Emergency Cardiovacular

Care (ECC)
Dr. Erwin Sukandi, SpPD, K-KV,
FINASIM
Cardiology Division
Internal Medicine Department

ECC
Acute Coronary Syndrome
Unstable Angina Pectoris
Non ST Elevation Myocardial Infarction
ST Elevation Myocardial Infarction

Acute Heart Failure

Malignant Arrhythmia

ACUTE CORONARY SYNDROMES

LEARNING OBJECTIVES

Define acute coronary syndromes (ACS)

Understand the pathophysiology
Be capable of risk stratification
Aware of medications and strategies
employed to manage ACS
Use basic principles of ECG interpretation
and infarct localization
Apply knowledge to case studies

Acute Coronary Syndrome

Unstable Angina Pectoris
Non-ST segment elevation
myocardial infarction (NSTEMI,
usually non Q wave MI)
ST segment elevation myocardial
infarction (STEMI, usually Q wave MI)

Goal of ACS Management:

REDUCE PATIENT SYMPTOMS
REDUCE MORTALITY
LIMIT MYOCARDIAL DAMAGE
PRESERVE LV FUNCTION

TIME IS MUSCLE

ACUTE CORONARY SYNDROMES

Stable Angina

Does not predict acute events

Marker of established coronary artery disease (CAD)
Fixed lesion / partially occluded vessel
Mismatch in oxygen supply and demand

Precipitants:
Exercise
Cold
Stress

Duration:
</= 15 to 20 minutes

Relief:
Rest
Nitroglycerine

ACUTE CORONARY SYNDROMES

Unstable Angina

Clinical Presentation:

I. New Onset Angina

Within past 1-2 months
CCS III or IV

II. Crescendo Angina

Previous stable angina which has become more
frequent, severe, prolonged, easily induced or less
responsive to nitroglycerine

III. Rest Angina

Angina occurring at rest and lasting more than 15-20
minutes

ACUTE CORONARY SYNDROMES

Unstable Angina/NSTEMI
UA/NSTEMI

Patent culprit artery, ulcerated plaque and associated

thrombus
Significant risk of of thrombotic reocclusion

Unstable Angina = ACS without abnormal levels

of serum biomarkers for myocardial necrosis
(Ti,Tt,CK-MB)

NSTEMI = ACS with positive markers

ACUTE CORONARY SYNDROMES

STEMI
STEMI
Complete thrombotic occlusion of a major epicardial artery

Presentation:
Characteristic symptoms of cardiac ischemia
More prolonged and severe symptoms
Little response to nitroglycerine

Specific EKG changes on serial EKGs

Elevation of serum markers for cardiac injury
WHO definition of AMI

ACUTE CORONARY SYNDROMES

ETIOLOGY

Atherosclerotic plaque rupture *

inflammation
thrombosis

Vasospasm
Dissection
Decreased oxygen delivery (e.g. anemia,hypotension)
Increased oxygen consumption (e.g. sepsis, thyrotoxicosis)

Diagnosis
Cardiac Chest pain
ECG chages
Cardiac enzymes

Symptoms -Angina Pectoris

Pain
Substernal
Squeezing/Crushing/Heaviness
May radiate to arms, shoulders,
jaw, upper back, upper abdomen
back
May be associated with shortness
of breath, nausea, sweating
13

Symptoms -Angina Pectoris

Pain usually associated with
3Es
Exercise
Eating
Emotion

14

Symptoms -Angina Pectoris

Pain seldom lasts > 30
minutes
Pain relieved by
Rest
Nitroglycerin

15

Symptoms -Angina Pectoris

Great anxiety/Fear
Fixation of the body
Pale, ashen, or livid face
Dyspnea (SOB) may be
associated
16

Symptoms -Angina Pectoris

Nausea
Diaphoresis
BP usually up during attack
Dysrhythmia may be present

THE ELECTROCARDIOGRAM
12 lead EKG
Cornerstone of initial evaluation
Within 10 minutes of presentation

Previous EKG tracings

Compare

Serial EKGs
Essential

THE ELECTROCARDIOGRAM
1. ST segment elevation 2mm
true posterior ischemia

(2 contiguous leads),

new LBBB,

STEMI

EMERGENT REPERFUSION
2. ST depression >1mm, marked symmetrical T wave
inversions >2 mm or Wellens pattern, dynamic ST-T
changes with pain
UA/NSTEMI LIKELY

