2th scenario Mr.

Alis Angina

14B Members
Zulherman
Ikrima Ainal Qalbi
Nurul Husna Muchtar
Ridhatul Amalia C.A
Puji Aulia Zani
Wulan Purnama Sari
Fatmi Eka Putri
Vani Morina Kasim
Afifah Ikhwan

Terminology
1. SKA (Acute Coronary Sindrom) : acute coronary
syndrome (ACS) refers to any group of clinical
symptoms compatible with acute myocardial ischemia
and includes unstable angina (UA), nonST-segment
elevation myocardial infarction (NSTEMI), and STsegment elevation myocardial infarction (STEMI).
2. Nitrat medicine group : drugs known as nitrates is one
of a class of drugs used for angina pectoris who works
by vascular dilatation
3. Troponin T : a protein produced by cells of the heart
muscle necrosis were used as markers of myocardial
necrosis
4. Clinical Chemistry : Clinical examinations were
performed for screening and diagnosis of disease

Problem Identification and

Problem Analyses
1. How is the corelation of age and gender with
condition that experienced by Mr. Ali?
Coronary Heart Disease is most commonly
suffered by man than woman. Estrogen in
woman thought to play a role in this case.
2. Why was Mr. Ali (56 years old) complained of
squeezed chest and shortness of breath? It
caused by lack of oxygen in tissue and hypoxia
of myocardium.

3. Why was doctor lay the patient and give

oxygen? to reduce the heart's work, accelerate
the blood flow back to the heart and replenish
the supply of oxygen to the tissues
4. Why was Mr. Ali complained heavy chest, cold
sweat, and vomiting? because plaque will loose
stuck and clog the blood vessels and reduces
blood flow to the tissues and tissue ischemia
and lead to myocardial infarction

5. How is the corelation of Mr. Alis condition and

Acute Coronary Sindrome that suffered by his
brother? a family history of exogenous factors
that cause heart disease
6. why after being given oxygen reduced the pain?
because after the administration of oxygen, the
oxygenation of tissues for the better and the
pain will be reduced

7.how the interpretation of an examination by a

doctor? classified as hypertensive blood pressure
and ECG results within normal limits can be a
state of angina pectoris
8. how the results of troponin T levels? test results
show that the presence of tissue necrosis large
enough so that the heart muscle cells to produce
an enzyme

9. why after Mr.Ali heal recommended to change

lifestyle? for prevention in order to avoid the
next heart attack

Scheme
Vomiting

Sesak Napas
Tn. Ali

Hipertension

Angina

Nitrat

Sport

Plaque

Chemistry
examination

Eating form

Obstruksi

Treatment

Life style

Preventive

Learning Objectives
Epidemiology, Etiology, Risk Factors, Clinical
Manifestation, Pathogenesis, Pathofisiology,
Diagnose, Differential Diagnose, Treatment,
Prognosis of Coronary Heart Disease

STABLE ANGINA PECTORIS

Angina Pectoris
Classic angina is characterized by substernal
squeezing chest pain, occurring with stress and
relieved with rest or nitroglycerin.
May radiate down the left arm
May be associated with nausea, vomiting, or
diaphoresis.

Stable Angina
Classification

Exertional
Variant
Anginal Equivalent Syndrome
Prinzmetals Angina
Syndrome-X
Silent Ischemia

Angina: Exertional
Coronary artery obstructions are not sufficient to
result in resting myocardial ischemia. However,
when myocardial demand increases, ischemia
results.

