1. Heart failure is defined as the inability of the heart to pump enough blood to meet the body's needs. It can occur when the heart muscle is damaged or weakened. 2. The document discusses the pathogenesis, stages, evaluation, and management of heart failure. Compensatory mechanisms initially help the heart function but eventually cause harm through remodeling if the underlying issue is not addressed. 3. Treatment involves controlling risk factors, using medications like ACE inhibitors and beta blockers, and devices like ICDs and CRT for more advanced cases. Ongoing monitoring is important as the condition can progress despite treatment.

1. HEART FAILURE -
PATHOGENESIS AND
CURRENT
MANAGEMENT
Dr Subhasish Deb
Dept. of General Medicine
Burdwan Medical College

2. Definition
 “Heart (or cardiac) failure is the
patho-physiological state in which the
heart is unable to pump blood at a
rate to commensurate with the
requirements of the metabolizing
tissues or can do so only from an
elevated filling pressure”
- Eugine Braunwald

3. Disease Burden
 Reliable estimates of heart failure are
lacking in India because of the
absence of a surveillance program to
track incidence and prevalence
 Prevalence in developed countries =
2%
 Among people over 65yr = 6-10%

4. Etiology
1.

5. 2.

6. 3.

7. CO = HR * stroke volume
Intrinsic health of
myocardium
Preload
Afterload

8. AFTERLOAD
EDV
EDV
PRELOAD
INTRINSIC ACTIVITY

9. Pathogenesis
 Described in the context of 3 phases:
1. The Index event
2. Compensatory mechanism activation
a) Advantages
b) Disadvantages
3. LV Remodeling

10. INDEX EVENT
 Anything that causes a loss of
functioning cardiac myocytes
 My be abrupt in onset (MI) or insidious
(chronic volume or pressure overload
states)
 It ultimately causes a decline in
pumping capacity of the heart

11. Compensatory mechanism
 These are activated in the presence of
cardiac injury, allowing patients to
sustain and modulate LV function for a
period of months to years

12. I. Activation of sympathetic system:
CCF decreased BP in carotid sinus
stimulation of CNS inc. sympatheic
outflow
Advantages:
1. Stimulates SA node – inc HR
2. Symp outflow acts as inotrope – inc CO
3. Adrenals stimulated – release of adrenaline –
inc HR & CO
4. Venoconstriction – inc EDV – inc stroke
volume

13. II. Activation of RAAS
Stimulus : decreased renal perfusion due
to
1. dec CO
2. inc vasoconstriction due to
sympathetic activity

15. Advantages:
1. Angio II is a venoconsrtictor – inc EDV
2. Simulates symp nerve endings
3. Acts on ZG of adrenals – aldosterone –
retension of salt and water (intinaly good)

16. 3. ADH/vasopressin release:
 Retention of water
 Veno and arteriolo constriction
4. ANP & BNP release:
 Beneficial as they counter the dangerous
effects of other compensation mechanisms.
 When more salt retained – natriuresis
 When more water retained – diuresis
 If vasoconsriction is too much – vasodilatation

17. Disadvantages of neurohumoral
activities
 If we allow the compensatory mechanisms to
go chronic, don’t correct the underlying cause
and do not correct these comp. mechanisms
pharmacologically, they bring about
disadvantages.
1. Chronic salt and water retension = chronic
preload
2. Chronic arterioloconstriction = chronic
afterload
These chronic preload and afterload cause
rmodeling of the heart

18. Remodeling
 Chronic stress causes altered genomic
expression of myocardium which starts
producing altered proteins which are not good
functionally
 Ex of altered protein : CaATPase
Calcium handling is abnormal

19. Pathophysiology in relation to
ventricular function curve
CO
EDV
5
140
In L/min
In ml
2
3
200 250
LVEF =50%
HR=72/min
A
B
C
D
A= normal
B= uncompensated
C= compensated
D= decompensated

20. Effect of drugs on ventricular
function curve
CO
EDV
5
140
In L/min
In ml
2
3
200 250
LVEF =50%
HR=72/min
A
B
C
D
inotrope
Does not ascend in the same pa
when drugs given

21. Laplace’s Law
 Pressure = Tension/Radius
 Diuretic/ACEi/ARB : radius decreases so
pressure generated inc.
 Inotrope: increases the tension so pressure in
creases.

