2. Congestive heart failure by Dawit.pptx

Objectives
 Definition
 Epidemiology
 Forms of HF
 Causes
 Pathophysiology
 C/F, evaluation,
 severity classification
 Investigation
 Management
 Prognosis
Heart Failure(Dr. Dawit)

DEFINITION —
Heart failure (HF) is a complex clinical syndrome that can
result from any structural or functional cardiac disorder (of an
inherited or acquired) that impairs the ability of the ventricle
(heart) to fill with or eject blood.
The final pathway for myriad (many) disease that affect the heart.
It is characterized by specific symptoms, such as dyspnoea
and fatigue, and signs, such as those related to fluid
retention(edema and rales).
There are many ways to assess cardiac function.
However, there is no diagnostic test for HF, since it is
largely a clinical dx that is based upon a careful hx & P/E.

Heart Failure
• ~ is a clinical syndrome which develops and progresses
with time resulting in failure of the heart to function
adequately.
• Could be acute or chronic (with 2 phases Sx & Asx)
• The development and disease progression of HF has 4
different stages
( Risk ----- Refractory HF )( Stage A, B,C D)
• The disease progression
• Could be fast or slow
• can be slowed or stopped by Rx
• may reverse spontaneously

Epidemiology
HF is
• Common
• costly
• disabling
• fatal (potentially)
Eg. In USA
• Prevalence 5 million pt
• Incidence 0.55 mill/yr
• Death 0.05 mill/yr
• 1-3 mill admissions /yr
• $ 28 bill /yr

Epidemiology
• A major public health problem in industrialized nations.
• US – ~ 5 million have HF & >55,000 Dxed for 1st
time each year
- HF is responsible for ~1 million hospital
admissions & 50,000 deaths annually.
• More in elderly (incidence ~1% of popn, 20% of all hospital
admissions in >65yrs of age, ~ 80% of hospitalizn for HF) ;
likely to increase as Popn. ages.

Epidem. Cont.
 5 years survival rate of less than 40% from the
time of diagnosis
 Higher mortality in the African-American
population, people over 65 yrs
 Once symptomatic at rest, 1-yr mortality of
50%
 In those with symptoms at rest and CAD, 1 and
3 yrs survival of 43% and 18%
Ethiopia: 3.7% of MICU admission
and
3.6% of total deaths (case fatality
ratio of 30.5% [ 40 of 131 CHF

Nearly any form of heart disease may ultimately
lead to the HF syndrome
The clinical syndrome may result from disorders of
the pericardium, myocardium, endocardium, valves
or great vessels, but many of the symptoms are
caused by LV dysfunction.
• LV dysfunction is wide in spectrum
• EF reduction
• Dilated LV size
• Systolic/diastolic dysfunction

Heart Failure as a Symptomatic Disorder
 The degree of functional limitation imposed
by HF is quantified (graded) 1 to 4
functional classes, first by NYHA -
depending on the degree of effort needed to
elicit symptoms:
 Class I - Sxs on ‘vigorous’ exertion as normal
person
 Class II - Sxs on ordinary activities
 Class III - Sxs on < ordinary activities
 Class IV - Sxs a rest
 be associated with a wide spectrum of LV
functional abnormalities,

Left Ventricular Dysfunction
• Begins with injury to or stress on the myocardium
• Is generally a progressive process
• The progression is mainly manifestation by a change in the
geometry and structure of the LV, such that
• the chamber dilates and/or
• hypertrophies and
• becomes more spherical—a process referred to as Cardiac
Remodeling.
↓
↑Hemodynamic stresses on the walls of the failing heart
Depresses its mechanical performance and
Regurgitant flow through the mitral valve.
↓
Sustain and exacerbate the remodeling process.
↓
Appearance and worsening of Symptoms
(HF)

