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Heart Failure

Gagal Jantung

B. Rudy Utantio
7
2
O
c
t
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b
e
Introduction

❖ Morbidity and mortality in heart failure patients remain


unacceptably high despite major advances in treatment
options

❖ The natural history of heart failure is characterized by


acute decompensation episodes

❖ Acute heart failure (AHF) is a life-threatening disease


requiring urgent treatment
THE BURDEN OF HEART FAILURE
NUMBER of PATIENTS ECONOMIC BURDEN
21 MILLION adults worldwide In 2012, the overall worldwide
are living with heart failure cost of heart failure was nearly
This number is expected to $108 BILLION.6
rise.1,2
MORTALITY
50% of heart failure patients die
within 5 years from diagnosis.5

REHOSPITALISATION COMORBIDITIES: The vast


Heart failure is the NUMBER 1 majority of HF patients has 3 or
cause of hospitalisation for more comorbidities 3
patients aged >65 years.4

1. Mozaffarian D et al. Circulation. 2015;131(4):e29-e322.


2. Mosterd A et al. Heart. 2007;93(9):1137-1146.
3. http://www.cms.gov/Research-Statistics-Data-and-Systems/Statistics-Trends-and-Reports/Chronic-Conditions/Downloads/2012Chartbook.pdf
4. Cowie MR et al. Oxford PharmaGenesis; 2014. http://www.oxfordhealthpolicyforum.org/AHFreport. Accessed February 18, 2015.
5. Fauci AS et al. Harrison's Principles of Internal Medicine. 17th ed. New York: McGraw-Hill; 2008.
6. Cook C et al. Int J Cardiol. 2014;171(3):368-376.
GAGAL JANTUNG

 Masalah kesehatan yang progresif


 Angka mortalitas dan morbiditas yang tinggi
di negara maju maupun negara berkembang
termasuk Indonesia.

Di Indonesia, usia pasien gagal jantung relatif lebih


muda dibanding Eropa dan Amerika disertai dengan
tampilan klinis yang lebih berat.
Gagal jantung (akut dan kronik) merupakan
masalah kesehatan yang menyebabkan :

1. Penurunan kualitas hidup


2. Tingginya rehospitalisasi karena
kekambuhan yang tinggi dan
peningkatan angka kematian.
AETIOLOGY OF HF
VALVULAR HEART DISEASE MYOCARDIAL DISEASE
• Coronary artery disease
• Mitral
• Hypertension
• Aortic
• Cardiomyopathy
• Trisuspid
• Pulmonary
ENDOCARDIAL DISEASE
PERICARDIAL DISEASE • With/without hypereosinophilia
• Constrictive pericarditis • Endocardial fibroelastosis
• Pericardial effusion
HEART
ARRHYTHMIA
HIGH OUTPUT STATES FAILURE • Tachyarrhythmia
• Anaemia • Atrial
• Sepsis • Ventricular
• Thyrotoxicosis • Bradyarrhythmia
• Paget‘s disease • Sinus node dysfunction
• Arteriovenous fistula CONDUCTION DISORDERS
• Atrioventricular block
VOLUME OVERLOAD
• Renal failure
• Iatrogenic (e.g. post-
CONGENITAL
operative fluid infusion HEART DISEASE McMurray et al. Eur Heart J 2012;33:1787–847
MOST COMMON CAUSES OF HEART FAILURE
Etiology
• Coronary heart disease • Congenital heart
disease
• Hypertension
• Pericardial disease
• Valvular disease
• Hyperkinetic states
• Cardiomyopathy
• Anemia
• Idiopathic cardiomyopathy
• Arterio-venous fistula
• Alcoholic cardiomyopathy
• Beriberi
• Toxin-related cardiomyopathy
e.g. adriamycin
• Post-partum cardiomyopathy
• Hypertrophic obstructive
cardiomyopathy
• Tachyarrhythmia-induced
cardiomyopathy
*Others: Including hypertension, diabetes, exposure to cardiotoxic agents,
• Infiltrative disorders (e.g. peripartum cardiomyopathy, etc.

