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
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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 medical attention
CHARACTERISTICS OF TYPICAL ANGINAL CHEST PAIN (ADAPTED
FROM ROSEN’S, 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
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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
Electrocardiography
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 QRS–T-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 V1 (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
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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
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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 STsegment 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.