ACUTE CORONARY

SYNDROMES

Dr. Ravi Kant

Assistant Professor
Department of General Medicine

LECTURE OUTLINE
INTRODUCTION
EPIDEMIOLOGY/PREVALENCE/DEFINITION
PATHOPHYSIOLOGY OF ACUTE CORONARY
SYNDROMES
APPROACH TO SUSPECTED ACUTE
CORONARY SYNDROME GUIDELINE
UPDATE
TREATMENT/MANAGEMENT UPDATE

INTRODUCTION
Coronary Artery Disease leading cause of
morbidity & mortality in industrialized
nations.
Although decrease in cardiovascular
mortality still major cause of morbidity
& burden of disease.

DEFINITIONS
CAD is a continuum of disease.
Angina -> unstable angina -> AMI ->
sudden cardiac death
Acute coronary syndrome encompasses
unstable angina, NSTEMI, STEMI
Stable angina transient episodic chest
pain d/t myocardial ischaemia,
reproducible, frequency constant over
time.usually relieved with rest/NTG.
Classification of angina Canadian
Cardiovascular Society classification.

Canadian Cardiovascular Association

Classification of Angina
CLASS 1

NO PAIN WITH ORDINARY

PHYSICAL ACTIVITY

CLASS 2

SLIGHT LIMITATION OF PHYSICAL

ACTIVITY PAIN OCCURS WITH
WALKING, CLIMBING
STAIRS,STRESS

CLASS 3

SEVERE LIMITATION OF DAILY

ACTIVITY PAIN OCCURS ON
MINIMAL EXERTION

CLASS 4

UNABLE TO CONDUCT ANY

ACTIVITY WITHOUT PAIN, PAIN AT
REST

UNSTABLE ANGINA

Pain occurring at rest duration > 20min,

within one week of first visit
New onset angina ~ Class 2 severity,
onset with last 2 months
Worsening of chest pain increase by at
least 1 class, increases in frequency,
duration
Angina becoming resistance to drugs that
previously gave good control.
NB! ECG normal, ST depression(>0.5mm),
T wave changes

ACUTE MYOCARDIAL
INFARCTION
ECC/ACC DEFN rise and fall in cardiac
enzymes with one or more of the following:
Ischaemic type chest pain/symptoms
ECG changes ST changes, pathological Q
waves
Coronary artery intervention data
Pathological findings of an acute MI
NSTEMI = UNSTABLE ANGINA
SYMPTOMS/FINDINGS + POSITIVE CARDIAC
ENZYMES
STEMI = ST ELEVATION ON ECG + SYMPTOMS

APPROACH
Identifying those with chest pain suggestive of
IHD/ACS.
Thorough history required:
Character of pain
Onset and duration
Location and radiation
Aggravating and relieving factors
Autonomic symptoms
TYPICAL VS ATYPICAL HISTORY
Failure to recognise symptoms other than
chest pain -> approx 2 hr delay in seeking

CHARACTERISTICS OF TYPICAL ANGINAL CHEST

PAIN (ADAPTED FROM ROSENS, EMERGENCY
MEDICINE)
CHARACTERISTIC

SUGGESTIVE OF
ANGINA

LESS SUGGESTIVE OF
ANGINA

TYPE OF PAIN

DULL
PRESSURE/CRUSHING
PAIN

SHARP/STABBING

DURATION

2-5 MIN, <20 MIN

SECONDSTO
HOURS/CONTINUOUS

ONSET

GRADUAL

RAPID

LOCATION/CHEST
WALL TENDERNESS

SUBSTERNAL, NOT
TENDER TO PALP.

LATERAL CHEST
WALL/TENDER TO PALP.

REPRODUCIBALITY

WITH
EXERTION/ACTIVITY

WITH
BREATHING/MOVING

AUTONOMIC
SYMPTOMS

PRESENT USUALLY

ABSENT

TOOLS USED IN RISK

STRATIFICATION
HISTORY
ECG
BIOCHEMICAL MARKERS

ECG
First point of entry into ACS algorithm
Abnormal or normal
Neither 100% sensitive or 100% specific
for AMI
Single ECG for AMI sensitivity of 60%,
specificity 90%
Normal ECG does not exclude ACS 1-6%
proven to have AMI, 4% unstable angina

 GUIDELINES:
Initial 12 lead ECG goal door to ECG time
10min, read by experienced doctor.
If ECG not diagnostic/high suspicion of ACS
serial ECGs initially 15 -30 min intervals.
ECG adjuncts leads V7 V9, RV 4
Continuous 12 lead ECG monitoring
reasonable alternative to serial ECGs.

Thanking You

Electrocardiograph
y

Dr. Ravi Kant

Assistant Professor
Department of General
Medicine

Introduction
An electrocardiogram (ECG or EKG) is a
graphic recording of electric potentials
generated by the heart.
The signals are detected by means of metal
electrodes attached to the extremities and
chest wall and then are amplified and
recorded by the electrocardiograph.
ECG leads actually display the
instantaneous differences in potential
between the electrodes.

ECG Waveforms and

Intervals
The ECG waveforms are
labelled alphabetically,
beginning with the P
wave, which represents
atrial depolarization .
The QRS complex
represents ventricular
depolarization, and the
ST-T-U complex
represents ventricular
repolarization.

 The J point is the junction between

the end of the QRS complex and the
beginning of the ST segment.
The QRS-T waveforms of the surface
ECG correspond in a general way with
the different phases of simultaneously
obtained ventricular action potentials,
the intracellular recordings from
single myocardial fibber's.

