Gagal Jantung_ukdw_okt2014.pdf

HEART FAILURE

Beberapa Istilah

Gagal Jantung Payah Jantung Decompensatio Cordis Heart Failure Congestive Heart Failure Ventricular Failure dll

Pendahuluan

Merupakan masalah yang sangat serius Menyebabkan pasien sering keluar masuk RS Di USA:

Terdapat 43.000 kematian per hari akibat gagal jantung

400.000 kasus baru per tahun Total terdapat 4,9 juta penderita gagal jantung

Menurut Braunwald Gagal Jantung adalah suatu keadaan patofisiologis adanya kelainan fungsi jantung yang berakibat jantung gagal memompakan darah untuk memenuhi kebutuhan metabolisme jaringan dan/atau kemampuannya hanya ada kalau disertai peninggian tekanan pengisian ventrikel kiri (volume diastolik).

Definisi

Menurut Sonnenblik: Secara singkat Gagal Jantung terjadi apabila jantung

tidak lagi mampu memompakan darah yang cukup untuk memenuhi kebutuhan metabolik tubuh pada tekanan pengisian yang normal, padahal aliran balik vena (venous return) ke jantung dalam keadaan normal.

Definisi

Definition:

A state in which the heart cannot provide sufficient cardiac output to satisfy the metabolic needs of the body

Definition of Heart Failure HF is a clinical syndrome in wich patients have the following feature: 1. Symptoms typical of HF

breathlessness at rest or on exercise fatique tiredness ankle swelling AND

2. Signs typical of HF tachycardia, tachypneu, pulmonary rales, pleural e f fus ion , r a i sed JVP , pe r iphera l oedema , hepatomegaly AND

3. Objective evidence of a structural or functional abnormality of the heart at rest (cardiomegaly, third heart sound, cardiac murmurs, abnormality of echocardiography, raised Natriuretic peptide concentration)

FORMS OF HEART FAILURE

Gagal Jantung Backward & Forward

Hipotesis backward failure pertama kali diajukan oleh James Hope pada tahun 1832: Apabila ventrikel gagal memompakan darah

maka darah akan terbendung dan tekanan di atrium serta vena-vena di belakangnya akan naik

Gagal Jantung Backward & Forward

Hipotesis forward failure diajukan oleh Mackenzie 80 tahun setelah hipotesis backward failure: Manifestasi gagal jantung timbul akibat

berkurangnya aliran darah (cardiac output) ke sistem arterial, sehingga terjadi pengurangan perfusi pada organ-organ yang vital dengan segala akibatnya

BACKWARD VERSUS FORWARD HEART FAILURE

backward HF one or the other ventricle fails to discharge its

contents or fails to fill normally

forward HF the clinical manifestations of HF result directly from

an inadequate discharge of blood into the arterial system

Gagal Jantung Right sided & Left sided

Gagal Jantung Kiri (Left Heart Failure) Ventrikel kiri gagal menjalankan fungsinya Infark ventrikel kiri, hipertensi, kelainan pada

katub aorta maupun mitral Terjadi kongesti pulmonal

Gagal Jantung Kanan (Right Heart Failure) Ventrikel kanan gagal menjalankan fungsinya Terjadi bendungan sistemik: edema tungkai,

ascites, hepatomegali, efusi pleura

RIGHT-SIDED VERSUS LEFT-SIDED HEART FAILURE

left-sided HF For example, patients in whom the left ventricle is

hemodynamically overloaded (e.g., aortic stenosis) or weakened (e.g., postmyocardial infarction) develop dyspnea and orthopnea as a result of pulmonary congestion

right-sided HF the underlying abnormality affects the right ventricle primarily

(e.g., congenital valvular pulmonic stenosis or pulmonary hypertension secondary to pulmonary thromboembolism),

symptoms resulting from pulmonary congestion are uncommon,

edema, congestive hepatomegaly, and systemic venous distention

Gagal Jantung Low Output & High Output

Gagal Jantung pada golongan ini menunjukkan bagaimana keadaan curah jantung (cardiac output) apakah tinggi atau rendah sebagai penyebab manifestasi klinik gagal jantung

Contoh gagal jantung low output: Penyakit jantung bawaan, hipertensi, kelainan katup,

koroner, kardiomiopati dll)

Contoh gagal jantung high output: Tirotoksikosis, Pagets Disease, beri-beri, anemia

