Conduction abn Flashcards
What is a fascicular block
- LBB: divide into anterior and posterior fascicles → pass at the base of corresponding papillary muscle
o LV depol shift toward blocked fascicle
o Hemiblock: involves 1 of the division of LBB
What type of conduction disturbance HCM cats
L anterior fascicular block
L anterior fascicular block is common in
in cats with HCM → turbulent flow in LVOT, myocardial fibrosis
Why is anterior LBB fascicle in more vulnerable
o Different blood supply
o Longer/thinner
o Located in turbulent LVOT
What vector is affected in ventricular depol by L anterior fascicular block
- Affect 3rd vector of ventricular depol: 3a
o Initial: block remove initial sup and L activation
1st vector downward and R - Q wave appear in lead I and aVL
- R wave in lead II, III, aVF
Alter initial portion of QRS toward +80-90
o Late: activation spread to LVFW in sup/L direction
Depol of anterosuperior portion of LV → slight prolongation, but small effect does not alter QRS duration
Prominent R wave in lead I, aVL (qR)
↑R wave peak time: impulse reach LV later
Prominent S wave in lead II, II, aVF (rS)
ECG characteristics of LAFB
o Normal QRS duration
o Marked L axis deviation: MEA -30 to -60
aVR usually isoelectric
o qR pattern: small Q wave + tall R wave in lead I and aVL
From early activation of LV posterior wall
o Deep S wave in lead II, III, aVF
ECG characteristics for RBBB + LAFB
o ↑ QRS duration
o Marked L axis deviation
o Small Q wave + tall R wave in lead I and aVL
o Deep S wave in lead I, II, III, aVF
L posterior fascicular block
Less common: anatomic organization makes L posterior fascicle ↓ risk to be damaged
Which vector is affected by LPFB
- Affect 3rd vector of ventricular depol: 3b
o Slight delay + antero-posterior direction
o Early activation of anterior wall → axis deviation of initial portion of QRS to -60
ECG characteristics LPFB
not possible to diagnose on surface ECG
o Normal QRS duration
o R waves in lead I, aVL
o Q waves in lead II, III, aVF
What are the 3 types of bifascicular blocks
Complete LBBB
RBBB w/ LAFB
RBBB w/ LPFB
What does LBBB usually indicates and consequences
severe myocardial damage
o Deteriorated LV systolic fct → worsens intra/interventricular dyssynchrony
ECG characteristics complete LBBB
Normal MEA
↑QRS duration from wide R wave
Q wave can remain present → early electrical activation from lateral RV wall
ECG characteristics RBBB + LAFB
o Posterior to superior direction of septal activation apparent
o ECG characteristics
↑QRS duration
MEA: inferior to sup axis btw -60 and -90
Largest negative deflection in lead I, II, III, aVF
ECG characteristics RBBB + LPFB
o Deviate axis to the R and superiorly
1st vector: upward, to the L → early activation of anterolateral wall of LV
2nd vector: upward, to the R → late activation of RVFW
o ECG characteristics
Complete RBBB characteristics
Q wave in leads II, III, aVF, no Q wave in leads I, aVL
Trifascicular block
- Interruption of impulse propagation alternate btw 3 subdivisions
- From extensive damage of conduction system → can progress to 3AVB
- Different patterns:
o LBBB alternating with RBBB
o RBBB with LAFB alternating w complete LBBB
o Bifascicular block + Mobitz type II 2AVB
Causes of SA block
impaired automaticity, conduction or both
1st degree SA block
- Cannot be recognized on surface ECG
- Prolongation of interval btw sinus impulse and P wave
2nd degree SA block
- Type I (Wenckebach periodicity): progressively shorter PP followed by a longer PP interval including blocked P
o Analogous to progressive ↓RR in 2AVB
o SA interval is analogous to PR interval - Type II: dropped P waves during sinus rhythm
o Pauses are multiple of basic PP interval
3rd degree SA block
- Escape rhythm
Demonstrate why the distal chamber (i.e., the atria) accelerates in “classic” Wenckebach periodicity. SA block
o Analogous to progressive ↓RR in 2AVB
↓PP before the block = acceleration of atrial depol
Related to increment at which S-A interval progressively increase is smaller → translate into progressive ↓ P-P duration before block
2AVB mobitz 1
- Progressive slowing of conduction velocity
o ↑delay in sinus impulse propagation across AV node until impulse blocked
