Pemicu KGD 1

MEIDY REGIANTO
Scenario
A 58-year-old man came to the Emergency Department with severe chest
pain extending to his jaw and left arm. He suddenly felt the chest pain 3
hours ago while he was watching television, accompanied by excessive
cold sweat, nausea, and vomiting. He also felt shortness of breath since
an hour ago.
He has a history of hypertension, diabetes mellitus and
hypercholesterolemia in the past 3 years. He is not taking his medication
regularly, has been smoking since the last 10 years and never exercises.
Previosly, he had suffered an episode of mild chest pain but the symptom
disappeared after resting. No history of stroke in the past.
Physical examinationsd result : compos mentis (GCS 15), looks in pain,
agitated, overweight and having mild-dyspneu. Blood pressure 170/90
mmHg, heart rate 120 beats per minute (regular with enough volume and
firmness), afebrile and slight increases in JVP.
Inspection, palpation and percussion of the heart are in normal limits; S1
& S2 in heart auscultation are normal, no murmur is found. Inspection,
palpation and percussion of the lungs are in normal limits but fine rales at
the basis of the lung can be heard in auscultation. Abdomen examination
is normal. His extremities are warm.
ECG examination results : tachycardia sinus rhythm, QRS rate
130x/minute, QRS axis LAD, normal P-wave, P-R interval 0,12 sec, QRS
duration 0,08 sec, Q-pathologic (-), ST-segment elevation in V1-V6 lead,
inverted T-wave(-) and LVH (-).

What can you learn from this problem?
ACS
UNSTABEL ANGINA
MISTEMI and NSTEMI

ACS : Algorithm
ACS : Algorithm
ANGINA-CORONARY OCCLUSION
CORONARY OCCLUSION
CORONARY CIRCULATION
Most tissues can increase O2 extraction with
demand.
Heart extracts near maximal amount of O2 at
rest.
Therefore can increase O2 demand by
increasing the Coronary Blood Flow.

Various Coronary Arteries of Heart
Types Of Angina Pectoris

1. Stable Angina
2. Unstable Angina
3. Variant Angina (Prinzmetals Angina)
4. Anginal Equivalent Syndrome
5. Syndrome- X
6. Silent Ischemia
UNSTABLE ANGINA
This is characterized by Pain that occurs with less
excertion , cumulating pain at rest.
platelet-fibrin thrombus associated with a
ruptured atheromatous plaque without
complete occulation of the vessels.
The risk of infraction is
subtanial, and the main aim
of therapy is to reduce this.

Unstable angina
is that characterized by rapidly
worsening chest pain on minimal
exertion or at rest.
= ulcerated atheroma+ thrombus
formation>>> reduction of coronary
blood flow caused by thrombus>>
angina at rest
Unstable angina
Recent onset (less than 1 month).
Increase frequency and duration of episode.
Angina at rest not responding readily to
therapy.
If the pain more than 20 min.
MI
The Canadian Cardiovascular Society grading
scale
is used for classification of angina severity, as
follows:

Class I : Angina only during strenuous or prolonged
physical activity
Class II : Slight limitation, with angina only during vigorous
physical activity
Class III : Symptoms with everyday living activities, ie,
moderate limitation
Class IV : Inability to perform any activity without angina
or angina at rest, ie, severe limitation
N.A.N 2009
The New York Heart Association classification
is also used to quantify the functional limitation
imposed by patients' symptoms, as follows:

Class I : No limitation of physical activity (Ordinary physical
activity does not cause symptoms.)
Class II : Slight limitation of physical activity (Ordinary physical
activity does cause symptoms.)
Class III : Moderate limitation of activity (Patient is comfortable
at rest, but less than ordinary activities cause symptoms.)
Class IV : Unable to perform any physical activity without
discomfort, therefore severe limitation (Patient may be
symptomatic even at rest.)

