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Austin K

on 26 March 2014

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Transcript of THE EKG

The depolarization of atrial myocytes leading to atrial contraction
Initiation begins at the SA node (60-100 bpm)
Gen Atria: 60-80 bpm
1st half is the Right Atrium
2nd half is the Left Atrium
PR Interval
Represent the time from the initiation of atrial contraction to ventricular depolarization
Normal duration: 0.12 to 0.2 seconds
P Wave
Is the depolarization of septal myocytes as the conduction signal flow down the bundle of HIS
PR Segment
Is the result of a pause in conducion, this pause occurs at the AV node
(Junctional rhythm: 40-60 bpm)
It is also the period from th end of atrial depolarization to the start of ventricular depolarization
R,S segment
The initial portion is the depolarization of the Left Ventricle (ascending portion)
This is followed by the depolarization of the right ventricle (decending portion
QRS interval <0.12 sec
ST segment
Respresent the time from the end of ventricular depolarization to the start of ventricular repolarization.
T Wave
Represents the ventricular repolarization
The process requires a great deal of energy unlike the largely passive depolarization
QT Interval
The time from the start of ventricular depolarization to the end of ventricular repolarization
Composes ~40% of the cardiac cycle
Rhythms With Abnormal P Waves
Terminal Width > 0.04 s in lead II
Height > 2.5 mm in lead II
No Urgent Intervention Required
Right atrial enlargement
Possible right axis deviation of P wave
No Urgent Intervention Required
Contraction initiated by AV node
no p wave (retrograde p is possible)
Abscent P wave resulting in Junctional Rhythm
Early depolarization of Atria : PAC
No Urgent Intervention Required
Left atrial enlargement
No significant axis deviation of P wave
No Urgent Intervention Required
P wave shape and axis may differ from the adjacent p waves as its location of origin is likely different
Rhythms With P-R Abnormalities
Short PR interval
, less than 3 small squares (0.12 sec)

bundle of Kent
, between the left atria & left ventricle
slurred upstroke to the QRS indicating pre-excitation
delta wave
Wide QRS
PSVT & WPW ( AV reciporcating tachycardia)
due to reentrant loop
Atrial Fibrillation in WPW
Bundle of Kent acts as a free conduit for chaotic atrial activity
300 bpm
Lethal !
Short PR interval
Long PR interval / AV node conduction issuses
long P-R interval > 0.2 sec
long P-R interval > 0.2 sec and successive increasing delay due to AV node
Dropped QRS "dropped beat"
Paroxysmal Supraventricular Tachycardia : PSVT
No Urgent Intervention Required
Atrial or Junctional in origin (p wave is buried in the QRS)
Is a regular rhythm & can also be known as AV nodal reentrant tachycardia
Very difficult to tell apart from

Atrial Flutter
Atrial Fibrillation
Rate of 250 - 350 bpm
Sawtooth pattern
AV node cannot handle the number of p-waves (2:1 is the most common)
Carotid massage will not terminate the rhythm
Rate of 500 impulses per minute from atria
Result is 120-180 bpm
No true P-wave can be seen
Irregularly irregular appearance of QRS
Multifocal Atrial Tachycardia
Need to ID three different P-wave
Irregular Rhythm with rate of 100-200 bpm
Resulting from random firing from multiple ectopic atrial foci
<100 bpm = wandering atrial pacemaker
Common in paitnets with severe lung disease
Carotid massage has no effect
Rhythms With QRS Abnormalities
Premature Ventricular Contractions: PVCs
QRS complex > 0.12 sec
Irregular Rhythm
PVC is followed by compensatory pause
Ratios, 1NSR beat : 1 PVC (bigeminy)
Trigeminy = 2NSR: 1PVC
Ventricular Tachycardia: V-Tach
Three or more PVCs in a row qualify as V-Tach
ACLs protocol should be followed
120-200 bpm (can be irregular)
Ventricular Fibrillation: V-Fib
ACLs protocol should be followed
Pre-terminal event (dying heart)
No true QRS complex
Coarse V-Fib
Fine V-fib
As potassium begins to rise, T waves across the entire 12-lead begin to peak
Easily confused with infarct changes which are isolated
As Potassium serum levels continue to rise
PR interval becomes prolonged
P wave gradually flattens & eventually disappears
Ultimately the QRS widens until it merges with T
Ventricular Fibrillation may develop (can be rapid)

Accelerated Idioventricular Rhythm
Benign rhythm
Rarely requires treatment
50 - 100 bpm
Multiple P Waves per QRS
No P Wave
Varying P Waves
Torsade de Pointes
Seen in patients with prolonged QT intervals
Result of prolonged ventricular repolarization (lenthened T wave)
No progressive lengthening of P-R interval ***
Dropped QRS "dropped beat"
(P : QRS ratios, 2:1, 3:2, ...)
Wide QRS
T Wave Abnormalities
Right Bundle (RBBB)
Wide QRS >0.12 sec
V1,V2 : "Rabbit ear" /or/ R'
Reciprocal late deep S waves
Lead 1, aVL, V5, V6
Acute PE
Large S wave in Lead I
Deep Q in Lead III
T in Lead III inverted (possible)
Left Bundle (LBBB)
Wide QRS >0.12 sec
Tall R Waves
Lead 1, aVL, V5, V6
Wolf-Parkinson-White syndrome
Lown Ganong Levine Syndrome
First degree Heart Block
Second degree Heart Block type III (Wenckebach)
Second degree Heart Block type II (Mobitz)
P Wave Size Variations
Short PR interval, less than 3 small squares (0.12 sec) & no delta wave

James fibers
(intranodal) bypass the delay within the AV node
Peaked T Waves
Flattened T Waves
T wave flattening
ST segment depression
Apperance of a U wave (not itself diagnostic)
U wave: term given to wave appearing after the T wave (appears in Ant. leads)

Everything slows down
PR, QRS, QT, etc may all become prolonged
ST segment elevation may be seen
J wave or Osborn wave
Various arrhythmias may ultimately supervene
Slow Atrial Fibrillation is most common
Muscle tremor artifact (shivering)
Do not confuse with atrial flutter
Multiple Interval Changes
Digitalis (treats SVT)
The digitalis effect more prominent in leads with tall R waves
ST segment depression
very gradual downslope (unique to digitalis)
T wave flattening /or/ inversion
Toxic levels
SA node suppression
AV node suppression
Can result in 1st, 2nd, 3rd degree heart blocks
ST segment changes
Antiarrhythmic agents :
sotalol, quinidine, procainamide, disophyramide, amiodarone, dofetilide, dronedarone
Other agents:
Tricyclic antidepressants, phenothiazines, erythromycin, quinolone antibiotics and various antifungals
Q-T Interval Changes
long Q-T
ST Elevation
T wave Flattening --> Inverstion
These changes tend to be diffuse (seen in multiple leads)
T wave inversion occurs after ST segments have returned to baseline (opposite for an Infarction)
Q wave formation does not occur
P-R interval is sometimes depressed
Inverted T Waves
Full transcript