CHEST PAIN

SCENARIO 3
GROUP 10

Ain,Latifah,Rafika,Nunung,Aishah,
Amalina,Miqdad,Harry,
Andhika,Fadli,Nova,Rina

SCENARIO
A collapse 60 years old bus driver was brought into casualty
complaining of severe,sustained crushing pain in a band across
the chest spreading into arms. Previously he had been
well,though he smoked 10 cigarettes a day. On examination he
was pale, with cold,sweaty skin. His pulse was weak,with
occasional extrasystole(ventricular ectopic beats). His arterial
blood pressure was 90/75 mmHg. Heart sound were normal. An
ECG revealed large Q wave and ST segment elevation. He was
admitted with a provisional diagnosis of myocardial infarction
due to coronary artery thrombosis. Plasma analysis showed
raised
cardiac
enzymes(
lactic
dehydrogenase,creatine
phosphokinase,aspartate aminotransferase). He was given O2
and morphine. A streptokinase infusion was set up to lyse the
coronary thrombus and he was also started on regular,low dose
aspirin.

KEYWORD
Collapse
Severe sustained crushing pain in band
across chest spreading into arm
Previously been well
Pale,cold, sweaty skin
Pulse weak with occasional extrasystole
Artery BP 90/75
Large Q wave, ST elevation
Plasma analysis: raised cardiac enzymes

QUESTION
1) Why the patient suffered a crushing pain that
spread to the arm?
2) Why occasional extrasystole occur ?
(pathomechanism)
3) What is the relationship between smoking and
occasional extrasystole?
4) Indication for large Q wave and ST elevation. What
are the relationship of these findings with chest pain?
5) Indication for increasing cardiac enzymes.
6) What are the relationship between myocardial
infarction with the symptoms? (why he is having weak
pulse)

http://www.emedicinehealth.com/cogestive_heart_
failure

DIFFERENTIAL DIAGNOSIS
STEMI

CAD

yes

yes

yes

no

Large Q wave and

ST elevasi

yes

no

Hypotension

yes

yes

yes

yes

SIGN AND
SYMPTOM
Crushing pain at
chest spreading
to arm
Occasional
extrasystol

Provisional
diagnosis MI due
to coroner arteri
trombosis

INTRODUCTION
STEMI "ST segment elevation myocardial infarction, is a
type of heart attack. This is determined by an ECG test.
Myocardial infarctions(heart attacks) occur when
acoronay arterysuddenly becomes at least partially
blocked by a blood clot, causing at least some of the
heart muscle being supplied by that artery to become
infarcted (that is, to die). Heart attacks are divided into
two types, according to their severity.
A STEMI is the more severe type.
http://heartdisease.about.com/ STEMI - ST Segment Elevation Myocardial
Infarction ByRichard N. Fogoros, M.D.

BASIC

EKG

Normal heart

Myocardial Infarction
Two to three days after an MI, the myocytes show that they are irreversibly damaged. They've lost their
nuclei. PMNs (polymorphonuclear leukocytes) are the first inflammatory cells on the scene. They will
begin to clear away the necrotic tissue. Later the macrophages will finish the job. These dying myocytes
will eventually be replaced with scar tissue.

http://www.kumc.edu/instruction/med
icine/anatomy/histoweb/path/path01.
htm

http://www.google.com/imgres?hl=en&gl=id&biw=1366&bih=624&tbm=isch&tbnid=KajG2
QEK1-M4mM:&imgrefurl=http://www.medicinenet.com/heart_attack_pathology_photo_e
ssay/page3.htm&docid=CZHmHLYLNv9ueM&imgurl=http://images.medicinenet.com/image
s/illustrations/myocardial_infarction_1.jpg&w=400&h=308&ei=8_KDUK3PH8nlrAeTzYH
wBw&zoom=1&iact=hc&vpx=398&vpy=128&dur=3820&hovh=197&hovw=256&tx=206&ty=150&si
g=116867615274730240580&page=2&tbnh=151&tbnw=196&start=21&ndsp=27&ved=1t:429,r
:23,s:20,i:206

