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ECG
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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 are then
amplified and recorded by the electrocardiograph.
Cardiac conduction system
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cardiac pacemaker cells
specialized conduction tissue
heart muscle
Cardiac conduction system
Sequence of depolarisation
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sinus node (spontaneous depolarization)
the right and left atria (atrial contraction)
AV junction
The bundle of His bifurcates (the right and left bundles)
The main left bundle bifurcates into two primary
subdivisions, a left anterior fascicle and a left posterior
fascicle
The right and left ventricular myocardium by way of Purkinje
fibers.
The depolarization wavefronts then spread through the
ventricular wall, from endocardium to epicardium, triggering
ventricular contraction
Remember!
The ECG records only the depolarization
(stimulation) and repolarization
(recovery) potentials generated by the
atrial and ventricular myocardium.
12 conventional ECG leads
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Electrodes are placed on the surface of the body
These leads are divided into two groups: six
extremity (limb) leads and six chest (precordial)
leads
The ECG leads are configured so that a positive
(upright) deflection is recorded in a lead if a wave
of depolarization spreads toward the positive pole
of that lead, and a negative deflection if the wave
spreads toward the negative pole
12 conventional ECG leads
ECG WAVEFORMS AND INTERVALS
ECG WAVEFORMS AND INTERVALS
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The ECG waveforms are labeled alphabetically
P wave (atrial depolarization)
The QRS complex (ventricular depolarization)
the ST-T-U complex (ST segment, T wave, and U
wave) (ventricular repolarization)
The J point is the junction between the end of the
QRS complex and the beginning of the ST
segment..
ECG WAVEFORMS AND INTERVALS
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The normal P wave will be positive in
lead II and negative in lead aVR (P from
sinus node)
The PR interval measures the time
(normally 120 to 200 ms) between atrial and
ventricular depolarization
ECG WAVEFORMS AND INTERVALS
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The QRS interval (normally 100 ms or less) reflects the duration of
ventricular depolarization.
V1 - a small positive deflection followed by a larger negative deflection (S
wave)
V6 - a small negative deflection followed by a relatively tall positive
deflection (R wave)
Intermediate leads show a relative increase in R-wave amplitude (normal Rwave progression) and a decrease in S-wave amplitude progressing across
the chest from the right to left. The precordial lead where the R and S waves
are of approximately equal amplitude is referred to as the transition zone
(usually V3 or V4)
The QRS pattern in the extremity leads may vary considerably from one
normal subject to another depending on the electrical axis of the QRS
An axis more negative than -30° is referred to as left axis deviation, while an
axis more positive than +100° is referred to as right axis deviation
ECG WAVEFORMS AND INTERVALS
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The QT interval (ventricular depolarization and repolarization)
varies inversely with the heart rate.
A rate-related (“corrected”) QT interval, QTc, is normally
≤0.44 s.
Normally, the mean T-wave vector is oriented roughly
concordant with the mean QRS vector.
!Repolarization normally proceeds in the reverse direction from
depolarization (i.e., from ventricular epicardium to
endocardium)!
The normal U wave - a small, rounded deflection (≤1 mm) that
follows the T wave (usually has the same polarity as the T
wave).
How to read ECG?
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The electrocardiogram is ordinarily recorded on special
graph paper which is divided into 1-mm2 gridlike boxes.
ECG paper speed is generally 25 mm/s (sometimes 50
mm/s),
the smallest (1 mm) horizontal divisions correspond to
0.04 s (40 ms), with heavier lines at intervals of 0.20 s
(200 ms).
Vertically, the ECG graph measures the amplitude of a
given wave or deflection (1 mV = 10 mm)
The heart rate (beats per minute) can be readily computed
from the interbeat (R-R) interval by dividing the number of
large (0.20 s) time units between consecutive R waves into
300 or the number of small (0.04 s) units into 1500.
14 points should be analyzed
carefully in every ECG
(1) standardization (calibration) and
technical features (including lead placement
and artifacts); (2) heart rate; (3) rhythm;
(4) PR interval; (5) QRS interval; (6) QT
interval; (7) mean QRS electrical axis; (8) P
waves; (9) QRS voltages; (10) precordial Rwave progression; (11) abnormal Q waves;
(12) ST segments; (13) T waves; (14) U
waves.