22. Pathophysiology in a nutshell
Index event/ increased work load on heart
Activation of compensatory mechanisms
Compensated HF
Self-defeating effects of compensatory mechanisms
Decompensated HF

23. Stages of heart Failure
 NYHA classification:
I. Asymptomatic
II. Symptoms at moderate physical activity
III. Symptoms on mild activity
IV. Symptoms at rest

24. ACC/AHA stages of Heart Failure
A
Risk Factors
Risk Factors
+
Structural/
Functional
changes
Risk Factors
+
Structural/
Functional
Changes
+
Has clinical
Features / on
trearment
Very frequently
Hospitalized
And cannot be
Discharged Safely
or
Cannot wean off
From IV ionotropes
or
On mechanical assist devic
or
Waiting for heart transplant
B
C
D
SYMPTOMATIC
•HTN
•DM
•h/o Cardiotoxic drug
•Rhumatic fever
•f/o cardiomyopathy
•Wall Hypertrophy
•Fibrosis
•Dilatation
•RWMA
•Valve lesion
•Post MI
(scarred heart)
Refractory

26. AHA stages vs NYHA
1. No criteria to treat pts early (stage A)
2. NYHA is subjective so cannot be uniform
(pts tell you the symptom)
3. Cannot develop a proper prognosis
(pt on NYHA III can go to II after treatment.
But once in Stage C can never go back
to Stage B. No jumping of stages)

27.  This classification system is intended to
complement but not to replace the New York
Heart Association (NYHA) functional
classification, which primarily gauges the
severity of symptoms in patients who are in
stage C or D.

28. Management of Heart failure
1. Initial and serial evaluation of the H
2. Treatment through stages A to D
3. Acute Heart Failure

29. Initial and serial evaluation of
the HF patient
1. History and Physical Examination
2. Diagnostic tests
3. Biomarkers in ambulatory/outpatients
4. Biomarkers in hospitalized pts
5. Non invasive cardiac imaging
6. Invasive cardiac imaging

30. History and physical
examination
 Thorough history and physical exam should
be obtained/performed to identify cardiac and
non cardiac disorders
 A 3 generation family hist. in pts with idiopathic
DCM
 Assessment of volume status and vital signs
 Weight
 Peripheral edema
 JVP estimate
 Orthopnea

31. Diagnostic tests
 Initial labs:
I. CBC
II. Urine r/e
III. Electrolytes (including Ca & Mg)
IV. BUN, Cr
V. FBS, PPBS
VI. LFT
VII. Fasting lipid
VIII. TSH
Serial monitoring with electrolytes and RFT

32. Biomarkers in
ambulatory/outpatients
 BNP and NT-proBNP for supporting clinical
decision making regarding diagnosis
 BNP and NT-proBNP for prognosis

33. Biomarkers in
Acute/Hospitalized
 BNP and NT-proBNP for supporting clinical
decision making regarding diagnosis
 BNP and NT-proBNP for prognosis

36. Non invasive cardiac imaging
 CXR to assess cardiac size, pulmonary
congestion and to detect other cardiac or non
cardiac disease
 2D echo with doppler to asses:
1. EF
2. Wall thickness
3. Wall motion
4. Valve function
 Repeat measurement of EF in:
1. HF pts with significant change in clinical status
2. Who have recovered from a clinical event

38. Invasive cardiac imaging
 Invasive hemodynamic monitoring with
pulmonary artery catheter should be
performed to guide therapy in patients who
have reparatory distress or clinical evidence of
impaired perfusion in whom adequacy or
excess of intracardiac filling pressure cannot
be determined from clinical assessment

40. Management of Heart failure
1. Initial and serial evaluation of the HF p
2. Treatment through stages A to D
3. Acute Heart Failure

42. STAGE A
 Htn and lipids should be managed as per
contemporary guidelines
 Other risk factors such as DM, tobacco
smoking, obesity, cardiotoxic agents should be
controlled or avoided

43. STAGE B
 Pts with recent or remote h/o of MI or ACS and
reduced Ef, ACEi should be used to prevent
symptomatic HF and reduced mortality
 For all pts. with a recent or old h/o of MI or
ACS and reduced EF, evidence based beta
blockers should be used to reduce mortality
 For all pts. with a recent or old h/o of MI or
ACS statins should be used to reduce
symptomatic HF and cardiovascular events

44.  In patients with structural cardiac
abnormalities, including LV hypertrophy, in the
absence of a history of MI or ACS, blood
pressure should be controlled in accordance
with clinical practice guidelines for
hypertension to prevent symptomatic HF
 ACE inhibitors should be used in all patients
with a reduced EF to prevent symptomatic HF,
even if they do not have a history of MI
 Beta blockers should be used in all patients
with a reduced EF to prevent symptomatic HF,
even if they do not have a history of MI

46. STAGE C – Non pharmacological
t/t

51. Device therapy in HFrEF
 ICD for primary prevention of SCD in
1. HFrEF, 40 days post MI
2. NYHA class II or III
3. LVEF <= 35%
4. On chronic GDMT and expected to live >1 yr
 ICD for primary prevention of SCD in
1. HFrEF, 40 days post MI
2. NYHA class I
3. LVEF <=30%
4. On chronic GDMT and expected to live >1 yr

52. Sudden Cardiac Death
 Sudden cardiac death (SCD) is an
unexpected death due to cardiac causes that
occurs in a short time period (generally within
1 hour of symptom onset) in a person with
known or unknown cardiac disease.

