Heart Failure

 Current AHA definition of HF

 HF is a complex clinical syndrome that results from
structural or functional impairment of ventricular filling
or ejection of blood, which in turn leads to the

 cardinal clinical symptoms of dyspnea and fatigue and

signs of HF, namely edema and rales
 > 37.7 million people affected worldwide
 prevalence of HF in the adult population in
developed countries is 2%.

 In developing countries the prevalence of HF is

not known but it is increasing

 The prevalence and incidence of HF increases

steeply with age
The human heart contains four valves
Two atrioventricular valves (AV valves) between the atria and the
ventricles:
o Tricuspid valve between the right atrium and the right
ventricle.
o Mitral valve between the left atrium and the left ventricle.

Two semilunar valves:

o Aortic valve between the left ventricle and the aorta.

o Pulmonary valve between the right ventricle and the

pulmonary trunk.

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 HF broadly classified in to
 HF with depressed EF (systolic HF)
 HF with preserved EF (Diastolic HF)

 Industrialized countries
 CAD is the predominant cause , responsible for 60-70%
 HTN contributes to the development of HF in 75% of patients, including most patients
with CAD

 Developing countries
 RHD is the commonest cause
 HTN is also an important cause
 CAD incidence is rising
(1) Cardiac compensation
– increased HR and cardiac contractility
– Cardiac dilatation
– Myocardial hypertrophy
(2) Systemic compensation
– Increase the blood volume
– Redistribution of blood flow
– Increased ability of tissues to utilize oxygen
(3) Neurohormonal compensation
– Sympathetic nervous system
– Renin-angiotensin system
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 Neurohormonal Mechanisms
 Remodeling: is a process by which
mechanical, neurohormonal and possibly
genetic factors alter ventricular size,
shape and function
 Symptoms Signs
• Exercise intolerance • Cardiomegaly
• Anorexia • Peripheral edema
• Nausea (e.g., pedal edema,
• Bloating which is swelling of
feet and ankles)
• Ascites
• Jugular venous
distension (JVD)
• Hepatojugular reflex
(HJR)
• Hepatomegaly

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 Stages of HF: ACC/AHA
Stage A
High Risk for developing
Heart failure (CAD,
hypertension,
and diabetes mellitus.)

Stage B
Asymptomatic
LV dysfunction NYHA Functional Class
Class I
symptoms at activity levels that
would limit normal individuals
Stage C Class II
Past or current symptoms of HF with
ordinary exertion
Symptoms of HF Class III
symptoms of HF with less
than ordinary exertion

Stage D Class IV
End-stage HF Symptoms of HF at rest
 CBC, BUN, Cr, TROPONIN, LFT, TSH, U/A
 CXR: useful screening test: Useful for detection of cardiac
enlargement, pulmonary edema, and pleural effusions.
 ECG: To assess HR, rhythm, LVH, conduction, previous MI (Q waves)
 Echo: Used to assess LV size, valve function, pericardial effusion,
wall motion abnormalities, and ejection fraction
 BNP
 Major criteria  Minor criteria
 PND  Extremity edema
 Neck vein distension  Night cough
 +ve HJR  Exertional dyspnea
 Bibasal rales  Hepatomegaly
 Cardiomegally  Pleural effusion
 S3 gallop  Tachycardia(≥100)
 Raised JVP
 2 major or 1 major + 2 minor criteria establish
clinical DX of HF.
 DDX include:
 Renal failure
 Hypovolemic shock
 Chronic lung diseases
MANAGEMENT OF HF WITH DEPRESSED LV
FUNCTION(EF<40%)
Desired Therapeutic Outcomes

• There is no cure for HF.

• The general management goals for chronic HF include

 preventing the onset of clinical symptoms or

 reducing symptoms, preventing or reducing hospitalizations,

 slowing progression of the disease,

 Improving quality of life, and prolonging survival.

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 Treatment of underlying disease
 Correction of precepitating factors
 General measures
 Treatment of the congestive
state(management of fluid status)
 Increase myocardial contractility
 Preventing disease progression
 screen for and treat comorbidities
 advise to stop smoking and to stop or limit
alcohol consumption
 Avoid extremes of temperature and heavy
physical exertion

 Certain drugs are known to make HF worse and

should also be avoided
 immunization with influenza and pneumococcal
vaccines to prevent respiratory infections
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 Routine and modest exercise is beneficial in patients with
NYHA Class I to III HF
 Dietary restriction of sodium

 Fluid restriction is generally unnecessary unless the patient

has
 Hyponatremic (sodium less than 130 mEq/liter)
 Fluid retention that difficult to control despite high doses of
diuretics and sodium restriction

 educate the patient and family about HF, the importance

of proper diet, as well the importance of compliance with
the medical regimen
 Arterial hypertension
 Coronary heart disease
 VHD
 Congenital heart disease
 Pericardial construction
 Tachycardia
 Bradycardia
 Thyroid gland dysfunction
 Alcoholic cardiomyopathy
 Chronic anemia
 Hypertrophic cardiomyopathy
LBBB (desyncronisation)
hypertensive therapy
revascularisation (CABG, PCI)
reconstruction of the valve
sugery, ballon valvuloplasty
surgery
pharmacological therapy,
cardioversion, ablation
pacemaker therapy
euthyreosis
stopping the misuse
diagnosis and correction
resection of LVOT
resynchronisation therapy
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MANAGEMENT OF THE CONGESTIVE STATE
 Diuretics differ in their potency and
pharmacologic properties

 Fractional excretion of Na
 Loop diuretics:  by 20–25%
 Thiazide diuretics:  by only 5–10%