Interpretation
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All 14 points ought to be assessed
Important clinical correlates or
inferences should be mentioned
Comparison with previous ECGs is
essential
The clinical utility of the ECG
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arrhythmias
conduction disturbances
myocardial ischemia
metabolic disturbances (e.g., hyperkalemia)
increased susceptibility to sudden cardiac death
(e.g., QT prolongation syndromes)
toxicity of drugs
MAJOR ECG ABNORMALITIES
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CARDIAC ENLARGEMENT AND
HYPERTROPHY
BUNDLE BRANCH BLOCKS
METABOLIC FACTORS AND DRUG
EFFECTS
MYOCARDIAL ISCHEMIA AND
INFARCTION
CARDIAC ENLARGEMENT AND
HYPERTROPHY
BUNDLE BRANCH BLOCKS
METABOLIC FACTORS AND
DRUG EFFECTS
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Hyperkalemia (narrowing and peaking
(tenting) of the T waves; AV conduction
disturbances, diminution in P-wave
amplitude, widening of the QRS interval.
cardiac arrest)
Hypokalemia (prolongation of ventricular
repolarization, prominent U waves)
Drug-induced prolongation of the QT interval
ECG changes
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electrolyte and acid-base disturbances
infectious processes
central nervous system disorders
endocrine abnormalities
Ischemia
hypoxia
MYOCARDIAL ISCHEMIA AND
INFARCTION
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the nature of the process [reversible (i.e.,
ischemia) vs. irreversible (i.e., infarction)],
the duration (acute vs. chronic)
extent (transmural vs. subendocardial)
localization (anterior vs. inferoposterior)
presence of other underlying abnormalities
(ventricular hypertrophy, conduction defects).
MYOCARDIAL ISCHEMIA AND
INFARCTION
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A 12-lead ECG recorded at rest is normal in about
half the patients with typical angina pectoris!
* signs of an old myocardial infarction
* ST-segment and T-wave changes
* left ventricular hypertrophy
* intraventricular conduction
* Typical ST-segment and T-wave changes that
accompany episodes of angina pectoris and
disappear thereafter
STRESS TESTING
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12-lead ECG before, during, and after exercise, usually on a
treadmill.
a standardized incremental increase in external workload
Monitoring of the symptoms, ECG, and arm blood pressure
Discontinuation upon evidence of chest discomfort, severe
shortness of breath, dizziness, severe fatigue, ST-segment
depression > 0.2 mV (2 mm), a fall in systolic blood pressure
>10 mmHg, or the development of a ventricular
tachyarrhythmia, increase in blood pressure beyond safety
limits
The normal response to graded exercise includes progressive
increases in heart rate and blood pressure.
Positive and highly positive
results
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Flat depression of the ST segment >0.1 mV below
baseline (i.e., the PR segment) and lasting longer
than 0.08 s
Failure of the blood pressure to increase or an
actual decrease with signs of ischemia
The development of angina and/or severe (>0.2
mV) ST-segment depression at a low workload
ST-segment depression that persists for >5 min
after the termination of exercise
A positive test for ischemia
What do we measure during
the exercise stress test?
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total duration of exercise
the times to the onset of ischemic ST-segment
change and chest discomfort
the external work performed (generally expressed
as the stage of exercise),
the internal cardiac work performed, i.e., by the
heart rate–blood pressure product
The depth of the ST-segment depression and the
time needed for recovery of these ECG changes.
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Ischemia exerts complex time-dependent effects on the
electrical properties of myocardial cells. Acute ischemia
lowers the resting membrane potential and shortens the
duration of the action potential
A voltage gradient between normal and ischemic zones
Deviation of the ST segment
Transmura acute ischemia - ST elevations, tall, positive
so-called hyperacute T waves (the earliest stages) over the
ischemic zone
Subendocardium ischemia - ST-segment depression (with
ST elevation in lead aVR)
Profound ST elevation or depression in multiple leads
usually indicates very severe ischemia
Localizing of ischemia
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The ECG leads are more helpful in localizing regions of
ST elevation than non-ST elevation ischemia.
Acute transmural anterior (including apical and lateral)
wall ischemia is reflected by ST elevations or increased Twave positivity) in one or more of the precordial leads (V1
to V6) and leads I and aVL.
Inferior wall ischemia produces changes in leads II, III,
and aVF.
Right ventricular ischemia usually produces ST elevations
in right-sided chest leads
ECG in STEMI