HIGH-OUTPUT VERSUS LOW-OUTPUT HEART FAILURE

low-output HF occurs secondary to ischemic heart disease,

hypertension, dilated cardiomyopathy, and valvular and pericardial disease

high-output HF is seen in patients with HF and hyperthyroidism,

anemia, pregnancy, arteriovenous fistulas, beriberi, and Paget's disease

In clinical practice, however, low-output and high-output HF cannot always be readily distinguished

Gagal Jantung Akut & Menahun

Menunjukkan saat atau lamanya gagal jantung terjadi atau berlangsung

Apabila terjadi mendadak, misal pada infark jantung yang luas, dinamakan gagal jantung akut

Apabila terjadi secara perlahan maka dinamakan gagal jantung menahun

ACUTE VERSUS CHRONIC HEART FAILURE

acute HF sudden development of a large myocardial

infarction or rupture of a cardiac valve in a patient who previously was entirely well

Chronic HF patients with dilated cardiomyopathy or

multivalvular heart disease that develops or progresses slowly

Gagal Jantung Sistolik & Diastolik

Apabila gagal jantung yang terjadi merupakan akibat abnormalitas fungsi sistolik, yaitu kemampuan mengeluarkan darah dari ventrikel maka dinamakan gagal jantung sistolik

Apabila gagal jantung yang terjadi merupakan akibat abnormalitas fungsi diastolik, yaitu kemampuan pengisian darah pada ventrikel maka dinamakan gagal jantung diastolik

SYSTOLIC VERSUS DIASTOLIC FAILURE

relates to whether the principal abnormality is the inability of the ventricle to contract normally and expel sufficient blood (systolic failure) or to relax and/or fill normally (diastolic failure). The major clinical manifestations of systolic failure relate to an inadequate cardiac output with weakness, fatigue, reduced exercise tolerance, and other symptoms of hypoperfusion, while in diastolic HF the manifestations relate principally to the elevation of filling pressures. Many patients, particularly those who have both ventricular hypertrophy and dilatation, exhibit abnormalities both of contraction and relaxation coexis

Diastolic HF may be caused by increased resistance to ventricular inflow

and reduced ventricular diastolic capacity (constrictive pericarditis and restrictive, hypertensive, and hypertrophic cardiomyopathy), impaired ventricular relaxation (acute myocardial ischemia), and myocardial fibrosis and infiltration (restrictive cardiomyopathy)

Etiology

It is a common end point for many diseases of cardiovascular system

It can be caused by : -Inappropriate work load (volume or pressure overload)

-Restricted filling -Myocyte loss

Causes of left ventricular failure Volume over load : Regurgitate valve

High output status Pressure overload : Systemic hypertension Outflow obstruction

Loss of muscles : Post MI, Chronic ischemia Connective tissue diseases Infection, Poisons

(alcohol,cobalt,Doxorubicin)

Restricted Filling : Pericardial diseases, Restrictive cardiomyopathy, tachyarrhythmia

Health conditions that either damage the heart or make it work too hard

Coronary artery disease Heart attack High blood pressure Abnormal heart valves Heart muscle diseases (cardiomyopathy) Heart inflammation (myocarditis)

What Causes Heart Failure?

Congenital heart defects Severe lung disease Diabetes Severe anemia Overactive thyroid gland (hyperthyroidism) Abnormal heart rhythms

What Causes Heart Failure?

Heart Failure

What Causes Heart Failure? Coronary artery disease

Cholesterol and fatty deposits build up in the hearts arteries

Less blood and oxygen reach the heart muscle

This causes the heart to work harder and occasionally damages the heart muscle

Heart Failure

What Causes Heart Failure? Heart attack

An artery supplying blood to the heart becomes blocked

Loss of oxygen and nutrients damages heart muscle tissue causing it to die

Remaining healthy heart muscle must pump harder to keep up

Heart Failure

What Causes Heart Failure? High blood pressure

Uncontrolled high blood pressure doubles a persons risk of developing heart failure

