Case 1

GROUP 13
FACULTY OF MEDICINE TARUMANAGARA
UNIVERSITY

2013

Acute Coronary
Syndrome

Definition
Any condition brought on by sudden, reduced blood
flow to the heart.
ST-segment elevation myocardial infarction (STEMI)
nonST-segment elevation myocardial infarction
(NSTEMI) or in unstable angina

Epidemiology
ACS is almost always associated with rupture of an
atherosclerotic plaque and partial or complete
thrombosis of the infarct-related artery.
It's important to recognize the patient with unstable
angina, because 5-17% suffer an MI within a week
after admission & 3-15% die within a year.

Etiology
Acute coronary syndrome (ACS) is caused
primarily by atherosclerosis.
Most cases of ACS occur from disruption of a
previously nonsevere lesion (an atherosclerotic
lesion that was previously hemodynamically
insignificant yet vulnerable to rupture).

Risk Factors
Older age (older than 45 for men and older than 55 for
women)
High blood pressure
High blood cholesterol
Cigarette smoking
Lack of physical activity
Type 2 diabetes
Family history of chest pain, heart disease or stroke

Pathophysiology
Normal

Fatty
streak

Fibrous
plaque

Atherosclerotic
plaque

Plaque
rupture/
fissure &
thrombosis

Unstable
angina

Ischemic
stroke/TIA

Clinically silent
Stable angina
Intermittent claudication

Critical leg
ischemia
Cardiovascular
death

Increasing age

Atherothrombosis: a Generalized and Progressive Process

Sign & Symptoms

Chest pain (angina) that feels like burning, pressure or
tightness and lasts several minutes or longer
Pain elsewhere in the body, such as the left upper arm or
jaw (referred pain)
Nausea
Vomiting
Shortness of breath (dyspnea)
Sudden, heavy sweating (diaphoresis)

Assessment
Onset

Signs and symptoms

Provocation

Allergies

Quality

Medications

Radiation
Severity
Time

Past medical history

Last meal
Events leading up to the
illiness

Criteria Diagnose
History
ECG changes
Serial changes in cardiac enzymes (detectors of
myocardial damage)

History
Palpitations
Pain, feels like pressure, squeezing, or a burning
sensation across the precordium & may radiate to the
neck, shoulder, jaw, back, upper abdomen or arm
Exertional dyspnea that resolves with pain or rest
Diaphoresis
Nausea

 Decreased exercise tolerance

Hypotension
Hypertension
Pulmonary edema & other signs of left heart failure
Jugular venous distention
Coold, clammy skin
A third heart sound (S3) may be present & frequently, a
fourth heart sound (S4) exists.

ECG
Changes that may be seen during anginal episodes
include the following:
Transient ST-segment elevations
Dynamic T-wave changes - Inversions, normalizations,
or hyperacute changes
ST depressions - May be junctional, downsloping, or
horizontal

Differential Diagnosis

Aortic Stenosis
Asthma
Cardiomyopathy
Myocardial Infarction
Myocarditis
Pericarditis and Cardiac Tamponade

Complications

Pulmonary edema

Rupture of the papillary muscle, left ventricular free

wall, and ventricular septum

Myocardial Infarct

MYOCARDIAL
INFARCTION
Myocardial necrosis due to blood flow
to the heart muscle impaired
Non-ST elevation Myocardial Infarction
ST elevation Myocardial Infarction

NON-ST ELEVATION
MYOCARDIAL
INFARCTION
a subtotally blockage in the coronary
artery in the first few hours and
disappear over time and there is
evidence myocardial infarction
(elevated cardiac biomarker)

Pathophysiology
oxygen supply or myocardial
oxygen demand superimposed on a
lesion (coronary arterial obstruction
atherothrombotic coronary plaque)

4 pathophysiologic processes development

of NSTEMI

1. plaque rupture or erosion NSTEMI

(embolization of platelet aggregates
or atherosclerotic debris)
2. dynamic obstruction (coronary spasm)
3. progressive mechanical obstruction
4. increased myocardial oxygen demand
and/or decreased supply (e.g.,
tachycardia, anemia)

Myocardial
Infarction
RISK FACTOR:
1.Smoking
2.Hypertension
3.hypercholesterolemia
Myocardial Infarction
thrombus coronary artery

Coronary artery Occlus

Aggregasi platelet

Decrease coronary artery blood flow

Arterosklerosis plaque

Ruptur plaque

Tromboxan A2

Thrombosit activation
Agonis (kolagen, ADP, epinefrin dan serotonin)

