Ethiology & Pathophysiology

of
Congestive Heart Failure
 Heart failure

Normal heart function

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 Congestive Heart Failure
Definition
• Impaired cardiac pumping such that
heart is unable to pump adequate
amount of blood to meet metabolic needs
• Not a disease but a “syndrome”
• Associated with long-standing HTN and
CAD

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 Factors Affecting Cardiac Output
Preload

Cardiac Output Stroke Volume

= Heart Rate X
CO SV

Afterload Contractility

SV: the volume of blood pumped from one ventricle of the heart with each
beat
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 Factors Affecting Cardiac Output
• Heart Rate
– In general, the higher the heart rate, the lower the cardiac
• E.g. HR x Systolic Volume (SV) = CO
» 60/min x 80 ml = 4800 ml/min (4.8 L/min)
» 70/min x 80 ml = 5600 ml/min (5.6 L/min)
– But only up to a point. With excessively high heart rates,
diastolic filling time begins to fall, thus causing stroke volume
and thus CO to fall

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 Heart Rate Stroke Volume Cardiac Output
60/min 80 ml 4.8 L/min
80/min 80/ml 6.4 L/min
100/min 80/ml 8.0 L/min
130/min 50/ml 6.5 L/min
150/min 40/ml 6.0 L/min
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 Factors effecting
heart pump
effectiveness Preload
• Volume of blood in ventricles at end diastole
• Depends on venous return
• Depends on compliance

Afterload
•Force needed to eject blood into circulation
•Arterial B/P, pulmonary artery pressure
•Valvular disease increases afterload
 Factors Affecting Cardiac Output
• Preload
– The volume of blood/amount of fiber stretch in the ventricles
at the end of diastole (i.e., before the next contraction)

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 Factors Affecting Cardiac Output
• Preload increases with:
• Fluid volume increases
• Vasoconstriction (“squeezes” blood from vascular system into heart)
• Preload decreases with
• Fluid volume losses
• Vasodilation (able to “hold” more blood, therefore less returning toheart)

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 Factors Affecting Cardiac Output
• Starling’s Law
– Describes the relationship between preload and cardiac output
– The greater the heart muscle fibers are stretched (b/c of increases in
volume), the greater their subsequent force of contraction – but only up to a
point. Beyond that point, fibers get over-stretched and the force of
contraction is reduced
• Excessive preload = excessive stretch → reduced contraction →
reduced SV/CO

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 Factors Affecting Cardiac Output
• Afterload
– The resistance against which the ventricle must pump. Excessive
afterload = difficult to pump blood → reduced CO/SV
– Afterload increased with:
• Hypertension
• Vasoconstriction
– Afterload decreased with:
• Vasodilation

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 Factors Affecting Cardiac Output
• Contractility
– Ability of the heart muscle to contract; relates to the strength of
contraction.

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 Factors Affecting Cardiac Output
• Contractility decreased with:
– infarcted tissue – no contractile strength
– ischemic tissue – reduced contractile strength.
– Electrolyte/acid-base imbalance
– Negative inotropes (medications that decrease contractility, such as beta
blockers).
• Contractility increased with:
– Sympathetic stimulation (effects of epinephrine)
– Positive inotropes (medications that increase contractility, such as digoxin,
sympathomimmetics)

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 Definition-Heart Failure (HF)
Key Concepts
• CO = SV x HR-becomes insufficient to
meet metabolic needs of body
• SV- determined by preload, afterload
and myocardial contractility
• EF< 40% (need to understand)
• *Classifications HF
– Systolic failure- dec. contractility
– Diastolic failure- dec. filling
– Mixed
90/140= 64% EF- 55-65 (75) normal
•Keys to understanding HF
• All organs (liver, lungs, legs, etc.) return blood to heart
• When heart begins to fail/ weaken> unable to pump blood forward-fluid backs up >
Inc. pressure within all organs.
• Organ response
• LUNGS: congested > “stiffer” , inc effort to breathe; fluid starts to escape into
alveoli; fluid interferes with O2 exchange, aggravates shortness of breath.

• Shortness of breath during exertion, may be early symptoms > progresses > later
require extra pillows at night to breathe > experience "P.N.D." or paroxysmal
nocturnal dyspnea .
• Pulmonary edema
• Legs, ankles, feet- blood from feet and legs > back-up of fluid and pressure in these
areas, heart unable to pump blood as promptly as received > inc. fluid within feet
and legs causes fluid to "seep" out of blood vessels ; inc. weight
Heart Failure
 Classifications- (how to describe)