Heart must pump harder to keep blood circulating

Over time, chamber first thickens, then gets larger and weaker

Heart Failure

What Causes Heart Failure? Abnormal heart valves Heart muscle disease

Damage to heart muscle due to drugs, alcohol or infections

Congenital heart disease Severe lung disease

Heart Failure

What Causes Heart Failure? Diabetes

Tend to have other conditions that make the heart work harder

Obesity Hypertension High cholesterol

Heart Failure

What Causes Heart Failure? Severe anemia

Not enough red blood cells to carry oxygen Heart beats faster and can become overtaxed with

the effort Hyperthyroidism

Body metabolism is increased and overworks the heart

Abnormal Heart Rhythm If the heart beats too fast, too slow or irregular it may

not be able to pump enough blood to the body

Manifestasi Klinis Manifestasi klinis gagal jantung sangat

beragam dan bergantung pada banyak faktor a.l. Etiologi kelainan jantung Umur pasien Berat atau ringannya Terjadinya secara mendadak atau perlahan

dan menahun Ventrikel mana yang menjadi pencetus

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

New York Heart Association (NYHA) Functional Classification

CLINICAL MANIFESTATIONS OF HEART FAILURE

DYSPNEA Orthopnea Paroxysmal (Nocturnal) Dyspnea

CHEYNE-STOKES RESPIRATION FATIGUE AND WEAKNESS ABDOMINAL SYMPTOMS

Anorexia and nausea associated with abdominal pain and fullness

CEREBRAL SYMPTOMS confusion, difficulty in concentration, impairment of memory,

headache, insomnia, and anxiety. Nocturia

Shortness of Breath (dyspnea) WHY?

Blood backs up in the pulmonary veins because the heart cant keep up with the supply an fluid leaks into the lungs

SYMPTOMS Dyspnea on exertion or at rest Difficulty breathing when lying flat Waking up short of breath

Signs and Symptoms of Heart Failure

Persistent Cough or Wheezing WHY?

Fluid backs up in the lungs SYMPTOMS

Coughing that produces white or pink blood-tinged sputum


Edema WHY?

Decreased blood flow out of the weak heart Blood returning to the heart from the veins

backs up causing fluid to build up in tissues SYMPTOMS

Swelling in feet, ankles, legs or abdomen Weight gain


Tiredness, fatigue WHY?

Heart cant pump enough blood to meet needs of bodies tissues

Body diverts blood away from less vital organs (muscles in limbs) and sends it to the heart and brain

SYMPTOMS Constant tired feeling Difficulty with everyday activities


Lack of appetite/ Nausea WHY?

The digestive system receives less blood causing problems with digestion

SYMPTOMS Feeling of being full or sick to your stomach


Confusion/ Impaired thinking WHY?

Changing levels of substances in the blood ( sodium) can cause confusion

SYMPTOMS Memory loss or feeling of disorientation Relative or caregiver may notice this first


Increased heart rate WHY?

The heart beats faster to make up for the loss in pumping function

SYMPTOMS Heart palpitations May feel like the heart is racing or throbbing


Common clinical manifestation of HF

Dominant clinical feature Symptoms Signs

Peripheral oedema / conges2on

Breathlessness Tiredness, fa2que Anorexia

Peripheral oedema Raised JVP Pulmonary oedema Hepatomegaly, ascites Fluid overload (conges2on) Cachexia

Pulmonary oedema Severe breathlessness at rest Crackles or rales over lungs, eusion Tachycardia, tachypnoea

Cardiogenic shock (low output syndrome)

Confusion Weakness Cold periphery

Poor peripheral perfusion Systolic BP < 90 mmHg Anuria or oliguria

High BP (hypertensive HF) Breathlessness Usually raised BP, LVH and preserved EF

Right HF Breathlessness Fa2que

Evidence of RV dysfunc2on Raised JVP, peripheral oedema, hepatomegaly, gut conges2on

Physical examination

The physical examina2on can provide important informa2on concerning the degree to which the cardiac output is reduced as well as the degree of volume overload, ventricular enlargement, and pulmonary hypertension

Heart sounds An S3 gallop have been associated with leS atrial pressures exceeding 20 mmHg, increased leS ventricular end-diastolic pressures (>15 mmHg)


Decreased cardiac output patients compensate for a fall in cardiac output

by increasing sympathetic outow sinus tachycardia, diaphoresis, and peripheral

vasoconstriction. manifested as cool, pale, and sometimes cyanotic

extremities (due to the combination of decreased perfusion and increased oxygen extraction)


Volume overload There are three major manifestations of volume

overload in patients with HF: pulmonary congestion, peripheral edema, and elevated jugular venous pressure

BLOOD TESTS

A complete blood count since anemia can exacerbate preexis2ng HF

Serum electrolytes and crea2nine as a baseline to follow when ini2a2ng therapy with diure2cs and/or angiotensin conver2ng enzyme inhibitors.

Liver func2on tests, which may be aected by hepa2c conges2on.

