENDATION
1. Indicated in all patient with congestion
2. Tolvaptan only if HYPONATREMIA (no benefit : EVEREST)
3. Loop +/- thiazide +/- eNaC inhibitors
4. Reduce symptoms, Hospitalization, increases excercise tolerance.
5. No mortality benefit.
SE:
1. Hypokalemia
2. Hyponatremia (in excessive doses)

37. DIURETICS

38. ARB (Angiotensin receptor
Blocker)
RECOMMENDATION
1. Use if ARNi/ACEi not tolerated (incessant cough) and patient is receiving beta blockers.
2. Higher doses are more efficacious.
SE:
1. Rise in serum creatinine
2. Hyperkalemia
CHARM - Alternative - CANDESARTAN
Val - HEFT - ACEi = ARB

39. ARB

40. H- ISDN (Hydralazine- ISDN) [ISOLAZINE]
RECOMMENDATION
(Class- 2A)
1. Response to ACEi/ ARB is suboptimal in blacks. H-ISDN shows better results.
2. If HFrEF who is already on ACEi + BB + MRA; but still NYHA 3 or 4. And (EF </= 35% or EF < 45% with dilated LV).
(Class - 2 B)
1. If HFrEF who is already on ACEi + BB + MRA; but refractory hyperkalemia cause discontinuation of (ACEi/ ARB/ MRA)
SE:
1. Reflex tachycardia (as reduce blood pressure- Baroreceptor Reflex) -> angina/ ACS
2. Headache/ flushing
V- HeFT ½
A- HeFT
MOA: Hydralazine: decrease afterload by arteriolo-dilatation (decreased systemic vascular resistance). Hence
improved stroke volume and cardiac output. This occurs by 3 mechanisms:
1. K+ channel opening —> Hyperpolarization of smooth muscle —> No action potential
2. Inhibit IP-3 induced Ca2+ release —> no contraction of vessel smooth muscle
3. Increase NO bioavailability (given by ISDN), and thus, cGMP mediated vasodilation.

41. H- ISDN (Hydralazine- ISDN)

42. IVABRADINE
RECOMMENDATION (Class- 2)
1. EF <35%
2. HR >70 bpm
3. Sinus Rhythm
4. On maximum beta blocker dose / not tolerating
beta blocker
5. Also receiving ACEi/ARNi + MRA already.
6. Decreases hospitalization and mortality.
7. Target HR =50- 60 bpm
SE:
1. Bradycardia/ Sinus arrest/ heart blocks. Esp. if used with Verpamil/ Diltiazem as they are CYP 3A4 inhibitors.
2. Atrial fibrillation
3. Visual effects (phosphenes), Rash, Fetal toxicity
SHIFT - IVABRADINE
MOA: Blocks funny Na+ current channels (If )of PHASE-4, slowing down the spontaneous depolarization.

43. IVABRADINE
● Titrate up by 2.5mg BD

44. DIGOXIN
RECOMMENDATION (Class 2)
1. Consider if AF in HFrEF.
2. Caution if: Age>70, Hypokalemia, Hypomagnesemia
(increase toxicity)
3. Maintain serum level <1.2 ng/ml (0.5 - 0.9 ideally)
4. Reduce symptoms and hospitalization.
5. No effect on Mortality.
SE:
1. Angina/ ACS (as increase contractility)
2. AV blocks (Vagal stimulation to AV node)
DIG
MOA: Inhibit Na+- K+ ATPase. So, Na+- Ca2+ exchanger brings more Ca2+ in. More contraction.

45. DIGOXIN

46. sGC+ (soluble guanine cyclase stimulator)
RECOMMENDATION (Class 2B)
1. If with use of 4 first line agents, patient is still symptomatic (NYHA 3,4 class)
SE:
1. Hypotension ( as vessels relax)
2. Headache, nausea, vomitings
VICTORIA - VERICIGUAT
MOA: Soluble guanine cyclase (cGMP) helps in smooth muscle relaxation. Stimulating this
pathway increase cGMP and its sensitivity to nitrates.

