Kegawatan Jantung

Dr. Andreas Arie Setiawan, SpPD-KKV

CHEST PAIN?
CHEST PAIN
 Laki-laki, 45 thn
 Nyeri dada kiri mendadak setelah lari pagi,
lama >20 menit, lemas, keringat dingin,
sesak
 Merokok, hipertensi
 Pemeriksaan fisik: tampak kesakitan,
T= 170/100, N=75x/mnt, RR 28x/mnt
ANGINA PECTORIS
Pembuluh darah yang mengalami aterosklerosis & trombosis
Diagnosis

Diagnosis is traditionally made on presence of two

out of three criteria
 History

characteristic chest pain

 Raised Cardiac enzymes

 ECG

ST elevation

For the purposes of diagnosis in the Emergency Dept.

only the first two criteria are useful
 Myocardial infarction is determined by the
specified cTn value, and at least one of the
five following diagnostic criteria:

1. Symptoms of ischemia
2. New (or presumably new) significant ST/T wave
changes or LBBB
3. Development of pathological Q waves on ECG
4. Imaging evidence of new loss of viable myocardium or
regional wall motion abnormality
5. Identification of intracoronary thrombus by angiography
or autopsy

New Universal Definition Of MI ESC 2012

 Enzymes Elevation
50
Myoglobin
Multiples of the AMI cutoff Limit

20 Cardiac Troponin
CK-MB
10
Cardiac Troponin after unstable angina
5

1
AMI decision limit
Upper normal limit
0
0 1 2 3 4 5 6 7 8
Days after MI Onset
 CLINICAL SUSPICION OF ACS
Physical examination
ECG monitoring, Blood sample

Persistent No Persistent Undetermined

ST-elevation ST-elevation Diagnosis

Thrombolysis ASA, LMWH

PCI
Clopidogrel, betablockers, Nitrate

High Risk Low Risk

Second troponin measurement

GpIIb/IIIa Positive Twice negative

Cor.Angiography
Stress test
PCI, CABG or Medical management Coronary angiography
Contraindications to fibrinolytic therapy1–3

ABSOLUTE RELATIVE

• Previous intracranial hemorrhage or stroke of • Transient ischemic attack in the preceding 6

unknown origin at any time month
• Ischemic stroke in the preceding 6 months • Oral anticoagulant therapy
• Central nervous system damage or neoplasms • Pregnancy or within 1 week postpartum
or arteriovenous malformation • Refractory hypertension
• Recent major trauma/surgery/head injury • Advanced liver disease
(within the preceding 3 weeks) • Infective endocarditis
• Gastrointestinal bleeding within the past mo • Active peptic ulcer
• Prolonged or traumatic resuscitation
• Known bleeding disorder (excluding menses)

• Aortic dissection
• Non-compressible punctures in the past 24 h
(e.g. liver biopsy, lumbar puncture)
• Ischemic stroke more than 6 months ago
1. Ibanez B et al. Eur Heart J 2017. https://academic.oup.com/eurheartj/article/4095042; Accessed November 6, 2017; 2. O’Gara PT et al. Circulation 2013;127:e362–e425; 3. Morse
MA et al. Drugs 009;69:1945–1966
Oral Antiplatelet Agents

Antiplatelet Agent Class Binding Dosing

Aspirin[1] Thromboxane inhibitor Irreversible QD
Clopidogrel[2] ADP receptor antagonist Irreversible QD
ADP receptor antagonist
Prasugrel[3] (more potent than Irreversible QD
clopidogrel)
ADP receptor antagonist
Ticagrelor[4] (more potent than Reversible BID
clopidogrel)

ADP : Adenosine diphospat

1. Aspirin [package insert]. 2. Clopidogrel [package insert]. 3. Prasugrel [package insert]. 4. Ticagrelor [package insert].
Cardiac
Arrest
Epidemiology
• Nearly 400,000 out-of-hospital sudden
cardiac arrests occur annually
• 88 percent of cardiac arrests occur at home
• Failure to act in cardiac emergency can lead
to unnecessary deaths
• Effective bystander CPR provided
immediately after sudden cardiac arrest can
double or triple a victim’s chance of survival.
• Less than 8 percent of people who suffer
cardiac arrest outside the hospital survive.
Electrical
Therapies
 • Early defibrillation is critical to
survival from sudden cardiac arrest