 Thiazides tend to lose their effectiveness in

patients with moderate or severe renal
insufficiency (creatinine >2.5 mg/dL)
 In patients who are volume overloaded, a reasonable goal is
weight reduction of 1.0 kg/day
 Duration of therapy: once begun, diuretic therapy is generally
continued indefinitely unless cardiac function improves
 subpopulation of stable patients with less severe disease who can be withdrawn from
diuretics

 No history of hypertension

 Left ventricular ejection fraction (LVEF) above 27 percent

 Have been controlled on a furosemide dose of 40 mg/day or

less
 Follow up: subjective complaint,signs of congestion,daily weight
measurement,input and output,RFT and serum electrolyte
 Electrolyte and metabolic disturbances
 Neurohormonal activation
 Hypotension and azothemia
 Ototoxicity
 Hyperuricemia
 Hypersensitivity reactions
PREVENTING DISEASE PROGRESSION
 should be used in symptomatic and asymptomatic patients
with a depressed EF (<40%).
 are corner stones in the management of HF
 All ACEIs are equaly effective

 stabilize LV remodeling, improve symptoms, reduce

hospitalization, and prolong life

 Start with low dose and titrate to the target dose used in
the clinical trials or the MAXIMUM TOLERATED DOSE

 Dose adjustement is every 1or 2wks

 Serum K, RFT 2wks after initiation then after periodically
 Hypotension
 Hyperkalemia
 Nonproductive cough (10–15% of
patients) and angioedema (1% of
patients)
 Adverse effects during pregnancy
 appear to be as or possibly slightly less effective than ACEI when
compared directly

 ARB should be used in symptomatic and asymptomatic patients

with an EF <40% who are ACE-intolerant for reasons other than
hyperkalemia or renal insufficiency

 Have the same side effect profile as that of ACEIs except for cough

 Dosage can be uptitrated every 3 to 5 days

 As with ACEIs, BP, RFT, and K levels should be reassessed within 1 -

2 wks after initiation and followed closely after changes in dose
 ßB (carvedilol, metoprolol, or bisoprolol ) reverse the
process of LV remodeling, improve patient symptoms,
prevent hospitalization, and prolong life.

 are indicated for patients with symptomatic or

asymptomatic HF and a depressed EF <40% unless
contraindicated

 Prior to initiation of therapy, the patient should have no or

minimal evidence of fluid retention and should not have
required recent intravenous inotropic therapy.

 may lead to an increase in symptoms for 4 to 10 wks

before any improvement is noted
 should be initiated in low doses followed by gradual
increments in the dose if lower doses have been well
tolerated to max tolerated doses

 If worsening fluid retention does occur, it is likely to do

so within 3–5 days of initiating therapy
 can usually be managed by increasing the dose of diuretics
 In some patients the dose of the beta blocker may have to
be reduced

 Duration of therapy: life long

 Heart rate <60 bpm
 Symptomatic hypotension
 Greater than minimal evidence of fluid
retention
 Signs of peripheral hypoperfusion
 PR interval >0.24 sec
 Second- or third-degree AV block
 History of asthma or reactive airways
 PAD with resting limb ischemia
 Worsening of HF symptoms
 Negative chronotropic effect
 Beta blocker withdrawal
 Increased air way resistance
 Exacerebation of PAD
 Facilitation of hypoglycemia
 Depression, fatigue, sexulal dysfunction
 Weight gain
 recommended for patients with
NYHA class IV or class III
(previously class IV) HF who have
a depressed EF (<35%) and are
receiving standard therapy,
including diuretics, ACE
inhibitors, and beta blockers

 in patients who had an MI within

the preceding two weeks and
who had an LVEF<= 40%
 Hyperkalemia (Aldosterone antagonists are not
recommended when the serum creatinine is >2.5 mg/dL (or
creatinine clearance is <30 mL/min) or when the serum
potassium is >5.0 mmol/l

 Painful gynecomastia may develop in 10–15%

of patients who use spironolactone
Management of Patients Who
Remain Symptomatic
 recommended as part of standard therapy in
addition to beta blockers and ACE inhibitors for
African Americans with NYHA class II–IV HF
 Considered in patients with refractory symptoms
despite standard therapy
 Death or hospitalization
 recommended for patients for worsening HF
with symptomatic LV systolic
dysfunction who have
concomitant
atrial fibrillation,
 should be considered for

patients who have signs or

symptoms of HF while All-cause
receiving standard therapy, mortality
including ACE inhibitors and
beta blockers

NEJM 1997;336:525.
 Intravenous inotrops and
vasodilators
 Hemofiltration

 Mechanical circulatory support

 Surgery

 Cardiac transplantation
 Despite the wealth of information with respect
to the evaluation and management of HFrEF,
there are no proven therapies for the
management of patients with HFpEF

 it is recommended that initial treatment

efforts should be focused, wherever possible,
on the underlying disease process
 Precipitating factors, such as tachycardia or atrial
fibrillation, should be treated as quickly as possible

 Dyspnea may be treated by

 reducing total blood volume (dietary sodium restriction and
diuretics),
 decreasing central blood volume (nitrates),

 Treatment with diuretics and nitrates should be

initiated at low doses to avoid hypotension and fatigue
 The evaluation of therapy is influenced by the ability
of treatment to successfully reduce symptoms,
decrease frequency of hospitalizations for HF, reduce
disease progression, improve quality of life and
prolong survival.
 The major outcome parameters focus on:
 (1) volume status;
 (2) exercise tolerance;
 (3) overall symptoms/quality of life;
 (4) adverse drug reactions; and
 (5) disease progression and cardiac function.
 THANK you

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