47. sGC INHIBITORS (soluble guanine cyclase inhibitor)
Available in India: By Bayer Zydus , cost approx
Rs.130 per tablet

48. AF
1. Rate control non inferior to rhythm control. Use beta blockers > digoxin/amiodarone
(slight risk of rhythm reversal)
2. CRT : If for rate control, ablation of AV node with ventricular pacing is being planned, its
better to go for CRT.
3. Rhythm control: [Class 2A] if severe symptoms or reversible cause. Use amiodarone/
external cardioversion with pulmonary vein isolation.
4. Anticoagulation: Direct Oral anticoagulants > Vit. K antagonist [except mod - severe
MS or metallic prosthetic valves.
CARE-HF Companion
RAFT-MADIT-CRT
ANTICOAGULATION: Not indicated unless AF/ Thrombus. [WARCEF - WARFARIN]

49. IV FERROUS CARBOXYMALTOSE
RECOMMENDATION (Class 2A) - reduces symptoms, hospitalization
1. EF < 50% (in hospitalised patient) / EF < 45% (in ambulatory patient) with Iron Deficiency:
● Ferritin <100 ug/L
● Ferritin 100-299 ug/L with transferrin saturation < 20%
Benefit of IV Iron : FAIR- HF, CONFIRM-
HF , EFFECT - HF , AFFIRM - HF
RED HF - No benefit of EPO
MOA: Oxygen delivery to cardiac myocytes is better as it is myoglobin based.

50. ICD (Implantable cardioverter defibrillator)
SCD-HeFT
MADIT II
Reduction of Sudden Cardiac Death due to arrythmias.
PREVENTION SUBCLASS RECOMMENDATION
Secondary
● includes VT/ VF > 48 hr of MI
● Life expectancy > 1 year
● Cause of arrhythmia is
irreversible
CLASS 1
Primary
● symptomatic even after
optimum medical management
and EF < 35%
NYHA class 2,3 Ischaemic cause (CLASS 1)
[ except MI <48hr]
Non - ischaemic (CLASS 2A)
NYHA class 4 Not indicated (as progressive heart failure is
itself a cause of mortality) except if patient is a
candidate for heart transplant.

51. CRT (Cardiac Resynchronisation Therapy)
1. Patient symptomatic even after optimum medical management with EF </= 35%
CARE- HF - Companion
RAFT MADIT II - CRT
MOA: Reduces electrical and mechanical heterogeneity among myocytes of failing heart.
QRS LENGTH SINUS RHYTHM with RECOMMENDATION
>/= 150 ms LBBB CLASS 1
Non LBBB CLASS 2A
130 - 149 ms LBBB CLASS 2A
Non LBBB CLASS 2B
2. Regardless of QRS duration, if a patient of EF </= 35% has a higher degree AV blocks/ AF needing pacing
with or already having RV pacing, PERFORM/ UPGRADE to CRT.
COMPLICATIONS: pneumothorax, pocket hematoma, infection, lead migration, coronary artery dissection

52. HFrEF
1.ACEi /ARNi /ARB
2. Beta blocker
3. Mineralocorticoid receptor
antagonist
4. SGLT2 Inhibitors
5. Diuretics
If still symptomatic
NYHA CLASS II, III, IV

53. EF < 35% but no
indication for device
therapy
EF<35% EF<35% WITH BROAD
QRS COMPLEX
(CRT)
QRS<130ms
CRT not indicated
Class II
recommendatio
n
c IC
D
Primary
Secondar
y
IIA
H-ISDN
IIB
* Digoxin
* Ivabradine
* sGC
inhibitor
QRS 130-
149 ms
QRS>150
ms
LBBB IIA
NON
LBBB
IIB LBBB I
NON LBBB IIA

54. THANK YOU