Fas2ng blood glucose to detect underlying diabetes mellitus

CHEST X-RAY

is a useful rst diagnos2c test, par2cularly in the evalua2on of pa2ents who present with dyspnea

Findings sugges2ve of HF include: cardiomegaly (cardiac-to-thoracic width ra2o above 50 percent), cephaliza2on of the pulmonary vessels, Kerley B-lines, and pleural eusions

ELECTROCARDIOGRAM

arrhythmias

ischemic heart disease

AV block

LeS ventricular hypertrophy

ECHOCARDIOGRAPHY

should be performed in all pa2ents with new onset HF and can provide important informa2on about ventricular size and func2on

KRITERIA DIAGNOSIS KRITERIA FRAMINGHAM

KRITERIA MAYOR: Paroxysmal Nocturnal

Dyspneu Distensi vena-vena leher Peningkatan vena jugularis Ronki Kardiomegali Edema paru Galop S3

KRITERIA MINOR: Edema ekstremitas Batuk malam Sesak pada aktivitas Hepatomegali Efusi pleura Takikardia (>120x/mnt)

Diagnosis ditegakkan bila terdapat paling sedikit satu kriteria mayor dan dua kriteria minor

DIAGNOSIS BANDING Penyakit Paru:

Pneumonia PPOK Asma eksaserbasi akut Infeksi paru berat misal ARDS, emboli paru

Penyakit Ginjal: Gagal Ginjal Kronik Sindrom Nefrotik

Penyakit Hati: Sirosis Hepatis

Precipitating Factors

In evaluating patients with HF, it is important to identify: not only the underlying but also the precipitating cause

PRECIPITATING CAUSES 1. Infection 2. Anemia 3. Thyrotoxicosis and pregnancy 4. Arrhythmias 5. Rheumatic, viral, and other forms of myocarditis 6. Infective endocarditis 7. Physical, dietary, fluid, environmental, and emotional

excesses 8. Systemic hypertension 9. Myocardial infarction 10.Pulmonary embolism.

Terapi

Treatment Options

The more common forms of heart failure cannot be cured, but can be treated

Lifestyle changes Medications Surgery

Lifestyle changes Stop smoking

Loose weight Avoid alcohol Avoid or limit caffeine Eat a low-fat, low-sodium diet Exercise Reduce stress Limit fluid intake

TERAPI Non Farmakologi Anjuran Umum:

Edukasi: terangkan hubungan keluhan, gejala dan pengobatan

Aktivitas sosial dan pekerjaan diusahakan agar dapat dilakukan seperti biasa sesuai kemampuan fisik yang masih bisa dilakukan

Gagal jantung berat harus menghindari penerbangan panjang

TERAPI Non Farmakologi Tindakan Umum:

Diet (hindarkan obesitas, rendah garam 2 gram pada gagal jantung ringan dan 1 gram pada gagal jantung berat, jumlah cairan 1 liter pada gagal jantung berat dan 1,5 liter pada gagal jantung ringan

Hentikan rokok Hentikan alkohol Istirahat baring pada gagal jantung akut, berat dan

eksaserbasi akut.

Myocardial Damaged

Myocardial Failure

Cardiac Output Ventricular Filling Pressures

Preload +

Afterload

Compensatory Mechanism Vasopresin RAA sympathetic activity

Na / H2O retention Venoconstriction

+ systemic vascular

resistance

Inotropic Agent (Digitalis)

ACE Inhibitors

Fluid restriction Low sodium diet Diuretic vasodilator

Mekanisme Kompensasi Gagal Jantung

Symptomatic HF + reduced ejection fraction

Persis2ng signs and symptoms

Diuretic + ACE I (or ARB) titrate to clinical stability

Betablocker

No

No

Yes

Yes

Yes

No Yes

LV EF < 35%?

Add aldosteron or ARB

Persis2ng symptoms

No further treatment Consider ICD

Consider: digoxin, hydralazine/nitrate LVAD

Consider: CRT or CRT-D

No

QRS dura2on > 120 sec

Detect major co-morbidi2es and precipita2ng factors Non cardiovascular Anemia Pulmonary disease Renal dysfunc2on Thyroid dysfunc2on Diabetes Cardiovascular IHD / CAD HT, AF, VT, Bradicardia

TERAPI Farmakologi Diuretik :

Kebanyakan membutuhkan diuretik dosis rendah untuk mencapai tekanan vena jugular normal dan menghilangkan edema

Permulaan dapat digunakan loop diuretik atau tiazid.