Risk Factors
age > 65 years
three or more risk factors for CAD (carotid
artery disease),
documented CAD at catheterization,
development of UA/NSTEMI while on
aspirin,
more than two episodes of angina within
the preceding 24 h
ST deviation 0.5 mm, and an elevated
cardiac marker

Clinical manifestation
chest pain
located in the substernal region or
sometimes in the epigastrium, that
radiates to the neck, left shoulder,
and/or the left arm
dyspnea and epigastric discomfort

Clinical manifestation

Diaphoresis
cool skin
sinus tachycardia
a third and/or fourth heart sound
basilar rales (crackles) inflamation,
fluid or infection.
Hypotension resembling the
findings of large STEMI.

Diagnosis
clinical history
ECG
Cardiac markers (recognize or
exclude MI )
Stress testing (coronary imaging is
an emerging option).

Electrocardiogram
ST-segment depression, transient STsegment elevation, and/or T-wave
inversion occur in 30 to 50% of
patients

Cardiac Biomarkers
elevated biomarkers of necrosis,
such as CK-MB > 3 ng/ml and
troponin >0.4 ng/ml
High risk mortality if troponin
incrase.

Prognosis
NSTEMI exhibit a wide spectrum of
early (30 days) risk of death, ranging
from 1 to 10%, and of new or
recurrent infarction of 35% or
recurrent ACS (5-15%).

ST ELEVATION
MYOCARDIAL
INFARCTION
a complete blockage in the coronary
artery

ETIOLOGI
coronary artery occlusion caused by
coronary emboli
congenital abnormalities
coronary spasm
wide variety of systemicparticularly
inflammatorydiseases

Pathophysiology
coronary artery thrombus (rapidly) at a site of
vascular injury surface atherosclerotic plaque
disrupted (rich lipid core and a thin fibrous cap )
thrombus forms coronary artery occlusion
coronary blood flow.
thrombotic occlusion (atherosclerosis) or
stenosis (slowly) coronary artery coronary
blood flow.
Vascular injury cigarette smoking,
hypertension, and lipid accumulation

Ruptur
plaque

Ruptur initial
monolayer platelet
form

collagen, ADP,
epinephrine,
serotonin

resistance to
fibrinolysis

tromboksan A2
(vasoconstrictor)

platelet activator

platelet cross-linking
and aggregation and
fibrin strands

high affinity for

soluble adhesive
proteins (i.e.,
integrins) such
as fibrinogen.

change in the
glycoprotein
IIb/IIIa receptor

coagulation
cascade
activated
Factors VII and X
are activated

prothrombin to
thrombin
And
fibrinogen to fibrin

myocardial damage caused

by coronary occlusion
1. supplied by the affected vessel
2. whether or not the vessel becomes totally
occluded
3. the duration of coronary occlusion
4. the quantity of blood supplied by collateral
vessels to the affected tissue
5. the demand for oxygen of the myocardium
whose blood supply has been suddenly limited
6. endogenous factors that can produce early
spontaneous lysis of the occlusive thrombus
7. the adequacy of myocardial perfusion in the
infarct zone when flow is restored in the
occluded epicardial coronary artery

RISK FACTORS

Unstable angina
Hypercoagulability
collagen vascular disease
cocaine abuse
intracardiac thrombi or masses that
can produce coronary emboli.
diabetes mellitus and age

Clinical manifestation
Precipitating factor
present before STEMI (vigorous physical
exercise, emotional stress, or a medical or
surgical illness).

Pain (deep, visceral, heavy,

squeezing,rushing, stabbing or burning).
commonly occurs at rest but when it
begins during a period of exertion, it does
not usually subside with cessation of
activity

 is usually more severe, and lasts longer

circadian variations are seen in the
morning within a few hours of awakening
Typically, the pain involves the central
portion of the chest, epigastrium and
radiates to the arms, abdomen, back,
lower jaw, and neck.
frequent location of the pain beneath the
xiphoid and epigastrium

 weakness, sweating, nausea,

vomiting, anxiety, and a sense of
impending doom
breathlessness, which may progress
to pulmonary edema
sudden loss of consciousness
unexplained drop in arterial pressure
Pallor
Coolness of the extremities

Physical examination
Chest Pain (persisting for >30 min)
anterior infarction sympathetic
nervous system hyperactivity
(tachycardia and/or hypertension),
abnormal systolic pulsation
inferior infarction show evidence of
parasympathetic hyperactivity
(bradycardia and/or hypotension).

 ventricular dysfunction include fourth

and third heart sounds
transient midsystolic or late systolic
apical systolic murmur dysfunction
of the mitral valve
pericardial friction rub is heard
transmural STEMI
carotid pulse (volume) stroke
volume

LABORATORY
1. acute (first few hours7 days)
2. healing (728 days)
3. healed (> 29 days)
ECG, serum cardiac biomarkers,
cardiac imaging, nonspecific indices
of tissue necrosis and inflammation.

