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GAGAL

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+

Heart Failure: a major public health


problem

The number of CHF patients will almost double


between the years 1990-2030, from these 3 million
cases of overt CHF to about 6 million.

ESTIMATED DIRECT AND


INDIRECT COSTS OF HF IN US
Hospitalization
$13.6

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

*Lost future earnings of persons who will die in 2004, discounted by 3%


AHA. Heart Disease and Stroke Statistics2004 Update

CAUSES OF HOSPITAL READMISSION


FOR CONGESTIVE HEART FAILURE

Over 2/3 of HF Hospitalizations Preventable


Diet Noncompliance
24%

16%
Inappropriate Rx

Rx Noncompliance
24%

19%
Failure to Seek
Care

Annals of Internal Medicine 122:415-21, 1995

17%
Other

PROGNOSIS WITH HEART FAILURE: MORE

Overall
5-year mortality 50%

Survival %

MALIGNANT THAN CANCER !


100
90
80
70
60
50
40
30
20
10
0

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

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

13

Associated with long standing HTN and CAD

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)

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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

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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Heart Rate

FACTORS AFFECTING
CARDIAC OUTPUT
Preload

18

The volume of blood/amount of fiber


stretch in the ventricles at the end of
diastole (i.e., before the next contraction)

FACTORS AFFECTING
CARDIAC OUTPUT
Preload increases with:
Fluid volume increases
Vasoconstriction (squeezes blood from
vascular system into heart)

Preload decreases with

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Fluid volume losses


Vasodilation (able to hold more blood,
therefore less returning toheart)

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

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Excessive preload = excessive stretch


reduced contraction reduced SV/CO

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:

21

Vasodilation

FACTORS AFFECTING
CARDIAC OUTPUT
Contractility

22

Ability of the heart muscle to contract;


relates to the strength of contraction.

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:

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Sympathetic stimulation (effects of epinephrine)


Positive inotropes (medications that increase
contractility, such as digoxin, sympathomimmetics)

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

Myocardial hypertrophy: walls of heart thicken to


provide more muscle mass stronger contractions

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:

32

Aldosterone release Na retention and


water retention (via ADH secretion)
Peripheral vasoconstriction

PATHOPHYSIOLOGY
OF CHF
Compensatory mechanisms may restore
CO to near-normal.

33

But, if excessive the compensatory


mechanisms can worsen heart failure
because . . .

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

Excessive tachycardia d diastolic


filling time d ventricular filling
d SV and CO

THE VICIOUS CYCLE OF


CONGESTIVE HEART FAILURE

LV Dysfunction causes
Decreased cardiac output

Decreased Blood Pressure


and
Decreased Renal perfusion

Stimulates the Release


of renin, Which allows
conversion of
Angiotensin
to Angiotensin II.
Angiotensin II stimulates
Aldosterone secretion
which
causes retention of
Na+ and Water,
increasing filling pressure

TYPES OF CONGESTIVE
HEART FAILURE

LEFT SIDE HEART FAILURE

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Most common form


Blood backs up through the left
atrium into the pulmonary veins
Pulmonary congestion and edema
Eventually lead to biventricular failure

TYPES OF CONGESTIVE
HEART FAILURE

LEFT SIDE HEART FAILURE


Most common cause
HTN
Cardiomyopathy
Valvular disorder
CAD
37

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

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TYPES OF CONGESTIVE
HEART FAILURE
RIGHT SIDE HEART FAILURE

39

Venous congestion
Peripheral edema
Hepatomegaly
Splenomegaly
Jugular Venous distension

RIGHT HEART FAILURE

Signs and Symptoms

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

Primay cause is left-sided failure


Cor pulmonale
RV dilation and hypertophy
caused by pulmonary pathology

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)

Systolic
heart
failure
vs
Diastolic
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

ACUTE VS. CHRONIC HEART FAILURE


FEATURE

ACUTE HEART FAILURE

DECOMPENSATED CHRONIC 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

Whole-body fluid volume load

No change or mild increase

Moderate to marked increase

Mild to marked increase

Cardiomegaly

Uncommon

Usual*

Common*

Ventricular systolic function

Reduced, normal, or
hypercontractile

Reduced*

Reduced*

Wall stress

Elevated

Markedly elevated

Elevated

Activation of sympathetic nervous system

Marked

Marked

Mild to marked

Activation of renin-angiotensin-aldosterone
system

Often increased

Marked

Mild to marked

Reparable, reversible causative lesion(s)

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

Underlying causes/risk factors


Ischemic heart disease (CAD)
hypertension
myocardial infarction (MI)
valvular heart disease
congenital heart disease

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

Low sensitivity, but highly specific

Cool, pale, cyanotic extremities

Have sinus tachycardia, diaphoresis and peripheral vasoconstriction

Crackles or decreased breath sounds at bases (effusions) on


lung exam
Elevated jugular venous pressure
Lower extremity edema
Ascites
Hepatomegaly
Splenomegaly
Displaced PMI
Apical impulse that is laterally displaced past the midclavicular line is
usually indicative of left ventricular enlargement>

MEASURING JUGULAR
VENOUS PRESSURE

What does this


show?

What is present in this extremity, common to right sided HF?

LAB ANALYSIS IN
HEART FAILURE
CBC

Since anemia can exacerbate heart failure

Serum electrolytes and creatinine

before starting high dose diuretics

Fasting Blood glucose

To evaluate for possible diabetes mellitus

Thyroid function tests

Since thyrotoxicosis can result in A. Fib,


and hypothyroidism can results in HF.

To screen for hereditary hemochromatosis as cause of heart failure.

To evaluate for possible lupus

Iron studies
ANA
Viral studies

If viral mycocarditis suspected

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 EDEMA DUE


TO HEART FAILURE

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.

NYHA Functional Classification


None
I

II

III

IV
D

Refractory HF requiring specialized


interventions.

No limitation of physical activity.


Ordinary physical activity does not cause
symptoms of HF.
No limitation of physical activity.
Ordinary physical activity does not cause
symptoms of HF.
Slight limitation of physical activity.
Comfortable at rest, but ordinary physical
activity results in symptoms of HF.
Marked limitation of physical activity.
Comfortable at rest, but less than ordinary
activity causes symptoms of HF.
Unable to carry on any physical activity
without symptoms of HF, or symptoms of
HF at rest.

MANAGEMENT

BASUKI RAHMAT, MD
DEPARTMENT OF CARDIOLOGY AND VASCULAR MEDICINE
FACULTY OF MEDICINE MATARAM UNIVERSITY - MATARAM HOSPITAL WEST NUSA TENGGARA

HEART FAILURE MANAGEMENT


U

Upright Position

Nitrates

Lasix

Oxygen

ACE, ARBs, Amiodorone

Dig, Dobutamine

Morphine Sulfate

Extremities Down

GOALS OF TREATMENT-ADHF/PULMONARY

EDEMA)

MAD DOG
Improve gas exchange

Start O2/elevate HOB/intubate


Morphine dec anxiety/afterload
A- (airway/head up/legs down)
D- (Drugs) Dig not first now- but drugs as
IV nitroglycerin; IV Nipride, Natrecor

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%

HF lead to severe hepatomegaly, especially with RV failure


Fibrosis and cirrhosis - develop over time

Renal insufficiency or failure

TERIMAKASIH

IN SUMMARY..

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