Definition of a pathologic Q wave

Any Q-wave @ leads V2V3 0.02s or QS complex in leads V2 and V3

Q-wave 0.03 s and > 0.1 mV deep or QS complex in leads I, II, aVL, aVF,
or V4V6 in any two leads of a contiguous lead grouping (I, aVL,V6; V4V6; II, III, and aVF)
R-wave 0.04 s in V1V2 and R/S 1 with a concordant positive T-wave
in the absence of a conduction defect
STT = ST Seg
EKG Morphology
= ventricular repolarization
Repolarization follows Contraction and Depolarization.

During Repolarization
-Cardiomyocytes elongate and prepare for the next heartbeat
-Repolarization takes much more time than the depolarization.
-Elongation is not passive

Repolarization Starts @ J point, Ends @ T wave. Normally the STs @ or near the isoelectric line
**Minor STT changes are not necessarily associated with cardiac ischemia[1].

P-Wave? The
The
The
T
T
T
wave
wave
wave
is
is
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usually "CONCORDANT" e.g. QRS = T-Wave for a given lead
normally in Lead I, II, AVL, AVF, V3-V6.
normally in V1 & AVR.

PTa Seg? The T wave

The T wave angle

is in V2 (in Blacks V3)

QRS Morphology LV Endocardium repolarizes 22msec slower LV Epicardium

QRS? 1.
2.
Are there any pathological Q waves as a sign of previous MI? Yes/No?
Are there signs of LV or RV Hypertrophy: Yes/No?
Repolarization = Current from the Endocardium Epicardium
Interpreted as a signal on the ECG

ST Elevation in Various Syndromes STT Elevation

STT?
3. Does the QRS complex show Microvoltage (< 5mV): Yes/No?
4. Is the Conduction normal or prolonged ( > 0.12s): Yes/No? #1 = Acute Ischemia
5. Is the R wave propagation normal? Early Repolarization
**(Normal R waves become larger from V1-V5 (Max @ V5)) Acute Pericarditis: SE Elevation @ All Leads (Except AVR)
Pulmonary Embolism: St Elevation @ V1 + AVRr

T-Wave?
a. Is R-Wave amplitude @ V2 > R-Wave amplitude @ V3?
Yes? could be a sign of a (previous) posterior MI + others Hypothermia: St Elevation @ V3, V4, V5, V6, II, III, + AVF
*If all these items are normal you can go on to the next step: ST morphology HCM @ V3, V4, V5, (V6)
K (Hyperkalemia): @ V1, V2 (V3)
During Acute Neurologic Events: @ All Leads, (Primarily V1-V6)
Acute Sympathic Stress: @ Leads Leads, (Especially V1-V6)
Brugada Syndrome.
Cardiac Aneurysm
Cardiac Contusion
LV-Hypertrophy
Idioventricular Rhythm Including Paced Rhythm

PTa seg STT Depression

= between the p wave and QRS complex
#1 = Ischemia
Atrial infarction or Pericarditis Reciprocal STsD (If one lead shows STsE another must show STsD
Elevation or Depression Straining LV-Hypertophy
of the PTa segment Digoxin effect
K, Mg
Post tachycardia)
During acute neurologic events

The T wave
= morphologically variable but give hints

Flat T wave < 0.5 mm / Concordance @ Leads I, II, V3, V4, V5 or V6

Inverted T wave > 0.5 mm @ leads I, II, V3, V4, V5 or V6

Early repolarization Possible causes of T wave changes:

P Wave Morphology
Ischemia & MI
= STE w/o without underlying disease. Pericarditis
Probably has nothing to do with actual early repolarization. Myocarditis
can reveal RA-Hypertrophy, LA-Hypertrophy + Atrial arrhythmias Commonly seen in young and understand that ER Ischemia Cardiac Contusion
best determined @ leads II and V1 during sinus rhythm.
Acute Neurologic event (ex SAH)
Normal P-Wave: Early Afterdepolarization vs ST-Elevation Mitral valve prolapse (MVP)
Digoxin effect
P-Wave max height = 2.5 mm @ leads II or III
Straining RV/LV-Hypertrophy
P-Wave duration < 0.12 seconds
P-Wave: Lead II: , AVF: , V1: Biphasic

Abnormal P wave
1. Elevation or Depression of the PTa segment
PTa seg = between the p wave and QRS complex
can result from atrial infarction or pericarditis.
2. If the p-wave is enlarged, the Atria are enlarged.
3. Inverted P-Wave = ectopic atrial rhythm

Early After Depolarizations