Electrocardiogram
initial stage, total occlusion of an
epicardial coronary artery ST-segment
elevation
Depresion Q waves
ST-segment elevation will not develop Q
waves the obstructing thrombus is not
totally occlusive
transmural MI Q waves or loss of R
waves and nontransmural MI only
transient ST-segment and T-wave changes

Cardiac Biomarkers
Cardiac-specific troponin T (cTnT)
and cardiac-specific troponin I (cTnI)
troponin >0.4 ng/ml elevated
for 710 days after STEMI.
CKMB > 3 ng/ml

Cardiac Imaging
detected accurately with highresolution cardiac MRI

Initial Management

MANAGEMENT STRATEGIES

Management in the Emergency

Department

Control of Discomfort
Nitroglycerin three doses of 0.4 mg
at about 5-min intervals
myocardial oxygen demand (by
lowering preload) and myocardial
oxygen supply (vasoditasion).
KI : low systolic arterial pressure (<90
mmHg)

Fibrinolysis

tissue plasminogen activator (tPA),

streptokinase,
tenecteplase (TNK),
reteplase (rPA)

If contraindication fibrinolysis PCI

(percutaneus coronary intervention)

Hospital Phase
Management
Coronary Care Unit
The cardiac ritm of each patient and
hemodynamic monitor in selected
patients

Activity
Factor that increase the work of the
heart increase the size of the infarct.
Bed rest for the first 12 h.

 Diet
30% total calories
fat and cholesterol 300 mg/d
high potassium, magnesium, and fiber,
low in sodium

Bowel management
Bed rest Conspations dioctyl
sodium sulfosuccinate (200 mg/d)

Sedation
Diazepam (5 mg),
oxazepam (1530 mg),
lorazepam (0.52 mg),
given 34 times daily

DD
acute pericarditis (Radiation of
discomfort to the trapezius )
pulmonary embolism
acute aortic dissection
Costochondritis
gastrointestinal disorders

Complication
Ventricular Dysfunction
Hemodynamic Assessment
Hypovolemia

UNSTABLE
ANGINA

UNSTABLE ANGINA
it occurs at rest (or with minimal exertion),
usually lasting >10 minutes.
it is severe and of new onset (i.e., within the
prior 46 weeks).
it occurs with a crescendo pattern (i.e.,
distinctly more severe, prolonged, or frequent
than previously).

Etiology
Atherosclerotic narrowing of coronary
vessels
Vasospasm, although this is usually at
rest and considered unstable if new onset
Microvascular angina or abnormal
relaxation of vessels with diffuse vascular
disease
Plaque disruption
Thrombosis

Arteritis:
Lupus
Takayasu disease
Kawasaki disease
Rheumatoid arthritis
Anemia:
Hemoglobin <8 g/dL
Hyperbarism or elevations in carboxyhemoglobin
Coronary artery gas embolus
Thyroid storm
Structural abnormalities of coronary arteries:
Radiation fibrosis
Aneurysms
Ectasia

 Cocaine- or amphetamine-induced
vasospasm
Cardiac risk factors include:
Hypercholesterolemia
Diabetes mellitus
Hypertension
Smoking
Family history in a first-degree relative less
than age 55
Men: age >55 years
Postmenopausal women

Diagnosis
Signs and Symptoms
Unstable angina is defined by either:
New-onset symptoms
Symptoms that occur at rest
A change in the patient's usual pattern
of angina

 Chest pain:
Most common
presentation of
myocardial
infarction
Substernal pressure
Heaviness
Squeezing
Burning sensation
Tightness

Occasional anginal
equivalents:

Abdominal pain
Syncope
Diaphoresis
Nausea or vomiting
Weakness

 May localize or radiate to arms, shoulders, back,

neck, or jaw
May be associated with dyspnea, syncope, fatigue,
diaphoresis, nausea, or vomiting
Symptoms are usually reproduced by exertion,
eating, exposure to cold, or emotional stress.
Symptoms commonly last 15 minutes or more.
Usually improved or relieved with rest or
nitroglycerin
Symptoms generally unchanged with position or
inspiration
Positive Levine sign or clenched fist over chest is
suggestive of angina
Blood pressure (BP) is usually elevated during
symptoms.