Diuretik hemat kalium, spironolakton 25-50 mg/hari dapat mengurangi mortalitas pada pasien gagal jantung sedang sampai berat yang disebabkan gagal jantung sistolik

Diuretics (water pills) Prescribed for fluid build up, swelling or

edema Cause kidneys to remove more sodium and

water from the bloodstream Decreases workload of the heart and edema Fine balance removing too much fluid can

strain kidneys or cause low blood pressure

Medications used to treat Heart Failure

Diuretics

Diure2cs are recommended in pts with clinical signs or symptoms of conges2on

Diure2cs provide relief from the symptoms and signs of pulmonary and systemic venous conges2on

Diure2cs cause ac2va2on of renin-angiotensin-aldosterone system and should be used in combina2on with an ACE-I / ARB

Class of recommenda6on I, level of evidence B

Aldosterone antagonists

The addi2on of aldosterone antagonist is recommended in all pts with an EF 35%, severe symptoma2c HF without hyperkalemia or signicant renal dysfunc2on

Aldosterone antagonists reduce hospital admission for worsening HF and increased survival when added to exis2ng therapy, including ACE-I

Class of recommenda6on I, level of evidence B

In such hospitalised pa2ents, treatment with an aldosterone antagonist should be ini2ated before discharge

Practical considerations in treatment with loop diuretics

Problems Suggested ac6ons

Hypokalemia/hypomagnesaemia

Increase ACE-I/ARB dosage Add aldosterone antagonist Potassium supplements Magnesium supplements

Hyponatremia Water restric2on Stop thiazide diure2c or switch to loop diure2c, if

possible Reduce dosage/stop loop diure2cs if possible i.v. inotropic support Consider ultraltra2on

Hyperuricemia/gout Consider allopurinol For symptoma2c gout use colchicine for pain relief Avoid NSAIDs

Hypovolemia/dehydra2on

Asses volume status Consider diure2c dosage reduc2on

Practical considerations in treatment with loop diuretics

Problems Suggested ac6ons

Insucient response or diure2c resistance

Check compliance and uid intake Increase dosage of diure2c Consider switching from furosemide to

bumetanide or torasemide Add aldosteron antagonist Combine loop diure2c and thiazide Admister loop diure2c twice daily or on empty

stomach Consider short-term i.v. infusion of loop diure2c

Renal failure Check for hypovolaemia/dehydra2on Exclude use other nephrotoxic agents e.g. NSAIDs,

trimethoprim Withhold aldosterone antagonist If using concomitant loop and thiazide diure2c,

stop thiazide diure2c Consider reducing dose of ACE-I/ARB Consider ultraltra2on

TERAPI Farmakologi Penghambat ACE:

Bermanfaat untuk menekan aktivasi neurohormonal dan pada gagal jantung akibat disfungsi sistolik ventrikel kiri

Pemberian dimulai dengan dosis rendah, dititrasi selama beberapa minggu sampai dosis yang efektif

Dapat mencegah secara dini terjadinya hipertrofi, dilatasi dan remodeling ventrikel yang menyebabkan disfungsi ventrikel yang pada akhirnya menyebabkan gagal jantung

ACE Inhibitors Cornerstone of heart failure therapy Proven to slow the progression of heart

failure Vasodilator cause blood vessels to

expand lowering blood pressure and the hearts work load


ACE Inhibitor

An ACE-I is recommended in all pa2ents with symptoma2c HF and an EF 40%

Treatment with an ACE-I improves LV func2on, pa2ent well being, reduces hospital admission for worsening HF and increases survival

Class of recommenda6on I, level of evidence A

In hospitalised pa2ents, treatment should be ini2ated before discharge

Angiotensin Receptor Blockers (ARBs)

An ARB is recommended in all pts with HF and EF 40% WHO: Remain symptoma2c despite op2mal Rx with an ACE-I and beta blocker As an alterna2ve in pts, intolerant of an ACE-I

Unless pts are treated with an aldosterone antagonist

Treatment with an ARB improves LV func2on, pa2ent well being and reduces hospital admission for worsening HF


Treatment reduces the risk of CV death

Class of recommenda6on IIa, level of evidence B

In hospitalised pa2ents, treatment with ARB should be ini2ated before discharge

TERAPI Farmakologi Penyekat beta:

Bermanfaat sama seperti penghambat ACE Pemberian mulai dosis kecil Biasanya diberikan bila keadaan mulai stabil

Angiotensin II antagonis reseptor:

Dapat digunakan bila ada kontraindikasi penggunaan penghambat ACE

Blocker

A blocker should be used in all pts with symptoma2c HF and an EF 40%

Lower the heart rate and blood pressure Decrease the workload of the heart

blockade improves ventricular func2on and pts well being, and reduces hospital admission for worsening HF and increases survival