N.A.N 2009
Causes:
Decrease in myocardial blood supply due to
increased coronary resistance in large and small
coronary arteries:

1. Significant coronary atherosclerotic lesion
2. Coronary spasm (ie, Prinzmetal angina)

N.A.N 2009
Causes:
3. Abnormal constriction or deficient endothelial-
dependent relaxation of resistant vessels
associated with diffuse vascular disease (ie,
microvascular angina)
4. Syndrome X
5. Systemic inflammatory or collagen vascular
disease, (scleroderma, systemic lupus
erythematous, Kawasaki disease, polyarteritis
nodosa, and Takayasu arteritis)
N.A.N 2009
Risk factors:
Major risk factors for atherosclerosis: like
family history of premature CAD, cigarette
smoking,DM,hypercholesterolemia(Metabol
ic syndrome), or systemic HTN
Other risk factors: These include LV
hypertrophy, obesity,
N.A.N 2009
Precipitating factors:
These include factors such as severe anemia,
fever, tachyarrhythmias, catecholamines,
emotional stress, and hyperthyroidism, which
increase myocardial oxygen demand.
N.A.N 2009
Preventive factors:
Factors associated with reduced risk of
atherosclerosis are a high serum HDL
cholesterol level, physical activity, estrogen,
and moderate alcohol intake (1-2 drinks/d).

N.A.N 2009
Stable Angina
Exercise Testing
The goal of exercise testing is to induce a
controlled, temporary ischemic state during
clinical and ECG observation

N.A.N 2009
ECG
ST segment depression with or without T
wave inversion that reverse after ischemia
disappears.


N.A.N 2009
ECG
Elevation of ST segment in prinzmentals
angina.

N.A.N 2009
ECG
The resting ECG may be normal between
attacks however it may show old MI, heart
block or LVH
N.A.N 2009
Exercise Testing
Contraindications
MIimpending or acute
Unstable angina
Acute myocarditis/pericarditis
Acute systemic illness
Severe aortic stenosis
Congestive heart failure
Severe hypertension
Uncontrolled cardiac arrhythmias

N.A.N 2009
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
thrombus coronary artery
Decrease coronary artery blood flow
Arterosklerosis plaque
Ruptur plaque
Thrombosit activation
Agonis (kolagen, ADP, epinefrin dan serotonin)
Tromboxan A2
Aggregasi platelet
Myocardial Infarction
Coronary artery Occlusion


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 ST-segment
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%).
STEMI
1. Definition of AMI
The actual definition includes the following,
either one of these criteria satisfies the
diagnosis for an acute, evolving, or recent MI :
1. Typical rise and gradual fall (troponin) or
more rapid rise and fall (isoenzyme of creatine
kinase with muscle and brain subunits [CK-
MB]) of biochemical markers of myocardial
necrosis with at least one of the following:
a. Ischemic symptoms;
b. Development of pathologic Q waves on the
ECG;
c. ECG changes indicative of ischemia (T wave
changes or ST segment elevation or
depression); and/or
d. Coronary artery intervention.
2. Pathologic findings of an AMI.
AMI is further classified by findings on the ECG
at presentation, as either ST elevation MI
(STEMI) or non-ST elevation MI (NSTEMI).
The differentiation between STEMI and
NSTEMI has important implications in terms of
management, therapeutic intervention,
outcome, and prognosis for patients with AMI.
2. Etiology
Atherosclerotic narrowing of coronary vessels
Vasospasmalthough 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
Prolonged hypotension
Anemia
Hemoglobin <8 g/dL
Hyperbarism or elevations in carboxyhemoglobin

Coronary artery gas embolus
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
55 years old
Men, age >55 years
Postmenopausal women

3.Pathofisiology
The underlying pathophysiology of ACS is
myocardial ischemia as a result of inadequate
perfusion to meet myocardial oxygen demand.
Myocardial oxygen consumption is
determined by heart rate, afterload,
contractility, and wall tension.
Inadequate perfusion most commonly results
from coronary arterial vessel stenosis as a
result of atherosclerotic CAD.
a. Probable cause is the generation of a total
coronary occlusion or functional collateral
circulation:
Often indicates an complete ischemic event
b. Coronary plaque disruption:
Endothelial disruption exposes subendothelial
collagen and other platelet-adhering ligands, von
Willebrand factor (vWF), and fibronectin.

