CHF.ppt it is internal medicine part 2016 Ambo

Objectives
• Definition
• Epidemiology
• Causes (etiology)
• Pathophysiology
• C/F, evaluation,
• severity classification
• Investigation
• Management
• Prognosis
Dr MATHEWOS
2/3/2024

DEFINITION —
Heart failure (HF) is a complex clinical syndrome that can
result from any structural or functional cardiac disorder
that impairs the ability of the ventricle to fill with or eject
blood.
The final pathway for myriad disease that affect the heart.
It is characterized by specific symptoms, such as
dyspnea and fatigue, and signs, such as those related to
fluid retention.
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.
Dr MATHEWOS
2/3/2024

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 b Rx
– may reverse spontaneously
Dr MATHEWOS
2/3/2024

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.
Dr MATHEWOS
2/3/2024

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 yo
• 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
admissions] ) Dr MATHEWOS
2/3/2024

 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
– Ejection fraction reduction
– Dilated LV size
– Systolic/diastolic dysfunction
Dr MATHEWOS
Epidem. Cont
2/3/2024

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 at rest
 be associated with a wide spectrum of LV functional
abnormalities.
Dr MATHEWOS
2/3/2024

Left Ventricular Dysfunction
• Begins with injury to or stress on the myocardium
• Is generally a progressive process
• The progression is mainly 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)
Dr MATHEWOS
2/3/2024

Dr MATHEWOS
Forms of heart failure
 Systolic/Diastolic/ *combined
 High output/low output
 Forward/backward
 Right sided/left sided
 Acute/chronic
2/3/2024

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.
Dr MATHEWOS
2/3/2024

• functional regurgitation = disruption of the
normal papillary muscle architecture
• Arbitrarily EF < 40-45% is systolic dysfunction
and EF > 60% is diastolic dysfunction.
Dr MATHEWOS
2/3/2024

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 pressure at any volume
• Preserved systolic func. with small LV cavity
• In aging population, mostly female
Dr MATHEWOS
2/3/2024

Etiologic Risk Factors for HF
Major risk factors
• CAD or history of MI
• Hypertension
• Valvular heart disease
• Alcoholism
• Diabetes
• Congenital heart defects
Additional
• Other:
– Obesity
– Age
– Reduced or falling vital
capacity
– Smoking
– High or low hematocrit level
2/3/2024 Dr MATHEWOS
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
Dr MATHEWOS
2/3/2024

Precipitating causes
• Infection
• Arrhythmias
• Physical, Dietary, Fluid, Env’tal, and Emotional
excesses
• MI
• Pulmonary embolism
• Anemia
• Thyrotoxicosis and Pregnancy
• Aggravation of HTN
• Rheumatic , Viral , and Other forms of Myocarditis
• Infective Endocarditis
Dr MATHEWOS
2/3/2024

Dr MATHEWOS
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
Mechanisms 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
2/3/2024

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)
Dr MATHEWOS
2/3/2024

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
Dr MATHEWOS
2/3/2024

Heart Failure Pathophysiology
Dr MATHEWOS
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
2/3/2024

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
Dr MATHEWOS
AT1 = angiotensin I; ANP = atrial natriuretic peptide; BNP = B-type natriuretic peptide.
Burnett JC Jr. J Hypertens. 1999;17(suppl 1):S37–S43.
2/3/2024

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 Sxs
Dr MATHEWOS
2/3/2024

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 √
Dr MATHEWOS
2/3/2024

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.
Dr MATHEWOS
Subjective assessment; doesn’t consider natural
progression; can change frequently over short
periods of time.
2/3/2024

OTHER Approach to the Classification of
Heart Failure (ACC/AHA Staging)
Dr MATHEWOS
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.)
2/3/2024

Classification of HF: Comparison Between ACC/AHA HF Stage
and NYHA Functional Class
Dr MATHEWOS
ACC/AHA HF Stage NYHA Functional Class
A At high risk for heart failure but without
structural heart disease or symptoms
of heart failure (eg, 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
2/3/2024

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
Dr MATHEWOS
2/3/2024

Cont…
B type Natriutric peptide
~ is a 32 amino acid polypeptide containing a 17
amino acid ring structure
o Secreted from cardiomyocytes in response to
ventricular wall stretch.
o Major source are the cardiac ventricles
o Have a fundamental role in CVS remodeling,
volume homeostasis & the response to ischemia
Dr MATHEWOS
2/3/2024

Cont…
• Guide to treatment of HF
• Predicte the response to therapeutics
interventions &
• Predicte prognosis.
Dr MATHEWOS
2/3/2024

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
Dr MATHEWOS
2/3/2024

Cont…
ECG
ABG
PULSE oximetriy
Dr MATHEWOS
2/3/2024

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 benfit 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
– Hyperkalemia
– Renal artery stenosis
– Past Angioendema
• Persistent dry cough can affect compliance

• ALDOSTERONE ANTAGONISTS
 SPIRNOLACTONE
 EPLRENONE
• MECANISM OF BENEFIT
Reduce urinary K loss maintaining a higher
plasma K concn & 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 decompensation 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 antiendothelin 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%

Thank you
Dr MATHEWOS
2/3/2024

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