Presentation on Heart failure and its management

2. Definition
 Complex clinical syndrome that results from
structural or functional impairment of ventricular
filling or ejection of blood , which in turn leads to
cardinal clinical symptoms of dyspnea and fatigue and
signs like edema and rales

3. Epidemiology
 More than 20 million affected worldwide
 Higher incidence in men than women
 Increasing prevalence is attributed to improved
medical care for MI, valvular heart disease ,
arrhythmia pts
 RHD leads in Africa and Asia
 Chagas in south America

4. Categorisation
 HFrEF ( EF less than 40 )
 HFpEF ( EF more than 50)
 Older terminologies like systolic and diastolic heart
failure are abandoned

5. Etiology
 Any condition that alters LV function or structure can
predispose to HF
 CAD is the dominant cause
 Hypertension comes next
 CAD, HTN, DM interact to augment risk of HF

6. Etiology cont..
 Some remain without etiology, called as non ischemic
dilated or idiopathic cardiomyopathy
 Viral infection , toxins like alcohol or
chemotherapeutic agents may also lead to HF
 Genetic defects also plays a major role
 HF also associated with muscular dystrophies

7. HFrEF etiology
 CAD
 Pressure overload – HTN, Obstructive valvular lesions
 Volume overload – Regurgitant lesions, intra cardiac
and extracardiac shunting
 Cor pulmonale
 Non ischemic dilated cardiomyopathy
 Toxic
 Chronic brady and tachyarrhythmia

8. HFpEF etiology
 Aging
 Restrictive ( infiltrative and storage disorders )
 EMF
 Pathologic hypertrophy ( HOCM , SHTN )

9. High output states
 Thyrotoxicosis
 Nutritional like beriberi
 Chronic anemia
 Arteriovenous shunting

10. Prognosis
 30-40 die within 1 year
 50-70 die within years
 NYHA I-II = annual mortality of 5-10
 NYHA III-IV = 30-70

11. Pathogenesis
 Index event – damages the myocytes
 Ultimately results in declining cardiac contractility
 Pts remain asymptomatic in the initial period due to
compensatory mechanisms
RAAS
Adrenergic nervous systems
Increased cardiac contractility
Vasodilatory molecules (
ANP,BNP,PGE2,PGI2, NO)

12. Cardiac remodelling
 Transition from asymptomatic to symptomatic period
is marked by increasing compensatory mechanisms
which ends in cardiac remodeling
 Remodeling refers to changes in LV mass, shape,
volume and composition of heart
 Contributes independently to progression
 So one of the main goal for therapy for HF is prevent or
reverse remodelling

13. Mechanism of cardiac failure
 LV remodeling results in
myocyte hypertrophy
loss of contractile properties
loss of myocytes due to necrosis and apoptosis
B adrenergis desensitisation
replacement of organised matrix with interstitial
collagen

14. Clinical manifestations : symptoms
 Fatigue – due to low cardiac output
 Dyspnea – pulmonary congestion, decreased
pulmonary compliance, anemia
 Dyspnea becomes less frequent with the onset of RHF
and TR
 Orthopnea
 PND
 Cheyne stokes respiration
 Acute pulmonary edema

15. Cont…
 Anorexia, nausea, vomiting due to bowel wall edema
and congested liver
 RUQ pain due to capsule stretching
 Confusion, disorientation due to cerebral ischemia in
severe cases

16. Physical examination
 Determine the cause and severity
 Narrowed pulse pressure due to decreased stroke volume
 Cool peripheries
 Central cyanosis
 Elevated JVP
 Basal crepts ( may be absent in chronic cases due to
augmented lymphatic drainage )
 Wheeze in cardiac asthma
 Pleural effusions

17. Cont..
 Cardiomegaly
 Down and out apical impulse
 S3 , S4
 Left parasternal impulse due to RVH
 MR and TR
 Hepatomegaly ( systolic pulsation in TR )
 Jaundice
 Ascites
 Peripheral dependent edema
 Cardiac cachexia

18. ECG
 Sinus tachycardia
 Atrial arrhythmia
 QRS voltage
 QRS duration
 Low voltage complexes
 Conduction abnormalities
 QT interval

19. Diagnosis
 CBC
 RFT with electrolytes
 LFT
 Urinalysis
 FLP
 FBS,PPBS
 TFT
 ECG – assess rhythm and determine QRS width