Release of tissue factors activates factor VII and extrinsic
pathway
c. Thrombus generation:
Platelet adhesion via glycoprotein (GP) Ia/IIa to
collagen; GP Ib to vWF:
Platelet activation: release of ADP, thromboxane A
2
,
and serotonin alters the platelet GP IIb/IIIa receptor;
also causes local vasoconstriction


Platelet aggregation: GP IIb/IIIa receptor binds
fibrinogen molecules, cross-links platelets forming local
platelet plug
d. Platelet stabilization: thrombin converts
fibrinogen to fibrin, provides fibrin mesh,
stabilizes platelet aggregate

4. Signs and Symptoms
Chest pain:
Most common presentation of myocardial
infarction (MI)
Substernal pressure
Heaviness
Squeezing
Burning sensation
Tightness

Anginal equivalents (MI without chest pain):
Abdominal pain
Syncope
Diaphoresis
Nausea or vomiting
Weakness
May localize or radiate to arms, shoulders,
back, neck, or jaw

Associated symptoms:
Dyspnea
Syncope
Fatigue
Diaphoresis
Nausea
Vomiting
Symptoms are usually reproduced by exertion,
eating, exposure to cold, or emotional stress

Symptoms commonly last 30 minutes or more.
Symptoms may occur with rest or during exertion.
Often preceded by crescendo angina
May be 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.

5. Diagnosis
Essential Workup:
ECG
Cardiac markers
Chest radiograph

Lab
Cardiac markers:
Troponins: specific indicators of myocardial infarction,
positive 3- 6 hours after MI, peaks at 9-10 days
Creatine kinase (CK): rises following infarction in 4-8
hours, peaks at 18-24 hours, subsiding at 3-4 days;
isoenzyme CK-MB more specific for cardiac origin
Myoglobin: rises within 2-6 hours, returns to baseline
within 24 hours, highly sensitive but very nonspecific
LDH: rises within 24 hours, peaks at 3-6 days, baseline
at 8-2 days

CBC
Serum electrolytes including magnesium
ESR: nonspecific marker of inflammation, rises
within 3 days, elevated for several weeks
PT/PTT/INR for patients on warfarin

Imaging
ECG:
ST-segment elevation indicates increased risk (ST
segment elevation may become evident. Morphologic
variations of ST segment elevation can be seen from
the J (or junction) point at the end of the QRS complex
to the apex of the T wave)
And Q waves letter
Chest radiograph:
To assess heart size, pulmonary edema/congestion or
identify other causes of chest pain

Echocardiography:
To identify wall motion abnormalities and assess
left ventricular function
Radionuclide studies:
Thallium or sestamibi scanning: identifies viable
myocardium
Technetium 99: identifies recently infarcted
myocardium


6. Treatment
Pre Hospital
IV access
Oxygen administration
Cardiac monitoring and treatment of arrhythmias
Aspirin, analgesia, anxiolytics
Initial Stabilization
Oxygen administration
IV access
Cardiac monitoring and treatment of arrhythmias

Anti-ischemic therapy to reduce myocardial
demand and increase myocardial supply of
oxygen:
Beta-blockers
Nitrates
Oxygen
Morphine sulfate
Calcium channel blockers
(nondihydropyridinese.g., diltiazem, verapamil)
may be used in patients with ongoing ischemia and
contraindications to beta-blockade.

Antiplatelet therapy to decrease platelet aggregation:
Aspirin
Clopidogrel
GP IIb/IIIa inhibitors (eptifibatide, tirofiban):
When catheterization and PCI is planned
Ongoing ischemia
Positive initial cardiac markers
Antithrombotic therapy to prevent thrombus
propagation:
Low molecular weight heparin (specifically enoxaparin)
preferred over unfractionated heparin
Anxiolytics to suppress sympathomimetic release

Reperfusion:
Door to baloon inflation (PCI) , target : 90 minute
Door to nedle ( fibrinolisis) , target : 30 minute
7. Complication
Bradydysrhythmia and atrioventricular (AV)
Tachydysrhythmias
Cardiogenic shock
Pericarditis
Hemorraghic Stroke

8. DD
Non ST-elevation myocardial infarction
Pulmonary embolus
Aortic dissection
Acute pericarditis
Pneumothorax
Pancreatitis
Pneumonia
Esophageal spasm/gastroesophageal reflux
Esophageal rupture
Musculoskeletal pain (diagnosis of exclusion)

