ACUTE CORONARY SYNDROME

Ali Nafiah Nasution MD,FIHA

Department of Cardiology and Vascular Medicine
Faculty of Medicine University of Sumatera Utara
H. Adam Malik Hospital
MEDAN

Acute Coronary Syndrome (ACS)

Sindroma Koroner Akut (SKA)
Terminologi yang digunakan untuk menggambarkan
spektrum klinis akibat terjadinya iskemia miokard
akut
Angina pektoris tidak stabil/APTS (unstable angina/UA)
Infark miokard gelombang non-Q atau infark miokard tanpa elevasi
segmen ST (Non-ST elevation myocardial infarction/ NSTEMI)
Infark miokard gelombang Q atau infark miokard dengan elevasi
segmen ST (ST elevation myocardial infarction/STEMI)

Insiden
Sindroma Koroner Akut (SKA)

1,57 juta pasien dirawat dengan SKA

UA/NSTEMI

STEMI

1,24 juta pasien

Setiap Tahun

0,33 juta pasien

Setiap Tahun

Nomenklatur

The Dysfunctional Endothelium

Stable and Vulnerable Atherosclerotic Plaque

Patofisiologi Sindroma Koroner Akut

Activated
Macrophages
Matrix
Degradation

Vulnerable Plaque
Reduced Colagen
Content
Thinning &Weakening
of Plaque-Cap

SMC
Density
SMC
Function
Matrix
Synthesize
Tiggers

Plaque
Disruption

Myocardial Oxygen Supply and Oxygen Demand

Evaluasi Awal

Anamnesis
Pemeriksaan Fisik
Elektrokardiografi
Pemeriksaan Enzim

10 Menit

Nyeri Dada Kardiak

Lokasi: Dada kiri/Substernal
Sifat:

Seperti ditusuk/diremas2
Tertimpa beban berat
Rasa terbakar
Rasa tercekik
Nyeri eigastrium

Ada penjalaran
Lamanya: > 2o menit
Disertai mual, muntah,
keringat dingin, sesak nafas

Nyeri Dada Non Iskemia/Atipikal

Nyeri dada pleuritik

Nyeri dada yang dapat ditunjuk dengan jari
Nyeri timbul karena pergerakan, penekanan
dada atau lengan
Nyeri yang sangat singkat (beberapa detik)
Nyeri yang menjalar sampai ekstremitas bawah

Penyebab Nyeri Dada Bukan Angina

Cardiac

Pulmonary

Haematological

Vascular

Gastrointestinal

Orthopaedic/
infectious

Myocarditis

Pulmonary
embolism

Sickle cell crisis

Aortic
dissection

Oesophageal
spasm

Cervical discopathy

Pericarditis

Pulmonary
infarction

Anaemia

Aortic aneurysm

Oesophagitis

Rib fracture

Cardiomyopathy

Pneumonia
Pleuritis

Cerebrovascular
disease

Peptic ulcer

Muscle injury/
inflammation

Valvular disease

Pneumothorax

Pancreatitis

Costochondritis

Cholecystitis

Herpes zoster

Tako-Tsubo
cardiomyopathy
Cardiac trauma

UAP/NSTEMI
Tiga Presentasi Klinis

Rest Angina

Angina yang timbul saat istirahat

lamanya > 20 menit

New-onset Angina

Angina berat yang pertama kali timbul

setidaknya CCS III

Crescendo Angina

Telah diketahui angina, namun nyeri

dirasakan makin sering, makin lama, dan
timbul dengan aktivitas yang lebih ringan

Faktor Risiko PJK

Pemeriksaan Fisik
Faktor pencetus iskemia miokardium
Tanda vital dan kardiovaskular
Biasanya normal
Tanda gagal jantung atau syok kardiogenik
Komplikasi infark miokard (ruptur septum ventrikel,
regurgitasi mitral akut

Elektrokardiografi
STEMI

NSTEMI

10 Menit

Sadapan EKG dan Lokasi Infark

Waktu Pelepasan Enzim Jantung

Myoglobin

Enzim Jantung

Kriteria Diagnosis Infark Miokard Akut

(IMA)
Nyeri dada khas kardiak
Perubahan pada EKG
Peningkatan enzim
jantung

Bila ada 2 dari 3 hal tersebut di atas

Pengobatan
Penderita SKA memerlukan perawatan RS dan
monitor koroner ICCU
Riwayat penyakit, Pem.Fisik, EKG ,Pem. Lab
merupakan diagnostik yg penting.
Tirah baring, Oksigen, Aspirin, Clopidogrel,Obat
antikoagulan, Nitrat , Analgetik Opiat
Trombolitik (STEMI).Sbg Pengobatan awal SKA
Stratifikasi resiko membantu pasien dgn resiko tinggi
yg membutuhkan Gp IIb/IIIa inhibitor dan angiografi
koroner.