PATHOPHYSIOLOGY
OF
ST-ELEVATION
MYOCARDIAL
INFARCTION (STEMI)

myocardial infarction
A myocardial
infarction is
defined as

Elevated blood
levels of cardiac
enzymes (CKMB or
Troponin T)

The patient
has typical
complaints

One of the
following criteria
are met

The ECG
shows ST
elevation or
depression

pathological
Q waves
develop on
the ECG

 PATHOPHYSIOLOGY MI
A prolonged imbalance between
myocardial oxygen supply and
demand leads to the death of
myocardial tissue. Coronary
atherosclerosis is an essential part of
the process in most patients.
Ischemic heart disease seems to progress
through stages of fatty-streak deposition
in coronary arteries to development of
fibro-fatty plaque, which then increases in
size until it causes luminal obstruction,
leading to exertional angina.
any stages in this process, the
atherosclerotic lesion may erode,
ulcerate, fissure, or rupture,
thereby exposing subendothelial
vessel wall substances to the
circulating blood

Procoagulant factors (such as tissue

factor) reside within the plaque itself
and, in the absence of
counterbalancing antithrombotic
factor (eg, heparin, tissue-factorinhibitor) and fibrinolytic activities
(tissues plasminogen activator [t-PA]
and single-chain urokinase-type
plasminogen activator) within the
endothelial cells of the coronary
artery, can cause thrombosis

This potent procoagulant stimulus

results in thrombus development in
this region. In general, acute MI
occurs when this thrombosis
propagates and occludes flow within
the artery, resulting in ischemia of
cardiomyocytes distal to the
obstruction

. Recent work suggests that

inflammation may play a pivotal role in
the genesis of plaque rupture. Total
thrombotic occlusion occurs most
commonly in proximal coronary
arteries; its presence has been
documented during the first 4 hours
after infarction in more than 85% of the
patients with ST segment elevation
(Crawford, M.H. (2009)).

Angina
pectoris

Neck
Shoulder
Arms

discomfort often refer to

other region of the C7
through dermatome

ischemic myocardial cells

release mediator such as
adenosine and lactate from
into local nerve endings

provocative substances
continue to accumulate and
active afferent nerve for
longer period

ischemic in acute MI persist

and proceed to necrosis

HYPOTENSION
May trigger a dramatic sympathetic nervous
system response
Systemic sign of subsequent catecholamine
release include diaphoresis (sweating),
tachycardia, and cool and clammy skin
cause of vasoconstriction

Systolic
Dysfuncti
on

J receptors effects a reflex

that results in rapid,
shallow breathing and
evokes the subjective
feeling of dyspnea

Decrease lungs
compliance and
stimulates juxtacappilary
receptors

Ischemia affects large

amount of
myocardium

Left ventricle
contractility can be
reduced

Decreasing the stroke

volume and causing the
diastolic volume and
pressure within the LV to
rise

Increase in LV pressure ,
compounded by the ischemia
induced stiffness of the
chamber (diastolic
dysfunction) is conveyed to
the left atrium and
pulmonary veins

SERUM MARKER OF INFARCTION

Detection of cardiac-specific troponins and creatine
kinase MB isoenzyme

Intracellular macromolecules leak into the cardiac

interstitium and ultimately into the bloodstream

Necrosis of myocardial tissue Cause by disruption of

the sarcolemma

TYPICAL
SYMPTOM:
- Crushing chest
pain, more severe
and wider than
usual angina

MYOCARDIAL
INFARTION

STEMI

SERUM BIOMARKS:
Creatine kinase
Troponin

ECG initial finding

- St elevation
- Q Wave

Left Ventricular Function

Systolic Function

Upon interruption of antegrade flow in an epicardial coronary artery, the

zone of myocardium supplied by that vessel immediately loses its ability
to shorten and perform contractile work. Four abnormal contraction
patterns develop in sequence:
(1) dyssynchrony, that is, dissociation in the time course of contraction
of adjacent segments;
(2) hypokinesis, reduction in the extent of shortening;
(3) akinesis, cessation of shortening; and
(4) dyskinesis, paradoxical expansion, and systolic bulging.
Hyperkinesis of the remaining normal myocardium initially accompanies
dysfunction of the infarcting segment. The early hyperkinesis of the
noninfarcted zones likely results from acute compensations including
increased activity of the sympathetic nervous system and the FrankStarling mechanism. A portion of this compensatory hyperkinesis is
ineffective work because contraction of the noninfarcted segments of
myocardium