Cardiac Arrest
Condition of blood circulation stops due to failure
of the heart to contract effectively
Characterized by the absence of pulse and other signs of circulation
Cardiac abnormalities can be caused by 4
rhythms :
Ventricular Fibrillation (VF)
Pulseless Ventricular Tachycardia (PVT)
Pulseless Electrical Activity (PEA)
Asystole
VF / PVT
The wave different shapes and
amplitude of waves
look : QRS complex, ST segment, T
wave
Smooth fibrillation wave amplitude
<0,2 mv often in the case of long-VF
like asystole
Etiology VF/PVT
Coronary heart disease, the accumulation of
Ca ions, free radicals, cell metabolic disorders,
autonomic modulation, etc
Ischemic cell trigger
Other : electrolyte disturbances (hypo K and
Mg), drug toxicity (digitalis, phenotiazine,
tricyclic and tetrasiklik, antidepressants)
PVT VF

Clinical manifestations
Heart only vibrate, unable to work as a pump
Clinical death biological death
Patients are not aware of no response

PEA / Asystole
PEA there is a electrical picture on the
monitor ECG, but no palpable pulse at A. carotid
ECG : wide QRS complex with a low frequency (
20 40x / min) idioventrikular rhythm

Asystole the heart stops contracting
ECG : a straight line without ventricular activity
( QRS complex)

ETIOLOGY FREQUENCY
Coronary Artery Disease
Acute Coronary Syndrome
Chronic Myocardial Scar
Approximately 80%
Cardiomyopathie
Dilated Cardiomyopathies
Hypertrophic Cardiomyopathies
Approximately
10% to 15%
Uncommon Causes
Valvular/Congenital Heart Disease
Myocarditis, Genetic Ion-Channel
Abnormalities, etc.
< 5%
Contributing Causes Of Cardiac Arrest
6H 5T
Hypovolemia
Hypoxia
Hydrogen ion (acidosis)
Hypokalemia/Hyperkalemia
Hypothermia
Hypoglycemia
Toxins
Tamponade, cardiac
Tension, pneumothorax
Thrombosis (coronary or pulmonary)
Trauma
symptomp
the heart stops beating and blood is not
supplied to the body
The presentation is not subtle
immediate loss of consciousness occurs not
aroused fall over
No pulse will be able to be palpated and no
signs of breathing
pulses paradoxus, elevated jugular venous
pulsation, distant heart sounds, and electrical
alternans on ECG
Heart attack warning sign
Chest discomfort (center of the chest that lasts
more than a few minutes, or that goes away and
comes back. It can feel like uncomfortable
pressure, squeezing, fullness or pain)
Discomfort in other areas of the upper body (one
or both arms, the back, neck, jaw or stomach)
Shortness of breath
Other signs: cold sweat, nausea or
lightheadedness
PATOFISIOLOGI
diagnosis
Sudden cardiac arrest is an unexpected death
in a person who had no known previous
diagnosis of a fatal disease or condition. The
person may or may not have heart disease.
DIFFERENTIAL DIAGNOSIS
Acute insults (hypoxia, ischemia, acidosis, electrolyte
imbalances, and toxic effects of certain drugs)
DRUGS:
tricyclic antidepressants
neuroleptics
macrolide and quinolone antibiotics
antifungal agents
procainamide, quinidine, disopyramide (class IA
antiarrhythmics)
sotalol, dofetilide, and ibutilide (class III antiarrhythmics)
treatment


Epinephrine
n a- and b-receptor agonist
increased peripheral vascular resistance via the
stimulation of a-receptors of the blood vessels.
redistribution of blood flow from visceral organs to
the heart and brain.
Atropine
asystole and slow PEA along with epinephrine and
vasopressin
Vasopresin, amiodarone, lidocaine
PROGNOSIS
related to the frequency of coronary artery
disease.
In the adolescent population, increased
awareness of hypertrophic cardiomyopathy
and appropriate screening may decrease the
frequency of sudden death.
Public education and widespread availability
of AEDs will increase survival.

