PMT, Johnston - AV, BBB, Hemiblocks, Hypertrophy Flashcards
Normal PRi
Normal QRS
- 2sec (5 small box)
0. 06-0.12sec (2 small boxes)
Etiology of 1st degree AV Block (AVB)
atherosclerosis, HTN, diabetes, fibrosis CHD, degeneration of conduction system
Thyroid, SLE, infiltrative (amyloid, sarcoid), mitral/aortiv valvular calcificaiton, myocarditis
ECG of 1st degree AVB
PRi constantly greater than 0.2sec
2nd degree AVB Mobitz 1 (Wenckebach) - what do you see?
- Progressive PRi prolongation prior to dropped QRS.
- “Grouped beats”.
- Narrow QRS
What causes a Mobitz 1?
Digitalis toxicity, ischemic events (Inferior MI due to RCA), myocarditis
Mobitz 1 (Wenckebach) - what is it?
2nd degree AVB
- INFERIOR aMI (RCA).
- Level of block is at AVN, resulting in transient, impairment of AVN conduction.
Etiology of 2nd degree AV Block - Mobitz 2
- IHD
- ANTERIOR MI (LAD)
- Degeneration of conduction system
2nd degree AVB Mobitz 2 - what do you see?
- PRi is uniform
- Dropped QRS
2nd degree AVB Mobitz 2 - what level does it occur at and what is it seen with?
- Distal to AVN: Bundle of His, both bundle branches, fascicular branches.
- Seen with ANTERIOR MI.
Does Mobitz 1 or 2 have worse prognosis?
Mobitz 2 is progressive and worse, irreverisble.
Third degree heart block looks like what, on ECG?
Two independent rhythms - p waves never related to QRS, so rate of atria and vents are different. Waves are normal size.
Where do third degree heart blocks occur?
Above or below the AVN.
- Above = Junctional rhythm, narrow QRS, rate 40-60
- Below AVN = Ventricular pacemaker, wide QRS, rate 20-40
Etiology of third degree heart block
- Ischemic
- Infiltrative diseases
- Cardiac surgery (bypass, valve replacement, myocarditis, degenerative)
How do you treat a third degree AVB?
Pacemaker!
What direction is the septum normally activated?
In LBBB, which ventricle is activated first?
- Left to right
- Right
Common features of BBB
- Wide QRS (greater than 0.12sec)
- ST segment - T waves slope off in opposite direction to QRS
What side of the septum is activated first in RBBB? LBBB?
RBBB - Left is first
LBBB - Right is first
RBBB see what on ECG?
V1 has small(er) R and larger S than in LBBB
V1, V2 = R - S(deep/big) - R’
- *V1rSR or rsR
- *L1 or V6 slurred S wave
Sequence of ventricular activation in LBBB.
Septum activated from R side, nearly same time as RV activated. Strong septal force, so negative deflection in V1. Positive deflection V6 results in monophasic R.
What issues is LBBB more apt to occur with?
- HTN
- Ischemia
- AS
- Cardiomyopathy (**LBBB + Right axis deviation)
LBBB + LAD is associated with what?
LBBB + RAD** is associated with what?
- Myocardial dysfunction, conduction system disease.
- Congestive Cardiomyopathy**
In addition to V1, what two other leads have the same features in BBB?
1 and AVL
What leads do you look at in LBBB and what do you see?
V5 and V6, see the notched R-R’
Why is there T wave change in BBB (T wave opposite of QRS)?
Polarity is opposite QRS direction. If T wave polarity is in the same direction of QRS, it is a PRIMARY T wave change, usually due to ISCHEMIA.
LBBB on ECG looks like what?
- L1/V6 upright monophasic or notched QRS
- V1 has negative QRS
- QRS > 0.12
- V5-V6 tall R-R’
Which two limb leads look like V6 in LBBB?
Lead 1 and AVL
What is a hemiblock?
Blockage of one of the two main divisions of the left bundle branch block.
Hemiblock: LAH (more common), LPH
Criteria for LAH
- Left axis deviation (greater than -60 degrees).
- Small Q in leads 1 and AVL
- Small R in 2, 3, AVF
- Normal QRS duration or slightly widened Q1S3
Criteria for LPH
- Right axis deviation (greater than +120 degrees=AVR+, L3 smallest).
- Small r in leads 1 and AVL
- Small Q in 2, 3, AVF
- S1Q3
- No evidence of RVH
Etiology of LAH
- Disease in conduction system.
- Often associated with MI (LAD occlusion)
Etiology of LPH
Disease in conduction system
P wave in RAE and LAE
RAE: L2, L3, aVF have P tall, pointed (L3 taller than L1), P-pulmonale
LAE: P broad, notched (L1 taller than L3), P-mitrale, diphasic P in V1 or L3
RAE is associated with what?
Pulmonary HTN, caused by COPD, PE, MS, MR
P-wave in RAE (p-pulmonale) on ECG
- L2, L3, AVF = pointed and taller than 0.25
- V1, V2 = taller than 0.1
- P wave is pointed and tall
P-wave in LAE (p-mitrale) onECG
V1 = Broad, notched P wave duration >0.11sec of terminal negativity
- P wave is “M-sign” or diphasic
Causes of LAE
MS, MR
Most common cause of LVH
HTN (other: AS, AI, hypertrophic cardiomyopathy, coarctation of the aorta)
Sokolow Lyon Criteria for LVH
- R-wave in L1 + S-wave in L3 > 25mm
- R-wave in AVL > 11mm
- R-wave in V6 > 26mm
LVH: Rule of 35 and 12
Deepest S (V1 or V2) + Tallest R (V5 or V6) >35
OR
R>12 in AVL
Causes of RVH
- Chronic lung disease, like COPD.
- RVOT obstruction, VSD
- Congenital = Tet of Fallot, PS, trasnposition
- MS, TR
RVH on ECG
- R waves prominent in RIGHT precordial leads
- Deep S waves in LEFT precordial leads
- R:S >1
- *RAD
- *V1 = Tall R wave with inverted T wave
- *low voltage
Causes of Dominant R waves in V1
RVH, Posterior or lateral MI, WPW, hypertrophic cardiomyopathy, muscular dystrophy, normal variant
Strain (ST depression) associated with what change in the heart?
Hypertrophy
See what in ECG of LVH with strain?
See what in ECG of RVH with strain?
LVH with strain, see ST-morphological changes and R:S>1 (positive) in LEFT chest leads.
RVH with strain, see ST-morphological changes and R:S>1 (positive) in RIGHT chest leads.
What pulls ST-segment down?
Digitalis or hypertrophy strain (and t wave inversion).
