ECG OVERVIEW

DEFINITION

The electrocardiogram (ECG or

EKG) is a diagnostic tool
that is routinely used to
assess the electrical and
muscular functions of the
heart. While it is a
relatively simple test to
perform, the interpretation
of the ECG tracing requires
significant amounts of
training. Numerous
textbooks are devoted to
the subject.

The heart is a two stage

electrical pump and the
heart's electrical activity
can be measured by
electrodes placed on the
skin. The
electrocardiogram can
measure the rate and
rhythm of the heartbeat,
as well as provide indirect
evidence of blood flow to
the heart muscle.

Ten electrodes are needed to

produce 12 electrical views
of the heart. An electrode
lead, or patch, is placed on
each arm and leg and six
are placed across the chest
wall. The signals received
from each electrode are
recorded. The printed view
of these recordings is the
electrocardiogram.

atrium, passes through the

atrioventricular node down into
the bundle of His and into the
Purkinje fibers, spreading down
and to the left throughout the
ventricles. This orderly pattern
of depolarization gives rise to
the characteristic ECG tracing.
ECG LEADS
Electrode leads on the chest
wall are able to detect
electrical impulses that are
generated by the heart
recorded over a period of time
(usually 10 seconds).. Multiple
leads provide many electrical
views of the heart. By
interpreting the tracing, the
physician can learn about the
heart rate and rhythm as well
as blood flow to the ventricles
(indirectly).

NORMAL ECG
WAVES

HEALTHY ECG
During each heartbeat, a
healthy heart has an orderly
progression of depolarization
that starts with pacemaker
cells in the sinoatrial node,
spreads out through the
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To briefly summarize the

components of a normal ECG
tracings, it consist of waveform
components which indicate
electrical events during one
heart beat. These waveforms
are labeled P, Q, R, S, T and U.
P wave is the first short upward
movement of the ECG tracing. It
indicates that the atria are
contracting, pumping blood into
the ventricles.
The QRS complex, normally
beginning with a downward
deflection, Q; a larger upwards
deflection, a peak (R); and then
a downwards S wave. The QRS
complex represents ventricular
depolarization and contraction.
The PR interval indicates the
transit time for the electrical
signal to travel from the sinus
node to the ventricles.
T wave is normally a modest
upwards waveform
representing ventricular
repolarization.

million cases of MI occur

annually in the United States.

Myocardial infarction (MI)

usually results from an
imbalance in oxygen supply and
demand, which is most often
caused by plaque rupture with
thrombus formation in an
epicardial coronary artery,
resulting in an acute reduction
of blood supply to a portion of
the myocardium.

The vast majority (~80%) of

inferior STEMIs are due to
occlusion of the dominant right
coronary artery (RCA).
Less commonly (around 18% of
the time), the culprit vessel is a
dominant left circumflex artery
(LCx).

MAYOCARDIAL INRFACTION
(MI)
BACKGROUND
Myocardial infarction (MI) (ie,
heart attack) is the irreversible
death (necrosis) of heart
muscle secondary to prolonged
lack of oxygen supply
(ischemia). Approximately 1.5
3

DIAGNOSIS
a patient is diagnosed with MI if
two (probable) or three
(definite) of the following
criteria are satisfied:
1. Clinical history of ischemictype chest pain lasting for
more than 20 minutes
2. Changes in serial ECG
tracings
3. Rise and fall of serum
cardiac biomarkers

PHYSICAL EXAMINATION
The general appearance of
patients may vary according to
the experienced symptoms; the
patient may be comfortable, or
restless and in severe distress
with an increased respiratory
rate. A cool and pale skin is
common and points to
vasoconstriction. Some patients
have low-grade fever (38
39 C). Blood pressure may be
elevated or decreased, and the
pulse can become irregular.

ECG (MI)

How to recognize an inferior

STEMI
1) ST elevation in leads II, III
and aVF
2) Progressive development
of Q waves in II, III and aVF
3) Reciprocal ST depression in
aVL ( lead I)
MI is considered part of a
spectrum referred to as acute
coronary syndrome (ACS). The
ACS continuum representing
ongoing myocardial ischemia or
injury consists of unstable
angina, nonST-segment
elevation MI (NSTEMI)
collectively referred to as non
ST-segment acute coronary
syndrome (NSTE ACS)and STsegment elevation MI (STEMI).
Patients with ischemic
discomfort may or may not
have ST-segment or T-wave
changes denoted on the
electrocardiogram (ECG). ST
elevations seen on the ECG
reflect active and ongoing
transmural myocardial injury.
Without immediate reperfusion
therapy, most patients with
STEMI develop Q waves,
reflecting a dead zone of
myocardium that has
undergone irreversible damage
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and death.

CARDIAC ENZYME AND

MARKERS
Those without ST elevations are
diagnosed either with unstable
angina or
NSTEMIdifferentiated by the
presence of cardiac enzymes.
Both these conditions may or
may not have changes on the
surface ECG, including STsegment depressions or T-wave
morphological changes.
Cardiac markers or cardiac
enzymes are proteins that leak
out of injured myocardial cells
through their damaged cell
membranes into the
bloodstream.
The markers most widely used
in detection of MI are MB
subtype of the enzyme creatine
kinase and cardiac troponins T
and I as they are more specific
for myocardial injury.
Cardiac troponins T and I are
the preferred markers for
myocardial injury as they have
the highest sensitivities and
specificities for the diagnosis of
acute myocardial infarction.
Peak circulating enzyme levels
tend to occur earlier and are
often higher following
successful thrombolytic
therapy.