BAD !!
Brain death and permanent death start to
occur in just 4 to 6 minutes after someone
experiences cardiac arrest
more than 95 percent of cardiac arrest victims
die before reaching the hospital

Factors Associated With Improved Outcomes in Cardiac Arrest
Presenting rhythm of VT/VF Presenting rhythm of VT/VF
Early/bystander CPR Early/bystander CPR
Early defibrillation Early defibrillation
CPR prior to defibrillation in the circulatory phase of cardiac arrest Minimal
interruptions to chest compressions
In-hospital and out-of-hospital use of AEDs
Amiodarone use in shock-resistant VT/VF
Therapeutic hypothermia in comatose cardiac arrest victims
ECG
Emergency ECG
Ventricular fibrillation
Pulseless Electrical Activity
Asystole
Ventricular fibrillation
reentrant pattern of excitation in the ventricles -> poorly synchronized and
inadequate myocardial contractions.
The heart consequently immediately loses its ability to function as a
pump.
As the initial reentrant pattern of excitation breaks up into multiple
smaller wavelets, the level of disorganization increases.
Sudden loss of cardiac output + subsequent tissue hypoperfusion ->
global tissue ischemia; brain and myocardium are most susceptible.
VF is the primary cause of sudden cardiac death (SCD).
Ventricular fibrillation is shown in the rhythm
strip below.
Epidemiology
Frequency
Ventricular fibrillation also is prevalent worldwide, with a reported
predominance in the northern hemisphere. Among some European
populations, the annual incidence of cardiac arrests exceeds 6 cases per
10,000 people.
Race
Black males have the highest incidence of sudden cardiac death.
Sex
Sudden cardiac death is more common among males than females,
although the rates become similar for patients older than 70 years.
Age
Incidence initially peaks during the first 6 months of life, then rapidly
declines until a second peak in those aged 45-75 years.

History
Ventricular fibrillation (VF) often occurs without
forewarning.
The following symptoms, while not necessarily specific
for sudden cardiac death or VF, may develop before
any major cardiac event :
Chest pain and other angina equivalents
Dyspnea
Easy fatigue
Palpitations
Syncope
Immediately preceding acute cardiac arrest, possible
increase in heart rate, presence of premature ventricular
contractions (PVCs), or period of VT

Physical
No pulse or respiration.
Patients in cardiac arrest have absent or
abnormal (gasping) respirations.
Unconsciousness
Wide and chaotic QRS complexes on cardiac
monitor

Causes
Cardiac, structural heart disease
Cardiac, no structural heart disease
Myocardial ischemia or infarction
due to coronary artery disease:
Coronary atherosclerosis
Cardiomyopathy: dilated,
hypertrophic, or arrhythmogenic
right ventricular cardiomyopathy
or dysplasia.
Aortic stenosis
Aortic dissection
Pericardial tamponade
Congenital heart disease
Myocarditis
Catecholaminergic polymorphic
ventricular tachycardia and right
ventricular outflow tract
tachycardia
Mechanical (commotio cordis)
[4]
or electrical accidents
Preexcitation (including Wolff-
Parkinson-White syndrome)
Heart block
Drug-induced QT prolongation
with torsades de pointes
Channelopathies: long QT
syndrome, short QT syndrome, or
Brugada syndrome

Causes
Noncardiac respiratory Metabolic or toxic
Bronchospasm
Aspiration
Sleep apnea
Primary pulmonary
hypertension
Pulmonary embolism
Tension pneumothorax
Electrolyte disturbances and
acidosis
Medications or drug ingestion
Environmental poisoning
Sepsis
Neurologic Seizure
Cerebrovascular accident -
Intracranial hemorrhage or
ischemic stroke
Drowning
Differential Diagnoses
Hyperkalemia
Hypokalemia
Torsade de Pointes
Toxicity, Antidepressant
Toxicity, Cocaine
Toxicity, Digitalis
Ventricular Tachycardia

Laboratory Studies
Serum electrolyte levels, including calcium
and magnesium
Cardiac enzymes to identify myocardial injury
Complete blood count (CBC) to detect
contributing anemia
Arterial blood gases (ABGs) to assess degree
of acidosis or hypoxemia
Toxicologic screens and levels as clinically
indicated

Imaging Studies
Chest radiography may identify aspiration
pneumonia, pulmonary edema, cardiomegaly,
and injury (eg, secondary to cardiopulmonary
resuscitation [CPR]).


