dr. David D Ariwibowo, Sp.

JP
Fakultas Kedokteran
Universitas Tarumanagara
2011

Review of
Circulatory
System

Cardiovascular
Emergencies
1. Acute Coronary Syndrome.
2. Cardiac Arrhythmias
3. Cardiac Tamponade
4. Acute Heart Failure
a. Hypertensive Heart Failure (Hypertensive Emergency)
b. Acute Pulmonary Edema
c. Right Ventricular Failure
d. Cardiogenic Shock
5. Cardiorespiratory Arrest
6. Aortic dissection
7. Acute Limb Ischemic
8. Etc.

Acute Coronary
Syndrome
Kompetensi

3A
Mampu membuat diagnosis klinik berdasarkan pemeriksaan fisik dan pemeriksaan
tambahan (misalnya : pemeriksaan laboratorium sederhana atau X-ray).
Dokter dapat memutuskan dan memberi terapi pendahuluan, serta merujuk ke
spesialis yang relevan (bukan kasus gawat darurat).
3B
Mampu membuat diagnosis klinik berdasarkan pemeriksaan fisik dan pemeriksaan
(misalnya : pemeriksaan laboratorium sederhana atau X-ray).
Dokter dapat memutuskan dan memberi terapi pendahuluan, serta merujuk ke
spesialis yang relevan (kasus gawat darurat).

STANDAR KOMPETENSI DOKTER, KONSIL KEDOKTERAN INDONESIA 2008

Acute Coronary
Syndrome
1. Unstable Angina Pectoris (UAP)
2. Acute Non ST-Elevation Myocardial infarction

(NSTEMI)
3. Acute ST-Elevation Myocardial infarction
(STEMI)

Patophysiology
Atherosclerosis Timeline
Foam
cells

Fatty
streaks

Intermediate
lesion

Atheroma

Fibrous
plaque

Complicated
lesion rupture

Endothelial Dysfunction
From First Decade

From 3rd decade

From 3rd decade

Growth mainly by lipid accumulation

From 4th decade

From 4th decade
Smooth
muscle and
collagen

Thrombosis
hematoma

Definition
Normal

Fatty
streak

Fibrous
plaque

Atherosclerotic
plaque

Plaque
rupture/
fissure &
thrombosis

Unstable
angina

NSTEMI
STEMI
Ischemic
stroke/TIA

Clinically silent
Stable angina
Intermittent claudication

Critical leg
ischemia
Cardiovascular
death

Increasing age

Atherothrombosis: a Generalized and Progressive

Diagnosis
Presentati
on
Working Dx

ECG
Cardiac
Biomarke
r
Final Dx

Ischemic Discomfort
Acute Coronray Syndrome

No ST
Elevation
UA

UA

ST
Elevation

NSTEMI

NQMI

QwMI

Presentation
Angina klasik
Rasa tidak nyaman / nyeri di daerah sternal > 20 menit.
Menjalar ke lengan kiri, leher, rahang, punggung.
Dapat bersifat tajam (ditusuk, terbakar) atau tumpul (seperti ditekan, diperas).
Disertai keringat dingin, mual / muntah, kesulitan bernapas, berdebar-debar.

Angina Equivalent
Tidak ada nyeri / rasa tidak nyaman di dada yang khas.
Gejala gagal jantung mendadak (sesak napas).
Aritmia ventrikular (palpitasi, presinkop, sinkop)

Presentation
Faktor Risiko :
Usia : Tua > Muda
Gender : Laki-laki > Perempuan
Riwayat Keluarga ( PJK )
Hipertensi
Diabetes Mellitus
Peningkatan Kadar Kolesterol Total dan LDL
Kadar Kolesterol HDL Rendah
Obesitas
Kurang Aktivitas Fisik
Diet : Tinggi Lemak Jenuh dan Kolesterol
Merokok

Differential Dx
Cardiac

Stable Angina
MVP
Aortic Stenosis
Hypertrophic cardio
myopathy
5. Pericarditis
1.
2.
3.
4.

Lungs
1.
2.
3.
4.

Lung Emboli
Pnemonia
Pneumothorax
Pleuritis

Gastrointestinal
1. Reflux esofagus
2. Ruptur esofagus
3. Gall bladder disease
4. Peptic Ulcer
5. Pancreatitis

Vascular

1. Aortic dissection

Others

1. Musculoskeletal
2. Herpes zoster

ECG
To detect ischaemic changes or arrhythmias.
Initial ECG has a low sensitivity for ACS.
A normal ECG does not rule out ACS.
ECG is the sole test required for emergency

reperfusion selection (fibrinolytic or primary

PCI).

