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JANTUNG
BASUKI RAHMAT, MD
DEPARTMENT OF CARDIOLOGY AND VASCULAR MEDICINE
FACULTY OF MEDICINE MATARAM UNIVERSITY - MATARAM HOSPITAL WEST NUSA TENGGARA
HEART FAILURE
OUTLINE
Prevalence and cost
Definition
Physiology
Pathophysiology
Cause
Clinical Assesment
Management
PREVALENCE
AND COST
BASUKI RAHMAT, MD
DEPARTMENT OF CARDIOLOGY AND VASCULAR MEDICINE
FACULTY OF MEDICINE MATARAM UNIVERSITY - MATARAM HOSPITAL WEST NUSA TENGGARA
PENDAHULUAN
Walaupun terjadi
penurunan progesifitas kematian
akibat PJK dan penyakit jantung
hipertensi o.k usia, TAPI insidensi
dan prevalensi HF akan terus
meningkat
PREVALENCE OF HF
INCREASES WITH AGE
10
Population (%)
Males
8
Females
6
4
2
0
2024
2534
3544
4554
5564
Age (yr)
US, 19881994
AHA. Heart Disease and Stroke Statistics2004 Update
6574
75+
Total Cost
$25.8 billion
53%
14%
Nursing Home
$3.5
7%
8%
8%
10%
Physicians/Other
Professionals
$1.8
Drugs/Other
Home Healthcare Medical Durables
$2.1
$2.7
Lost Productivity/
Mortality*
$2.1
16%
Inappropriate Rx
Rx Noncompliance
24%
19%
Failure to Seek
Care
17%
Other
Overall
5-year mortality 50%
Survival %
Women
Men
10
Years
Survival after the onset of congestive heart failure in Framingham Heart Study subjects
AHA, 1998 Heart and Statistical Update
NCHS, National Center for Health Statistics
Ho Circulation 1993;88:107-115
COST OF
HEART FAILURE
Total pengeluaran AS pertahun
untuk HF adalah $ 33 milyar.
Beban biaya rawat inap HF 2,4 x
lebih besar dibandingkan kanker
dan 1,7 x dibandingkan semua IMA
yang dirawat dirumah sakit
DEFINITION
BASUKI RAHMAT, MD
DEPARTMENT OF CARDIOLOGY AND VASCULAR MEDICINE
FACULTY OF MEDICINE MATARAM UNIVERSITY - MATARAM HOSPITAL WEST NUSA TENGGARA
DEFINITION
13
PHYSIOLOGY
BASUKI RAHMAT, MD
DEPARTMENT OF CARDIOLOGY AND VASCULAR MEDICINE
FACULTY OF MEDICINE MATARAM UNIVERSITY - MATARAM HOSPITAL WEST NUSA TENGGARA
FACTORS AFFECTING
CARDIAC OUTPUT
Preload
Heart Rate
Afterload
Stroke Volume
SV
Contractility
15
Cardiac Output
CO
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)
16
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
17
Heart Rate
FACTORS AFFECTING
CARDIAC OUTPUT
Preload
18
FACTORS AFFECTING
CARDIAC OUTPUT
Preload increases with:
Fluid volume increases
Vasoconstriction (squeezes blood from
vascular system into heart)
19
FACTORS AFFECTING
CARDIAC OUTPUT
Starlings 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
20
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
21
Vasodilation
FACTORS AFFECTING
CARDIAC OUTPUT
Contractility
22
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).
23
PATHOPHYSIOLOGY
BASUKI RAHMAT, MD
DEPARTMENT OF CARDIOLOGY AND VASCULAR MEDICINE
FACULTY OF MEDICINE MATARAM UNIVERSITY - MATARAM HOSPITAL WEST NUSA TENGGARA
PATHOPHYSIOLOGY
OF CHF
Pump fails decreased stroke volume
/CO.
Compensatory mechanisms kick in to
increase CO
SNS stimulation release of epinephrine/norepinephrine
Increase HR
Increase contractility
Peripheral vasoconstriction (increases afterload)
31
PATHOPHYSIOLOGY
OF CHF
Hormonal response: d renal perfusion interpreted by
juxtaglomerular apparatus as hypovolemia. Thus:
32
PATHOPHYSIOLOGY
OF CHF
Compensatory mechanisms may restore
CO to near-normal.