Other Tests
Electrocardiography (ECG) to help identify
ischemic or proarrhythmic conditions

Pulseless Electrical Activity
A clinical condition characterized by
unresponsiveness and lack of palpable pulse
in the presence of organized cardiac electrical
activity.
Epidemiology
The use of beta-blockers and calcium channel blockers
may increase the frequency of PEA, presumably by
interfering with cardiac contractility.
Females are more likely to develop PEA than males.
The average patient age is 70 years. Older patients are
more likely to have PEA as an etiology of cardiac arrest.
Whether the patient outcome differs based on age is not
known; however, advanced age is likely associated with a
worse outcome.

Etiology
severe prolonged hypoxia or acidosis or
extreme hypovolemia or flow-restricting
pulmonary embolus.
exacerbated by worsening acidosis, hypoxia,
and increasing vagal tone
inadequate mechanical activity, even though
electrical activity is present
Hypoxia : preload, afterload, or contractility
often result in PEA.

Decreased preload
decreased venous return to the left atrium),
the left ventricle is unable to generate
sufficient pressure to overcome its afterload.
Cardiac tamponade may also cause decreased
ventricular filling.
Increased afterload
Afterload is inversely related to cardiac
output.
Severe increases in afterload pressure cause a
decrease in cardiac output.
Decreased contractility
Calcium influx and binding to troponin C is
essential for cardiac contraction.
If calcium is not available (eg, calcium channel
blocker overdose) or
if calcium's affinity to troponin C is decreased (as
in hypoxia), contractility suffers.

Decreased contractility
Depletion of intracellular adenosine
triphosphate (ATP) reserves increase in
adenosine diphosphate (ADP bind calcium,
reducing energy reserves.
Excess intracellular calcium can result in
reperfusion injury severe damage to the
intracellular structures, predominantly the
mitochondria.

Additional etiologic factors
Hypovolemia
Hypoxia
Hydrogen ion (acidosis)
Hypokalemia/hyperkalemia
Hypoglycemia
Hypothermia
Toxins
Cardiac tamponade
Tension pneumothorax
Thrombosis (coronary or pulmonary)
Trauma

Differential Diagnoses
Accelerated Idioventricular Rhythm
Acidosis
Cardiac Tamponade
Drug overdose
Hypokalemia
Hypothermia
Hypovolemia
Hypoxemia
Myocardial Ischemia
Pulmonary Embolism
Syncope
Tension pneumothorax
Ventricular Fibrillation

Prevention
The following measures may prevent some
cases of in-hospital pulseless electrical
activity:
Patients who have been on prolonged bed rest -
Should receive deep venous thrombosis (DVT)
prophylaxis
Patients who are on ventilators - Should be
monitored carefully for auto-PEEP development
Hypovolemia - Should be treated aggressively,
especially in patients with active bleeding

Asystole
Asystole is cardiac standstill.
No cardiac output & no ventricular
depolarization.
Eventually occurs in all dying patients.
Epidemiology
Children
Women
higher in women than in men
more common in males until around age 75
years.

Pathophysiology
Primary asystole occurs when the heart's
electrical system intrinsically fails to generate
a ventricular depolarization.
Secondary asystole occurs when factors
outside of the heart's electrical conduction
system result in a failure to generate any
electrical depolarization.

History
Immediate diagnosis of asystole requires the
recognition of a full cardiac arrest and a
confirmed flat-line rhythm in 2 perpendicular
leads.
Lightheadedness or syncope may precede
asystole when it follows a bradyasystolic
rhythm.

Physical Examination
If the rhythm is truly asystole and has been
present for more than several seconds, the
patient will be unconscious and unresponsive.
A few agonal (final gasping) breaths may be
noted, but detectable heart sounds and
palpable peripheral pulses are absent.