MEDICAL MANAGEMENT +/- URGENT IMAGING

3. Non-diagnostic or normal ECG
ACS LESS LIKELY

RISK STRATIFY

THE ELECTROCARDIOGRAM
INFARCT LOCATION
II, III, AVF
: Inferior
V1 - V4
: Anteroseptal
I, aVL
: High lateral
I, aVL, V5-V6
: Lateral
I,aVL, V1-V6
: Extensive anterior
V1-V2 tall R, ST depression : True
posterior

ELECTROCARDIOGRAM

Anterior Myocardial
Infarction
Occlusion of the
left coronary artery
left anterior
descending branch
ECG changes: ST
segment elevation
with tall T waves
and taller-thannormal R waves in
leads V3 and V4

Inferior Myocardial
Infarction
Occlusion of the
right coronary
arteryposterior
descending branch
ECG changes: ST
segment elevation
in leads II, III, and
aVF

Lateral Myocardial Infarction

Occlusion of the
left coronary artery
circumflex
branch
ECG changes: ST
segment elevation
in leads I, aVL, V5,
and V6

Septal Myocardial Infarction

Occlusion of the
left coronary artery
left anterior
descending branch
ECG changes:
pathological Q
waves; absence of
normal R waves in
leads V1 and V2

Posterior Myocardial Infarction

Occlusion of the right
coronary artery
(posterior descending
branch) or the left
circumflex artery
Tall R waves and ST
segment depression
possible in leads V1,
V2, V3, and V4
ST segment elevation
in true posterior leads,
V8 and V9

Cardiac enzyme Marker

Cardiac
enzyme
Marker

Initial
elevation
after AMI

Mean time
to peak
elevations

Time to
return to
baseline

Myoglobin

1-4hr

6-7hr

18-24hr

CTnI

3-12hr

10-24hr

3-10 day

CTnT

3-12hr

12-48hr

5-14 day

CKMB

4-12 hr

10-24hr

2-3day

TCK

2-6 hr

4.7hr(3-5)

72hr(50-96)

KILLIP SCORE

Management of Cardiac Chest

Pain

MANAGEMENT STEMI ACS

Urgent reperfusion:
FIBRINOLYSIS
PERCUTANEOUS CORONARY INTERVENTION

ACUTE PULMONARY EDEMA

Most commonly due to left ventricular dysfunction
Usually occurs in the setting of chronic congestive
heart failure
Also commonly occurs with myocardial infaction
(usually anterior infarction)
Less frequently due to acute valvular dysfunction
(mitral or aortic)
SVT or AF can cause APE
Acute myocarditis can also cause APE
Always associated with elevated pulmonary
venous pressure

Precipitating Factors

Chronic LV dysfunction, most commonly

Na and or fluid overload
Viral and or bacterial infection
Myocardial ischemia
New arrhythmia: atrial fibrillation
Acute valvular dysfunction
Acute ischemia precipitating or
worsening mitral regurgitation

Diagnosis
Broad differential for acute dyspnea
Dyspnea due to CHF
BNP level > 100 pg/mL in patient with
acute dyspnea carry 12X risk of CHF
etiology
BNP level > 500 pg/mL, CHF is nearly
certain and therapy ca be instituted

Chest X-ray
Cardiomegaly
Cephalization of vessels
Interstitial edema

BNP level and ches x-ray finding are

independent predictor for CFF etiology

Treatment

Treat precipitating factors

Preload reduction
Intravenous nitrates
Diuretics
Afterload reduction (if blood pressure
telerates)
Inotropic agents

Treatment
LMNOP
Furosemide (Lasix)
Morphine, intravenous, caution with
nausea
Nitrates, most important agents
Oxygen
Posture (upright

Malignant Arrhythmia
Supraventriclar Arrhythmia
Atrial Fibrillation
Atrial Flutter
Supraventricular Tachycardia

Ventricular (Lethal) Arrhythmia

Ventricular Tachycardia
Ventricular Fibrillation
PEA (Pulseless Electrical Activity)
Asystole

SUPRAVENTRICULAR
ARRHYTHMIA

VENTRICULAR ARRHYTHMIA