In hospitalised pa2ents, treatment with a blocker should be ini2ated cau2ously before discharge

TERAPI Farmakologi digoksin:

Digunakan untuk pasien simtomatik dengan gagal jantung disfungsi sistolik ventrikel kiri dan terutama yang dengan fibrilasi atrial

Digunakan bersama-sama dengan diuretik, penghambat ACE dan penyekat beta

Digitalis preparations Increases the force of the hearts

contractions Relieves symptoms Slows heart rate and certain irregular heart

beats


Class I recommendations for drugs in patients with symptomatic systolic dysfunction

ACE-I All pa6ents* Class I Level A ARB ACE intolerant/persis2ng signs or

symptoms on ACE-I / B-blokade* Class I Level A

B-Blocker All pa2ents* Class I Level A Aldosterone antagonist

Severe symptoms on ACE-I* Class I Level A

Diure6c All pts with signs or symptoms of conges2on

Class I Level B

Management of Hypertention in pts with HF

In hypertensive pts with evidence of LV dysfunc6on

Systolic and diastolic BP should be carefully controlled with a therapeu2c target of 140/90 and 130/80 mmHg in diabe2cs and high risk pts

An2-hypertensive regimens based on renin-angiotensin system antagonists (ACE-I or ARBs) are preferable

Acute HF

Is dened as rapid onset or change in the signs and symptoms of HF, resul2ng in the need of urgent therapy

It may present as new HF or worsening HF in the presence of Chronic HF

It may be associated with worsening symptoms or signs or as a medical emergency such as acute pulmonary oedema

Mul2ple cardiovascular and non cardiovscular morbidi2es may precipitate AHF

Causes and precipitating factors of AHF

Ischaemic Heard Disease ACS Right ventricular infarc6on

Circulatory failure Sep6caemia Thyrotoxicosis Anaemia Tamponade Pulmonary embolism

Valvular Valve stenosis Valvular rregurgita2on Endocardi2s Aor2c dissec2on

Myopathies Postpartum cardiomyopathiy Acute myocardi2s

Decompensa2on of preexis2ng chronic HF Volume overload Infec2on, especially pneumonia Surgery Renal dysfunc2on Asthma, COPD

Hypertension / arrhythmia Hypertension Acute arrhythmia

A clinical assessment of pts with AHF

DRY AND WARM

WET AND WARM

DRY AND COLD

WET AND COLD

Pulmonary Congestion

Tiss

ue P

erfu

ssio

n

Clinical Cassifications

Goals of treatment in AHF Immediate (ED/ICU) Improve symptoms Restore oxygena2on Improve organ perfusion an haemodynamics Limit cardiac/renal damage Minimize ICU Length of stay

Intermediate (in hospital) Stabilize pts and op2mize treatment strategy Ini2ate appropriate (live saving) pharmacological therapy Minimize hospital LOS

Long-term and predischarge management Educate and ini2ate appropriate lifestyle adjustments Prevent early readmission Improve quality of life and survival

Prognosis

Annual mortality rate depends on patients symptoms and LV function

5% in patients with mild symptoms and mild in LV function

30% to 50% in patient with advances LV dysfunction and severe symptoms

40% 50% of death is due to SCD

SUMMARY

A thorough history and physical examina2on are the ini2al steps in the evalua2on of pa2ents with suspected HF.

The absence of dyspnea on exer2on makes the diagnosis of HF unlikely, while a history of myocardial infarc2on and a displaced apical impulse, or S3 on physical examina2on, strongly suggest the diagnosis.

Ini2al blood tests should include a complete blood count, plasma electrolytes, BUN and crea2nine, liver func2on tests, and urinalysis

SUMMARY

A chest x-ray and electrocardiogram should be performed in all pa2ents.

The presence of pulmonary vascular conges2on and cardiomegaly on chest x-ray support the diagnosis of HF; chest x-ray is also useful for ruling out pulmonary disease in pa2ents who present with dyspnea.

A normal ECG is unusual in pa2ents with symptoma2c systolic dysfunc2on (98 percent nega2ve predic2ve value).

SUMMARY

Echocardiography should be performed in all pa2ents with new onset HF.

Echocardiography has a high sensi2vity and specicity for the diagnosis of myocardial dysfunc2on, and may also establish the e2ology of HF

Terima Kasih

Documents

Gagal Jantung_ukdw_okt2014.pdf