amyloidosis)
Krum and Gilbert. Lancet 2003;362:147–58; Colucci (Ed.). Atlas of Heart Failure, 5th ed. Springer 2008;
Dickstein et al. Eur Heart J 2008;29:2388–442
PATHOPHYSIOLOGY OF HF
Injury to myocytes
due to myocardial ELECTRICAL INSTABILITY
infarction or other VENTRICULAR
cause REMODELING
REDUCTION of EF

NEUROHUMORAL
IMBALANCE

An imbalance occurs in three key neurohumoral systems:


• The renin–angiotensin–aldosterone system
• The sympathetic nervous system
• The natriuretic peptide system

The systemic responses in the renin–angiotensin–aldosterone and sympathetic nervous systems cause further
myocardial injury, and have detrimental effects on the blood vessels, and various organs, thereby creating a
pathophysiological ‘vicious cycle’. The natriuretic peptide system has a protective function, which can
counterbalance
1. these
McMurray JJ. N Engl J Med detrimental effects.
2010;362:228–238
2. Shah AM. Lancet 2011;378:704–712
SYMPTOMS AND SIGNS
Clinical The diagnosis of HF can be difficult,
manifestations especially in the early stages
Tiredness
• Main symptoms Shortness of breath

• Breathlessness - DOE Pumping action Coughing


of the heart
• Orthopnea grows weaker Fluid retention
• Paroxysmal Nocturnal Dyspnea
• Reduced exercise tolerance Pleural effusion
• Fatigue
• Ankle swelling

• Main signs
• Elevated jugular venous pressure
Swelling of feet,
• Hepato-jugular reflux ankles, abdomen
and lower back
• Third heart sound area
• Laterally displaced apical impulse
• Cardiac murmur

Pulmonary edema

McMurray et al. Eur Heart J 2012;33:1787–847


Clinical FREQUENCY OF SYMPTOMS AND SIGNS
manifestations
Symptoms and signs in 4,537 residents of Worcester, Massachusetts, USA,
hospitalized for acute HF between 1995 and 2000
100

80
Patients (%)

60

40

20

Goldberg et al. Clin Cardiol 2010;33:e73–80


HEMODYNAMIC PROFILE (The Stevenson four quadran
diagram)
Skenario klinik:

Seorang laki-laki umur


50 tahun datang dengan
keluhan sesak napas,
kedua kaki bengkak
dan cepat lelah
B. Rudy Utantio
SESAK NAPAS
16

10/7/2019
SESAK NAPAS
17

10/7/2019
18

SESAK NAFAS ORGAN JANTUNG  DYSPNEA


Kriteria dispnea :

1. Frekwensi nafas  (Tachypnea)


2. Pernafasan Cuping Hidung
3. Terlihat Kontraksi Otot-Otot Nafas Bantu
4. (Amplitudo Nafas )

10/7/2019
Hasil Anamnesis (Subjective)

Keluhan
 Sesak pada saat beraktifitas - dyspneu d’effort
 Gangguan napas pada posisi tidur terlentang - ortopneu
 Sesak napas malam hari - paroxysmal nocturnal dyspneu

Keluhan tambahan: lemas, mual, muntah dan gangguan mental


pada orangtua
20

DYSPNEA

 DYSPNEU D’EFFORT

 PAROXYSMAL NOCTURNAL
DYSPNEU (PND)
 ORTHOPNEU
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21

SESAK NAFAS  DYSPNEA


• Dyspnea ≠ Hypernea
• Hyperpnea=Tachypnea = Hyperventilation

• Kriteria dispnea :
1. Frekwensi nafas 
2. Pernafasan Cuping Hidung
3. Terlihat Kontraksi Otot-Otot Nafas
Pembantu
4. Amplitudo Nafas 

10/7/2019
Dyspneu d’effort
EDEMA
Pitting Edema
1
0
/
7
/
2
0
33 1
9
DEFINISI GAGAL JANTUNG (1)
Gagal jantung adalah jantung dengan penurunan fungsi
sistolik (fraksi ejeksi) dan atau penurunan fungsi diastolik
(fungsi sistolik atau fraksi ejeksi normal)

