Penyakit Jantung Koroner  The discomfort experienced when the

heart muscle is deprived of adequate

PENYAKIT JANTUNG ISKEMIK oxygen is called angina pectoris

PENDAHULUAN FAKTOR RISIKO

- Peny. Jantung Iskemik

 Kondisi dimana terjadi imbalans antara
suplai dan kebutuhan oksigen yang
mengakibatkan hipoksia miokardium
dan penumpukan sisa metabolit. Paling
sering karena aterosklerosis arteri
koroner.
- Ischemia : inadequate blood supply
(circulation) to a local area due to blockage
of the blood vessels supplying area.
 Ischemic means that an organ (e.g the
heart) is not getting enough blood and
oxygen
FAKTOR PENCETUS
 Ischemic heart disease / coronary heart
disease / coronary artery disease - Aktifitas / olah raga
 Caused by narrowed heart (coronary) - Emosi
arteries that supply blood to the heart - Makan
muscle - Hipotermi
- Patofisiologi - Ejakulasi

DIAGNOSIS

- Nyeri dada angina

 Lokasi
 Retrosternal
 Radiasi
 Leher, rahang bawah-gigi, bahu-
lengan kiri (ulnar), punggung
 Karakter/kualitas
 Tertekan/tertindih, terikat, terbakar
 Catatan : – nyeri tumpul
 Systole = arteri coroner cenderung  Durasi
menutup  <15 menit ; >15 menit pada SKA
 Diastole = mengalir melewati arteri  Ada faktor pencetus : 5E
coroner  Pereda
 Arteri coroner di belakang katup  istirahat, relaksasi, nitrat SL
 Diastole = otot jantung lemes, dia  Gejala penyerta
mengembang, darah bisa mengalir  Keringat dingin, pusing, pingsan,
sampe arteriole dan kapiler mual, muntah, sesak nafas
 The narrowing can be caused by a blood - Klasifikasi angina
clot or by constriction of the blood
vessel, most often it is caused by
buildup of plaque, called atherosclerosis
 When the blood flow to the heart musle
is completely blocked, the heart muscle
cells die, which is termed a heart attack
or myocardial infarction (MI).
  Decreased blood flow to part of heart
TATALAKSANA
 This is a dynamic process composed of
SINDROMA KORONER AKUT
PENDAHULUAN
- Sindroma Koroner Akut (SKA) : Spektrum
Klinis Yang Menggambarkan Kejadian
Iskemik Miokard Akut Karena Ruptur Plak
Aterosklerosis
- Acute coronary syndrome (ACS) refers to a
group of conditions that include ST-
elevation myocardial infarction (STEMI),
non-ST elevation myocardial infarction
(NSTEMI), and unstable angina.
 Myocardial infarction (MI) / heart
attack : occurs when blood flow
decreases or stops in one of the
coronary arteries of the heart, causing
infarction (tissue death) to the heart
muscle.
- ACS is a manifestation of CHD (coronary
heart disease) and usually a result of plaque
disruption in coronary arteries.
- Patofisiologi
GEJALA DAN TANDA
musculature which is usually secondary
to plaque rupture and formation of
thrombus.
 Sometimes ACS can be secondary
to vasoopasm with or without
underlying atherosclerosis
 The result is decreased blood flow
to a part of heart musculature
resulting first in ischemia and the
infarction of that part of the heart
four phases that result in thrombus
formation:
1. Initiation and formation of the
platelet plug, which is composed of
three stages: the initiation phase,
involving platelet adhesion; the
extension phase, including
activation, additional recruitment,
and aggregation; and the
perpetuation phase, characterized
by platelet stimulation and
stabilization of the thrombus.
2. Propagation of the clotting process.
This is driven by sequential
activation of coagulation factors,
resulting in significant stepwise
response amplification to the
activation of thrombin (factor II),
which has a central role in the
conversion of fibrinogen in fibrin,
forming the hemostatic plug. In
addition, thrombin also promotes
platelet activation and aggregation
via protease activated receptors
(PARs).
3. Termination of clotting by
antithrombotic control
mechanisms.
4. Removal of the clot by fibrinolysis.
 - Nyeri dada TERAPI AWAL
 Substernal
 Menjalar leher, punggung, bahu dan - Morfin
lengan kiri (ulnar)  Meredakan nyeri dan kecemasan
 Seperti tertindih, terikat, teriris  Menurunkan preload dan afterload
 Durasi >15 min - Oksigen
 Berkurang sedikit/tidak hilang dengan  Terutama jika terjadi gagal jantung akut
istirahat. - Nitrat
- Tidak dipengaruhi batuk, nafas dalam dan  Dilatasi arteri koroner – memperbaiki
pergerakan. kolateral
 Menurunkan preload – kebutuhan O2
menurun
 Meredakan nyeri
- Aspirin & Clopidogrel
 Antiagregasi platelet – manghambat
trombosis