Angina: Variant Angina

Transient impairment of coronary blood supply
by vasospasm or platelet aggregation
Majority of patients have an atherosclerotic
plaque
Generalized arterial hypersensitivity
Long term prognosis very good

Angina: Anginal Equivalent Syndrome

Patients with exertional dyspnea rather than
exertional chest pain
Caused by exercise induced left ventricular
dysfunction

Angina: Prinzmetals Angina

Spasm of a large coronary artery

Transmural ischemia
ST-Segment elevation at rest or with exercise
Not very common

Angina: Syndrome X
Typical, exertional angina with positive exercise
stress test
Anatomically normal coronary arteries
Reduced capacity of vasodilation in
microvasculature
Long term prognosis very good
Calcium channel blockers and beta blockers
effective

Angina: Silent Ischemia

Very common
More episodes of silent than painful ischemia in
the same patient
Difficult to diagnose
Holter monitor
Exercise testing

Etiology and pathogenesis

Symptoms are results of myocardial ischemia
due to insufficient blood flow through
atherosclerotically changed coronary vessels

Clinical symptoms

Patient history is agolden standard

Retrosternal pain
Dyspnea
Nausea
Arrhythmia
Restlessness
Levine sign
Pain eased after taking nitrates

Physical examination

Hypertension
Obesity
Hyperglycemia
Hyperlipidemia
Auscultation

Investigations
Laboratory tests (leukocytes, hemoglobin,
thyroid hormones, troponin I and T, MB-CPK)
Resting ECG
Excercise ECG
Cardiac scintigraphy
Echocardiography
Coronary angiography

treatment
Prognostic therapy: Aspirin, lipid-lowering
therapy
Symptomatic treatment: GTN, beta-blockers,
long-acting nitrates, calcium-channel blockers,
ACEI
Percutaneous coronary intervention, coronary
artery bypass grafting

UNSTABLE ANGINA PECTORIS

 Epidemiology : In the United States each year 1

million patients hospitalized for unstable angina
pectoris.
Unstable angina was defined as angina pectoris (or
equivalent discomfort in ischemic-type chest) with
one of the clinical appearance:
1. Occurs at rest (or minimal activity) and usually
lasts more than 20 minutes (if no nitrates or
analgesic use).
2. Severe pain and obvious.
3. Usually gain weight (eg pain that awakens the
patient from sleep or is getting worse, continuous or
more frequent than before).

 Pathophysiology:
1. Plaque rupture or plaque erosion with nonocclusive thrombus (this causes the greatest
role in the occurrence of UAP).
2. Dynamic obstruction caused by:
a. Coronary artery spasm epicardium, as in
Prinzmetal variant angina.
b. Coronary vascular resistance.
c. Local vasoconstrictor thromboxane A2
such, which is released from platelets.
d. Disfunction of coronary endothelial.
e. Adrenergic stimuli including cold and
cocaine.

3. Great narrowing of the lumen of the coronary

arteries caused by the formation of
atherosclerotic progression and restenosis postpercutaneous coronary intervention.
4. Inflammation.
5. Secondary unstable angina pectoris, which
causes an increase or decrease in oxygen 'needs
oxygen supply (eg in case of tachycardia, fever,
hypotension, or anemia).

Investigations:
1. Electrocardiography (ECG)
The presence of new ST segment depression
indicating the possibility of acute ischemia.

2. Exercise test
Patients who have been stabilized with medical
therapy and showed signs of high risk need
examination by a treadmill exercise test.
3. Echocardiography
This examination does not provide data for
diagnosis of unstable angina directly. But when it
appears the disturbance of the left ventricle
physiology, the presence of mitral insufficiency
and cardiac regional wall motion abnormalities
indicating poor prognosis.

4. Chest X-ray
Chest radiograph was instrumental to identify the
presence of pulmonary congestion or edema,
which usually occurs in patients with UAP
extensive involving the left ventricle, causing left
ventricular dysfunction.

Management:
1. Bed rest.
2. Given a sedative
3. Oxygen
4. Anti ischemia
5. Anti agregation platelet.
6. Antitrombin

ACUTE MYOCARDIAL INFARCTION

 NSTEMI (NonST-segment elevation

myocardial infarction) and STEMI (ST-segment
elevation myocardial infarction) are commonly
known as heart attack. But they are different
from each other in some extent. NSTEMI
account for about 30% and STEMI about 70% of
all heart attack (myocardial infarction).