Physical Exam
Physical exam is usually unrevealing.
Occasional physical findings include:
S3 or S4 due to left ventricular systolic
or diastolic symptoms
Papillary muscle dysfunction resulting in
mitral regurgitation
Diminished peripheral pulses

Tests
ECG:
Will be normal approximately 50% of the time
ST segment changes or T-wave inversions most
often will be unchanged from previous tracings.
Must be compared to prior tracings if available
New ST segment changes or T-wave inversions
are suspicious for unstable angina.
Serial ECG tracings that remain unchanged
may assist in differentiating stable from
unstable angina.
1-mm depression of the ST segment below the
baseline, 80 msec from the J point, is
characteristic of angina

Lab

CK-MB and troponin I or T

Hematocrit
Coagulation profile
Creatinine

Imaging
Chest radiograph:
Usually normal
May show cardiomegaly
Congestive heart failure is suggestive of
unstable angina.
May identify other etiologies of chest pain
such as pneumonia

Rest echocardiography may establish

the diagnosis of acute coronary
insufficiency (ACI):
Has a sensitivity of 70% and specificity of
87% for ACI

 Technetium Tc-99 sestamibi (rest):

Has a sensitivity of 81% and specificity of 73%
for ACI

Exercise stress testing may help establish

the diagnosis of angina and provide
prognostic information when the clinical
presentation is equivocal:
Exercise stress testing with ECG alone has a
sensitivity of 68% and specificity of 77%.
Exercise stress testing with echocardiography
has a sensitivity of 85% and specificity of 77%.

 Exercise stress testing with thallium-201 or

technetium Tc-99m sestamibi has a
sensitivity of 87% and specificity of 64%.
1-mm depression of the ST segment below
the baseline, 80 msec from the J point, in
three consecutive beats and two consecutive
leads is characteristic of cardiac ischemia.
Early positive (within 3 minutes) stress tests
are worrisome for unstable angina.

Differential Diagnosis

Acute MI
Anxiety
Aortic dissection
Biliary colic
Costochondritis
Esophageal reflux
Esophageal spasm
Herpes zoster

Panic disorder
Peptic ulcer disease
Pneumonia
Psychogenic
Pulmonary embolus
Hiatal hernia
Mitral valve prolapse
MI

Treatment
Pre Hospital
IV access
Aspirin
Oxygen
Cardiac monitoring
Sublingual nitroglycerin for symptom
relief

Initial Stabilization
IV access
Oxygen
Cardiac monitoring
Oxygen saturation
Continuous BP monitoring and pulse
oximetry

Drugs
Aspirin
Enoxaparin
Glycoprotein IIb/IIIa
inhibitors:
Eptifibatide
(Integrilin):
Tirofiban
(Aggrastat):
Abciximab (ReoPro):

Heparin
Metoprolol

Morphine
Nitroglycerin
Nitroglycerin
Nitropaste

CARDIAC
ARREST

8686

Epidemiology
50% of all cardiac deaths are sudden & unexpected, at
least two-thirds of which are first cardiac events or
occur among population subsets with previously known
heart disease.

Signs & Symptoms

Unresponsiveness
Pulselessness
Shallow, gasping respirations may persist for a few minutes
Occasionally preceded by chest pain, dyspnea, palpitation,
seizure activity
Immediately prior to arrest :
Shock or hypotension
Impaired mentation

Diagnostic Tests
Laboratory tests :
Electrolytes
Blood urea nitrogen/creatinine
Creatinine kinase with isoenzymes, cardiac troponin
Arterial blood gas
CBC
Therapeutic drug levels
Toxicological testing

 ECG :
Establish or rule out acute coronary syndrome
Pericardial effusion
Wall motion abnormality
Valvular dysfunction

CXR :
Endotracheal tube position
Cardiac silhouette
Pneumothorax

Differential Diagnose
Sudden loss of consciousness with a palpable pulse:
Syncope
Seizure
Acute stroke
Hypoglycemia
Acute airway obstruction
Head trauma & toxins

Management
The initial response : basic life support & public
access defibrillation (if available)
Advanced life support
Post-resuscitation care
Long-term management

Management (Pre-Hospital)

Prompt

initiation

of

standard

CPR

active

compression-decompression CPR (ACD-CPR)

Confirm underlying rhythm

Early defibrillation of ventricular tachycardia (VT) or

ventricular fibrillation (VF):
- Automated external defibrillator
- EMT-D or layperson

Consider CPR before defibrillation, if arrest >5

minutes.