DRUGS for AMI

MONACo greets all MI patients
M = Morphine
O = Oxygen
N = Nitrate
A = Aspirin
Co= Clopidogrel

27

Intervensi Koroner Perkutan

PTCA + Stent

PTCA

Coronary Artery Bypass Graft (CABG)

ACUTE PULMONARY EDEMA

Congestive Heart Failure

or
Acute Pulmonary Edema

INTRODUCTION
Congestive Heart Failure (CHF)??? :
A syndrome resulting from the inability of the
heart to pump blood forward at a sufficient rate to
meet the metabolic demands of the body (forward
failure), or the ability to do so only if the cardiac
filling pressures are abnormally high (backward
failure), or both.
Results in retention of fluid congestion.

PULMONARY CIRCULATION
Blood flows from the right ventricle
through the pulmonary artery
Blood reaches the capillaries surrounding
alveoli where gas exchange occurs
Oxygenated blood returns by pulmonary
veins to the left ventricle where it is
pumped into systemic circulation

ETIOLOGY AND
PATHOPHYSIOLOGY
Syndrome usually results from LV
dysfunction and compensatory mechanisms
Cardiac performance is a function of 4
primary factors. What are they?

4 FACTORS DETERMINING
CARDIAC PERFORMANCE
1.
2.
3.
4.

Preload
Afterload
Contractility
Heart Rate

Compensatory Mechanisms to
Maintain Cardiac Output:
The Frank-Starling mechanism
Myocardial hypertrophy

Increased sympathetic tone

All result in increased myocardial O2 demand!

Kidneys

CAUSES OF
Congestive Heart Failure
Conditions that increase preload, e.g. aortic
regurgitation, ventricular septal defects, fluid
overload
Conditions that increase afterload, e.g. aortic
stenosis, systemic hypertension (vasoconstriction),
Conditions that decrease myocardial contractility,
e.g. MI, cardiomyopathies, pericarditis,
tamponade

SIGNS &SYMPTOMS OF
Congestive Heart Failure
Exertional dyspnea usually with Crackles
- fatigue may be the first sign
Increased respiratory rate and effort
Orthopnea and/or PND
Cyanosis and pallor
Tachycardia
JVD
Dependant edema

Framingham Criteria
Major Criteria:

PND
JVD
Rales
Cardiomegaly
Acute Pulmonary Edema
S3 Gallop
Positive hepatic Jugular reflex
venous pressure > 16 cm H2O

Framingham Criteria
Minor Criteria:

Extremitas edema
Night cough
Dyspnea on exertion
Hepatomegaly
Pleural effusion
vital capacity by 1/3 of normal
Tachycardia
Weight loss 4.5 kg over 5 days management

CATEGORIZING FAILURE
Left or Right sided heart failure
Forward or Backward ventricular failure
Backward failure is secondary to elevated
systemic venous pressures.
Forward ventricular failure is secondary to left
ventricle failure and reduced flow into the aorta
and systemic circulation

LV BACKWARD EFFECTS
Decreased emptying of the left ventricle

Increased volume and end-diastolic pressure in

the left ventricle

Increased volume (pressure) in the left atrium

Increased volume in pulmonary veins

LV BACKWARD EFFECTS cont

Increased volume in pulmonary capillary bed =
increased hydrostatic pressure

Transudation of fluid from capillaries to alveoli

Rapid filling of alveolar spaces

Pulmonary edema

LV FORWARD EFFECTS
Decreased cardiac output

Decreased perfusion of tissues of body

Decreased blood flow to kidneys and glands

Increased reabsorption of sodium and water and

vasoconstriction

LV FORWARD EFFECTS cont

Increased secretion of sodium and waterretaining hormones

Increased extracellular fluid volume

Increased total blood volume and increased

systemic blood pressure

RV BACKWARD EFFECTS
Decreased emptying of the right ventricle

Increased volume and end-diastolic pressure in the

right ventricle

Increased volume (pressure) in right atrium

Increased volume and pressure in the great veins

RV BACKWARD EFFECTS cont

Increased volume in the systemic venous
circulation
Increased volume in distensible organs
(hepatomegaly, splenomegaly)
Increased pressures at capillary line
Peripheral, dependant edema and serous infusion