• Systolic versus diastolic

– Systolic- loss of contractility get dec. CO
– Diastolic- decreased filling or preload
• Left-sided versus right –sided
– Left- lungs
– Right-peripheral
• High output- hypermetabolic state
• Acute versus chronic
– Acute- MI
– Chronic-cardiomyopathy
 Heart Failure
Etiology and Pathophysiology
• Systolic failure- most common cause
– Hallmark finding: Dec. in *left ventricular ejection
fraction (EF)
• Due to
– Impaired contractile function (e.g., MI)
– Increased afterload (e.g., hypertension)
– Cardiomyopathy
– Mechanical abnormalities (e.g., valve disease)
 Heart Failure
Etiology and Pathophysiology
• Diastolic failure
– Impaired ability of ventricles to relax and fill
during diastole > dec. stroke volume and CO
– Diagnosis based on presence of pulmonary
congestion, pulmonary hypertension, ventricular
hypertrophy
– *normal ejection fraction (EF)- Know why!
 Heart Failure
Etiology and Pathophysiology
• Mixed systolic and diastolic failure
– Seen in disease states such as dilated
cardiomyopathy (DCM)
– Poor EFs (<35%)
– High pulmonary pressures
• Biventricular failure (both ventricles may be
dilated and have poor filling and emptying
capacity)
 Congestive Heart Failure
Types of Congestive Heart Failure

• Left-sided failure
– Most common form
– Blood backs up through the left atrium
into the pulmonary veins
• Pulmonary congestion and edema
– Eventually leads to biventricular failure

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 Congestive Heart Failure
Types of Congestive Heart Failure

• Left-sided failure
– Most common cause:
• HTN
• Cardiomyopathy
• Valvular disorders
• CAD (myocardial infarction)

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 Congestive Heart Failure
Types of Congestive Heart Failure

• Right-sided failure
– Results from diseased right ventricle
– Blood backs up into right atrium and venous
circulation
– Causes
• LVF
• Cor pulmonale: failure
failure of
of the
the right
right side
side of
of the
the heart
heart brought
brought on
on
by
by long-term
long-term high
high blood
blood pressure
pressure in
in the
the pulmonary
pulmonary arteries
arteries and
and right
right
ventricle
ventricle of
of the
the heart
heart
04/11/2009 • RV infarction 24
 Congestive Heart Failure
Types of Congestive Heart Failure

• Right-sided failure
– Venous congestion
• Peripheral edema
• Hepatomegaly
• Splenomegaly
• Jugular venous distension

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 Congestive Heart Failure
Types of Congestive Heart Failure

• Right-sided failure
– Primary cause is left-sided failure
– Cor pulmonale
• RV dilation and hypertrophy caused
by pulmonary pathology

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Cardiomegaly/ventricular remodeling occurs as heart overworked> changes in size, shape, and
function of heart after injury to left ventricle. Injury due to acute myocardial infarction or due to
causes that inc. pressure or volume overload as in Heart failure
American Heart Assn-Media files Animations
 Pathophysiology of CHF
• Pump fails → decreased stroke volume /CO.
• Compensatory mechanisms kick in to increase CO
– SNS stimulation → release of epinephrine/nor-epinephrine
• Increase HR
• Increase contractility
• Peripheral vasoconstriction (increases afterload)
– Myocardial hypertrophy: walls of heart thicken to provide more muscle
mass → stronger contractions

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 Pathophysiology of CHF
– Hormonal response: ↓’d renal perfusion interpreted by
juxtaglomerular apparatus as hypovolemia. Thus:
• Kidneys release renin, which stimulates conversion of
antiotensin I → angiotensin II, which causes:
– Aldosterone release → Na retention and water retention (via ADH
secretion)
– Peripheral vasoconstriction

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 Pathophysiology of CHF
• Compensatory mechanisms may restore CO to near-
normal.
• But, if excessive the compensatory mechanisms can worsen
heart failure because . . .

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 Pathophysiology of CHF
• Vasoconstriction: ↑’s the resistance against which heart has to
pump (i.e., ↑’s afterload), and may therefore ↓ CO

• Na and water retention: ↑’s fluid volume, which ↑’s preload. If

too much “stretch” (d/t too much fluid) → ↓ strength of
contraction and ↓’s CO

• Excessive tachycardia → ↓’d diastolic filling time → ↓’d

ventricular filling → ↓’d SV and CO

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 Congestive Heart Failure
Risk Factors

• CAD
• Age
• HTN
• Obesity
• Cigarette smoking
• Diabetes mellitus
• High cholesterol
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• African descent 33
 Heart Failure
(AKA-congestive heart failure)
• Pathophysiology
• A. Cardiac compensatory mechanisms
– 1.tachycardia
– 2.ventricular dilation-Starling’s law
– 3.myocardial hypertrophy
• Hypoxia leads to dec. contractility
 Pathophysiology-Summary
• B. Homeostatic Compensatory mechanisms
• Sympathetic Nervous System-(beta blockers block this)
– 1. Vascular system- norepinephrine- vasoconstriction
(What effect on afterload?)
– 2. Kidneys
• A. Dec. CO and B/P > renin angiotensin release. (ACE)
• B. Aldosterone release > Na and H2O retention
– 3. Liver- stores venous volume (ascites, +HJR,
Hepatomegaly- can store 10 L. check enzymes
Counter-regulatory-
• Inc. Na > release of ADH (diuretics)
• *Release of atrial natriuretic factor > Na and H20
excretion, prevents severe cardiac decompensation
• What is BNP? What drug is synthetic form BNP?
 Heart Failure
Etiology and Pathophysiology
• Compensatory mechanisms- activated to
maintain adequate CO
– Neurohormonal responses: Endothelin -stimulated by
ADH, catecholamines, and angiotensin II >
• Arterial vasoconstriction
• Inc. in cardiac contractility
• Hypertrophy
 Heart Failure
Etiology and Pathophysiology
• Compensatory mechanisms- activated to maintain
adequate CO
– Neurohormonal responses: Proinflammatory cytokines (e.g.,
tumor necrosis factor)
• Released by cardiac myocytes in response to cardiac injury
• Depress cardiac function > cardiac hypertrophy, contractile
dysfunction, and myocyte cell death
 Heart Failure
Etiology and Pathophysiology
• Compensatory mechanisms- activated to
maintain adequate CO
– Neurohormonal responses: Over time > systemic
inflammatory response > results
• Cardiac wasting
• Muscle myopathy
• Fatigue
 Heart Failure
Etiology and Pathophysiology
• **Counter regulatory processes
– Natriuretic peptides: atrial natriuretic peptide (ANP) and
b-type natriuretic peptide (BNP)- *also dx test for HF