Terjadi myocardial remodeling yang akan berlanjut dan


menimbulkan sindroma klinis gagal jantung.
DEFINISI GAGAL JANTUNG (2)
Gagal jantung adalah kumpulan gejala yang kompleks dimana seorang
pasien memiliki tampilan berupa:
1. 1. Gejala gagal jantung (nafas pendek yang tipikal saat istrahat atau
2. saat melakukan aktifitas disertai / tidak kelelahan);
3. 2. Tanda retensi cairan (kongesti paru atau edema pergelangan
4. kaki);
5. 3. Adanya bukti objektif dari gangguan struktur atau fungsi jantung
6. saat istrahat.
AN ABNORMALITY OF CARDIAC STRUCTURE
Heart failure
definition
OR FUNCTION
From myocardial infarction (MI) to HF: Ventricular Remodeling after MI

Fibrous scar Myocyte hypertrophy

Acute
infarction
Increased
interstitial
collagen

Infarct zone thinning Spherical ventricular


and elongation dilation

Konstam MA, et al. J Am Coll Cardiol Img 2011;4:98–108


THE PATHOPHYSIOLOGY OF CHRONIC
HF
Damage to cardiac myocytes and extracellular
matrix leads to changes in the size, shape and
function of the heart (remodeling) and cardiac wall
stress

These changes lead to systemic neurohormonal


imbalance

This may lead to fibrosis, apoptosis, hypertension,


hypertrophy, cellular and molecular alterations,
myotoxicity

Remodeling and Hemodynamic


progressive worsening alterations, salt and
of LV function water retention

Morbidity and mortality HF symptoms


arrhythmias, pump failure dyspnea, edema, fatigue

LV=left ventricular
McMurray. N Engl J Med 2010;362:228–38; Francis et al. Ann Intern Med 1984;101:370–7; Krum, Abraham. Lancet 2009;373:941–55
38

7-Oct-19
TERMINOLOGY RELATED TO LEFT
VENTRICULAR
Heart failure definition EJECTION FRACTION

Diastole
ventricles relaxing

Systole
ventricles contracting
Amount of blood
pumped out of
the ventricle
Total amount of = Ejection fraction (%)
blood in
the ventricle

McMurray et al. Eur Heart J 2012;33:1787–847; Dickstein et al. Eur Heart J 2008;29:2388–442
(NEW)
TERMINOLOGY OF HEART FAILURE
TERMINOLOGY used to describe HF

Related to EF*: HFrEF (reduced ejection fraction: EF<40%)


HFmEF (mildly impaired EF: EF 40-49%
HFpEF (preserved ejection fraction: EF ≥50%)*

Related to time-course: New onset, transient, chronic

Related to progression: Acute, stable, worsening


* There is no consensus concerning the cut-off for preserved EF2

Related to location: Left heart, right heart, combined


1. McMurray et al. Eur Heart J 2012;33:1787–847
2. Dickstein K et al. Eur Heart J 2008;29:2388–442
Tanda objektf gangguan struktur atau fungsional
jantung saat istrahat

- Kardiomegali
- Suara jantung ke tiga  S3 gallop
- Murmur jantung
- Ekokardiografi : abnormal
- Kenaikan konsentrasi peptida natriuretik
Hasil Pemeriksaan Fisik dan Penunjang Sederhana
(Objective)

Pemeriksaan Fisik:
 Peningkatan tekanan vena jugular
 Frekuensi pernapasan meningkat
 Frekuensi nadi dan regularitasnya
 Tekanan darah
 Kardiomegali
 Gangguan bunyi jantung (gallop)
 Ronkhi pada pemeriksaan paru
 Hepatomegali
 Asites
 Edema perifer
Pemeriksaan penunjang esential

 Rontgen thoraks :
 -Kardiomegali,
 -Gambaran edema paru/alveolar edema/butterfly appearance

 EKG :
 -Hipertrofi ventrikel kiri,
 -Atrial fibrilasi,
 -Perubahan gelombang T,
 -Gambaran abnormal lainnya.

Darah perifer lengkap


Foto Toraks
Merupakan komponen penting dalam diagnosis gagal jantung.
Rontgen toraks dapat mendeteksi :
1. Kardiomegali
2. Kongesti paru
3. Efusi pleura
4. Penyakit paru atau infeksi paru  sesak nafas.