ECG
Affecting all ECG featuring ventricles

ECG
T wave changes
A.Inverted T
Pada iskemia namun kurang

spesifik
Perubahan akhir pada
STEMI, terjadi setelah ST
elevasi kembali ke normal

B.Hyperacute T
Perubahan awal pada STEMI

ECG
ST Segment changes

A. With acute subendocardial ischemia the electrical forces (arrows) responsible for
the ST segment are deviated toward the inner layer of the heart, causing ST
depression in V5, which faces the outer surface of the heart
B. With acute transmural (epicardial) ischemia, electrical forces are deviated toward
outer layer of the heart, causing ST elevation in the overlying lead.

ECG
A. ST depresion

Bermakna bila > 1 mm di

bawah garis dasar PT di titik

J
Titik J adalah titik akhir
kompleks QRS dan
permulaan segmen ST
Bentuk segmen ST :
A.

Horizontal
Spesifik

B.

Down-sloping
Paling

C.

untuk iskemia.

spesifik.

Up-sloping
Tidak

spesifik

ECG
B. ST elevation
Occurs in the leads
facing the infarction
in the early stages
Slight ST elevation
may be normal in V1
or V2

ECG
Q wave
Q wave duration of more than 0.04 seconds (1
mm)
Q wave depth of more than 1/3 of ensuing R
wave

ECG
R

R
T

ST

ST

QS

1 minute after onset

1 hour or so

A few hours

R
ST

P
T

A day or so

ST

P
T

Later changes

A few months

Sequence of changes in evolving STEMI

ECG

ECG
I

aVR

aVL

V2

V3
III

INFERIOR

V4

SEPTAL

LATERAL
II

V1

aVF

Anatomi Koroner & EKG 12 sandapan

V1 & V2 menghadap septal area LV.
V3 & V4 menghadap dinding anterior LV
V5 & V6 + I & avL menghadap dinding lateral LV
II, III & avF menghadap dinding inferior LV

ANTERIOR
V5

LATERAL
V6

Laboratorium
Multiples of
the URL

10
0

Cardiac Biomarkers in
STEMI

5
0
2
0
1
0
5

Cardiac troponin-no
reperfusion
Cardiac troponin-reperfusion
CKMB-no reperfusion
CKMB-reperfusion

2
Upper reference
limit

1
0
8

Days After Onset of

STEMI

URL = 99th %tile of

Reference Control
Group

Alpert et al. J Am Coll Cardiol

2000;36:959.

Diagnosis Nomenclature
1. Timing at presentation :
Acute (0-7 days)
Recent (7-14 days)
Old (>14 days)

2. Infarct location
Septal, anterior, anteroseptal, anterolateral, anterior extensive
Inferior, inferolateral, lateral
Posterior, right ventricular infarct

Example
UAP
Acute NSTEMI
Acute Anterior STEMI
Recent inferolateral MCI
Old Inferior MCI

Anterior infarction

I II III

Left
coronary
artery

aVR aVL aVF

V1 V2 V3

V4 V5 V6

Inferior infarction

I II III

Right
coronary
artery

aVR aVL aVF

V1 V2 V3

V4 V5 V6

Lateral infarction

I II III

Left
circumflex
coronary
artery

aVR aVL aVF

V1 V2 V3

V4 V5 V6

Management
Treatment Delayed is Treatment Denied

Symptom
Recognition

Call to
Medical
System

PreHospital

ED

Increasing Loss of
Myocytes
Delay in Initiation of Reperfusion

Cath Lab

Management
Onset of STEMI
- Prehospital issues
- Initial recognition and management
in the Emergency Department (ED)
- Reperfusion

MONA
Morphin 2- 5 q 5 min titrate to response and side

effects.
O2 Nasal cannula 4 L/mnt
Nitrat: ISDN 5 mg SL 3 times
Aspirin 160-320 mg

Options for Transport of Patients

With STEMI and Initial Reperfusion
Treatment

Hospital fibrinolysis:
Door-to-Needle
within 30 min.

Not PCI
capable
Onset of
symptoms
of STEMI

9-1-1
EMS
Dispatc
h

EMS on-scene

Encourage 12-lead ECGs.

Consider prehospital fibrinolytic
if capable and EMS-to-needle
within 30 min.

EMS
Triag
e
Plan

GOALS

5
min.
Patient

InterHospital
Transfer

PCI
capable

8
EMS Transport
min.

EMS

Dispatc
h
1 min.

Prehospital
fibrinolysis
EMS-to-needle
within 30 min.

EMS transport
EMS-to-balloon within 90
min.
Patient self-transport
Hospital door-to-balloon
within 90 min.