• Released in response to inc. in atrial volume and ventricular

pressure
• Promote venous and arterial vasodilation, reduce preload
and afterload
• Prolonged HF > depletion of these factors
 Heart Failure
Etiology and Pathophysiology
• Counter regulatory processes
– Natriuretic peptides- endothelin and aldosterone
antagonists
• Enhance diuresis
• Block effects of the RAAS
– Natriuretic peptides- inhibit development of
cardiac hypertrophy; may have antiinflammatory
effects
Result of
Compensatory
Mechanisms >

Heart Failure
Heart Failure Exp
lained
 Pathophysiology-
Structural Changes with HF
• Dec. contractility
• Inc. preload (volume)
• Inc. afterload (resistance)
• **Ventricular remodeling (ACE inhibitors can prevent
this)
– Ventricular hypertrophy
– Ventricular dilation
Ventricular remodeling
 END RESULT
FLUID OVERLOAD > Acute Decompensated Heart
Failure (ADHF)/Pulmonary Edema

>Medical Emergency!
 Congestive Heart Failure
Classification

• Based on the person’s tolerance to physical

activity
– Class 1: No limitation of physical activity
– Class 2: Slight limitation
– Class 3: Marked limitation
– Class 4: Inability to carry on any physical
activity without discomfort
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 Heart Failure
Classification Systems
• New York Heart Association Functional
Classification of HF
– Classes I to IV
• ACC/AHA Stages of HF (newer)
– Stages A to D
ACC/AHA
Stages

NY ASSN Funct Class

 Congestive Heart Failure
Risk Factors

• CAD
• Age
• HTN
• Obesity
• Cigarette smoking
• Diabetes mellitus
• High cholesterol
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• African descent 50
 Heart failure

Underlying causes/risk factors

• Ischemic heart disease (CAD) 70
%
• hypertension

• myocardial infarction (MI)

• valvular heart disease

• congenital heart disease

• dilated cardiomyopathy

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 CHF-due to
– 1. Impaired cardiac function
• Coronary heart disease
• Cardiomyopathies
• Rheumatic fever
• Endocarditis
– 2. Increased cardiac workload
• Hypertension
• Valvular disorders
• Anemias
• Congenital heart defects
– 3.Acute non-cardiac conditions
• Volume overload
• Hyperthyroid, Fever,infection
 Heart Failure
Etiology and Pathophysiology
• Primary risk factors
– Coronary artery disease (CAD)
– Advancing age
• Contributing risk factors
– Hypertension
– Diabetes
– Tobacco use
– Obesity
– High serum cholesterol
– African American descent
– Valvular heart disease
– Hypervolemia
Can You Have RVF Without LVF?
• What is this called?
COR PULMONALE
 Heart Failure
Complications
• Pleural effusion
• Atrial fibrillation (most common
dysrhythmia)
– Loss of atrial contraction (kick) -reduce CO by
10% to 20%
– Promotes thrombus/embolus formation inc. risk
for stroke
– Treatment may include cardioversion,
antidysrhythmics, and/or anticoagulants
 Heart Failure
Complications
• **High risk of fatal dysrhythmias (e.g., sudden
cardiac death, ventricular tachycardia) with HF and
an EF <35%

– HF lead to severe hepatomegaly, especially with

RV failure
• Fibrosis and cirrhosis - develop over time
– Renal insufficiency or failure
 Congestive Heart Failure
Diagnostic Studies

• Primary goal is to determine underlying

cause
– Physical exam
– Chest x-ray
– ECG
– Hemodynamic assessment

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 Heart Failure
Diagnostic Studies
• Primary goal- determine underlying cause
– Hemodynamic assessment-Hemodynamic
Monitoring-CVP- (right side) and Swan Ganz (left and
right side)
– Echocardiogram-TEE best
– Stress testing- exercise or medicine
– Cardiac catheterization- determine heart
pressures ( inc.PAW )
– Ejection fraction (EF)
Transesophageal
echocardiogram
TEE
But