Ventricular Remodeling
As a consequence of STEMI, the changes in left ventricular size, shape,
and thickness involving both the infarcted and the noninfarcted segments
of the ventricle described earlier occur and are collectively referred to as
ventricular remodeling, which can in turn influence ventricular function
and prognosis.
A combination of changes in left ventricular dilation and hypertrophy of
residual noninfarcted myocardium causes remodeling.
After the size of infarction, the two most important factors driving the
process of left ventricular dilation are ventricular loading conditions and
infarct artery patency.
Elevated ventricular pressure contributes to increased wall stress and
the risk of infarct expansion, and a patent infarct artery accelerates
myocardial scar formation and increases tissue turgor in the infarct zone,
reducing the risk of infarct expansion and ventricular dilation.

AntmanEM,MorrowDA,McCabeCH,et al:
Enoxaparin versus unfractionated heparin with fibrinolysis for ST-elevation
myocardial infarction.
N Engl J Med2006;354:1477.

references
SLIDE 2: Alpert JS, Thygesen K, Antman E, and Bassand JP.
Myocardial infarction redefined--a consensus document of The Joint European Society of Cardiolog
y/American College of Cardiology Committee for the redefinition of myocardial infarction.
J Am Coll Cardiol 2000 Sep; 36(3) 959-69. pmid:10987628
Book of Pathophysiology of Heart Disease fourth edition, editor Leonard S.Lilly page :179184
ILMU PENYAKIT DALAM, Jilid II Edisi V, Editor Aru W.Sudoyo, Bambang Setiyohadi,
Idrus Alwi, page:1741-1744

ST elevation MI

ST segment elevation type of

acute myocardial infarction require
at least 1mm (0.1 mV) of ST
segment elevation in the limb
leads, and at least 2mm elevation
in the precordial leads

left ventricular
hypertrophy

These elevations must

be present in
anatomically
contiguous leads. (I,
aVL, V5, V6 correspond
to the lateral wall; V1V2 correspond to the
septal wall; V3-V4
correspond to the
anterior wall; II, III, aVF
correspond to the
inferior wall.)

left bundle branch

block
early repolarization
hyperkalemia
ventricular aneurysm

The clinician must therefore

be well versed in
recognizing the so-called
ECG mimics of acute
myocardial infarction which
include

12-lead electrocardiogram
showing ST-segment
elevation (orange) in I, aVL
and V1-V5 with reciprocal
changes (blue) in the
inferior leads, indicative of
an anterior wall myocardial
infarction

An acute STEMI involving

the inferior and right
ventricular wall.
Reciprocal changes are
seen in the anterior
leads

PATHOLOGIC OF Q-WAVE
Pathologic Q
waves

previous
myocardial
infarction

Any Q-wave in leads V2V3 0.02 s

or QS complex in leads V2 and V3
Q-wave 0.03 s and > 0.1 mV
deep or QS complex in leads I, II,
aVL, aVF, or V4V6 in any two leads
of a contiguous lead grouping (I,
aVL,V6; V4V6; II, III, and aVF)

result of absence of
electrical activity

The evolution of an
infarct on the ECG. ST
elevation, Q wave
formation, T wave
inversion, normalisation
with a persistent Q wave

PATHOMECANISM CHEST
PAIN
http://emedicine.medscape.com/article/150215-overview#2
Prof.Dr.Peter Kabo, Bagaimana Menggunakan Obat-obat
kardiovasculer secara Rasional