Golden Hour = first 60 min.

Total ischemic time: within 120 min.

Select Reperfusion Treatment.

If presentation is < 3 hours and there is no delay to an invasive
strategy, there is no preference for either strategy.

Fibrinolysis generally preferred

Early presentation ( 3 hours from symptom
onset and delay to invasive strategy)
Invasive strategy not an option

Cath lab occupied or not available

Vascular access difficulties
No access to skilled PCI lab

Delay to invasive strategy

Prolonged transport
Door-to-balloon more than 90 minutes

> 1 hour vs fibrinolysis (fibrin-specific agent) now

Select Reperfusion
Treatment.
Invasive strategy generally
preferred
Skilled PCI lab available with
surgical backup
Door-to-balloon < 90 minutes

High Risk from STEMI

Cardiogenic shock, Killip class 3

Contraindications to fibrinolysis,

including increased risk of bleeding

and ICH

Late presentation

> 3 hours from symptom onset

Diagnosis of STEMI is in doubt

Percutaneous Coronary Intervention

(PCI)

Percutaneous Coronary Intervention

(PCI)

Percutaneous Coronary Intervention

(PCI)

Percutaneous Coronary Intervention

(PCI)

Coronary Artery Bypass Graft (CABG)

Surgery

Acute Heart Failure

Kompetensi

3B
Mampu membuat diagnosis klinik berdasarkan pemeriksaan
fisik dan pemeriksaan (misalnya : pemeriksaan laboratorium
sederhana atau X-ray).
Dokter dapat memutuskan dan memberi terapi pendahuluan,
serta merujuk ke spesialis yang relevan (kasus gawat
darurat).

STANDAR KOMPETENSI DOKTER, KONSIL KEDOKTERAN INDONESIA 2008

Definition

AHF Rapid onset or change in the signs & symptoms of HF.

New or worsening of pre-existing chronic HF.

The European Society of Cardiology: Guidelines for the diagnosis and treatment of acute and chronic heart failure, 2008

Causes & precipitating factors of AHF

These aetiologies &
conditions often
interact should
be identified &
incorporated into
the treatment
strategy.

The European Society of Cardiology: Guidelines for the diagnosis and treatment of acute and chronic heart failure, 2008

Clinical presentation
Usually characterized by pulmonary congestion
cardiac output & tissue hypoperfusion may dominate the clinical presentation
Reflects a spectrum of conditions present in one of 6 clinical categories.
Figure demonstrates the potential overlap between these conditions

The European Society of Cardiology: Guidelines for the diagnosis and treatment of acute and chronic heart failure, 2008

Clinical presentation

The European Society of Cardiology: Guidelines for the diagnosis and treatment of acute and chronic heart failure, 2008

Diagnosis
Based on the presenting symptoms & clinical findings.
Confirmation by the history, physical examination, ECG, CXR,

echocardiography, laboratory investigation, with blood gases & specific

biomarkers.

The European Society of Cardiology: Guidelines for the diagnosis and treatment of acute and chronic heart failure, 2008

Goals of treatment in
AHF

The European Society of Cardiology: Guidelines for the diagnosis and treatment of acute and chronic heart failure, 2008

Immediate goals
tissue oxygenation & haemodynamics

permit further interventions by :

1. Reduce fluid volume & filling pressures.

2. Reduce systemic vascular resistance (SVR)
3. Increase cardiac output (CO)

Therapeutic Goal
Parameters
Clinical
Hemodynamic
1.
2.
3.
4.

SBP > 90 mmHg

Warm extremities
JVP < 8 cm
No orthopnea

1. SBP
2. SVRI

> 90 mm Hg
< 1200 dyne-s-

cm-5
3. PCWP < 15 mm Hg
4. RAP
< 8 mm Hg

Specific treatment
strategy
based on distinguishing the clinical
conditions

The European Society of Cardiology: Guidelines for the diagnosis and treatment of acute and chronic heart failure, 2008

Two Minutes Assessment of

Haemodynamic Profile
The Forrester classification is based on clinical signs &

haemodynamic characteristics.
Figure presents a modified from the Forrester classification.

Patient Treatment Selection

Fonarow GC. Rev Cardiovasc Med. 2001;2(suppl 2):S7S12.