RV Forward Effects
Decreased volume from the RV to the lungs

Decreased return to the left atrium and

subsequent decreased cardiac output

All the forward effects of left heart failure

Congestive Heart Failure Can Be

Defined Based on:
How rapid the symptoms onset
Which ventricle is primarily involved
Overall cardiac output

CARDIOGENIC SHOCK
The most extreme form of pump failure
Occurs when left ventricular function is so
compromised that the heart cannot meet the
metabolic needs of the body
Usually caused by extensive myocardial
infarction, often involving more than 40%
of the left ventricle, or by diffuse ischemia
MAP drops below 70mmHg

New York Heart Associations

functional classification of
CHF

CLASS I
A patient who is not limited with normal
physical activity by symptoms but has
symptoms with exercise.

CLASS II
Ordinary physical activity results in fatigue,
dyspnea, or other symptoms.

CLASS III
Characterized by a marked limitation in
normal physical activity.

CLASS IV
Defined by symptoms at rest or with any
physical activity.

Three Stages of Pulmonary Edema

Stage 1 - Fluid transfer is increased into the lung
interstitium; because lymphatic flow also increases,
no net increase in interstitial volume occurs.
Stage 2 - The capacity of the lymphatics to drain
excess fluid is exceeded and liquid begins to
accumulate in the interstitial spaces that surround the
bronchioles and lung vasculature (which yields the
roentgenographic pattern of interstitial pulmonary
edema).

Three Stages of Pulmonary Edema

Stage 3 - As fluid continues to build up,
increased pressure causes it to track into the
interstitial space around the alveoli.
Fluid first builds up in the periphery of the
alveolar capillary membranes and finally
floods the alveoli .
During stage 3 the x-ray picture of alveolar
pulmonary edema is generated and gas
exchange becomes impaired.

Acute Pulmonary Edema

May be CARDIAC or NON-CARDIAC in origin.
Results from conditions such as:
Increased pulmonary capillary pressure
Increased pulmonary capillary permeability
Decreased oncotic pressure
Lymphatic insufficiency
mixed or unknown mechanisms

Differential Diagnosis for APE:

Cardiac causes of acute CHF
COPD exacerbation
Non-cardiac pulmonary edema:
Tansudate vs. Exudate
fluid overload
infection
ARDS
High altitude
Pulmonary Embolism
Pneumonia

CLINICAL PRESENTATION:
History
Physical Exam
EKG
This should provide enough
information to establish a cardiac
etiology, if one exists!

Symptoms Suspicious of
Pulmonary Congestion
Any complaint of dyspnea/ decreased exercise
tolerance
PND/ Orthopnea
Feeling of suffocation or air-hunger
Restlessness and anxiety
Cyanosis/Diaphoresis
Pallor

Symptoms Suspicious of
Pulmonary Congestion

Crackles
Wheezing (Cardiac Asthma)
Tachypnea
Coughing (Dry cough may be med related)
Retractions, accessory muscle use
Frothy pink-tinged sputum

Physical Findings
JVD
Edema - ankle/pretibial vs sacral
Ascites
- Positive Hepato-jugular reflex test
BP and P are often markedly elevated
Cardiac exam
S3 or intermittent S4 may be present?
PMI may be shifted left

EKG Analysis:
Search for evidence of infarction or
ischemia
Non-specific findings may include:
hypertrophy
chamber enlargement
conduction disturbances

CHEST XRAY:
Usually demonstrates increased heart size
Progression of pulmonary congestion:
first: Cephalization
second : Interstitial edema
third: Pulmonary (alveolar) edema

Treatment of APE:
First and foremost is to increase oxygen
saturation
a reasonable approach is to base therapy on
the Systolic Blood Pressure
Decrease the preload on the heart
Shift and then eliminate excess fluids

Prehospital Management:

Patient sitting
Supplemental O2 provided
Cardiac monitoring/ Pulse oximetry
Initiate necessary supportive therapy
Nitroglycerin for APE if patient matches protocol
Be prepared to assist ventilations
PPV is an effective treatment

