-V to A pacing: PM mediated tachycardia, after pVC, retrograde P. PM waiting for QRS, when
it sees none it starts pacing
-Grouped beats: SA Exit block - Mobitz I - Mobitz II - Blocked PACs
LBBB: qS, rS in V1, V2 - Rs in I, V5, V6
-Similar to VPC in morphology
-Initiated by VPC
-AV dissociation: capture, fusion beats
-QRS> 0.14 secs if RBBB morphology
-QRS> 0.16 secs if LBBB morphology
-Concordance: QRS in precordial leads all + or all -
-R>R' in V1
.Cornell 1:
RaVL + SV3 > 28 M (> 20 F)
most sensitive: 35-50%
most specific
.Sokolow: RV5 + SV1 >40 M (> 48 F)
.RaVF > 21                SaVR > 15
V6 > 20
Sinus Arrhythmia
Longest / shortest (P-P) interval vary by > 160 ms or 10% of the P-P interval
QTc quick method from 60 bpm:
60 + 10: - 0.02 (+- 0.04)
60 - 10: + 0.02 (+- 0.04)
Prolonged ST: Hypocalcemia
Shortnened ST: Hypercalcemia (< 0.42)
Non Voltage crieria LVH
-ST depression and TWI in V5-V6
-ST elevation right precordials (V1-V3)
-U waves
-Intrinsicoid Deflection > 0.05
-Abnormal inferior Q
Low Voltage
limb leads < 5 mm
Precordials < 10 mm
-V1: Terminal negative portion of P > 0.04 secs in
length and > 1 mm in amplitude

'p pulmonale' with a P wave >0.25 mV in II and >0.15
mV in V1.
HCM:  Q in I, aVL, V4-V6
(septal hypertrophy)
Cor pulmonale
Lateral MI
ASD secundum

ECG is insensitive for pulmonary embolism and
would more like manifest as sinus tachycardia, atrial
arrhythmias, RBBB, or RV strain
ASD primum: (15-20%), associated to,
-Anomalous pulmonary venous drainage
-Down Sd
-RSR' in V1, iRBBB, LAD
-1st degree AVB (15-40%)
LBBB + Ischemia
Discordant ST elevations > 5mm
Concordant ST elevations > 1 mm
-Sinus Pauses or SAEB
-Tachy / Brady
-AF with slow VR
-Prolonged sinus node recovery after APC
-AV Junctional escape rhythm
2:1 Block

QRS normal
PR> 300 ms
CSM worsens
Atropine improves
Exercise improves

PR < 160 ms
CSM improves
Atropine worsens
Exercise worsens
Don't Code infarction Unless you see Q waves
Code the highest level of block you see if mixed
If R>S in V1 => Posterior infarct
QT measurement

-The accuracy levels of manual determination with a caliper is 20–40 ms.
-The QT measurement should be made in leads II and V5 or V6, with the longest value being used.
-In general,
biphasic T waves are frequently present in multiple leads, whereas discrete and separate low-
U waves are best seen in the lateral precordial leads. The end of the U wave is defined as the
intersection point of the descending limb of the U wave and the isoelectric baseline.
-In patients with bundle branch block, Class 1c antiarrhythmic drugs, or preexcitation, the measure of the JT
from the S wave offset to T wave end may be used, but normal standards for the JT interval are not well
A- T wave morphology is normal
B- T wave is followed by a distinct U wave
C- Biphasic T
D-Second low amplitude repolarization wave interrupts the terminal portion of the larger T wave
QT correction formulas
LAD occlusion proximal to S1: ST-elevation in lead aVR (ST1aVR), complete RBBB, ST-depression in lead V5  and ST elevation in V1 >2.5 mm
LAD occlusion distal to S1: Q-waves in V4–6 were associated with occlusion distal to S1
LAD occlusion proximal to D1: Q-wave in lead aVL
LAD occlusion distal to D1: ST depression in aVL
For both S1 and D1 inferior ST depression > 1.0 mm strongly predicted proximal LAD occlusion, whereas absence of inferior ST depression
predicted distal occlusion

Value of the ECG in detecting site of LAD occlusion - JACC 1999
the sensitivity of most RVH voltage criteria is <10%!  If you see ancillary findings
like right atrial enlargement, right axis deviation, and QRS widening, you should
consider the diagnosis.  There are a number of independent, voltage criteria
which are worth mentioning:
1. R in V1 > 0.7 mV
2. S in V5 or V6 > 0.7 mV
3. R in V1 + S in V6 >/= 1.0 mV
4. R/S ratio in V1 > 1
5. R/S ratio in V5 or V6 <1
The ST-T segment changes associated with RV hypertrophy essentially mirror
those seen in LV hypertrophy, except they're typically seen in the anterior
precordial leads, V1-V3.
T wave
LVH and LAFB if you see
1.) LAE 2.) ST-T wave changes consistent with
‘strain’ 3.) QRS 'widening' (but still <0.12 ms) 4.) an
axis <-45 degrees 5.) an 'S' wave in III > 1.5 mV
Ventriculophasic Sinus Arrhythmia

Longer PP intervals that surround a QRS complex. This is due to alternations in sinus nodal automaticity secondary to changes in blood pressure.
Each QRS complex is associated with an increase in blood pressure, which affects the baroreceptors. One needs to postulate that the
baroreceptor mediated slowing of the sinus rate occurs too late to affect the P wave immediately after the QRS complex, but does prolong the
subsequent SCL. Thus, the PP interval between the two QRS complexes is lengthened.