TERAPI SKA

- Antiplatelet :
 Awal : Aspirin 160-325mg, klopidogrel
300mg, ticagrelor 180mg
 Rumatan : Aspirin 80-160mg,
clopidogrel 75mg, ticagrelor 90mg

 tanya minum obat antiplatelet ga, kalua

minum stop 5 hari
- Antiangina :
 Langsung repertusi pake obat atau PCI  Nitrat : ISDN, Nitrogliserin
kalo ada estelevasi (?)  ß -bloker : metoprolol, bisoprolol,
 Troponin naik ada infark miokard carvedilol
 UA : unstable anginapectoris  CCB : diltiazem, verapamil
TARGET TERAPI SKA  Di bawah lidah lebih cpt krn masuk ke
vena, biar ga kena pencernaan dulu
- Meminimalisir area infark - Antikoagulan :
- Menyelamatkan area iskemik  Heparin, fondaparinux, enoxaparin,
- Menurunkan kebutuhan oksigen bivalirudin
- Meredakan nyeri dan cemas - Statin :
- Mencegah aritmia fatal  Atorvastatin, rosuvastatin
- Memperbaiki survival - Reperfusi :
  Farmakologis : streptokinase, alteplase  Gram (+), Gram (-)
 Mekanik : intervensi perkutan
primer (IKP) / percutaneus coronary EPIDEMIOLOGY
intervention (PCI) - Incidence :
DURASI TREATMENT  1.6 to 6.0 cases per 100,000 person –
years
 The rate is higher :
 After age 50; 15 per 100,000
person – years
 Patient with valvular hearth
disease, Prosthetic hearth valves,
Congenital hearth disease or
Intravenous drugs use.
- Prognosis
 IE is a life-threatening disease
 Antibiotic therapy 4 to 6 weeks reduce
mortality 20 to 50 percent ,
 Cardiac surgery further reduce 20 to 50
percent
Infective Endocarditis
PATHOGENESIS & PATHOLOGY
DEFINISI
- Endocardial Injury  Turbulent Flow &
- Disease caused by microorganism that Foreign Materials
infected endocardial surface of the hearth - Thrombus Formation  at site of injury
including endothelium of blood vessels. - Bacterial entry to the circulation
- Heart valves are most commonly affected  Access to the blood steam
but occasionally other part of endocardium  Survival in the circulation
can be affected.  Ability to adherence to endocardium
- Vegetation is a characteristic lesion - Bacterial adherence to the hospitable
endocardial surface
CLASSIFICATION & TERMINOLOGY
- Endocardial Injury and Thrombus formation
- Activity of the disease and recurrence: :NBTE (Sterile vegetation)
 Active IE - Bacterial entry and Bacterial
 Recurrent IE adherence :Infected Vegetation (IE) 
 Persistent IE Source of continuous bacteremia
- Diagnostic status (Modified Duke Criteria) - Complication
 Definite IE  Mechanical Cardiac Injury / local
 Possible IE destructive effect (Valve damage,
 Rejected IE Abscess formation, Erosion into cardiac
- Pathogenesis conducting system)
 Native Valve Endocarditis (NVE)  Thrombotic or Septic Emboli (Incite
 Prosthetic Valve Endocarditis (PVE) infection and Infarct; Brain, Ren, Lien
 Intra Venous Drug Abuse Endocarditis etc)
(IVDA)  Immune Injury – Type III Autoimmune
- Anatomical Site (Glomerulonephritis, arthritis, and
 Left Heart IE vacuities)
 Right Heart IE
- Microbiology
 StaphylococcusAureus Streptococcus
Viridan, HACEK group, etc
MICROBIOLOGY IN IE

