ECG Jose Gianni C.

Espada
Clinical Clerk
ELECTROCARDIOGRAM

Records the electrical activity of the heart,

providing a record of cardiac electrical
activity, as well as valuable information
about the hearts structure and function
Most information represents electrical
activity of contraction of the myocardium
Also yields information about the hearts
rate and rhythm
 Pic p 10
 Pic p 11-12
 SA Node pic p 18
 AV Node pic p 19, 22
 Purkinje fibers pic p 24

Na+ - fast
QRS complex
Ventricular contraction
 ST segment horizontal, flat
T wave ventricular repolarization
K+ leaving the myocytes
VENTRICULAR
SYSTOLE
QRS to end of T wave (QT interval)
spans depolarization and repolarization
of ventricles
 Ion movement pic p 33
RECORDING

Pic p 34, 37
LEADS

Leads p 39
AUGMENTED LEADS

AVR right arm positive

AVL left arm positive
AVF foot (left foot) positive
 Six limb leads pic p 46
 Pic p 50
CONTIGUOUS LEADS

II, III, aVF Inferior Wall

I, aVL High Lateral Wall
V1, V2 Septal Wall
V3, V4 Anterior Wall
V5, V6 Lateral Wall
READING EKG

I. Rate
II. Rhythm
III. Axis
IV. Hypertrophy
V. Infarction
Normal Values
P wave <0.12 (3 small boxes)
PR interval 0.12 0.2 (3-5 small
boxes)
QRS duration <0.11 to 0.12 (3 small
boxes)
Corrected QT interval 0.35 to 0.43;0.45
I. RATE

SA Node 60-100/min
AV Node (AV junction) 40-60/min
His bundle (Purkinje fibers) 20-40/min
*automaticity foci
RATE

Regular rhythm
Heart rate = 1500/# of small squares from
R to R

Irregular rhythm
HR = # of QRS complexes within 30 large
boxes x 10
II. RHYTHM

Sinus Rhythm
There is a P wave before every QRS
Distances between R-R intervals should
be equal
Sinus bradycardia - <60 bpm
Sinus tachycardia - >100 bpm
ARRHYTHMIAS

Irregular rhythm
A.Escape
B.Premature beats
C.Tachyarrythmias
IRREGULAR RHYTHM

Multiple active automaticity sites

Wandering Pacemaker
Multifocal Atrial Tachycardia
Atrial Fibrillation
 Pic p 111
 COPD
HR >100
 Continuous rapid firing of multiple atrial automaticity foci
Occasional, random atrial depolarization that reaches the AV node to be
conducted to the venricles, producing irregular QRS rhythm
A. ESCAPE
B. PREMATURE BEATS
 AV Node unreceptive to premature atrial depolarization stimulus
because it reached the AV node prematurely (while AV node is still in
refractory period), resulting in a non-conducted PAB
 Bigeminy PAB couples to the end of a normal cycle and repeats this process by
coupling a PAB to the end of each successive normal cycle
Trigeminy fires after 2 normal cycles
 Occur early in the cycle
Great width and enormous amplitude
Usually the opposite the polarity of the normal QRS
 Depolarize only the ventricles
Pause not caused by resetting of SA Node
Ventricles are still repolarizing
 6 or more PVCs per minute is considered pathological!
Hypoxic
 If VT lasts longer than 30 seconds, it is called
sustained VT
 Severe cardiac hypoxia
C. TACHYARRYTHMIA
 Coronary insufficiency (ischemia) or other causes of
hypoxia
 Caused by low K, meds that block K channels, or congenital problems
Rate: 250-350
 Baseline is lost between back-to-back flutter, saw tooth
 An abnormal, accessory AV conduction pathway, the bundle of
Kent, can short circuit the usual delay of ventricular conduction
in the AV node
 Blocks retard or prevent the conduction of depolarization
Can occur in the SA node, AV node, or in the larger divisions of
the ventricular conduction system
 No P wave
 PR interval greater than .2 second
PR prolongation is consistent in every cycle
 Occurs in AV node
PR interval gradually lengthens in successive cycles but the last
P wave of the series fails to conduct to to the ventricles (final P
lacks a QRS, then series repeats)
 Totally blocks a number of paced atrial depolarizations (P
waves) before conduction to the ventricles is successful,
producing 2:1 P:QRS AV ratios. The series repeats.
 One ventricle depolarizes slightly later than the
other, causing two joined QRS
III. AXIS

Refers to the direction of the movement of

depolarization, which spreads throughout
the heart to stimulate the myocardium to
contract
 V2 obtained by placing a positive electrode
on the chest along the L side of the sternum
4th ICS
 Most of the ventricular depolarization moves away from the
positive V2 electrode, toward the thicker and more posteriorly
positioned left ventricle
COMPUTATION OF FRONTAL
AXIS
Deduct negative deflections from positive
deflections in QRS complexes to derive the
values for aVF and I
If value in lead I is a negative integer, add 90
to computed axis

Axis = 90 x aVF/ |I| + |avF|

INTERPRETATION
Normal Examples
Value
Right Axis >100 to RVH, anterolateral wall MI,
Deviation 180 left posterior hemiblock,
pulmonary embolism,
normal variant (thin person)
Left Axis -30 to LVH, inferior wall MI, left
Deviation -90 anterior hemiblock, left
bundle branch block, normal
variant
Normal Axis -30 to
100
Extreme Axis -90 to
Deviation 180
IV. HYPERTROPHY

An increase in muscle mass

 Atrial enlargement
 Left ventricular wall is very thick, causing
great QRS deflections in the chest leads
 Large S in V1 and a large R in V5
 T wave inversion with T wave asymmetry
 V1 provides the most information concerning
hypertrophy of the hearts chambers
V. INFARCTION

Results from the complete occlusion of a

coronary artery
The infarcted area of myocardium
becomes necrotic so it cant depolarize or
contract
Commonly, it is the LEFT VENTRICLE that
suffers myocardial infarction
 Hereditary condition (dysfunctional cardiac Na+ channels) that
can cause sudden death in individuals without heart disease
RBBB with ST elevation in leads V1 to V3
 Any significant ST depression in leads where QRS is
upright indicates compromised coronary blood flow
until proven otherwise
CONTIGUOUS LEADS

II, III, aVF Inferior Wall

I, aVL High Lateral Wall
V1, V2 Septal Wall
V3, V4 Anterior Wall
V5, V6 Lateral Wall
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