Factors affecting Cardiac Remodeling
• Activation of endogenous neuro-hormonal systems
(nor epinephrine, angiotensin II, aldosterone, endothelin, vasopressin, and cytokines)
• increase the hemodynamic stresses on the ventricle by
• causing sodium retention and
• peripheral vasoconstriction
• Exert direct toxic effects on cardiac cells and
• Stimulate myocardial fibrosis,
↓
Alter the architecture and impair the performance of the
failing heart.
Alters the performance and phenotype of myocytes

Forms of heart failure
 Systolic/Diastolic/ *combined
 High output/low output
 Forward/backward
 Right sided/left sided
 Acute/chronic

Systolic Heart Failure
 Impaired contractility, weak systolic contraction
 Increased ventricular volume and pressure
 Cardiac dilatation
 Inadequate ventricular emptying
 Examples – DCMP, IHD, Valvular regurgitant lesions,
cardiogenic shock secondary to AMI.

Diastolic Heart Failure
• Typical SSxs of HF in pt with Normal LVEF
& no valvular abnormalities on Echo.
• At least 1/3rd of CHF pts
• Impaired diastolic(filling phase) function
regardless of EF (increased resistance to
inflow, impaired relaxation, myocardial
fibrosis).
• Elevated diastolic Po at any volume
• Preserved systolic func. with small LV cavity
• In aging population, mostly female

Etiologic Risk Factors for HF
• CAD or history of MI
• Valvular heart disease
• Congenital heart
defects
• Hypertension
• Diabetes
• Alcoholism
• Anemia
• Thyrotoxicosis
• Other:
• Obesity
• Age
• Smoking
• High or low hematocrit level
• Reduced or falling vital
capacity
CAD=coronary artery disease; LVH=left ventricular hypertrophy.

Other Etiologic Risk Factors for CHF
 Valvular cardiomyopathy
 Mostly regurgitation and not stenosis
 Idiopathic dilated cardiomyopathy
 Various genetic variants
 Idiopathic myocardial fibrosis
 Endomyocardial fibrosis
 Tropical eosinophilic endomyocardial fibrosis
 Commonly in South/Central America and Tropical/Subtropical
Africa
 Inflammatory (Autoimmune and infectious - HIV)
 Tachycardia Induced
 Metabolic, peripartum, and toxin exposure 
cardiomyopathy

Precipitating causes
• Aggravation of HTN
• Anemia
• Thyrotoxicosis
• Arrhythmias
• Pulmonary embolism
• MI
• Infection (Rheumatic fever, Endocarditis, Myocarditis
• Pregnancy
• Alcohol consumption
• Drug discontinuation (of HF)
• Stress (Physical, Dietary, Env’tal, and Emotional)
HATA PMI PADS

Pathophysiology of CHF
• CHF begins with an
injury and adaptive
response it induces
Myocardial infarction,
genetic mutation, valvular
lesion with volume or
pressure overload …
• Index event may result in
failure with decreased
cardiac efficiency and
reduced blood pressure
Mechanism
s
Causes
Hemodynamic
burden
Valvulopathy, cong
HD, HTN (Po or
volume overload)
Sustained
myocardial loss
(structural,
functional)
MI, infectious,
cardiomyopathy,
inflammatory,
infiltrative, genetic
mutation (HCM)
Depressed
contractility
Metabolic, drugs
Tachycardia
induced
depression
Arrhythmias

Frank-Starling curves in HF

Pathophysiology cont.
• Adaptive mechanism
• An increase in diastolic volume( Frank- Starling mechanism)
• Hypertrophy
• Redistribution of blood to the brain, heart and away from
muscle, skin, kidney and
• VC due to neurohumoral adjustment: to maintain arterial
perfusion in face of a sudden reduction of COP
Adaptive mechanisms well suited for acute CHF
• As adaptive response fails :
The process to the index event becomes maladaptive
perpetuating the heart failure
• The need for protection of BP and flow to vital organs activates
baroreceptors that control RAAS,SNS
• Elevation of endothelin and fibrotic cytokines (TNF-α)