CLINICAL MANIFESTATION

VASCULAR PHENOMENA

- Peripheral stigmata of endocarditis

MODIFIED CRITERIA FOR DIAGNOSIS

 - X ray : to provide evidence of Hearth
Failure, Septic emboli in Intravenous drug
use, widening of Aorta  mycotic aneurysm
- Fluoroscopy : partial dehiscence 
prosthetic valve
- MRI, Angiographic : Aneurysm in Brain
and elsewhere
- ECG : Hearth block and new arrhythmias
- Echocardiography : play a key role in
diagnosis, prognosis and management of IE

MANAGEMENT (PRINCIPLES)

LABORATORY INVESTIGATION

CARDIAC IMAGING & TEE

Gangguan Irama Jantung
  Fibrillasi
 Escape beat
 Arrest
 Wandering Pace-maker
- Gangguan penghantaran impuls (impuls
conduction) yang meliputi:
 Block, yaitu:
 SA block
 AV block
 Intra-ventricular block /B.B.B
 Accelerated conduction
 Syndroma Wolf-Parkinson-White

NORMAL SINUS RHYTHM (NSR)

AKTIVITAS KELISTRIKAN JANTUNG
- A sinus rhythm is a rhythm which originates
- Jantung memiliki kemampuan membentuk in and is controlled by the sino-atrial node.
depolarisasi spontan & potensial aksi sendiri - This rhythm is the normal cardiac rhythm .
 Sistem Penghantar Khusus (sel - Rate: 60-100 per minute
autoritmis) - Rhythm: R- R regular
- Sifat sistem penghantar khusus - P waves: Upright, similar
 Otomasi : kemampuan menghasilkan - P-R: 0.12 -0 .20 second & consistent
impuls scr spontan - qRs: 0.04 – 0.10 second
 Ritmis: keteraturan membangkitkan - P:qRs: 1P:1qRs
impuls
 Daya penerus : kemampuan
menghantarkan impuls
 Peka rangsang : kemampuan berespons
thd rangsang

SINUS TACHYCARDIA

- regular cardiac rhythm in which the heart

beats faster than normal.
- Rate: > 100
- Rhythm: R- R regular
- P waves: Upright, similar
- P-R: 0.12 -0 .20 second & consistent
- qRs: 0.04 – 0.10 second
- P:qRs: 1P:1qRs

KLASIFIKASI ARRHYTHMIA

Secara garis besar arrythmia disebabkan oleh :

- Gangguan pembentukan impuls (impuls

formation), yang meliputi:
 Extrasystole
 Abnormal tachycardia - Causes
 Flutter  Exercise
 Hypovolemia
  Medications - Rate: Atrial: 400-700
 Fever - Vent. 160-180/minute
 Hypoxia - Rhythm: Atrial: irregular;
 Substances - Vent.: irregular
 Anxiety, Fear - P waves: No identifiable Ps
 Acute MI - f waves: may be seen.
 Fight or Flight - PRI: unable to measure (No identifiable P)
 Congestive Heart Failure
- qRs: usually normal
ATRIAL FLUTTER

- the heart's upper chambers (atria) beat too

quickly. This causes the heart to beat in a
fast, but usually regular, rhythm.
- Rate: Atrial rate 250-350
- Vent 150 common
- Rhythm: Atrial = Regular
- Vent = Reg. or irreg
- P waves: Not identifiable
- F waves: Uniform (sawtooth or picket fence
)
- PRI: not measurable
- qRs: 0.04 – 0.10 second