20.  CXR - Cardiomegaly
 2D ECHO
 MRI
 Biomarkers – BNP and NT BNP ( ST2 and galectin 3 )
 Treadmill

21. DDs
 Renal failure
 ARDS
 Varicose veins

22. Cor pulmonale
 Altered RV structure or function in the context of
chronic lung disease

23. Etiology
 Parenchymal
COPD, IPF, LAM, PLCH, Cystic fibrosis
 Vasculature
PAH, CTEPH
 Hypoxia
Alveolar hypoventilation syndrome, obesity
hypoventilation syndrome, high altitude,
neuromuscular respiratory failure

24. Pathophysiology
 Development of pulmonary hypertension is the index
event
 Sustained pressure overload on RV eventually fails it
 Acute cor pulmonale – massive pulm embolus
 Chronic cor pulmonale – COPD, CF

25. Symptoms
 Dyspnea
 Orthopnea and PND are rare
 Abdominal pain and ascites
 Pedal edema

26. Signs
 Tachycardia
 Elevated JVP
 Hepatomegaly
 Pedal edema
 Prominant v in TR
 RV heave
 Carvallos sign

27. Diagnosis
 Mc cause is….. LHF
 ECG – P Pulmonale, RAD, RV hypertrophy
 Spirometry
 CT
 VQ scan for CTEPH
 2D echo
 MRI
 Rt heart catheterisation

28. Management

29. Management of HFrEF
 Initially renocentric
 Then hemodynamic
 Now disease modifying

30. ACE I and Beta
blockers are the
cornerstone

31. ACEI
 Mortality benefit
 Fluid retention can attenuate it's action, so optimise
diuretic first
 Hypotension may occur
 Start low , titrate every 3-5 days
 If hypotension develops , decrease diuretic dose if
volume overload is not seen and decrease ACEI if
volume overload is seen

32. ARB
 Used in ACEI intolerant pts

33. ARNI
 Combination of AR blocker and NEI
 Valsartan with sacubitril

34. Beta blockers
 Carvedilol, bisoprolol, sustained release metaprolol
 To be started at low dose and uptitrated slowly every 2
weeks
 Pt may develop fluid retention in the initial 3-5 days ,
increase diuretic dose during that period
 May lead to fatigue and increasing weakness
 Watch for heart block and bradycardia

35. Arteriovenous dilators
 Provides mortality benefit
 Hydralazine and nitrates
 Preferred in pts with contraindication for ACE I like
kyperkalemia

36. Heart rate modification
 Ivabradine if heart rate is more than 70/mt

37. Diuretics
 Loop diuretics preferred bcoz
 1. Higher solute diuresis 20-30%
 2. Acts even in advanced renal failure
 No mortality benefit
 Equivalent dose
 40 mg furosemide = 20 mg torsemide
 Oral bioavailability of furosemide is 40% whereas it is
80%with torsemide
 Ethacrynic acid can be used in sulfate allergy pts

38. Cont....
 Always use diuretics with neurohormonal antagonists
 Start with low dose and uptitrate to desired ECF
volume
 Only loop diuretics that is long acting is Torsemide
 Ototoxicity more with ethacrynic acid

39. Diuretic resistance
 Braking phenomenon
 Due to shorter duration of action ( except Torsemide ) ,
period of increased sodium absorption occurs
 So administer frequent doses of short acting or give long
acting drugs
 Increased sodium absorption occurs in distal tubule
which can be overcome by thiazide like diuretics
 Check for concurrent use of NSAIDs ,
thiazolidinediones, gentamicin, septran
 Don't decrease dose of loop diuretics while adding
second diuretic

40. Cont..
 Choose metalazone bcoz of its longer duration of
action, also acts in renal failure
 Continuous intravenous infusion may be tried to avoid
periods of Post diuretic salt reabsorption in
hospitalised pts
 Above said approach decreases ototoxicity, low
incidence of hypotension

41. MR antagonists
 Aldosterone breakthrough
 Start MRA when EF falls below 35 and are receiving
ACEI, diuretics, beta blockers
 Check potassium after 3 days and after 1 week and
monthly thereafter after MRA initiation,
 Contraindicated if creatinine is above 2.5, potassium is
above 5.5
 Painful Gynecomastia , go for eplerenone

42. Novel neurohumoral antagonist
 Omapatrilat – combines ACE I with neutral
endopeptodase inhibitor
 Risk of angioedema is higher with omapatrilat

43. Digoxin
 No mortality benefit
 Used as a last stand

44. Statins
 No use in nonischemic heart failure

45. Antiplatelets
 No difference between warfarin ant aspirin
 Use ASA in ischemic cardiomyopathy

46. Fish oil
 Omega 3 fatty acid improves clinical outcome

47. Microutrients
 Thiamine and selenium deficiency can affect heart
 Diuretics aggravates vit deficiency
 Not routinely recommended

48. EECP
 Reduces angina and improves exercise time

49. Thank You