Kardiomegali bisa tidak ditemukan pada gagal jantung akut dan


gagal jantung kronik
Elektrokardiogram (EKG)
Pemeriksaan elektrokardiogram harus dikerjakan pada semua
pasien diduga gagal jantung.
Abnormalitas EKG sering dijumpai pada gagal jantung
Abnormalitas EKG memiliki nilai prediktif yang kecil dalam mendiagnosis
gagal jantung
Bila EKG normal, diagnosis gagal jantung khususnya dengan disfungsi
sistolik sangat kecil (< 10%).
54

Left Ventricle Hypertrophy


(LVH)

07/10/2019
Penegakan Diagnostik(Assessment)

Diagnosis Klinis
Diagnosis ditegakkan berdasarkan
Kriteria Framingham minimal :

1 kriteria mayor dan 2 kriteria minor.


Kriteria Mayor:

 Sesak napas tiba-tiba pada malam hari


 (paroxysmal nocturnal dyspneu)
 Distensi vena-vena leher
 Peningkatan tekanan vena jugularis
 Ronkhi
 Terdapat kardiomegali
 Edema paru akut
 Gallop (S3)
 Refluks hepatojugular positif
Kriteria Minor:

− Edema ekstremitas
− Batuk malam
− Dyspneu d’effort (sesak ketika beraktifitas)
− Hepatomegali
− Efusi pleura
− Penurunan kapasitas vital paru sepertiga dari normal
− Takikardi >120 kali per menit
KLASIFIKASI
GAGAL JANTUNG
Klasifikasi berdasarkan kelainan struktural jantung Klasifikasi berdasarkan kapsitas fungsional (NYHA)

Stadium A Kelas I
Memiliki risiko tinggi untuk berkembang menjadi gagal Tidak terdapat batasan dalam melakukan aktifitas
jantung. fisik. Aktifitas fisik sehari-hari tidak menimbulkan
Tidak terdapat gangguan struktural atau fungsional kelelahan, palpitasi atau sesak nafas
jantung, tidak terdapat tanda atau gejala gagal jantung

Stadium B Kelas II
Telah terbentuk gangguan struktur jantung yang Terdapat batasan aktifitas ringan. Tidak terdapat keluhan
berhubungan dengan perkembangan gagal jantung saat istrahat, namun aktifitas fisik sehari-hari
Tidak terdapat tanda atau gejala gagal jantung menimbulkan kelelahan, palpitasi atau sesak nafas

Stadium C Kelas III


Gagal jantung yang simtomatik berhubungan dengan Terdapat batasan aktifitas bermakna.
penyakit struktural jantung yang mendasari Tidak terdapat keluhan saat istrahat, tetapi aktfitas fisik
ringan menyebabkan kelelahan, palpitasi atau sesak

Stadium D Kelas IV
Penyakit jantung struktural lanjut serta gejala gagal jantung Tidak dapat melakukan aktifitas fisik tanpa keluhan
yang sangat bermakna saat istrahat walaupun sudah Terdapat gejala saat istrahat.
mendapat terapi medis maksimal (refrakter) Keluhan meningkat saat melakukan aktifitas

Disadur dari ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2008 1
Diagnosis Banding

− Penyakit paru: Obstruktif kronik (PPOK), Asma, Pneumonia,


Infeksi paru berat (ARDS), Emboli paru

− Penyakit Ginjal: Gagal ginjal kronik, Sindrom nefrotik

− Penyakit Hati: Sirosis hepatik


Komplikasi

− Syok kardiogenik
− Gangguan keseimbangan elektrolit
TUJUAN TATALAKSANA GAGAL JANTUNG
1 . Prognosis Menurunkan mortalitas
. Morbiditas
2 Meringankan gejala dan tanda
Memperbaiki kualitas hidup
Menghilangkan edema dan retensi cairan
Meningkatkan kapasitas aktifitas fisik
Mengurangi kelelahan dan sesak nafas
Mengurangi kebutuhan rawat inap
Menyediakan perawatan akhir hayat
. Pencegahan Timbulnya kerusakan miokard
3

Perburukan kerusakan miokard


Remodelling miokard
Timbul kembali gejala dan akumulasi rawat inap
Disadur dari ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 20081
Penatalaksanaan
1. Modifikasi gaya hidup
 Pembatasan asupan cairan maksimal 1,5 liter (ringan), maksimal 1 liter

