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ACUTE CORONARY

SYNDROME
dr. Wisudawan, M.Kes, Sp.JP, FIHA

BAGIAN KARDIOLOGI DAN KEDOKTERAN VASKULAR


FAKULTAS KEDOKTERAN UNIVERSITAS MUSLIM INDONESIA
©2012 National Heart Foundation of Australia
CVD – the facts

• Heart disease is one of the leading cause of death.

• In Indonesia, coronary heart disease (CHD) and stroke are


estimated to cause more than 470 000 deaths annually

• The annual mortality rate per 100,000 people from


cardiovascular diseases in Indonesia has increased by
55.4% since 1990, an average of 2.4% a year.

©2012 National Heart Foundation of Australia

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ACUTE CORONARY SYNDROME

• ACS is a broad spectrum of clinical presentations, spanning


STEMI (heart attack) through an accelerated pattern of angina
without evidence of myonecrosis/infarction (muscle death).
• Myocardial infarction (MI) occurs when the blood supply to the
heart muscle is interrupted due to partial or complete occlusion
(thrombus) of the coronary artery. As a result, some of the
heart muscle becomes infarcted (dies).
• A heart attack can be confirmed by an electrocardiogram (ECG)
test.

©2012 National Heart Foundation of Australia

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Coronary Atherosclerotic Disease
is a diffuse process with focal
atherosclerotic material (plaque).

Some plaques are obstructive but


not thrombotic.
Others are potentially thrombotic
but not obstructive.

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©2012 National Heart Foundation of Australia
Angiography vs Pathology

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INITIAL ASSESMENT OF CHEST PAIN

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Signs and symptoms of ACS presentation

• chest discomfort (tightness, pressure, heaviness) at rest or for a prolonged period (> 10
minutes, not relieved by sublingual nitrates)
• recurrent chest discomfort
• discomfort associated with syncope/acute heart failure.

The pain may spread to other parts of the upper body, including:
• back, neck, jaw, arm(s), shoulder(s) or epigastric pain.

The person may also experience:


• dyspnoea (shortness of breath), diaphoresis (profuse perspiration), dizziness, nausea or
vomiting
• recent research shows that women, the elderly and people with diabetes are less likely
to experience chest pain as a symptom.

©2012 National Heart Foundation of Australia


Who Presents With Atypical Symptoms?

©2012 National Heart Foundation of Australia Antman EM, Anbe DT, Armstrong PW, et al. www.acc.org/clinical/guidelines/stemi/index.pdf. Updated 2004.
Accessed June 20, 2007.
Risk factors for Cardiovascular
Disease
Modifiable risk factors: Non-modifiable risk factors:
• smoking • gender
• poor diet • age
• high cholesterol • family history of CVD

• physical inactivity • diabetes

• high blood pressure


• being overweight
• depression, social isolation and
lack of social support.

©2012 National Heart Foundation of Australia


Risk factors for Cardiovascular
Disease

©2012 National Heart Foundation of Australia


©2012 National Heart Foundation of Australia
Important ECG Findings

©2012 National Heart Foundation of Australia


Example of ST-segment Elevation (STEMI) Example of ST-segment Depression (UA/STEMI)
J
poi
nt
ST
D

S
T
J
E
poin
Example of T-wave Inversion (UA/STEMI) t

T wave
change
©2012 National Heart Foundation of Australia
s
Normal 12-lead
LATERAL
ECG
ANTERIOR

LATERAL
INFERIOR

©2012 National Heart Foundation of Australia


http://www.uptodate.com/contents/image?imageKey=CARD%2F1617. Accessed Aug 6. 2011.
ST-segment elevation ST-segment depression

Early-Stage Acute MI (STEMI)

T-wave inversion

©2012 National Heart Foundation of Australia


ST-segment elevation T-wave inversion

3-Day-Old MI (STEMI)

©2012 National Heart Foundation of Australia


Time from symptom onset and likely outcome

< 1 hour
Aborted heart attack or only little heart muscle damage

Early response: treatment is1–2


time
hourscritical
Minor heart muscle damage only

2–4 hours
Some heart muscle damage with moderate heart muscle salvage

4–6 hours
Significant heart muscle damage with only minor heart muscle salvage

6–12 hours
No heart muscle salvage (permanent loss) with potential infarct
healing benefit

> 12 hours
Reperfusion is not routinely recommended if the patient is
asymptomatic and haemodynamically stable

In cases of major delay to hospitalisation (> 30 minutes) ambulance


crews should consider pre-hospital fibrinolysis.