Atherosclerosis

Productio
n of
adenosin

Diffuse to
extracellula
r space

Produce
endothelial
derived
constricting
factor (EDCF)
Aerobic
glycolysis
turn to
anerobic
glycolysis
Stimulate A1
receptor in
cardiac
afferent nerve
ending

Chest
pain

Increas
e tonus
artery
corona
ry

Ischemic
myocard

Bind with
somatic
cervico
thoracalis
nerve at
ascending
pathway in
medulla
spinalis

SMOKING

KILLS

Nicotine is a
sympathomimetic chemical
that promotes the release of
catecholamines and other
neurotransmitters

addition to its cardiovascular

effects such as elevated heart
rate, blood pressure and cardiac
output
nicotine has metabolic
effects, in particular
increased lipolysis

One might also expect that

the hemodynamic effects of
nicotine would contribute to
endothelial damage and
accelerate the progression of
atherosclerosis.
These effects could
potentially trigger
symptoms of ischemia in
such smokers.

Lipolyis - increased levels of

circulating free fatty acids
and glycerol in the blood and
the resulting increase in fat
metabolism drives a demand
for more oxygen, leading to
increased coronary blood
flow and myocardial oxygen
uptake.

SIGNS AND
SYMPTOMS

Chest pain

(pressure,tightness,heaviness and might

radiate to neck, arm)

Ingestion / heartburn
Nausea, Vomiting
Sweating
Weakness
Dizziness

http://www.cardiosmart.org/ManageCondition/Default.aspx?id=904
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2233977/

ADDITIONAL EXAMINATION
1. Physical examination
Gen appearance
Distress, Levine sign
Heart rate, pulse, respirrate variable
Blood pressure variable
Low-grade fever
Examination of jugular venous pulsations
Pulmonary Crackles
S4 gallop due to reduced LV compliance
S3 gallop if LV dysfunction present
Murmurs, Pericardial friction rubs

2. ECG
The key to rapid diagnosis
and risk stratification for the
patient with chest pain
To be obtained within 10
minutes of arrival to
Emergency Department
For STEMI ST-segment
elevation >1mm in 2+
contiguous leads OR new
left bundle branch block
(LBBB)
Location of Infarct:
Leads
Inferior MI II, III, aVF
Anterior MI V2-V4

3. Lab
studies
Cardiac
Biomarkers:
CK, CK-MB,
cTn
Serum
Chemistries
Renal
Function
Coagulatio
n Studies

Aspirin

TREATMENT

Rapidly blocks formation of

thromboxaneA2 in platelets by
cyclooxygenase inhibition
162-325mg chewed (promotes
buccalabsorption)
ISIS-223%
reduction in mortality, largely
Other Adjuvant
additive to the reduction in mortality from
Therapies
streptokinase
Analgesics
Nitrates
Beta-blockers
Ace Inhibitors
Oxygen
Heparin
IV Glycoprotein IIb/IIIaInhibitors

Thrombolytic Therapy
Common Agents:
TNK-tPA30-50mg IV bolus
Reteplase10U x 2 (each over 2 minutes) IV
Alteplaseup to 100mg in 90mins (based on weight)
Contraindications:
Absolute : Prior intracranial hemorrhage, known
cerebral
vascular
lesion,
malignant
intracranial
neoplasm, ischemic stroke within 3 months, suspected
aortic dissection, active bleeding, recent closed head
injury or facial trauma within 3months
Relative
:
History
of
chronic,
severe
HTN,
severe/uncontrolled HTN at presentation (>180/110),
history
of
ischemic
stroke
>3
months,
traumatic/prolonged CPR, recent internal bleeding (2-4
weeks), pregnancy, active peptic ulcer, current

Primary
PCI
PCI =
Percutaneous
Coronary
Intervention
PTCA =
Percutaneous
Transluminal
Coronary
Angioplasty
POBA = Plain

PROGNOSIS
Discharge usually 5 days after
admission
Smoking Cessation
Short and Long-term survival
depend upon resting LV function,
residual ischemic myocardium,
and susceptibility to ventricular
arrhythmias

THE END