Complications
Complications from asystole include
permanent neurologic impairment and
complications from cardiopulmonary
resuscitation (CPR) or invasive procedures (eg,
liver laceration, fractured ribs, pneumothorax,
hemothorax, air embolus, aspiration,
gastric/esophageal rupture).
Death often occurs.
Differential Diagnoses
Hyperkalemia in Emergency Medicine
Hypothermia
Syncope
Ventricular Fibrillation


AMERICAN HEART
ASSOCIATION
CHANGES IN THE 2010
GUIDELINES AFFECTING
ALL RESCUERS
AMERICAN HEART ASSOCIATION:
2010 GUIDELINES
Health Care Provider*
PUSH HARD AND PUSH FAST
At least 100 COMPRESSIONS / MINUTE*
Allow the chest to recoil -- equal compression and relaxation times
<10 seconds for pulse checks or rescue breaths
Compression Depth*
Adults 2
Child/Infant 1/3 depth of chest 1.5" infant 2" child
Avoid excessive ventilations
A-B-C changed to C-A-B*
Critical element is chest compressions
Delay in A-B
Avoidance of A & B
Early defib
If alone--call and retrieve AED
Exception asphyxial arrest
AMERICAN HEART ASSOCIATION:
2010 GUIDELINES
Cricoid pressure not recommended
Advanced airway = 1 every 6-8 seconds
Adult: 1 every 5-6 Peds: 1 every 3
With advanced airway- no pause
AMERICAN HEART ASSOCIATION:
2010 GUIDELINES
Dispatcher Identification
SCA = seizure & agonal gasps
Trained to ID ask if breathing is normal
Only gasping???
Provide CPR instructions
AMERICAN HEART ASSOCIATION:
2010 GUIDELINES
AHA ECC Adult Chain of Survival - New
Simplified Universal
BLS algorithm

AMERICAN HEART ASSOCIATION:
2010 GUIDELINES
CPR
CPR
Combines external chest compressions with
artificial ventilation
Provides 30% (or less) of normal circulation
Only effective for short period of time
CPR 1 Rescuer
Assess
responsiveness
Summon EMS
Position the patient

CPR 1 Rescuer
Open the airway

CPR 1 Rescuer
Look, listen, and feel
for breathing

CPR 1 Rescuer
If there is no
breathing, give two
breaths, each lasting
1 second

CPR 1 Rescuer
Check for a pulse (
10 seconds)

CPR 1 Rescuer
If there is no pulse,
find your landmarks,
lower half of the
sternum, between
the nipples

CPR 1 Rescuer
Begin chest
compressions

CPR 1 Rescuer
Perform 30 chest
compressions
Push hard
Push fast
Allow the chest to
recoil after each
compression

CPR 1 Rescuer
Administer two
ventilations then
return to
compressions

CPR 2 Rescuer
1
2
3
4
CPR - Children

Use heel of one
hand
Keep airway open
with other hand
30 compressions:2
ventilations if alone
(2 rescuers use 15:2)
CPR - Infant

Give chest thrusts and
puffs of air
30 compressions:2
ventilations if alone
15 compressions: 2
ventilations with 2
rescuers
AEDs
Safe, accurate &
lightweight
Easy to operate

What is public
access defibrillation?

PAD
AEDs in public
places
Training the public
in CPR/AED
Special Considerations
Children
Clothing
Body hair
Water
Transdermal medication
patches

Implanted defibrillators
or pacemakers
Metal surfaces
Jewelry and glasses
AED
Assess
Check your
patient

Universal Steps
Power

Patient

Analyze

Shock
Power
Turn the power
on

Patient
Apply pads to
patient

Analyze
Stay clear while
patients heart
rhythm analyzed
Clear
Head to toe and
toe to head:
everyone is clear!

Shock
Defibrillate

Patient
Standard is set of 1
shock
Immediately restart
CPR for 2 minutes
then check pulse

conclusion
We have discussed about UA, MI
(NSTEMI&STEMI), cardiac arrest, emergency
ECG, CPR.
Related to the case, this patient : STEMI.
suggestion
Adminisration defebrilation, PCI and lab
examination (Myoglobin, Troponin and CK-
MB)
REFERENCE
Subagjo,agus,dkk. BCLS (Basic cardiac life
support) ed.2011
ACLS (advance cardiac life support) ed.2011
Rossens
Harrison princple ed.18th