- risk factors

- causes
 Ischemic heart disease
 Hypoxia
 Acute MI
 Digitalis Toxicity
 Mitral or Tricuspid valve disease - Klasifikasi
 Pulmonary embolism  FA Paroksismal: FA < 48 jam
+ 50% FA paroksismal kembali ke
ATRIAL FIBRILATION irama sinus secara spontan dalam waktu
24 jam
- heart condition that causes an irregular and  FA Persisten: FA > 48 jam - < 7 hari
often abnormally fast heart rate Perlu kardioversi untuk kembali ke
- the electrical signals are fast, irregular and irama sinus
disorganized, and the heart may not pump as
efficiently
  FA Kronik:
Sukar sekali (resisten) dikonversi ke
irama sinus
CHA DS2DS-VASc
Table 82CHA -VASc score (1)
2 2
CHA2DS2-VASc score
Risk factors and definitions
C Congestive heart failure
Clinical HF, or objective
evidence of moderate to
severe LV dysfunction, or HCM
H Hypertension
or on antihypertensive therapy
A Age 75 years or older
Table 8 CHA2DS2-VASc score (2)
www.escardio.org/guidelines
CHA2DS2-VASc score
Risk factors and definitions
D Diabetes mellitus
Treatment with oral
hypoglycaemic drugs and/or
insulin or fasting blood glucose
>125 mg/dL (7 mmol/L)
S Stroke
Previous stroke, TIA, or
thromboembolism
Table 8 CHA2DS2-VASc score (3)
www.escardio.org/guidelines
CHA2DS2-VASc score
Risk factors and definitions
V Vascular disease
Angiographically significant
CAD, previous myocardial
infarction, PAD, or aortic
plaque
A Age 65−74 years
Sc Sex category (female)
Maximum score
www.escardio.org/guidelines
 Low risk stroke
1 (female)
 Moderate risk stroke : Score 1 (male);
2 (female)  Considered anticoagulant
 High risk stroke
(male); ≥3 (female)  Anticoagulant
recommended
FA > 7 hari COMPARISON ORAL AC
SUPRAVENTRICULAR TACHYCARDIA
- happens when the electrical system that
controls your heart rhythm is not working
properly. This causes your heart to suddenly
beat much faster. It can then slow down
abruptly.
- Supraventricular tachycardia (SVT) is a
Points Comment
awarded
1 Recent decompensated HF irrespective of LVEF (thus incorporating
dysrhythmia originating at or above the
HFrEF or HFpEF), or the presence (even if asymptomatic) of moderate-
severe LV systolic impairment on cardiac imaging; HCM confers a high atrioventricular (AV) node and is
stroke risk and OAC is beneficial for stroke reduction.
1 History of hypertension may result in vascular changes that predispose
to stroke, and a well-controlled BP today may not be well-controlled
defined by a narrow complex (QRS <
over time. Uncontrolled BP − the optimal BP target associated with the
lowest risk of ischaemic stroke, death, and other cardiovascular 120 milliseconds) at a rate > 100 beats
outcomes is 120−129/<80 mmHg.
2 Age is a powerful driver of stroke risk, and most population cohorts
show that the risk rises from age 65 years upwards. Age-related risk is
per minute (bpm)
a continuum, but for reasons of simplicity and practicality, 1 point is
given for age 65−74 years and 2 points for age ≥75 years. - Rhythm: Absolutely regular
©E SC
- Rate: > 150 per minute
2020 ESC Guidelines for the diagnosis and management of atrial fibrillation
(European Heart Journal 2020-doi/10.1093/eurheartj/ehaa612)
- P Waves: Not visible
Points Comment
awarded - (PR Interval not measurable)
1 Diabetes mellitus is a well-established risk factor for stroke, and more
recently stroke risk has been related to duration of diabetes mellitus
(the longer the duration of diabetes mellitus, the higher the risk of
- qRs: normal 0.04 – 0.10 sec
thromboembolism) and presence of diabetic target organ damage,