(berat)
 Pembatasan asupan garam maksimal 2 gram/hari (ringan), maksimal 1

gram/hari (berat) - Berhenti merokok dan konsumsi alkohol


2. Aktivitas fisik
 Pada kondisi akut berat: tirah baring

 Pada kondisi sedang atau ringan: batasi beban kerja sampai 70% sd 80%

dari denyut nadi maksimal (220 - umur)


1. Penatalaksanaan farmakologi pada gagal jantung
akut di Layanan Primer :

 - Terapi oksigen 2-4 ltr/mnt, posisikan semi-fowler


 - Pemasangan iv line untuk akses
 - Injeksi furosemid 20 s/d 40 mg bolus.
 - Cari pemicu gagal jantung akut.

  Segera rujuk !!!!


PATHOPHYSIOLOGY AND TREATMENT
STAGE OF HEART FAILURE
TREATMENT OVERVIEW
For symptoms For survival/morbidity
Continue ACE-inhibitor/ARB if
NYHA Reduce/stop previous ACE-inhibitor intolerant, continue
I diuretic aldosterone antagonist if post-MI,
add beta-blocker if post-MI
ACE-inhibitor as first-line
+/- Diuretic depending treatment/ARB if ACE-inhibitor
NYHA
intolerant, add Beta-blocker and
II on fluid retention Aldosterone antagonist if post-
MI
ACE-inhibitor or ARB
NYHA + Diuretics + Digitalis if ACE-inhibitor intolerant +
III if still symptomatic beta-blocker
add aldosterone antagonist

+ Diuretics + Digitalis Continue ACE-inhibitor/ARB,


NYHA
IV
+ consider temporary Beta-blocker
Inotropic support Aldosterone antagonist

67 Swedberg K, et al. Eur Heart J 2005; 26(11):1115-40.


Terapi gagal jantung kronik di Layanan Primer

 - Furosemid bila perlu dapat dikombinasikan thiazid (HCT)


 - Bila dalam 24 jam tidak ada respon rujuk ke
 Layanan Sekunder.

 - ACE Inhibitor (ACE-I) atau


 Angiotensine II receptor blocker (ARB)
 mulai dari dosis terkecil sampai tercapai dosis yang efektif

 Bila pengobatan sudah mencapai dosis maksimal dan


 target tidak tercapai  dirujuk !!!
 Beta Blocker (BB)
 mulai dari dosis terkecil dan titrasi dosis
 Bila pengobatan sudah mencapai
 dosis maksimal dan target tidak tercapai
  dirujuk !!!

Digoxin diberikan bila ditemukan fibrilasi atrial untuk


menjaga denyut nadi tidak terlalu cepat.
Next Step ……
Merujuk penderita !

