ECG Flashcards
Notching of QRS complex in inferior leads may suggest
ASD-Crochetage sign
Low atrial rhythm may be seen in
Sinus venous ASD
Acute Amlodipine intoxication
Rare CHD
How to differentiate between high / mid/ low junctional rhythm
High-look like low atrial rhythm
Mid- no visible p waves(in QRS)
Low- After QRS; inverted p seen in inferior leads
How to identify low left atrial rhythm
P will be inverted in lateral leads also. L
If the PR interval is short in a low atrial rhythm it indicates
It probably arise from junction and not the low atrial tissue
Criteria for RVH in V1
R >7mm or R/S >1
V5/6—>7 mm deep S or R/S <1
RBBB and RVH
RAD(axis derived from first 60ms of QRS)
R/S ratio in Lead l is <0.5
In incomplete RBBB if R’is 10 mm or more it suggests RVH
Similarities of RVH and LPHB ecg
- RAD
- qR in Ld 3
But as c/c LPFB is rare, this diagnosis is generally not used.
RAE and changes in V1-3 and young age favors RVH
Young age more likely RVH and old age more likely LPFB
Not easy to differentiate with ECG alone
Repolarisation abn in RVH is seen in
V1-3, aVF and III
Criteria for impending MI in LBBB
- ST elevn >1mm in Rwaved leads(OR-25.2)
- ST elevn>5mm in S waved leads(odds ratio-4.3)
- ST depression 1mm or more in V1-3(OddsRatio-6)
Criteria for completed MI in LBBB
- Q in V6,I,aVL or II and aVF
- RV1 >3mm with QV6
- CABRERA sign- V3 or 4 , ascending limb of S wave will show notching(more than 50 msec duration
Sinoventricular conduction in Hyperkalemia means
P waves are absent but the impulses reach AV node
DD of 2:1 AV Block
Blocked premature P
Differentiated by the premature occurrence .
This is also a dd for Sinus pause
ie look 👀 for a premature p in 2:1 block and in Sinus pause- This is wrong. In sinus pause the p should be conducted. Non conducted premature p is correct
Exercise parameters suggesting significant MS
MeanPG15 or more.PCWP-25 or more.PASP more than 60
Dobutamine mean should be more than 18
—-% of Brugada will develop dangerous arrhythmias
25% can have life threatening arrhythmias
If PR is <90 ms it is .———-
Unlikely to be a conducted p wave. May be junctional (high)
Type of SA exit block which can be assessed in ECG
second DEGREE -In type 2 pp interval will be multiples of basic pp.; but not in Type 1
First Degree-will look normal
Third Degree-may be exit block or Sinus arrest
In wenkebach RR interval of pause is ———-
LESS than 2 previous RR
Cornel Voltage criteria for LVH
SV3 + RaVL > 28 in males & >20 in females
95% specificity 40% sensitivity
Cornell PRODUCT is best for LVH but tedious. So use Voltage
SVERaL-28/20 NoV um NoS um
Sokolow-Lyon index for LVH
- R in aVL 11 or more
2.S in V1 or 2 plus R in V5or 6 is
35 or more
Lateral wall MI pattern with Q in I & aVL s/o which WPW
Left lateral wall (Not left free wall?? which will include LL,LAL,LPL, LP)
IWMI pattern with Q in II,III,aVF s/o Posteroseptal pathways :::
Coronary Sinus type also will have IWMI pattern
De Winter sign
ST depression with Peaked T waves in precordial leads
It’s AWMI equivalent
In patients with RBBB ST depression during TMT is normal in
V1-4
ST depression in V4-6, II and aVF suggests CAD
qR in aVL indicates
LAHB
R peak time in aVL in LAHB
45 ms or more
LPHB mimics
LWMI due loss of R in lateral leads
LAHB mimics IWMI due to loss of R waves
Opposite leads will show qR pattern. ie LAHB shows qR in lateral leads while LPHB shows qR in inferior leads
LAHB - LAD; LPHB- RAD
This is in terms of R wave but in terms of Q its opposite pattern. I think better it is Q based.
Low voltage limb leads means
QRS amplitude <5 mm in each of the 3 standard limb leads I,II,& III
1mv = 10 mm
Low voltage of ALL LEADS means
- Low voltage limb leads &
- Average voltage in chest leads less than 10 mm
This is uncommon. Usually only limb leads are of low voltage
Low voltage QRS causes
- Fat, Fluid, Air
- Infiltration- RCMP(Amyloidosis,Sarcoidosis,Hemochromatosis, Myxedema -MASH)
- DCMP-loss of myocytes due to any reason
- CP, Scleroderma
- PERED- conditions with Peripheral or Pulm edema
Anterior fascicle supplies which area of LV
Upper and Lateral wall
Ie why small R waves in lateral leads and small Q in inferior leads in LPHB. ( reverse of LAHB)
The delayed activation of upper and lateral wall masks corresponding normal activation in infr wall in LAHB
Prolonged QTc
Abnormally prolonged QTc (ACC/AHA)
Highly abnormal QTc
> 440/470
> 470/480
> 500
ECG doesn’t show any change in ………,pericarditis because…….