TREATMENT PHARMACOLOGY
REDUCTION OF AFTERLOAD
SUBLINGUAL NITROGLYCERIN: 0.4 mg REPEAT 1-5 MIN
IV NITROGLYCERIN: 10-30 micg/min TITRATE TO 200
micg/min
IV NITROPRUSSIDE: 2.5 micg/kg/min TITRATE
NESIRITIDE: ANTAGONIST TO RENIN- ANGIOTENSIN
AXSIS, 2 micg/kg BOLUS, IV DRIP 0.01 micg/kg/min

VASODILATORS NOT RECOMMENED FOR

HYPOTENSIVE PATIENTS, PATIENTS WITH
CARDIOGENIC SHOCK

CONTRAINDICATIONS TO
VASODIALATORS
PRELOAD DEPENDENT STATES

RIGHT VENTRICULAR INFARCTION

AORTIC STENOSIS
VOLUME DEPLETION
HYPERTROPHIC CARDIOMYOPATHY

REDUCTION OF HEART RATE AND

CONTRACTILITY WITH IV BETA
BLOCKERS IS THERAPY OF CHOICE

TREATMENT PHARMACOLOGY
FUROSEMIDE:
NO PRIOR USE: 40 mg IVP
PRIOR USE: DOUBLE LAST 24 HOUR USAGE: 80180 mg
NO RESPONSE IN 20-30 MIN RE-DOUBLE DOSE

BUMETANIDE:
1-3 MG DIURESIS BEGINS WITHIN 10 MIN

MONITORING OF ELECTROLYTES
ESSENTIAL

TREATMENT PHARMACOLOGY
ACE INHIBITORS
DECREASE MORTALITY AND HOSPITALIZATIONS
ALL HF PATIENTS SHOULD BE DISCHARGED WITH
ACEI (DECREASES MORTALITY IN CLASS 4 HF BY 31%)

BETA BLOCKERS
DECREASE MYOCARDIAL HYPERTROPHY,
AFTERLOAD AND MYOCARDIAL OXYGEN DEMAND
METOPROLOL DECREASES 1 YEAR MORTALITY IN
CLASS II-III BY 34%

Treatment Procedure
Patient in sitting
position
100% oxygen via
NRB or BVM
Cardiac monitor

Cardiac Arrest Arrhythmias

Cardiac Arrest
Mechanisms

Ventricular Fibrillation
Pulseless Ventricular Tachycardia
Asystole
Pulseless Electrical Activity (PEA)
A condition; Not an ECG rhythm

Cardiac Arrest
Most common rhythms
Adults: ventricular fibrillation
Children: Asystole, Bradycardic PEA
Pediatric V-fib suggests:
Drug toxicity
Electrolyte imbalance
Congenital heart disease

Cardiac Arrest
ABCs come first!
Airway - unobstructed? manually open
Breathing - no or inadequate ventilate
Circulation - no pulse in 5 sec chest
compressions

Do NOT wait on equipment

Assure effective BLS before going to ALS
Rise and fall of chest
Air movement in lung fields
Pulse with compressions

Cardiac Arrest
First ALS priority is defibrillation
Only cure for v-fib is defib
The quicker the better
Probability of resuscitation decreases 7-10% with
each passing minute

Cardiac Arrest
Vascular access
Antecubital space
Arm, EJ, Foot (last resort)
IO in peds < 6 y/o
14 or 16 gauge
LR or NS
30 sec - 60 sec of CPR to circulate drug

Cardiac Arrest
Intubation as time allows
Less emphasis today as compared to past
Epi, atropine, lidocaine may be administered
down tube
2x IV dose
IV is preferred

Analyze the Rhythm

Ventricular Fibrillation (VF)

Characteristics

Chaotic, irregular, ventricular rhythm

Wide, variable, bizarre complexes
Fast rate of activity
Multiple ventricular foci
No cardiac output
Terminal rhythm if not corrected quickly
Most common rhythm causing sudden cardiac
death in adults

Ventricular Fibrillation (VF) Treatment

ABCs
Witnessed arrest: Precordial thump
Little demonstrated value but worth a try

CPR until defibrillator available

Quick Look for VF or pulseless VT
Treat pulseless VT as if it were VF

Defibrillate
200 J, 300 J, 360 J
Quickly and in rapid succession

Identify cause if possible

Ventricular Fibrillation Treatment

If still in VF/VT arrest, continue CPR for 1 minute
Establish IV access and Intubate
If sufficient personnel, attempt both simultaneously
If not, quick attempt at IV access then attempt ETT