Secure airway and provide adequate respirations:

- Endotracheal intubation or Laryngeal mask airway

Post-resuscitation care:
- Identify cause of arrest
- 12-lead ECG
- Monitor vital signs

Transport to the closest facility:

If

return

of

spontaneous

circulation,

consider

transport to center equipped for interventional cardiac

care.

Pediatric critical care center for children

Termination of resuscitative efforts:

Persistent, confirmed asystole

Prolonged arrest

Initial Stabilization

Initiate advanced cardiac life support (ACLS)

Perform standard CPR as long as no pulse is

palpable

Consider ACD-CPR (stop CPR only briefly to check

cardiac rhythm or intubate)

Secure the airway

Obtain IV access

Cardiac monitor

Th/ based on the underlying rhythm according to

ACLS protocols

ED Treatment
Pulseless VT or VF
Immediate defibrillation with up to three countershocks:
200 J
200 - 300 J
360 J

If defibrillation is unsuccessful:
Epinephrine
Vasopressin

If refractory to defibrillation and epinephrine:

Amiodarone
Lidocaine
Procainamide
Magnesium for Torsades de Pointes

Asystole

Dismal prognosis if this is the presenting rhythm

Confirm in two or more leads

Epinephrine

Atropine

Consider transcutaneous pacing for severe bradyasystolic rhythm.

PEA

Epinephrine

Atropine

Treat for reversible cause :

- Pneumothorax
- Cardiac tamponade
- Hypoxia
- Pulmonary embolus
- Hypovolemia (hemorrhage)

Medication (Drugs)
Amiodarone

Magnesium

Atropine

Procainamide

Epinephrine

Sodium bicarbonate

Lidocaine

Vasopressin

Post Resuscitation
Treat the underlying cause of the arrest
Ventilatory support
Continue antidysrhythmic therapy
Correct electrolyte abnormalities

ECG Emergency

CARDIORESPIRATOR
Y RESUSCITATION

Definition
CPR is an organized, sequential response
to cardiac arrest, including
Recognition of absent breathing and circulation
Basic life support with chest compression and
rescue breathing
Advanced cardiac life support (ACLS) with
definitive airway and rhythm control
Postresuscitative care

Prompt initiation of chest

compression and early defibrillation
(when indicates) are the key of
success.

When to start CPR

Anyone who initiate resuscitation knowledge and
skills to initiate CPR when dealing with cases of
cardiac arrest.
A.Incidence of cardiac arrest who witnessed
If we are witnessing the cardiac arrest, was
should
immediately started CPR. However,
there are
circumstances like this some
underlying unnecessary
CPR started:
There is evidence of demand for family
CPR efforts will harm people who helped
Possible CPR can restore spontaneous circulation is
very small
Cardiac arrest happened on terminal illness who
have been treated to the maximum

B. Incidence of cardiac arrest was not witnessed

Helper ill cardiac know how long it's been
going on. For something like this we do not
need to start doing CPR if the state finds as
follows:
There is a sign that death does not change like
rigor mortis / bruised corpse
It's getting no signs of decay
Patients experiencing trauma that can not be
saved, such as charred, decapitation

When to stop CPR

There are several compelling reasons for rescuers to
stop CPR among other things:
Helpers are doing basic and advanced life support
optimal included:
CPR, defibrillation in patients with VF / VT without a
pulse, vasopressin / epinephrine IV, open the airway,
ventilation and oxygenation using airway aid and all
levels lanut rhythm after treatment performed.

Helpers are considering whether there is a

hypothermia patient. Helpers has established the
presence / absence of hypothermia by measuring
body temperature.

 Helpers have considered whether patients

exposed to toxic materials or an overdose
that inhibits CNS.
Helper was recorded through a monitor
systolic settled for 10 minutes or more.
The time interval pd cardiac resuscitation
efforts
were
unsuccessful
witnessed
restore spontaneous circulation was 25-30
minutes.

General Technique of CPR

continued
If alone, alternate 30 chest compressions
and 2 ventilations for any age patient
In two-rescuer CPR for infant/child,
alternate 15 compressions and 2
ventilations
Chest-encircling method in infant
Give each ventilation over 1 second
Follow local protocol regarding oxygen

Put hand(s) in correct position for

chest compressions

Give 30 chest compressions at rate

of 100 per minute
Then give 2 ventilations