B. Rudy Utantio
SUMMARY
• Heart Failure is an abnormality of cardiac structure or function leading
to failure of the heart to deliver sufficient oxygen to metabolizing
tissues1
• The most common cause of HF is coronary artery disease2
• The most frequently reported signs and symptoms of HF are dyspnea,
edema and cough3
• HF has a complex pathophysiology involving activation of two key
neurohormonal systems:4
• Renin–angiotensin–aldosterone system
• Sympathetic nervous system
• Natriuretic peptides counteract the detrimental effects of RAAS and
SNS activation5
RAAS: renin-angiotensin-aldosterone system; SNS: sympathetic nervous system
1. McMurray et al. Eur Heart J 2012;33:1787–847; 2. Lam et al. Eur J Heart Fail 2011;13:18–28;
2. Dickstein et al. Eur Heart J 2008;29:2388–442; 3. Goldberg et al. Clin Cardiol 2010;33:e73–80;
4. McMurray et al. Eur Heart J 2012;33:1787–847; 5. Levin et al. N Engl J Med 1998;339;321–8
1. The ACC/AHA/HFSA guideline update gives a Class I recommendation for the clinical strategy of inhibition of the renin-
angiotensin system with angiotensin-converting enzyme (ACE) inhibitors (Level of Evidence: A), OR angiotensin-receptor
blockers (ARBs) (Level of Evidence: A), OR angiotensin receptor–neprilysin inhibitors (ARNI) (Level of Evidence: B-R) in
conjunction with evidence-based beta blockers and aldosterone antagonists in selected patients with chronic heart failure
with reduced ejection fraction (HFrEF) to reduce morbidity and mortality.
1. The recommendation for ARNI is based on the PARADIGM trial, which reported a 20% reduction in the composite endpoint
of cardiovascular death or HF hospitalization—this composite endpoint of cardiovascular death or HF hospitalization was
consistent across subgroups.
2. The ACC/AHA/HFSA guideline update gives a Class I recommendation (Level of Evidence: B-R) to replace an ACE inhibitor
or ARB by an ARNI in selected patients with chronic symptomatic HFrEF (New York Heart Association [NYHA] class II/III)
with an adequate blood pressure who are already tolerating a reasonable dose of ACE inhibitor or ARB.
1. The use of ARNI is associated with the risk of hypotension,
renal insufficiency, and a low-frequency incidence of
angioedema. Clinical experience will provide further
information regarding the optimal titration and tolerability
of ARNI, particularly with respect to blood pressure,
adjustment of concomitant HF medications, and the rare
complication of angioedema.
2. To facilitate initiation and titration, the approved ARNI is
available in three doses, which includes a dose that was not
tested in the PARADIGM trial. See the package insert for
directions of use.
1. The ACC/AHA/HFSA guideline update gives a Class I
recommendation (Level of Evidence: A) for the use of ARBs
in patients with prior or current symptoms of chronic HFrEF
and who are intolerant to ACE inhibitors due to cough or
angioedema, to reduce morbidity and mortality. Head-to-
head comparisons of an ARB versus ARNI for HF do not
exist. The guideline update recommends the use of ARBs
for those patients in whom an ACE inhibitor or ARNI are
inappropriate.
2. The ACC/AHA/AFSA guideline update gives a Class III
(harm) recommendation (Level of Evidence: B-R), that is,
ARNI should not be administered concomitantly with ACE
inhibitors or within 36 hours of the last dose of an ACE
inhibitor.
3. The ACC/AHA/HFSA guideline update gives a Class III
(harm) recommendation (Level of Evidence: C-EO), that is,
ARNI should not be administered in patients with a history
of angioedema.
1. The ACC/AHA/HFSA guideline update gives a Class IIa
recommendation (Level of Evidence: B-R) for use of
ivabradine to reduce HF hospitalization in patients with
symptomatic (NYHA class II-III) stable chronic HFrEF
(LVEF ≤35%) receiving guideline-directed evaluation and
management, including a beta blocker at maximum
tolerated dose, and who are in sinus rhythm with a heart
rate of 70 bpm or greater at rest. The guideline
recommends that given the well-proven mortality benefits of
beta-blocker therapy, it is important to initiate and uptitrate
these agents to target doses, as tolerated, before assessing
the resting heart rate for consideration of ivabradine
initiation. It was noted that the study patients who had a
myocardial infarction within 2 months were ….
TQ for your attention
AN ABNORMALITY OF CARDIAC STRUCTURE
Heart failure
definition
OR FUNCTION
From myocardial infarction (MI) to HF: Ventricular Remodeling after MI

Fibrous scar Myocyte hypertrophy

Acute
infarction
Increased
interstitial
collagen

Infarct zone thinning Spherical ventricular


and elongation dilation

Konstam MA, et al. J Am Coll Cardiol Img 2011;4:98–108


Abnormalitas fototoraks yang umum ditemukan pada gagal jantung
Disadur dari ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 20081

Abnormalitas Penyebab Implikasi klinis


Kardiomegali Dilatasi ventrikel kiri, ventrikel kanan, Ekokardiograf, doppler
atria, efusi perikard
Hipertrofi ventrikel Hipertensi, stenosis aorta, kardiomiopati Ekokardiografi, doppler
hipertrofi
Tampak paru normal Bukan kongesti paru Nilai ulang diagnosis
Kongesti vena paru Peningkatan tekanan pengisian ventrikel Mendukung diagnosis gagal jantung kiri
kiri

Edema intersital Peningkatan tekanan pengisian ventrikel Mendukung diagnosis gagal jantung kiri
kiri

Efusi pleura Gagal jantung dengan peningkatan tekanan Pikirkan etologi nonkardiak (jika efusi
pengisian. banyak)
Jika efusi bilateral
Infeksi paru, pasca bedah/ keganasan
Garis Kerley B Peningkatan tekanan limfatik Mitralstenosis/gagal jantung kronik

Area paru hiperlusen Emboli paru atau emfsema Pemeriksaan CT, Spirometri, ekokardiografi

Infeksi paru Pneumonia sekunder akibat kongesti paru Tatalaksana kedua penyakit : gagal jantung
dan infeksi paru

Infltrat paru Penyakit sistemik Pemeriksaan diagnostik lanjutan


96

SIMPTOM KARDINAL PENYAKIT JANTUNG……..