33
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
34
LV Dysfunction causes
Decreased cardiac output
TYPES OF CONGESTIVE
HEART FAILURE
36
TYPES OF CONGESTIVE
HEART FAILURE
TYPES OF CONGESTIVE
HEART FAILURE
RIGHT SIDE HEART FAILURE
Result from diseased right ventricle
Blood backs up into right atrium and
venous circulation
causes
LVF
Cor Pulmonare
RV infarction
38
TYPES OF CONGESTIVE
HEART FAILURE
RIGHT SIDE HEART FAILURE
39
Venous congestion
Peripheral edema
Hepatomegaly
Splenomegaly
Jugular Venous distension
fatigue, weakness,
lethargy
wt. gain, inc. abd. girth,
anorexia, RUQ pain
elevated neck veins
Hepatomegaly +HJR
may not see signs of
LVF
TYPES OF CONGESTIVE
HEART FAILURE
RIGHT SIDE HEART FAILURE
41
HEART FAILURE
ETIOLOGY AND
PATHOPHYSIOLOGY
Systolic failure- most common cause
Hallmark finding: Dec. in *left ventricular ejection
fraction (EF)
Due to
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)
Systolic
heart
failure
vs
Diastolic
Heart
failure
CHRONIC HEART
FAILURE
Symptom severity
Marked
Marked
Mild to moderate
Pulmonary edema
Frequent
Frequent
Rare
Peripheral edema
Rare
Frequent
Frequent
Weight gain
None to mild
Frequent
Frequent
Cardiomegaly
Uncommon
Usual*
Common*
Reduced, normal, or
hypercontractile
Reduced*
Reduced*
Wall stress
Elevated
Markedly elevated
Elevated
Marked
Marked
Mild to marked
Activation of renin-angiotensin-aldosterone
system
Often increased
Marked
Mild to marked
Common
Occasional
Occasional
*Patients with diastolic heart failure may have little to no cardiomegaly and normal systolic function.
Clinical and pathophysiological characteristics of the two major categories of unstable heart failure (acute heart failure and decompensated chronic heart failure) are compared
with those of chronic heart failure.
Adapted from Leier CV: Unstable heart failure. In Colucci WS (ed): Heart Failure: Cardiac Function and Dysfunction. 2nd ed. In Braunwald E (series ed): Atlas of Heart Diseases,
vol 4. Philadelphia, Current Medicine, 1999, pp 9.19.17.
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
CAUSES
BASUKI RAHMAT, MD
DEPARTMENT OF CARDIOLOGY AND VASCULAR MEDICINE
FACULTY OF MEDICINE MATARAM UNIVERSITY - MATARAM HOSPITAL WEST NUSA TENGGARA
50
dilated cardiomyopathy
CLINICAL
ASSESMENT
BASUKI RAHMAT, MD
DEPARTMENT OF CARDIOLOGY AND VASCULAR MEDICINE
FACULTY OF MEDICINE MATARAM UNIVERSITY - MATARAM HOSPITAL WEST NUSA TENGGARA
PHYSICAL EXAMINATION
IN HEART FAILURE
S3 gallop
MEASURING JUGULAR
VENOUS PRESSURE
LAB ANALYSIS IN
HEART FAILURE
CBC
Iron studies
ANA
Viral studies
LABORATORY
ANALYSIS (CONT.)
BNP
With chronic heart failure, atrial mycotes secrete increase
amounts of atrial natriuretic peptide (ANP) and brain
natriuretic pepetide (BNP) in response to high atrial and
ventricular filling pressures
Usually is > 400 pg/mL in patients with dyspnea due to
heart failure.
CHEST X-RAY IN
HEART FAILURE
Cardiomegaly
Cephalization of the pulmonary vessels
Kerley B-lines
Pleural effusions
CARDIOMEGALY
PULMONARY VESSEL
CONGESTION
PULMONARY OEDEMA
KERLEY B LINES
CARDIAC TESTING IN
HEART FAILURE
Electrocardiogram:
May show specific cause of heart failure:
Ischemic heart disease
Dilated cardiomyopathy: first degree AV block, LBBB, Left
anterior fascicular block
Amyloidosis: pseudo-infarction pattern
Idiopathic dilated cardiomyopathy: LVH
Echocardiogram:
Left ventricular ejection fraction
Structural/valvular abnormalities
FURTHER CARDIAC
TESTING IN HEART FAILURE
Exercise Testing
Should be part of initial evaluation of all patients with CHF.
Coronary arteriography
Should be performed in patients presenting with heart failure
who have angina or significant ischemia
Reasonable in patients who have chest pain that may or may
not be cardiac in origin, in whom cardiac anatomy is not
known, and in patients with known or suspected coronary
artery disease who do not have angina.
Measure cardiac output, degree of left ventricular dysfunction,
and left ventricular end-diastolic pressure.
CLASIFICATION OF
HEART FAILURE
A
B
ACCF/AHA Stages of HF
At high risk for HF but without structural
heart disease or symptoms of HF.
Structural heart disease but without signs
or symptoms of HF.
Structural heart disease with prior or
current symptoms of HF.
II
III
IV
D
MANAGEMENT
BASUKI RAHMAT, MD
DEPARTMENT OF CARDIOLOGY AND VASCULAR MEDICINE
FACULTY OF MEDICINE MATARAM UNIVERSITY - MATARAM HOSPITAL WEST NUSA TENGGARA
Upright Position
Nitrates
Lasix
Oxygen
Dig, Dobutamine
Morphine Sulfate
Extremities Down
GOALS OF TREATMENT-ADHF/PULMONARY
EDEMA)
MAD DOG
Improve gas exchange
D- Diuretics
O- oxygen /measure sats;
Hemodynamics, careful observation
G- blood gases
COMPLICATION
BASUKI RAHMAT, MD
DEPARTMENT OF CARDIOLOGY AND VASCULAR MEDICINE
FACULTY OF MEDICINE MATARAM UNIVERSITY - MATARAM HOSPITAL WEST NUSA TENGGARA
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%
TERIMAKASIH
IN SUMMARY..