NORMAL HEART HEART FAILURE

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 Introduction
Heart failure is the pathological process in
which the systolic or/and diastolic function of
the heart is impaired, and as a result, cardiac
output decreases and is unable to meet the
metabolic demands of the body.

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 Cardiac Physiology

Preload Contractility Afterload

CO = SV x HR

HR: parasympathetic
and sympathetic tone Stroke Volume Heart Rate

SV: preload,
Cardiac Output
afterload,
contractility
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 Stroke Volume

z PRELOAD : Passive stretch of muscle prior to

contraction  function of LVEDP
z AFTERLOAD : Force opposing/stretching muscle
after contraction begins  measured by SVR
(Systemic Vascular Resistance)
z CONTRACTILITY : ability of the muscle to
contract at a given force for a given stretch,
independent of preload or afterload forces
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 Frank Starling Mechanism

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 Pathophysiology
Systolic dyfunctions :
The contractile state of the
myocardium
The preload of the ventricle
 The afterload applied to the
ventricle
The heart rate
Dysfunction of myocardium :
Myocardial damage :
myocardial infarction;
Cardiomyopathy;
Myocarditis
Metabolic disturbance :
ischemia and hypoxia;
diabetes

Overload for myocardium :

Pressure overload (afterload) : Hypertension, aortic stenosis;
Pulmonary hypertension
Volume overload (preload) : Mitral regurgitation
Restriction of cardiac dilation : Pericardial effusion
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 Ventricular Remodeling

 Ventricular remodeling is the process by which mechanical,

neurohormonal, and possibly genetic factors alter
ventricular size, shape, and function.
 Its hallmarks include hypertrophy, loss of myocytes, and
increased interstitial fibrosis.

Ventricular remodeling in diastolic and systolic heart

failure

Hypertrophied heart Dilated heart

Normal heart (systolic heart
(diastolic heart failure)
 Etiology of HF

Hypertensive heart disease

Coronary artery disease
Valvular disease
Heart inflammation : pericarditis, myocarditis.
Cardiomyopathy
Venous disease (deep vein thrombosis) right
heart failure

March 2013 ghennersdorf DGK ESC SES

 The precipitating causes
 Ischemia
 Arrhythmia : Tachycardia  atrial fibrillation
Bradycardia
 Infection : especially lung infection
 Excessive physical activity
 Pregnancy and delivery
 Anemia
 Administration of inappropriate drug
 Medication noncompliance
 Excess fluid intake
 Thyrotoxicosis
 Functional class of Heart Failure
New York Heart Association

Class % of Symptoms
patients
I 35% No symptoms or limitations in ordinary
physical activity
II 35% Mild symptoms and slight limitation during
ordinary activity
III 25% Marked limitation in activity even during
minimal activity. Comfortable only at rest
IV 5% Severe limitation. Experiences symptoms
even at rest
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 Stages of heart failure

Stage A: Asymptomatic with no heart damage but

have risk factors for heart failure
Stage B: Asymptomatic but have signs of structural
heart damage
Stage C: Have symptoms and heart damage
Stage D: End stage disease

ACC/AHA guidelines, 2001

 Clinical classification
According to the course of disease
Acute HF
Chronic HF
According to the cardiac output (CO)
Low-output HF
High-output HF
According to the location of heart failure
Left -side heart failure (LHF)
Right-side heart failure (RHF)
Biventricular failure (whole heart failure)
According to the function impaired
Systolic failure
Diastolic failure
 Acute versus Chronic
Acute heart failure
develops rapidly
can be immediately life threatening
due to lack of time to undergo
compensatory adaptations.
may result from CABG, acute
infection (sepsis), acute myocardial
infarction, valve dysfunction, severe
arrhythmias, etc.
can often be managed successfully
by pharmacological or surgical
interventions.
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Chronic heart failure
 a long-term condition
(months/years) that is
associated with the heart
undergoing adaptive responses
(e.g., dilation, hypertrophy) to
a precipitating cause.
 These adaptive responses,
however, can be deleterious in
the long-term and lead to a
worsening condition.
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 Systolic
SYSTOLIC versus Diastolic
DIASTOLIC
HEART FAILURE HEART FAILURE

Systolic– “can’t pump” Diastolic- “can’t fill”

Aortic Stenosis Mitral Stenosis
HTN Tamponade
Aortic Insufficiency Hypertrophy
Mitral Regurgitation Infiltration
Muscle Loss Fibrosis
Ischemia
Fibrosis
Infiltration
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Diastolic HF vs Systolic HF
What Are The Symptoms
of Heart Failure?