 Conditions that prolong phase 2

(amiodarone, hypocalcemia) increase
the QT interval.
In contrast, shortening of ventricular
repolarization (phase 2), such as by
digitalis administration or
hypercalcemia, abbreviates the ST
segment

ECG Leads
The 12 conventional ECG leads record the
difference in potential between electrodes
placed on the surface of the body.
These leads are divided into two groups:
six limb (extremity) leads and six chest
(precordial) leads.
The limb leads record potentials
transmitted onto the frontal plane and the
chest leads record potentials transmitted
onto the horizontal plane

Genesis of the Normal ECG

P Wave
The normal atrial depolarization vector is oriented downward and
toward the subject's left, reflecting the spread of depolarization
from the sinus node to the right and then the left atrial
myocardium.
Since this vector points toward the positive pole of lead II and
toward the negative pole of lead aVR, the normal P wave will be
positive in lead II and negative in lead aVR. By contrast,
activation of the atria from an ectopic pacemaker in the lower
part of either atrium or in the AV junction region may produce
retrograde P waves (negative in lead II, positive in lead aVR).
The normal P wave in lead V1 may be biphasic with a positive
component reflecting right atrial depolarization, followed by a
small (<1 mm2) negative component reflecting left atrial
depolarization.

QRS Complex
Normal ventricular depolarization proceeds as a rapid,
continuous spread of activation wave fronts.
This complex process can be divided into two major sequential
phases, and each phase can be represented by a mean
vector
The first phase is depolarization of the interventricular septum
from the left to the right and anteriorly (vector 1).
The second results from the simultaneous depolarization of
the right and left ventricles; it normally is dominated by the
more massive left ventricle, so that vector 2 points leftward
and posteriorly.
Therefore, a right precordial lead (V1) will record this biphasic
depolarization process with a small positive deflection (septal
r wave) followed by a larger negative deflection (S wave).

T Wave and U Wave

Normally, the mean T-wave vector is oriented roughly concordant with
the mean QRS vector (within about 45 in the frontal plane). Since
depolarization and repolarization are electrically opposite processes,
this normal QRST-wave vector concordance indicates that
repolarization normally must proceed in the reverse direction from
depolarization (i.e., from ventricular epicardium to endocardium).
The normal U wave is a small, rounded deflection (1 mm) that follows
the T wave and usually has the same polarity as the T wave.
An abnormal increase in U-wave amplitude is most commonly due to
drugs (e.g., dofetilide, amiodarone, sotalol, quinidine, procainamide,
disopyramide) or to hypokalemia.
Very prominent U waves are a marker of increased susceptibility to
the torsades de pointes type of ventricular tachycardia Inversion of
the U wave in the precordial leads is abnormal and may be a subtle
sign of ischemia.

Major ECG Abnormalities

Cardiac Enlargement and Hypertrophy

Right ventricular hypertrophy due to a pressure load (as from
pulmonic valve stenosis or pulmonary artery hypertension) is
characterized by a relatively tall R wave in lead V 1 (R S wave),
usually with right axis deviation alternatively, there may be a
qR pattern in V1 or V3R. ST depression and T-wave inversion in
the right-to-midprecordial leads are also often present.
This pattern, formerly called right ventricular "strain," is
attributed to repolarization abnormalities in acutely or
chronically overloaded muscle.
Prominent S waves may occur in the left lateral precordial
leads. Right ventricular hypertrophy due to ostium secundum
type atrial septal defects, with the accompanying right
ventricular volume overload, is commonly associated with an
incomplete or complete right bundle branch block pattern with
a rightward QRS axis.

Bundle Branch
Blocks

Clinical Interpretation of
the ECG
Accurate analysis of ECGs requires thoroughness and care.
The following 14 points should be analyzed carefully in every ECG:
1 standardization (calibration) and technical features (including lead
placement and artefact's)
2 rhythm
3 heart rate
4 PR interval/AV conduction
5 QRS interval
6 QT/QTc interval
7 mean QRS electrical axis
8 P waves
9 QRS voltages
10 precordial R-wave progression
11 abnormal Q waves
12 ST segments
13 T waves
14 U waves

Myocardial Ischemia and

Infarction
The ECG is a cornerstone in the diagnosis of acute and chronic ischemic heart
disease.
Ischemia exerts complex time-dependent effects on the electrical properties
of myocardial cells. Severe, acute ischemia lowers the resting membrane
potential and shortens the duration of the action potential.
These currents of injury are represented on the surface When the acute
ischemia is transmural, the ST vector usually is shifted in the direction of the
outer (epicardial) layers, producing ST elevations and sometimes, in the
earliest stages of ischemia, tall, positive so-called hyperacute T waves over
the ischemic zone. With ischemia confined primarily to the subendocardium,
the ST vector typically shifts toward the subendocardium and ventricular
cavity, so that overlying (e.g., anterior precordial) leads show ST-segment
depression (with ST elevation in lead aVR). Multiple factors affect the
amplitude of acute ischemic ST deviations. Profound ST elevation or
depression in multiple leads usually indicates very severe ischemia. From a
clinical viewpoint, the division of acute myocardial infarction into ST-segment
elevation and non-ST elevation types is useful since the efficacy of acute
reperfusion therapy is limited to the former group

ECG sequence with anterior

q wave infraction

ECG sequence with inferior q wave

infraction

Computerized
Electrocardiography
Computerized ECG systems are widely
used for immediate retrieval of thousands
of ECG records.
Computer interpretation of ECGs still has
major limitations.
Incomplete or inaccurate readings are
most likely with arrhythmias and complex
abnormalities. Therefore, computerized
interpretation should not be accepted
without careful clinician review.