• Purpose of defibrillation
– Does not restart the heart
– Defibrillation briefly terminates all
electrical activity (including VT and VF)

• Principle of early defibrillation

– A common initial rhythm in out-of-
hospital witnessed sudden cardiac arrest
– Electrical defibrillation is the most
Defibrillation effective way to treat VF
– The probability of successful
defibrillation decreases quickly over
time

• The earlier defibrillation occurs, the

higher the survival rate.
Shock 1st or CPR 1st ?
• Healthcare provider who treat cardiac
arrest in hospital should provide
immediate CPR until defibrillator is ready
for use
• Use the defibrillator as soon as it is
available.
• AHA strongly recommends performing
CPR while a defibrillator or AED is
readied for use and while charging for all
patients in cardiac arrest.
VF or Pulseless VT
Managing VF/Pulseless VT
Managing VF/Pulseless VT
Managing
VF/Pulseless VT
Application of the Cardiac Arrest Algorithm:
VF/VT Pathway
Minimal Interruption of Chest Compression
•Team member should continue to perform high-quality CPR until defibrillator arrives
and attached to patient
•Chest compressions should ideally be interrupted only for ventilation (unless an
advanced airway is placed), rhythm checks, and shock delivery.

Deliver 1 Shock
•The appropriate energy dose is determined by the identity of defibrillator –
monophasic or biphasic.
•Monophasic: a single 360-J shock
•Biphasic: use the manufacturer’s recommended energy dose (eg, initial dose 120 –
200 J)
•Immediately after the shock, resume CPR. Give 2 minutes (about 5 cycles) of CPR.

Resume CPR
Application of the Cardiac Arrest Algorithm:
Delivering Shock
Clearing for Defibrillation
• To ensure safety during defibrillation, always announce the shock warning
• State the warning firmly and in a forceful voice before delivering each shock
• “Clear. I am going to shock on three”
• Check to make sure you are clear of contact with patient with patient,
the stretcher, or other equipment.
• Make a visual check to ensure that no one is touching the patient or
stretcher.
• “One, two, three. Shocking”
• When pressing the SHOCK button, the defibrillator operator should face
the patient, not the machine.

Rhythm Check
• Conduct a rhythm check after 2 minutes (about 5 cycles) of CPR
• The pause in chest compressions to check the rhythm should not exceed 10
seconds.
• Perform a pulse check -- preferably during rhythm analysis – only if an
organized rhythm is present
Synchronized cardioversion
• Synchronized cardioversion
uses a sensor to deliver a shock
that is synchronized with a
peak of the QRS complex (eg.
The highest point of the R
wave)
• Synchronization avoids the
delivery of a shock during
cardiac repolarization (a period
of vulnerability in which a
shock can precipitate VF)
• Synchronize cardioversion uses
a lower energy level than
attempted defibrillation.
When to use synchronized
cardioversion
• Unstable AF

• Unstable SVT

• Unstable Atrial Flutter

• Unstable regular monomorphic

tachycardia with pulses
 Energy dose for cardioversion
• For unstable Atrial Fibrillation (AF)
– Monophasic cardioversion: deliver an initial 200-J synchronized
shock
– Biphasic cardioversion: deliver an initial 120-200 J synchronized
shock
– In either case, increase the energy dose in a stepwise fashion for
any subsequent cardioversion attempts

• For unstable Atrial Flutter and SVT

– An initial energy dose of 50 J-100 J with a monophasic or biphasic
waveform
– If the initial dose fails, increase the dose in a stepwise fashion

• For monomorphic VT
– An initial energy dose of 100 J
– If there is no response to the first shock, increase the dose in a
stepwise fashion.

• Polymorphic VT
– Treat as VF with high energy shock (defibrillation dose)
When to use Unsynchronized Shocks
• For patient who is pulseless
• For patient demonstrating clinical
deterioration (in prearrest), such as those
with severe shock or polymorphic VT
• When you are unsure whether
monomorphic or polymorphic VT is
present in the unstable patient
 Sebenarnya penyebab
sakit jantung adalah...

…karena orang itu

punya jantung…

04/11/2009 40
TERIMA KASIH