I. Troponins T and I
Troponin is a protein released
from myocytes when
irreversible myocardial damage
occurs. It is highly specific to
cardiac tissue and accurately
diagnoses myocardial infarction
with a history of ischaemic pain
or ECG changes reflecting
ischaemia. Cardiac troponin
level is dependent on infarct
size, thus providing an
indicator for the prognosis
following an infarction .
Troponin I and T are of equal
clinical value.
Serum levels increase within 312 hours from the onset of
chest pain, peak at 24-48
hours, and return to baseline
over 5-14 days.

II. Creatine kinase

Myocardial muscle creatine
kinase (CK-MB) is found mainly
in the heart.
CK-MB levels increase within 312 hours of onset of chest pain,
reach peak values within 24
hours, and return to baseline
after 48-72 hours.
Sensitivity and specificity are
not as high as for troponin
levels.
The diagnosis of myocardial
infarction requires two out of
three components (history,
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ECG, and enzymes). When

damage to the heart occurs,
levels of cardiac markers rise
over time, which is why blood
tests for them are taken over a
24-hour period. Because these
enzyme levels are not elevated
immediately following a heart
attack, patients presenting
with chest pain are generally
treated with the assumption
that a myocardial infarction has
occurred and then evaluated
for a more precise diagnosis.
MI COMPLICATIONS
Complications may occur
immediately following the heart
attack (in the acute phase), or
may need time to develop (a
chronic problem).

Complicatio
n type
ISCHEMIC

**VENTICULAR FIBRILLITION
The heart's electrical activity
becomes disordered. When this
happens, the heart's lower
(pumping) chambers contract in
a rapid, unsynchronized way.
(The ventricles "fibrillate"
rather than beat.) The heart
pumps little or no blood.
Collapse and sudden cardiac
arrest follows, which requires
immediate medical help (CPR
and defibrillation) .

Manifestations

Angina, reinfarction,
infarct extension
MECHANICA Heart failure,
L
cardiogenic shock,
mitral valve
dysfunction,
aneurysms, cardiac
rupture
ARRHYITHM Atrial or ventricular
IC
arrhythmias
(FIBRILLITION) , sinus
or atrioventricular
node dysfunction ,
EMBOLIC
Central nervous
system or peripheral
embolization
INFLAMMAT Pericarditis
ORY

MI Major Risk
Factors
Six primary risk factors
have been identified with
the development of
atherosclerotic coronary
artery disease and MI:
- hyperlipidemia
- diabetes mellitus
- hypertension
- tobacco use
- male gender

- family history of
atherosclerotic arterial
disease.
The presence of any risk
factor is associated with
doubling the relative risk
of developing
atherosclerotic coronary
artery disease.

MI Treatment
and
Management
Although the initial treatment
of the different types of acute
coronary syndrome (ACS) may
appear to be similar, it is very
important to distinguish
between whether the patient is
having an ST-elevation MI
(STEMI) or a nonSTEMI
(NSTEMI), because definitive
therapies differ between these
two types of MI. Particular
considerations and differences
involve the urgency* of therapy
and the degree* of evidence
regarding different
pharmacologic options.
The goals of therapy in acute
MI are the expedient
restoration of normal coronary
blood flow and the maximum
salvage of functional
myocardium. These goals can
be met by a number of medical
interventions and adjunctive
therapies. The primary
obstacles to achieving these

goals are the patient's failure

to recognize MI symptoms
quickly and the delay in seeking
medical attention. When
patients present to a hospital,
there are a variety of
interventions to achieve
treatment goals.

MEDICAL OPTIONS FOR EARLY

CARE

- Aspirin in a dose of 325 mg should be

administered immediately on recognition of MI
signs and symptoms

- Supplemental Oxygen
Oxygen should be administered to patients with
symptoms or signs of pulmonary edema or with
pulse oximetry less than 90% saturation.

- Nitrates
benefit of nitrates is derived from its vasodilator
effect.

- Pain Control
The agent of choice is morphine sulfate, given
initially IV at 5 to 15 minute intervals at typical
doses of 2 to 4 mg

-Beta Blockers
treatment with a beta blocker decreases the
incidence of ventricular arrhythmias, recurrent
ischemia, reinfarction, and, if given early
enough, infarct size and short-term mortality.
Beta blockade decreases the rate and force of
myocardial contraction and decreases overall
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myocardial oxygen demand.

- Unfractionated Heparin
Heparin has the added benefit of preventing
thrombus through a different mechanism than
aspirin.

- Warfarin
for at least 3 months in patients with left
ventricular aneurysm or thrombus

- Angiotensin-Converting Enzyme

Inhibitors and Angiotensin Receptor

Blockers.
ACE inhibitors are also recommended in
patients with NSTEMI who have diabetes, heart
failure, hypertension, or an ejection fraction less
than 40%.

Implantable Cardiac Defibrillators

-Statin Therapy
a benefit of starting patients on high-dose
therapy from the start

SURGICAL OPTIONS
Surgical Revascularization

The device is ,in general

,capable of correcting most lifethreatening cardiac
arrhythmias.