 CEPAT LELAH
NYERI DADA
 BENGKAK KAKI
 SESAK NAPAS (DYSPNEA) (EDEMA)
 BATUK – HEMOPTOE
BERDEBAR (PALPITASI)
 PINGSAN (SINKOPE)

10/7/2019
CONTENTS

Heart Failure Definition

Etiology & Patophysiology

Clinical Manifestation

Management
GAGAL JANTUNG
Dominant clinical feature Symptoms Signs

Peripheral oedema Raised jugular venous pressure


Peripheral oedema/congestion Breathlessness Tiredness, fatigue Anorexia Pulmonary oedema Hepatomegaly, ascites Fluid
overload (congestion) Cachexia

Crackles or rales over lungs, effusion Tachycardia,


Pulmonary oedema Severe breathlessness at rest
tachypnoea

Poor peripheral perfusion SBP <90 mmHgAnuria or


Cardiogenic shock (low output syndromes) Confusion Weakness Cold periphery
oliguria

High blood pressure (hypertensive heart failure) Breathlessness Usually raised BP, LV hypertrophy, and preserved EF

Evidence of RV dysfunction Raised JVP, peripheral


Right heart failure Breathlessness Fatigue
oedema, hepatomegaly, gut congestion
HEART FAILURE
DEFINITION
• HF is a clinical syndrome characterized by typical
symptoms :
- Breathlessness,
- Ankle swelling and
- Fatigue
May be accompanied by signs :
- Elevated jugular venous pressure,
Left
atrium
- Pulmonary crackles
Right
- Peripheral oedema atrium
Left
ventricle
Caused by :
Right
- Structural and/or functional cardiac abnormality ventricle

 resulting in a reduced cardiac output and/or


elevated intracardiac pressures at rest or
during stress.

2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure
Abnormalitas fototoraks yang umum ditemukan pada gagal jantung
Abnormalitas Penyebab Implikasi klinis

Kardiomegali Dilatasi ventrikel kiri, ventrikel kanan, atria, Ekokardiograf, doppler


efusi perikard

Hipertrofi ventrikel Hipertensi, Ekokardiografi, doppler


stenosis aorta,
kardiomiopati hipertrofi

Tampak paru normal Bukan kongesti paru Nilai ulang diagnosis


Disadur dari ESC Guidelines for the diagnosis and treatment of acute and chronic

Kongesti vena paru Peningkatan Mendukung


tekanan diag
pengisian ventrikel nosis
kiri gagal jantung kiri
Edema intersital Peningkatan Mendukung
tekanan diag
pengisian ventrikel nosis
kiri gagal jantung kiri
Efusi pleura Gagal jantung Pikirkan etologi
dengan nonkardiak (jika efusi
peningkatan banyak)
tekanan pengisian.
Jika efusi bilateral
Infeksi paru, pasca
bedah/ keganasan
Garis Kerley B Peningkatan Mitralstenosis/gagal
tekanan jantung kronik
limfatik
Area paru Emboli Pemeriksaan CT,
hiperlusen par Spirometri,
u ekokardiografi
ata
u emfsema
Infeksi paru Pneumonia Tatalaksana
sekunder ked
ua penyakit:
akibat
gagal
kongesti
jant
paru
ung dan
infeksi paru
Infltrat paru Penyakit sistemik Pemeriksaan
diagnostik lanjutan
Abnormalitas Penyebab Implikasi klinis
Sinus takikardia Gagal jantung dekompensasi, anemia, demam, Penilaian klinis
hipertiroidisme Pemeriksaan Laboratorium