Pathoph. Cont.
• Chronic elevation of renin, angiotensin, aldosterone and NE
have harmful effect on heart & other organs
• Maladaptive mechanism
• Excessive dilation
• Remodeling (the process by which mechanical, neurohormonal, and
possibly genetic factors alter ventricular size, shape [spherical-
decreases effectiveness of ejection], and function. Its hallmarks are
hypertrophy, loss of myocytes, and increased interstitial fibrosis).
Remodeling occurs in MI, CMP, HTN, VHD,…
• Persistent remodeling : decline in LV function
• Excess hypertrophy causing impaired filling
• Excess and prolonged neurohumoral effect causing increased after
load and myocyte death

Biochemical abnormality of CHF
• Reduced myocardial energy reserve
• Reduction of myosin ATPase activity
• Reduced delivery of Ca++ to the contractile site
• Abnormal neurohumoral and cytokine adjustment
• Increase hemodynamic burden and oxygen
consumption (maladaptive)

Biochemical abn. of CHF cont.
1.Adrenergic nervous system
• Raise vascular resistance
• May cause myocyte damage through Ca++ overload
• Cardiac arrhythmias
2. RAAS
• Vasoconstriction
• Water retention and volume overload
• Cardiac fibrosis
3. Endothelin excess : VC
4. Over expression of TNF-α
• myocardial reduced contractility, CHF, increased mortality
• Proinflammatory cytokines and oxidative stresses are cytotoxic to
myocardium.

Heart Failure Pathophysiology
Index Event
(MI, Valve Lesion, Mutation)
Fall in LV Performance
Activation of RAAS, SNS, ET,
and Others
Myocardial Toxicity
Peripheral Vasoconstriction
Hemodynamic Alterations
Remodeling and
Progressive
Worsening of
LV Function Heart Failure Symptoms
Morbidity and Mortality
Shah M et al. Rev Cardiovasc Med. 2001;2(suppl 2):S2–S6.
Adaptive Response

 CNS sympathetic outflow
 Cardiac sympathetic activity  Renal sympathetic activity
Activation
of RAS
Sodium retention
Myocyte hypertrophy
Myocyte injury
Increased arrhythmias
Disease progression
1
b1
How Sympathetic Activation Promotes
the CV Disease Continuum
b1 b2 1
 Vascular sympathetic activity
Vasoconstriction
1

RAS Pathophysiology
Angiotensin I
Angiotensin II
Increased Cellular Growth & Hypertrophy
Increased Sympathetic Activity
Apoptosis
Sodium Retension
Increased Aldosterone Release
Vasoconstriction
AT1 Receptor
ACE

Heart Failure Pathophysiology
Myocardial Injury Fall in LV Performance
Activation of RAAS, SNS, ET,
and Others
Myocardial Toxicity
Peripheral Vasoconstriction
Hemodynamic Alterations
Remodeling and
Progressive
Worsening of
LV Function Heart Failure Symptoms
Morbidity and Mortality
ANP
BNP
Shah M et al. Rev Cardiovasc Med. 2001;2(suppl 2):S2–S6.

The NPS Is Overwhelmed in
Decompensated Heart Failure
Adapted from Shah M et al. Rev Cardiovasc Med. 2001;2(suppl 2):S2–S6.
ANP
BNP
Endothelin
Aldosterone
Vasopressin
Angiotensin II
Norepinephrine
Excess
vasoconstriction
Compensation
Excess vasodilation

Physiologic Effects of the RAAS and NPS
RAAS (Renin-Angiotensin-Aldosterone System)
Activation of AT1 receptors Vasoconstriction
by angiotensin II Sodium retention
Increased aldosterone release
Increased cellular growth
Increased sympathetic nervous activity
NPS (Natriuretic Peptide System)
ANP, BNP Vasodilation
Sodium excretion
Decreased aldosterone levels
Inhibition of RAAS
Inhibition of SNS
Antiprolif. of vasc.smooth ms cells
AT1 = angiotensin I; ANP = atrial natriuretic peptide; BNP = B-type natriuretic peptide.
Burnett JC Jr. J Hypertens. 1999;17(suppl 1):S37–S43.