Think FACES...
Fatigue
Activities limited
Chest congestion
Edema or ankle swelling
Shortness of breath
 Modified Framingham Criteria
Diagnosis for Heart Failure

Major criteria Minor criteria

Neck vein distension Bilateral ankle edema
Orthopnea Night cough
Cardiomegaly on CXR Dyspnea on exertion
CVP > 12 mm Hg Hepatomegaly
Left Ventricular Pleural effusion
dysfunction on EKG Tachycardia (> 120
Weight loss beats/min)
Acute pulmonary edema
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 Clinical Data
HEART SOUNDS!!!
Systolic Murmurs
Mitral Regurgitation
Aortic Stenosis
Diastolic Murmurs
Mitral Stenosis
Mitral Stenosis
Aortic Insufficiency
S3: Rapid filling of a diseased ventricle
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 Clinical Data
CXR(Chest X-Ray)
Kerley’s lines : A and B
Pulmonary Edema
Cephalization
Pleural Effusions (bilateral)
EKG(Electrocardiogram)
Left atrial enlargement
Arrhythmias
Hypertrophy (left or right)
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 Clinical Data
Laboratory Data

Chemistry
Renal Function: Be Wary

BNP(Brain Natriuretic Peptide) Test

Used in ER departments the world over
Pulmonary versus cardiac dyspnea

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 Treatment Strategies of HF

Etiology therapy
 Treatment of etiology causes
 Treatment of precipitating causes
 Improve life-style
Lessen cardiac load
 Rest
 Limitation of salt intake
 Water intake
 Diuretics
Drug treatment for CHF
Diuretics, ACE inhibitors

Reduce the number of sacks on

the wagon
 Diuretics
Indicated in patients with symptoms of fluid retention

Initiated with low doses followed by increments in

dosage until urine output increases and weight decreases
by 0.5-1kg daily

Benefits :
Improves symptoms of congestion
Can improve cardiac output

Limitations :
Excessive volume depletion
Electrolyte disturbance
Ototoxicity
 ACE Inhibitor
 All patients with symptomatic heart failure and functional
class I with reduced LV function, unless contraindicated or
not tolerated
 Should be continued indefinitely and titrate to optimal
dosage in the absence of symptoms or adverse effects on
end-organ perfusion
 Increases exercise capacity and improves functional class
 Attenuation of LV remodeling post MI
 Beta-blockers
Limit donkey’s speed, thus saving
energy

 Initiate with low dosage

 Titration to target dosage
 Digitalis

Like the carrot placed in front of the

donkey
 Digitalis
 Enhances LV function, normalizes baroreceptor-mediated
reflexes and increases cardiac output at rest and during
exercise
 Should be used in conjunction with diuretics, ACE inhibitors
and beta-blockers
 Also recommended in patients with heart failure who have
atrial fibrillation
 Adverse effects include cardiac arrhythmias, GI symptoms
and neurological complaints (eg. visual disturbances,
confusion)
 CRT/CRT-D
Increase the donkey’s (heart) efficiency
CRT device:
Pts with NYHA Class Ⅲ/Ⅳ
Symptomatic despite optimal
medical therapy
QRS ≥ 130 msec

LVEF ≤ 35%
 Treatment Strategies of HF

 Aldosterone antagonist:
RALES, serious HF
 Angiotensin receptor blocker:
substitute, not replace
Triple Therapy for
most patients – ACE,
B-Blocker and MRA
 Heart failure:
More than just drugs.

 Dietary counseling
 Patient education
 Physical activity
 Medication compliance
 Aggressive follow-up
 Sudden death assessment
 Questions to determine therapeutic
strategy in CHF patients

Is heart failure present?

What caused the problem?

What precipitated deterioration?

How severe is the heart failure?

What is the best chronic therapeutic strategy?

Can the initiating/precipitating problem be cured, and can
the state of HF be attenuated?
What is the prognosis?
 ventricular filling occurs during this phase.

Intra atrial pressure recordings reveal two peaks and two descents. The a wave is the
atrial pressure generated during atrial systole immediately preceding ventricular systole.
The peak atrial pressure recorded during ventricular systole before the tricuspid and
mitral valves open is the v wave.

120 mmHg

Aortic Valve Opens Aortic Valve Closes

80 mmHg
Aortic Pressure

Mitral Valve Opens

Mitral Valve Closes LA Pressure

v
a wave
wave
10 mmHg
LV Pressure
Diastole Systole Diastole
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