Sinus bradikardia Obat penyekat β, anti aritmia, hipotiroidisme, Evaluasi terapi obat
sindroma sinus sakit Pemeriksaan laboratorium
(Sick Sinus Syndrome)

Atrial flutter / fbrilasi Hipertiroidisme, infeksi, gagal jantung dekompensasi, Perlambat konduksi AV, konversi medik, elektroversi,
infark miokard ablasi kateter, antikoagulasi

Aritmia ventrikel Iskemia, infark, kardiomiopati, miokardits, Pemeriksaan laboratorium, tes latihan beban,
hipokalemia, hipomagnesemia, overdosis digitalis pemeriksaan perfusi, angiografi koroner, ICD

Iskemia / Infark Penyakit jantung koroner Ekokardiografi, troponin, Angiografiikoroner ,

revaskularisasi
Gelombang Q Infark lama, kardiomiopati hipertrofi, LBBB, preexitasi Ekokardiografi, angiografii koroner

Hipertrofi ventrikel kiri Hipertensi, penyakit katup aorta, Ekokardiografi, doppler


kardiomiopati hipertrofi

Blok Atrioventrikular Infark miokard, Intoksikasi obat, miokarditis,


sarkoidosis, Penyakit Lyme Evaluasi penggunaan obat, pacu jantung,
penyakit sistemik

Mikrovoltase Obesitas, emfisema, efusi perikard, amiloidosis Ekokardiografi, rontgen toraks

Durasi QRS > 0,12detikdengan Disinkroni elektrik dan mekanik Ekokardiograf, CRT-P, CRT-D
Global Pandemic of Heart Failure

GLOBAL PANDEMIC > 26 mill people and increasing

Indonesia : > 500.000 cases

Ambrosy PA et al. The Global Health and Economic Burden of Hospitalizations for Heart Failure.
Lessons Learned From Hospitalized Heart Failure Registries. J Am Coll Cardiol. 2014;63:1123–1133.
Data Riset Kesehatan Dasar 2013, Badan Litbangkes Kementerian Kesehatan RI dan Data Penduduk
Sasaran, Pusdatin Kementerian Kesehatan RI
Bui AL, Horwich TB, Fonarow GC. Epidemiology and 54. risk profile of heart failure. Nat Rev Cardiol
SYMPTOMS AND SIGNS OF HF
The diagnosis of HF can be difficult, especially in the early stages

Symptoms Signs

Typical More specific

Breathlessness Elevated jugular venous pressure

Orthopnoea Hepatojugular reflux

Paroxysmal nocturnal dyspnoea Third heart sound (gallop rhythm)

Reduced exercise tolerance Laterally displaced apical impulse

Fatigue, tiredness, increased time to


Cardiac murmur
recover after exercise

Ankle swelling
McMurray et al. Eur Heart J 2012;33:1787–847

McMurray et al. Eur Heart J 2012;33:1787–847


Gejala Tanda

Tipikal Spesifik
 Sesak nafas  Peningkatan JVP
 Ortopneu  Refluks hepatojugular
 Paroxysmal nocturnal dyspnoe  Suara jantung S3 (gallop)
 Toleransi aktifitas yang berkurang  Apex jantung bergeser ke
 Cepat lelah lateral
 Begkak di pergelangan  Bising jantung
kaki

Tabel 2Manifestasi klinis gagal jantung


Heart failure
definition
HFREF & HFPEF
Systolic Diastolic
dysfunction dysfunction

HFrEF
HFrEF HFpEF
HFpEF
EF≤35–40%
EF≤40% EF>40–50%
EF>50%

Echocardiography is a useful method for evaluating left ventricular ejection fraction

HFpEF: heart failure with preserved ejection fraction


McMurray et al. Eur Heart J 2012;33:1787–847; Dickstein et al. Eur Heart J 2008;29:2388–442
DIAGNOSIS GAGAL JANTUNG DENGAN
FRAKSI EJEKSI NORMAL
(HFPEF)………….

• 1. Terdapat tanda dan / atau gejala gagal jantung


• 2. Fungsi sistolik ventrikel kiri normal atau sedikit terganggu
(Fraksii ejeksi > 45 – 50 %)
• 3. Terdapat bukti disfungsi diastolik
(relaksasi ventrikel kiri abnormal / kekakuan diastolik)
Classification Heart
Failure

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