to Dx Pt. Evaluation/ Approach
• Initial Evaluation of pts with HF:
1. Pts. Identification: Pt. can present with
(a) syndrome of decreased exercise tolerance
(b) syndrome of fluid retention
(c) no SSx (evid.of cardiac enlarg. or dysfunction)
2. Identification of a structural & functional abnormality
Hx, P/E, Dxic tool
3. Evaluation of cause
Hx, P/E, Lab. Test
• Ongoing evaluation: assessment of functional capacity, volume
status, lab, prognosis
• Discordance b/n EF & degree of functional impairement
• Outcomes of Dev’t of structural abnormalities:
1. Sxs controlled by Rx
2. Death from progressive HF
3. Death before dev’t of SxsHeart Failure(Dr. Dawit)

Clinical Manifestation
The cardinal Sxs of HF are
 dyspnea and fatigue,
○ which may limit exercise tolerance, and
 fluid retention,
○ which may lead to pulmonary congestion and
peripheral edema
 Both abnormalities can impair the
functional capacity and quality of life
Dyspnea and fatigue ≠ Fluid retention
CHF X HF √

Modified Framingham clinical criteria for the dx of HF
Major
 PND
 Orthopnoea
 Pulmonary rales
 Elevated JVP
 Third heart sound
 Cardiomegaly on CXR
 Pulm. edema on CXR
 Wt loss ≥4.5 kg in 5
days in response to
Rx of presumed HF
Minor
 Nocturnal cough
 Dyspnea on ordinary
exertion
 Tachycardia ( ≥120
bpm)
 Pleural effusion
 Hepatomegaly
 Bilateral leg edema
 Wt loss ≥4.5 kg in 5
days
Diagnosis
 2 major or 1 major + 2 minor criteria cannot be attributed to
another medical condition.

New York Heart Association Functional
Class
• Class I No limitations.
No symptoms with ordinary activities.
• Class II Slight limitations. Symptoms with
ordinary activities.
• Class III Marked limitations.
Symptoms with < ordinary activities.
• Class IV Symptoms at rest.
Subjective assessment; doesn’t consider natural progression; can
change frequently over short periods of time.

New Approach to the Classification of Heart
Failure (ACC/AHA Staging)
Stage Patient Description
A High risk for
developing heart
failure (HF)
Hypertension,
CAD
Diabetes mellitus
Family Hx of cardiomyopathy
B Asymptomatic HF Previous MI
LV systolic dysfunction
Asymptomatic valvular disease
C Symptomatic HF Known structural heart disease
Shortness of breath and fatigue
Reduced exercise tolerance
D Refractory
end-stage HF
Marked Sxs at rest despite
maximal medical therapy (eg,
those who are recurrently
hospitalized or cannot be safely
discharged from the hospital
without specialized interven.)

Classification of HF: Comparison Between ACC/AHA HF Stage
and NYHA Functional Class
ACC/AHA HF Stage NYHA Functional Class
A At high risk for heart failure but without
structural heart disease or symptoms
of heart failure (e.g. patients with
hypertension or coronary artery disease)
B Structural heart disease but without
symptoms of heart failure
C Structural heart disease with prior or
current symptoms of heart failure
D Refractory heart failure requiring
specialized interventions
I Asymptomatic
II Symptomatic with moderate exertion
IV Symptomatic at rest
III Symptomatic with minimal exertion
None

INVETIGATIONS
CBC → anemia ,leukocytosis
SERUM ELECTROLYTE
RFT → Normal in pt with mild to moderate HF
IN pt with sever HF those on large dose of
diuretics may have ↑BUN &Cr because of chronic
reduction of renal blood flow from ↓CO
LFT→ impaired in pt with congestive
hepatomegally & cardiac cirrhosis