Uremic pericarditis doesn’t affect the epicardium
Difference in ST/T in pericarditis and MI
ST segment elevation and T wave inversion DON’Toccur simultaneously in Pericarditis -Exceptions occur
Differentiate ECG of pericarditis and early repolarisation
Only 50% of early repolarisation have ST elevation in limb leads
In pericarditis it is seen in most cases
T inversion in inferolateral leads may be normal in
Black/African athletes
Tall T waves definition
> 10 mm in chest leads
> 5 mm in limb leads
ST elevation criteria in V2 and V3 in STEMI
2mm in males
1.5 mm in females
VPCs arising at same site of origin may have different morphologies
True
Coupling interval of VPCs can affect the morphology
Fixed coupled VPCs are usually considered
Reentrant
But not diagnostic of Ree try
Rarely Parasystole also appear fixed
Fixed coupled VPCs mean
Variation less than or equal to 80 ms at Any cycle length
ST/T ratio in early repolarisation
< 0.25
PR segment depression is seen in
- Pericarditis
2. Atrial infarction
If ECG sags or get elevated use the
Position control facility in the ECG machine
If ECG baseline is thick(50-60Hz interference)
Electrical interference. Check loose connection etc ; other electronic equipment interference; change socket etc
Highest voltage limb lead is
Ld 2
Ld2= Ld 1+Ld 3
….. leads indicate the true voltage at the site of placement
Unipolar leads. Since negative electrode is connected to the central terminal which is zero
Why unipolar limb leads are Augmented
Since the true voltage is relatively weak ,to be on par with other leads , they are augmented 1.5 times
Why lead 1?axis is taken as zero
Arbitrarily. Need to convey to another person how the axis is
ECG lead kept on midclavicular line
V4
Anterior/Posterior forces can be assessed from which precordial leads
V2
Right / Left forces can be assessed from which lead
V6
Normal resting myocardial cells have———charge outside and——-charge inside
Positive outside and Negative inside
When can we see the repolarisation of atria
In extreme bradycardia we may see a negative wave after the QRS
The anterior precordial leads are
V1&V2
Others are anterolateral or lateral
ie why negative P is not common in V3-6
How to differentiate a normal negative deflection of P in V1
Negative deflection will be SMALLER than the positive component of right Atrial P in V1
The part of ventricle to be first activated is the
SEPTUM
Septum is considered part of LV and is always activated from the LV side from Left bundle
ie L to R in normal cases
The third vector of Ventricular depolarization activates ….
Basal and Posterior aspects of Ventricles.
So Vector directed Superiorly and Posteriorly.
So small s in V1( submerged in large S) &V6
Normal duration of RA and LA depolarization
RA- ends in .02-.04 sec
LA- starts at 0.03 sec and ends in another.06 seconds
Idea not very clear in Pediatric cardiology by Santhosh kumar
Is PR interval affected by Heart rate
Faster the heart rate , shorter the PR interval
U wave amplitude is usually….of T wave
1/4th of T wave
QT dispersion is
Difference in QT interval in different leads ( because of differences in depolarization and repolarisation in different parts of myocardium)
Why beta blockers are useful in congenital long QT syndrome
Adrenergic stimulation precipitatesTorsades- Hence beta blockers are useful
QRS duration is best measured in a lead with
Lower QRS amplitude- eg- limb leads, V1-2
The mechanical properties of stylet may falsely increase QRS duration when amplitude is high
Bundle branch blocks cause wide QRS due to ………delay
TERMINAL delay
Commonest cause of intraventricular conduction delay is
Ventricular enlargement ( takes more time for travel)- as in LVH
In intraventricular conduction delay the qrs prolongation affects
Both initial and terminal portions
BBB-terminal
Why second r wave is seen in anterior Chest leads(V1,2)
- The RVOT is just beneath the Sternum
- This one of the last portion to be depolarized
Hence second r wave
This is smaller than first R wave
Sinus arrhythmia means RR interval variation is more than
120
160 ms according to some
ie 3-4 small divisions
Early transition (V2) is seen in
TOF
Low voltage QRS seen - think of
- Myocarditis- due to myocardial edema
- Emphysema
- Obesity
- Generalized edema etc
Small q is normally seen in
I,aVL,aVF, II,III,V4-6
Deep q in V4-6 indicates
Septal hypertrophy- which in turn indicates LV hypertrophy
Eg VSD with LVVO
Santhosh- Pediatric ECG
Absence of q in V6 indicates
- Single Ventricle
- cTGA
- LBBB
- Mirror image dextrocardia
Causes of ST depression
- Digoxin toxicity/ effect
2. Severe Anemia- possibly due to myocardial ischemia
How to measure axis in BBB
Controversial
- RBBB- initial 80-100 ms ( ie only LV forces considered)
- LBBB and IVCD- entire QRS or initial 80-100 ms
Short PR (<0.12s)with narrow QRS is seen in
LGL syndrome
Lown
Ganong
Levine
In the absence of tachycardia, it’s considered a benign variant
If tachy is present- no increase in mortality
All from Wiki
Tall T wave definition
More than 2/3 rd preceding QRS
Normal T is 6 mm in limb leads and 10 mm in precordial leads
Santhosh- pediatric ECG