manisfestasi klinik, patofisiologi

1. NORMAL HEART HEART FAILURE
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2. 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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3. Cardiac Physiology
CO = SV x HR
HR: parasympathetic
and sympathetic tone
SV: preload,
afterload,
contractility
Preload Contractility Afterload
Stroke Volume Heart Rate
Cardiac Output
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4. Stroke Volume
PRELOAD : Passive stretch of muscle prior to
contraction  function of LVEDP
AFTERLOAD : Force opposing/stretching
muscle after contraction begins  measured by
SVR (Systemic Vascular Resistance)
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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5. Frank Starling Mechanism
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6. 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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8. 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
Normal heart Hypertrophied heart
(diastolic heart
Dilated heart
(systolic heart

9. 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

10. 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

11.
Class % of
patients
Symptoms
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
Functional class of Heart
Failure
New York Heart Association
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12. 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

13. 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

14. 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
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
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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15. Systolic versus
Diastolic
Systolic– “can’t pump”
Aortic Stenosis
HTN
Aortic Insufficiency
Mitral Regurgitation
Muscle Loss
Ischemia
Fibrosis
Infiltration
Diastolic- “can’t fill”
Mitral Stenosis
Tamponade
Hypertrophy
Infiltration
Fibrosis
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SYSTOLIC
HEART FAILURE
DIASTOLIC
HEART FAILURE
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16. Diastolic HF vs Systolic
HF

17. What Are The Symptoms
of Heart Failure?
Think FACES...
Fatigue
Activities limited
Chest congestion
Edema or ankle swelling
Shortness of breath

18. Modified Framingham
Criteria Diagnosis for Heart
Failure
Major criteria
Neck vein distension
Orthopnea
Cardiomegaly on CXR
CVP > 12 mm Hg
Left Ventricular
dysfunction on EKG
Weight loss
Acute pulmonary edema
Minor criteria
Bilateral ankle edema
Night cough
Dyspnea on exertion
Hepatomegaly
Pleural effusion
Tachycardia (> 120
beats/min)
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20. Clinical Data
HEART SOUNDS!!!
Systolic Murmurs
Mitral Regurgitation
Aortic Stenosis
Diastolic Murmurs
Mitral Stenosis
Aortic Insufficiency
S3: Rapid filling of a diseased ventricle
Mitral Stenosis
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21. 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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22. 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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23. 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

24. Drug treatment for CHF

25. Diuretics, ACE
inhibitors
Reduce the number of sacks
on the wagon

26. 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

27. 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

28. Beta-blockers
Limit donkey’s speed, thus
saving energy
Initiate with low dosage
Titration to target dosage

29. Digitalis
Like the carrot placed in front of the
donkey

30. 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)

31. 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%

32. Aldosterone antagonist:
RALES, serious HF
Angiotensin receptor blocker:
substitute, not replace
Treatment Strategies of
HF

34. Triple Therapy forTriple Therapy for
most patients – ACE,
B-Blocker and MRA

36. Heart failure:
More than just drugs.
Dietary counseling
Patient education
Physical activity
Medication compliance
Aggressive follow-up
Sudden death assessment

37. 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?

39. 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.
Aortic Pressure
LV Pressure
120 mmHg
80 mmHg
10 mmHg
LA PressureMitral Valve Closes
Aortic Valve Opens Aortic Valve Closes
Mitral Valve Opens
Systole DiastoleDiastole
a
wave
v
wave
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