Cont…
B type Natriutric peptide
~ is a 32 amino acid polypeptide containing a 17 amino
acid ring structure
oSecreted from cardiomyocytes in response to
ventricular wall stretch.
oMajor source are the cardiac ventricles
oHave a fundamental role in CVS remodeling, volume
homeostasis & the response to ischemia
• Guide to treatment of HF
• Predict the response to therapeutics interventions &
• Predict prognosis. Heart Failure(Dr. Dawit)

Cont…
CXR
ECHO reliable in the dx of the cause or causes
of HF
Determine LV function ,wall thickness, chamber size
Regional wall motion abnormality
Presence of VHD, pericardial disease

Cont…
ECG
ABG
PULSE oximetriy

Goals of Heart Failure Therapy in the Symptomatic
Patient
• Relieve HF symptoms
• i.e., make patients feel better
• Improve overall clinical status
• Stabilize acute episodes of decompensation
• Decrease morbidity and mortality
• Slow and/or reverse disease progression
• Identify and treat reversible causes of
LV dysfunction

How Do We Make Heart Failure Patients
Feel Better?
• With hemodynamic interventions
• Diuretics
• Digoxin
• Vasodilators
• Positive inotropic agents
• Mechanical interventions that improve
hemodynamics (e.g., CRT, LVADs)

How Do We Make HF Pts Live Longer?
• With neurohormonal interventions
• ACE inhibitors
• Angiotensin receptor antagonists
(in ACE-inhibitor intolerant patients)
• Aldosterone antagonists
• Beta-Blockers
And with
• Mechanical interventions that improve LV
remodeling (e.g., CRT, LVADs)

ACEI
• All patients at all classes will benefit from ACEI
• Improved symptoms, decrease risk of death
and combined risk of death and hospitalization
Prevent disease progression
Should be used even in patients with structural
heart disease but no symptoms

ACEI
• All ACEI are equally effective
• Optimal dosage is controversial
• Ideally started at a low dose(Captopril 6.25, enalapril
2.5, lisinopril 2.5-5) and titrated up every 3 to 7 days
with a goal daily dose (Captopril 150mg, enalapril 20mg
and lisiniopril 20-40mg)
• If ACEI not tolerated
• Hydralazine/ isosorbide dinitrate combination
• ARB

ACEI
• Contraindications
• Symptomatic hypotension
• Renal failure
• Cautious use with renal insufficiency
• Renal artery stenosis
• Hyperkalemia
• Past Angioedema
• Persistent dry cough can affect compliance

• ALDOSTERONE ANTAGONISTS
 SPIRNOLACTONE
 EPLRENONE
• MECANISM OF BENEFIT
Reduce urinary K loss maintaining a higher
plasma K conc. & block deleterious effect of
aldosterone on the heart.
30% ↓ in overall mortality
35%↓ in hospitalization

RECOMMENDED
• In pts with moderately severe or severe HF
• Recent de-compensation or LV dysfunction after
MI
Check baseline K and RFT with follow up
monitoring
Spironolactone 12.5 -25 mg /day
Eplerenone 25-50 mg/day
• ALDOSTERONE ANTAGONISTS

Beta-blockers
• Most exciting advance in the last 15 years
• Reduce total mortality
• Slow left ventricular remodeling
• Reduce the size of the heart
• Improve ejection fraction by up to 8-10%
• Mild initial decline in EF and fatigue might be seen
• Patients feel better 3-12 wks after initiating therapy

Beta-blockers
• Unlike ACEI, NOT all beta-blockers are equally
effective
• Metoprolol and Carvedilol are the two commonly
used drugs
• Carvedilol is ideal since it is nonselective vasodilator with
antioxidant and anti-endothelin properties
• Metoprolol better in those with lower blood pressure

Beta-blockers
• Best candidates for beta-blockers are stable
patients with mild to moderate heart failure and
optimal fluid status
• Drugs initiated at a low dose (Carvedilol 3.125mg,
Toprol 12.5-25mg) and slowly and carefully up-
titrated every 2-4 weeks (Carvedilol 50-100mg
and Metoprol 100-200 mg/day)