e.g. retinopathy. Both type 1 and type 2 diabetes mellitus confer
broadly similar thromboembolic risk in AF, although the risk may be
slightly higher in patients aged <65 years with type 2 diabetes mellitus
compared to patients with type 1 diabetes mellitus.
2 Previous stroke, systemic embolism, or TIA confers a particularly high
risk of ischaemic stroke, hence weighted 2 points. Although excluded
from RCTs, AF patients with ICH (including haemorrhagic stroke) are at
very high risk of subsequent ischaemic stroke, and recent
observational studies suggest that such patients would benefit from
©ESC
oral anticoagulation.
2020 ESC Guidelines for the diagnosis and management of atrial fibrillation
(European Heart Journal 2020-doi/10.1093/eurheartj/ehaa612)
Points Comment
awarded
1 Vascular disease (PAD or myocardial infarction) confers a 17−22% VENTRIKEL FIBRILLATION
excess risk, particularly in Asian patients. Angiographically significant
CAD is also an independent risk factor for ischaemic stroke among AF
-
patients (adjusted incidence rate ratio 1.29, 95% CI 1.08−1.53).
Complex aortic plaque on the descending aorta, as an indicator of
significant vascular disease, is also a strong predictor of ischaemic
Fibrilasi ventrikular adalah kelainan irama
1
stroke.
See above. Recent data from Asia suggest that the risk of stroke may
jantung dengan tidak ditemukan depolarisasi
rise from age 50−55 years upwards and that a modified CHA 2DS2-VASc
score may be used in Asian patients. ventrikel yang terorganisasi sehingga
1 A stroke risk modifier rather than a risk factor.
9 ventrikel tidak mampu berkontraksi sebagai
©ESC
2020 ESC Guidelines for the diagnosis and management of atrial fibrillation
suatu kesatuan dengan irama yang sangat
: Score 0 (male); (European Heart Journal 2020-doi/10.1093/eurheartj/ehaa612)
kacau serta tidak terlihat gelombang P, QRS,
maupun T.
- Rate: ∅
- Rhythm: ∅ regularity,
: Score ≥2 - chaotic undulating
- waves
 - P Waves: ∅
- qRs: ∅
BLOCK
- ST/T Wave: ∅
- Organized activity: ∅
- No Cardiac Output or Pulse
- Causes
 Acute Myocardial Infarction
 Untreated Ventricular Tachycardia
 Hypothermia
 R-on-T PVCs
 Electrolyte imbalance
 Electrical shock
- Terapi
 DC shock dengan evaluasi dan shock
sampai 3 kali jika perlu dimulai dengan
200 Joule, kemudian 200-300 Joule dan
360 Joule.
 Resusitasi Jantung Paru  selama tidak
ada irama jantung yang efektif (pulsasi
di pembuluh nadi besar tidak teraba).
 Bila teratasi penatalaksanaan seperti
takikardia ventrikular.
 Usia > 40 tahun
- Sino atrial block (SA block)
 Impuls yang dibentuk di SA node
diblock pada batas SA node dengan
jaringan atria sekitarnya  tidak ada
aktivitas baik atrium maupun ventrikel.
 Gambaran EKG  tidak terlihat
gelombang P-QRS-T.
 Bila hambatan sementara  SA node
dapa mengaktifkan atrium dan ventrikel
lagi
 Maka pada EKG  terdapat suatu gap
yang intervalnya adalah kelipatan dari
interval normal
- Atrioventrikular block (AV block)
 Terdapat hambatan penyaluran impuls
dibatas atrium – ventrikel (AV junction)
 Klasifikasi AV block :
 Parsial AV block
 first degree AV block
 Second degree AV blok:
 Mobitz I (Weckenbach)
 Mobitz II
 Complete AV block (third degree
AV block)

VENTRIKEL EXTRASISTOLE (VES) /

PREMATURE VENTRIKEL CONTRACTION
(PVC)

- Tidak ada gelombang P didepan QRS yang

abnormal
- Kompleks QRS timbul prematur dan bentuk
bizzare (aneh)
- Perubahan pada segmen ST dan gelombang
Y yaitu depresi segmen ST dan T terbalik
- Masa kompensasi penuh

- Ciri VES yang berbahaya

 VES > 5 x/menit
 Multifokal
 R on T phenomen
 Timbul post exercise