Vasopressor Medication
Epinephrine
1 mg 1:10,000 IVP
Repeat every 3-5 mins as long as arrest persists

Vasopressin (alternative to Epinephrine)

40 units IVP one time only

Ventricular Fibrillation Treatment

Shock @ 360 J after each medication given as long
as VF/VT arrest persists
Alternate epi-shock & antidysrhythmic-shock sequence

Antidysrhythmic Medication

amiodarone 300 mg IVP single dose

lidocaine 1-1.5 mg/kg IVP, q 5 min, max 3mg/kg total
procainamide 100 mg IV, q 5 min, max 17 mg/kg total
magnesium 10% 1-2 g IV
if hypomagnesemic or prolonged QT

Ventricular Fibrillation Treatment

Consider NaHCO3 if prolonged
Only after effective ventilations

In many EMS systems, consider terminating

resuscitation efforts in consult with med
control

Ventricular Fibrillation
The ultimate unstable tachycardia
Shock early-Shock often
Sequence is drug-shock-drug-shock
Sequence of drugs is epi-antiarrhythmic-epiantiarrhythmic

Asystole
Characteristics
The ultimate unstable bradycardia
A terminal rhythm
poor prognosis for resuscitation
best hope if ID & treat cause

No significant positive or negative

deflections

Asystole
Possible Causes
Hypoxia: ventilate
Preexisting metabolic acidosis: Bicarbonate 1
mEq/kg
Hyperkalemia: Bicarbonate 1 mEq/kg, Calcium
1 g IV
Hypokalemia: 10mEq KCl over 30 minutes
Hypothermia: rewarm body core

Asystole
Possible Causes
Drug overdose

Tricyclics: Bicarbonate
Digitalis: Digibind (Digitalis antibodies)
Beta-blockers: Glucagon
Ca-channel blockers: Calcium

Asystole & PEA Differentials

(The 5Hs & 5Ts)
Hypovolemia
Hypoxia
Hydrogen ions
(Acidosis)
Hyper/hypo-kalemia
Hypothermia

Tablets (Drug OD)

Tamponade
Tension
Pneumothorax
Thrombosis,
Coronary
Thrombosis,
Pulmonary

Asystole Treatment
Primary ABCD
Confirm Asystole in two leads
Reasons to NOT continue?

Secondary ABCD

ECG monitor/ET/IV
Differential Diagnosis (5Hs & 5Ts)
TCP (if early)
Epinephrine 1:10,000 1 mg IV q 3-5 min.
Atropine 1 mg IV q 3-5 min, max 0.04 mg/kg
Consider Termination

PEA
Possibilities
Massive pulmonary embolus
Massive myocardial infarction
Overdose:

Tricyclics - Bicarbonate
Digitalis - Digibind
Beta-blockers - Glucagon
Ca-channel blockers - Calcium

PEA
Identify, correct underlying cause if possible
Possibilities:

Hypovolemia: volume
Hypoxia: ventilate
Tension pneumo: decompress
Tamponade: pericardiocentesis
Acute MI: vasopressor
Hyperkalemia: Bicarbonate 1mEq/kg
Preexisting metabolic acidosis: Bicarbonate 1mEq/kg
Hypothermia: rewarm core

PEA Treatment
ABCDs
ETT/IV/ECG monitor
Differential Diagnosis
Find the cause and treat if possible

Epinephrine 1:10,000 1 mg q 3-5 min.

If bradycardic,
Atropine 1 mg IV q 3-5 min, Max 0.04 mg/kg
TCP

In many systems, consider termination of

efforts

Managing Cardiac Arrest

Check pulse after any treatment or
rhythm change

Post-resuscitation Care
If pulse present:
Assess breathing

Present?
Air moving adequately?
Equal breath sounds?
Possible flail chest?

Post-resuscitation Care
If pulse present:
Protect airway
Position to prevent aspiration
Consider intubation

100% Oxygen via BVM or NRB

Vascular access

Post-resuscitation Care
Assess perfusion
Evaluate

Pulses
Skin color
Skin temperature
Capillary refill
BP

Key is perfusion, not pressure

Post-resuscitation Care
Management of Decreased Perfusion
Fluid challenge
Catecholamine infusion
Dopamine, or
Norepinephrine

Titrate to BP ~ 90 to 100 systolic

Cardiac Arrest kuliah 2013

106

Treat the patient,

not the monitor . . . . .
. . . .!!!