Indications and Contraindications of
Beta-blockers
Indications
• CHF
• To improve survival
and, also, to reduce
hospitalizations in
mild to severe CHF
• Ischemic or
cardiomyopathic origin
• Hypertension
• Can be used alone or
in combination with
other antihypertensive
agents, especially
thiazide-type diuretics
Contraindications
Bronchial asthma
Severe bradycardia, 2° or 3°
AV block, sick sinus syndrome
(unless a permanent
pacemaker is in place)
Cardiogenic shock
Decompensated HF requiring
use of IV inotropic therapy
Hypersensitivity to the drug
• Clinically manifest hepatic
impairment

Diuretics
• Pivotal in reliving the volume-overload states in CHF
• If no overt congestion, no need for chronic use
• Often volume overload can be due to inadequate
sodium and fluid restriction
• Generally the least toxic drug (HCTZ or chlorthalidone) at
the lowest dose is used
• If congestion worsens, long-acting loop diuretics
(furosemide, bumetanide, or torsemide) are prescribed
• For refractory edematous states, combination
diuretics may be tried

Diuretics
• Reduction in plasma volume might adversely
activate the RAAS & SNS.
• This paradoxically promotes fluid and sodium
retention and eventually contribute to the
progression of heart failure and remodeling.
• Therefore diuretics should not be used without
ACEI and beta-blockers +/- aldactone

Digoxin
• Has no significant mortality benefit
• Substantially improved heart failure symptoms
and reduced recurrent hospitalization
• Very beneficial in those with persistent symptoms
and atrial arrhythmias
• Lower doses(0.125-0.25mg) used with drug
combinations

Calcium Channel Antagonists
• Generally have negative inotropic effects
• To date, no symptomatic or mortality benefit
• At best, neutral effect for few drugs (amlodipine
and felodipine)
• However in ischemic heart failure, greater
chance of adverse effects seen with nifedipine
and diltiazem
• NO ROLE IN CHF MANAGMENT

Use of CHF drugs based on the
NYHA Functional Class
• Class I ACEI
• Class II ACEI, Beta-blocker, Diuretic
• Class III ACEI, BB, Diuretic, Digoxin, Aldactone(1)
• Class IV ACEI, BB, Diuretic, Digoxin , Aldactone(1)
1) Aldactone reserved for those with severe CHF who have
remained symptomatic despite conventional therapy of ABDD or
those with hypokalemia who don’t tolerate potassium
supplements

General Non-Pharmacologic Therapy
• 3 gm (mild CHF) or 2 gm (moderate to advanced CHF) sodium
diet
• Fluid restriction
• Avoidance of alcohol/nicotine
• Regular aerobic physical activity(3x/wk for 30min)
• Avoid NSAIDs and decongestants
• Weight control and low animal fat diet
• Education, compliance monitoring, self-management

Surgical and Mechanical
Interventions
• Contemporary medical therapy should be given
before and after surgical interventions
• Beta-blockers and ACEI can independently promote
reverse remodeling
• All new onset cardiomyopathy should be optimally
medically treated and the patient observed before
considering other interventions

Prognosis
• Depends on
the nature of underlying heart disease
presence or absence of precipitating factor that can be treated
• Factors associated with poor prognosis:
Severely depressed EF (< 15%)
Reduced maximal O2 uptake(10 ml/Kg/min)
Inability to walk on a level and at a normal pace for more than 3
minutes
Reduced serum Na conc.(< 133 mEq/L)
Reduced serum K (< 3 mEq/L)
Markedly elevated BNP (> 500 pg/ml)
Frequent ventricular extra systole

Mortality
• Main cause of death in patient with HF are:
 Sudden or arrhythmic death
Progressive pump failure
• Annual mortality
- Asymptomatic < 5%
- Mild 10%
- Moderate 20-30%
- Severe 30- 80%

2. Congestive heart failure by Dawit.pptx

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