Pathophysiology of NSTEMI vs STEMI:

Pathophysiologically, NSTEMI is somewhat different
from STEMI. NSTEMI occurs by developing a
complete occlusion of a minor coronary artery or a
partial occlusion of a major coronary artery
previously affected by atherosclerosis. This causes a
partial thickness damage of heart muscle.
STEMI occurs by developing a complete occlusion of
a major coronary artery previously affected by
atherosclerosis. This causes a full thickness damage
of heart muscle.

Symptoms of STEMI:
There is no difference between NSTEMI and
STEMI in clinical presentation. In both cases,
patients usually present with similar type of
symptoms such as chest pain, nausea, vomiting,
sweating, breathing difficulty.
- See more at: http://nstemi.org/nstemi-vsstemi/#sthash.IUAZpuaO.dpuf

ECGof STEMI:
STEMI shows ST segment elevation in ECG (due to
full thickness injury of heart muscle) and later
progress to a Q-wave. For this reason, it is also
called a Q-wave myocardial infarction (QWMI).
The ultimate ECG findings of STEMI are STsegment elevation, pathological Q-wave formation
and T-wave inversion.

Cardiac markers of NSTEMI vs STEMI:

Cardiac markers including CK-MB (creatine
kinase myocardial band), troponin I and
troponin T, all elevate both in cases. But the
elevation of these markers is often mild in
NSTEMI compared with STEMI.

Diagnosis STEMI:
The diagnosis of a STEMI is based on a typical
history of chest pain, ST segment elevation in ECG
plus elevation of cardiac markers in serum.

Diagnosis of NSTEMI:
DIAGNOSIS of HISTORY
Chest pain or epigastric pain which leads to great
myocardial ischemia: As squeezed heavy objects,
feels suffocated, Flavor pressed, punched, stabbed
burning.
- Stenum usually felt behind the entire chest ,
especially the left, can be to the nape, jaw,
shoulders, back, left arm or both arms
- Especially men> 35 years and Women> 40 years
- Often accompanied by nausea or vomiting, malaise
can also be accompanied by shortness of breath,
weakness, loss of consciousness, and sweat a lot
-

Additional checks
ECG
ECG features of acute myocardial infarction nonQ-wave (NSTEMI):
ST segment depression or inverted T waves in
leads sequentially 2
T wave inversion of at least 1 mm in 2 or more
consecutive leads.
ST segment changes when complaints and
returns to normal when the complaint was lost

Examination Markers Heart / Cardiac enzymes

(Cardiac Markers):

Common is CKMB, troponin T can

also (TnT) or troponin I (TNI)
Increased cardiac markers will be seen
in acute myocardial infarction Q-wave
(STEMI) and non-Q-wave (NSTEMI)

Complications STEMI:
Complications occur both in cases. But some
complications like cardiogenic shock, left
ventricular failure, severe mitral regurgitation
due to papillary muscle rupture, cardiac
tamponade due to ventricular wall rupture are
more in STEMI (due to full thickness heart
muscle damage) than NSTEMI.

Treatment of STEMI:
Antiplatelets (Aspirin, Clopidogrel, Ticagrelor),
anticoagulants (Enoxaparin, Dalteparin, Fondaparinux),
beta-blockers (atenolol, metoprolol, bisoprolol), nitrates
(isosorbide dinitrate, glyceryl trinitrate), statins
(atorvastatin, rosuvastatin, simvastatin, pitavastatin),
ACE inhibitors (ramipril, enalapril, captopril, lisinopril)
or ARBs (valsartan, candesartan, losartan, olmesartan)
are given both in NSTEMI and STEMI.
In case of reperfusion therapy, primary PCI
(percutaneous coronary intervention) is the treatment of
choice for STEMI.

Prognosis of NSTEMI vs STEMI:

Short-term (in-hospital or one month) mortality
is lower in NSTEMI (3-5%) compared to STEMI
(10-15%). Re-infarction rate (further heart
attack) is higher in NSTEMI (15-25%) after
hospital discharge compared to STEMI (5-8%).
Long-term mortality is similar or higher in
NSTEMI compared to STEMI (two year
mortality is approximately 30% in both cases).

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