Initial treatment
algorithm

The European Society of Cardiology: Guidelines for the diagnosis and treatment of acute and chronic heart failure, 2008

AHF treatment strategy according to

systolic BP

The European Society of Cardiology, Guidelines on the diagnosis and treatment of acute heart failure, 2005

Loop diuretics
In the presence congestion & volume overload.
Class I, level of evidence B

The European Society of Cardiology, Guidelines on the diagnosis and treatment of acute heart failure, 2005

Vasodilators

The European Society of Cardiology, Guidelines on the diagnosis and treatment of acute heart failure, 2005

Inotropic agents

The European Society of Cardiology, Guidelines on the diagnosis and treatment of acute heart failure, 2005

Cardiorespiratory
Arrest
Kompetensi

3B
Mampu membuat diagnosis klinik berdasarkan pemeriksaan
fisik dan pemeriksaan (misalnya : pemeriksaan laboratorium
sederhana atau X-ray).
Dokter dapat memutuskan dan memberi terapi pendahuluan,
serta merujuk ke spesialis yang relevan (kasus gawat
darurat).

STANDAR KOMPETENSI DOKTER, KONSIL KEDOKTERAN INDONESIA 2008

Cardiorespiratory
Arrest
suatu keadaan dimana pasien:
tidak sadar
tidak bernafas
tidak ada denyut nadi

Syarat dasar untuk hidup

Fungsi
Sirkulasi

Fungsi
Pernapasan

Terganggu

Terganggu

Henti
Jantung

Henti Napas

Sebab tersering: serangan jantung

Prevalensi
WHO (2004) 17,1 juta orang meninggal

karena penyakit jantung.

2030 23,6 juta kematian karena penyakit
jantung dan pembuluh darah
Eropa kasus henti jantung 700.000 / tahun.
Indonesia (2007) Prevalensi Nasional PJK
7,2% 1.
Prevalensi PJK di 16 Propinsi di Indonesia diatas

angka Nasional

Bantuan hidup jantung

Kematian akibat

penyakit jantung terutama

disebabkan henti jantung mendadak, dengan
irama terdokumentasi paling sering adalah
ventrikel fibrilasi (VF).
Pertolongan bantuan hidup dasar yang berhasil,
dilakukan dalam 5 menit pertama dengan
bantuan AED
Bantuan hidup jantung merupakan gabungan
pengamatan dan tindakan yang tidak terputus
yang disebut Chain of Survival

Chain of Survival

Bantuan hidup dasar

Serangkaian usaha awal untuk
mengembalikan fungsi pernafasan dan
atau sirkulasi pada seseorang yang
mengalami henti nafas dan atau henti
jantung.

LANGKAH-LANGKAH
Pastikan penolong dan korban dalam kondisi

aman
Tempatkan korban di atas alas yang keras
dalam posisi telentang
Lakukan langkah-langkah algoritme.

Cek Respons

Carilah tanda-tanda

sirkulasi:
Bergerak
Bersuara
Bernapas

Dengan cara

menepuk dengan
cukup kuat bahu/dada
korban sambil
memanggil korban

Minta tolong/panggil
bantuan
Bila seorang diri, telepon dulu sarana
kesehatan terdekat (RS, ambulans), ambil AED
bila ada.
Bila ada penolong lain, satu penolong
memanggil bantuan dan ambil AED, yang lain
langsung menolong korban
Meminta pertolongan harus jelas mengenai
kejadian, jumlah korban, lokasi dll

Mulai Resusitasi Jantung Paru (RJP)

Bila korban tidak memberi respons dan

tidak bernapas/bernapas tidak normal

segera lakukan RJP setelah memanggil
bantuan
RJP terdiri dari tindakan kompresi dada dan
pemberian napas bantuan
Dilakukan berulang 30 kali kompresi dada
diselingi 2 kali napas bantuan

A Change From A-B-C to

C-A-B
For adults, children, and infants (excluding the newly born)
The vast majority of cardiac arrests in adults & the highest

survival rates witnessed arrest and an initial rhythm of VF or

pulseless VT.
The critical initial elements chest compressions and early
defibrillation.
In the A-B-C, chest compressions are often delayed while the
responder opens the airway to give mouth-to-mouth breaths,
retrieves a barrier device, or gathers and assembles
ventilation equipment.
In the C-A-B, chest compressions will be initiated sooner and
the delay in ventilation should be minimal (ie, only the time
required to deliver the first cycle of 30 chest compressions, or
18 seconds)

Kompresi Dada

Tekan cepat dan kuat

(minimal 100x/menit)
(minimal dalamnya 5 cm)

Napas bantuan

Buka jalan
napas dengan
cara
menengadahkan

Beri 2 napas bantuan

Pertahankan posisi kepala
Satu kali napas 1 detik
Pastikan dada terangkat

30

30x

Ulangi kompresi dan pemberian napas

bantuan dengan perbandingan 30 kali
kompresi dan 2 kali napas bantuan

TERIMA KASIH