53. Implantable Cardiac Defibrillator
 ICD keeps track of each beat
 If heart goes into a fast rhythm
which is potentially life
threatening -- SHOCK

54. Cardiac Resynchronization
therapy
BACKGROUND:
 Approx 25% pts with CHF have
intraventricular conduction delay; commonly
LBBB
 Electrical activation of lateral aspect of LV can
be delayed in relation to that of RV and/or IV
septum
 This results in:
1. Dyssynchronous electrical activation and contraction
2. Unequal distribution of myocardial work load
3. Altered myocardial blood flow and metabolism

55. Lateral view X-ray of 1st successful
cardiac resynchronization therapy
University hospital of Rennes, 1994

56.  Simultaneous pacing of
RV & LV = BIVENTRICULAR
PACING
 Leads in RA, RV & LV
 LV paced via coronary
sinus

59. Stage D
 A subset of patients with chronic HF will
continue to progress and develop persistently
severe symptoms despite maximum GDMT.
 Various terminologies have been used to
describe this group of patients who are
classified with ACCF/AHA stage D HF,
including “advanced HF,” “end-stage HF,” and
“refractory HF.”

60.  In the 2009 ACCF/AHA HF guideline, stage D
was defined as “patients with truly refractory
HF who might be eligible for specialized,
advanced treatment strategies, such as MCS,
procedures to facilitate fluid removal,
continuous inotropic infusions, or cardiac
transplantation or other innovative or
experimental surgical procedures

62.  Fluid restriction (1.5 to 2 L/d) is
reasonable in stage D, especially in
patients with hyponatremia, to reduce
congestive symptoms.

63.  Ionotropes:
Until definitive therapy (eg, coronary
revascularization, 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.

64.  Cardiac transplant:
Evaluation for cardiac transplantation is
indicated for carefully selected patients with
stage D HF despite GDMT, device, and
surgical management

65. Management of Heart failure
1. Initial and serial evaluation of the HF p
2. Treatment through stages A to D
3. Acute Heart Failure

66. ACUTE HEART
FAILURE
ESC guidelines for diagnosis and treatment of acute

67.  AHF Definition:
Rapid onset or change in signs and symptoms
of heart failure, resulting in the need of urgent
therapy.
 It may present as new HF or worsening HF in
presence of chronic HF

72. Diuretic tit-bits
 Bumetanide – most potent
 Torsemide – longest T ½ (24 hr action)
 Drug interactions:
1. Thiazide/loop diuretic with Digitalis –
hypokalemia casing digitalis toxicity
2. ACEi with spironolactone – hyperkalemia can
cause cardiac arrest in diastole.
(*hypercalcemia causes cardiac arrest in
systole)
3. loop diuretic with aminogylcoside – ototoxicity
 Spironolactone in HF heart failure (provided

74. Some new drugs in HF
management
 Nesiritide:
 Synthetic form of BNP
 Causes natriuresis and diuresis
 Rapidly metabolized by vasopeptidase (a neutral
endopeptidase) thus given in infusion
 Carperitide:
 ANP analogue
 Uralitide:
 Analogue of Urodilatin which is a peptide like ANP
and BNP

75.  Ompatrilat & Sampatrilat:
 Inhibits neutral endopeptidase
 Also inhibits ACE
 Levosimendan & Pimobendan:
 Ca sensitisers
 Has phosphodiesterase III blocking property
(levosimendan)
 Isteroxine:
 Na K atpase pump (like digitalis)

76.  Cinacigaut:
 Nitrates act by stimulating guanyl cyclase to
produce NO for vasodilatation
 In guanyl cyclase resistant people direct
stimulaton by this compound
 Aka Bay compounds

78.  studied in 12 patients with severe congestive heart failure and
compared with those of dopamine in 10 clinically similar patients.
Dobutamine produced a distinct increase in cardiac index, while
lowering left ventricular end-diastolic pressure and leaving mean
aortic pressure unchanged. Dopamine also significantly improved
cardiac index, but at the expense of a greater increase in heart rate
than occurred with dobutamine.
 Because it has comparatively little effect on heart rate and aortic
pressure, both major determinants of myocardial oxygen
consumption, it may be of special value in patients with the low
output syndrome associated with coronary heart disease

80. THANK YOU