©2012 National Heart Foundation of Australia


©2012 National Heart Foundation of Australia
• Implement reperfusion strategy for patients presenting within 12 hours of onset of ischaemic symptoms
consistent with ACS (determined by physical examination):

Early response
immediate 12-lead ECG
▪ insert cannulae
▪ pain relief
▪ blood tests.
• Give aspirin 150–300 mg (unless already given, or contraindicated).

• Doctor sees patient within 10 minutes of arrival

• Oxygen therapy indicated only for patients with hypoxia (oxygen saturation < 93%) and those with
evidence of shock (Consensus).

©2012 National Heart Foundation of Australia


STEMI – what is it?

STEMI is defined as presentation with clinical symptoms consistent with an ACS


with ECG features including any of:
• persistent ST-segment elevation ≥ 1 mm in two contiguous limb leads
• ST-segment elevation ≥ 2 mm in two contiguous chest leads
• new left bundle branch block (LBBB) pattern.

©2012 National Heart Foundation of Australia


Choice of reperfusion therapy
• In general, PCI is the treatment of choice, providing it can be performed promptly by a qualified
interventional cardiologist in an appropriate facility.1
• All PCI facilities should be able to perform primary angioplasty within 90 minutes of patient presentation.

• Fibrinolysis should be considered early if PCI is not readily available.

• In cases of major delay to hospitalisation (> 30 minutes) consider pre-hospital fibrinolysis.

Reference
1. Acute Coronary Syndrome Guidelines Working Group. Guidelines for the management of acute coronary syndromes 2006. Med J
©2012 National Heart Foundation of Australia Aust 2006; 184(8 Suppl):S9–29.
NSTEACS – what is it?

• Non-ST-elevation ACS (NSTEACS) applies to patients with suspected ACS in the absence of other
plausible causes of troponin elevation (e.g. sepsis, pulmonary embolus).
• On physical examination, patients with NSTEACS may have a ‘normal’ ECG reading, or show minor
changes (occurs in up to 50% of patients).
• All patients with NSTEACS should have their risk stratified to direct management decisions.

• The management of patients with NSTEACS requires evolving risk stratification: clinical assessment,
assessment of cardiac biomarkers and time.

©2012 National Heart Foundation of Australia


©2012 National Heart Foundation of Australia
Management of patients with NSTEACS

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Medication regimen

©2012 National Heart Foundation of Australia


Before discharging a patient:
• discharge medication regimen

• Long-term management
provide tailored lifestyle advice to reduce risk of further
events, including:
▪ smoking cessation
▪ good nutrition and moderate alcohol intake
▪ physically active lifestyle and weight management as
relevant
▪ managing depression
▪ warning signs of a heart attack.
• Refer all patients to comprehensive cardiac
rehabilitation programs.

©2012 National Heart Foundation of Australia


ACUTE LUNG
OEDEMA

©2012 National Heart Foundation of Australia

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Definition

Pulmonary Edema is a condition characterized by fluid accumulation in the lungs caused by


extravasation of fluid from pulmonary vasculature in to theinterstitium and alveoli of the lungs.

©2012 National Heart Foundation of Australia


Patophisiology

• Imbalance of Starling forces


increased pulmonary
capillary pressure,
decreased plasma oncotic
pressure,
increased negative
interstitial pressure
• Damage to the alveolar-
capillary barrier
• Lymphatic obstruction
• Idiopathic (unknown)
mechanism

©2012 National Heart Foundation of Australia


Diagnosis And Causes
1• Symptoms: Dyspnea (on effort or at rest)/breathlessness, fatigue, orthopnea, cough, weight gain/ankle
swelling
2• Signs: Tachypnea, tachycardia, low or normal blood pressure, raised jugular venous pressure, 3rd/4th
heart sound, rales, oedema, intolerance of the supine position
3• Cardiovascular risk profile: Older age, HTN, diabetes, smoking, dyslipidemia, family history, history of
CVD
4• Precipitating factors: Myocardial ischemia, rhythm disturbances, medication (NSAID, negative inotropic
agents), infection, noncompliance
5• Differential diagnosis: Exacerbated pulmonary disease, pneumonia, pulmonary embolism, pneumothorax,
acute respiratory distress syndrome, (severe) anaemia, hyperventilation (acidosis), sepsis/septic shock,
redistributive/ hypovolemic shock
6• Likelihood: Depending on the site off presentation the underlying cause of acute heart failure is likely to
differ.
Diagnosis And Causes
©2012 National Heart Foundation of Australia
Management of dyspnea
Initial treatment (C) IV therapy
thank you…

BAGIAN KARDIOLOGI DAN KEDOKTERAN VASKULAR


FAKULTAS KEDOKTERAN UNIVERSITAS MUSLIM INDONESIA
©2012 National Heart Foundation of Australia

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