o Progressive prolongation of relative refractory period in AV node
α to prematurity of impulse traveling through it → rate of conduction depend on time the impulse arrives to AV node - Earlier impulse = longer to conduct
Impulses are arriving earlier and earlier in relative refractory period → prolongation of conduction delay → until one impulse arrive during absolute refractory period - RP-PR reciprocity or RP-dependent PR interval
- Period of rest for AV node by blocked impulse → normal conduction on subsequent beat
Absolute refractory period is normal
Max change in PR w/ 2AVB
2nd beat after blocked P
Characteristic of RR interval w/ 2AVB mobitzI
o ↓RR before block (↑HR)
* Progressive ↑PR associated to progressive ↓RR
- Increment by which it ↑ is progressively smaller → PR continues to prolong but ↓R-R interval
Atypical Wenckebach 2AVB
- Frequent with ratio of AV conduction >7:6
- Variable PR, maximum prolongation is NOT 2nd beat after block
- No ↓RR before block
Advanced 2AVB
- AV conduction ratio > 2:1
- Hisian or infra-Hisian
- ECG characteristics
o 2 or > consecutive blocked P waves
o Normal or ↑PR
o QRS is normal or prolonged if block is infra Hisian
Define “ventriculophasic sinus arrhythmia”
- Longer RR with a blocked P wave
- Variation of PP intervals induced by ventricular systole
- PP interval with QRS is shorter than PP interval w/o QRS
o 2:1 2 AVB or 3AVB
o Ventricularly paced rhythms
ALTERNATING WENCKEBACH
- 2:1 2nd degree AVB with progressive prolongation of PR for conducted waves
o Until block worsens to more advanced block (3:1, 4:1) - Mechanism: 2 points block
o Proximal in AV node
o Distal at His bundle → higher grade of block - Manifestation of functional block in SVT: Afib, Aflutter
Define AV dissociation
Atria and ventricles are independent → asynchronous activation
Causes of AV dossication
o Slowing of dominant PM → allow independent ventricular PM (junctional or ventricular escape rhythm)
o Acceleration of latent PM (↑ automaticity)
o Complete heart block
DDX
o HypoK+
o Vtach
o 3AVB
o Focal junctional tachycardia
o AIVR
Focal junctional tachycardia
- ↑ automaticity or triggered activity in junctional area
o Proximal to apex of Koch’s triangle
o Posterior to distal AV bundle
FJT most common in
Young labs
ECG FJT
o Regular ventricular rate 100-160bpm
o Isorhythmic AV dissociation
o Periods or retrograde ventriculo atrial activation 1:1 ratio
P’ waves in ST segment as pseudo S waves
o Gradual onset
IAVD
- 2 rhythms: one sinus, one junctional or ventricular
o Sinus P waves in close relation but not associated with QRS
o When atrial and ventricular rhythm are the same rate
What is accrochage
same rate for short or long periods
IAVD: types of synchronization
o Type I: continuous fluctuation of P-QRS interval
P wave marching toward and in the QRS
Suspected from BP variations: P waves moves closer to QRS until overlap → ↓ contribution of atrial contraction → small ↓ BP → stimulation baroR → ↑∑ tone → ↑ sinus d/c → ↓P-P
o Type II: fixed relationship of P-QRS
Mechanical stimulus from SA node artery pulsation → synchronizing effect on SA node, AV node and conduction system
IAVD: effect of retrograde activation
d/c of junctional PM > SA node → suppress SA node PM
Mechanism of ventriculo phasic arrhythmia
o BaroR reflex
↑ arterial BP with ventricular contraction (QRS) → nucleus tractus solitarius → ↑ vagal stimulation → ↓ SA node d/c
Effect begins 600ms after QRS and last 1s
* P wave just after QRS: occurs prior to p∑ effect
o Sinus arrhythmia
Potential common physiological pathway
Inspiration → ↑ ∑ stim → ↑ SA node d/c
Arrhythmia is abolished by atropine = support this mechanism
o Ventricular synchrony
Intrinsic complex (vs paced) → better ventricular synchrony
↑ ventricular contraction efficiency → ↑ SV → ↑ arterial BP
o Blood supply to SA node
Ventricular contraction may ↑ SA node blood supply → earlier SA node d/c after QRS
o Mechanical stimulation of SA node
Ventricular contraction → traction on atria → mechanical stimulation of atria → ↑ SA node d/c
Paradoxical ventriculo-phasic sinus arrhythmia
- PP interval including QRS are longer than PP w/o QRS
Mechanism of paradoxical ventriculo-phasic sinus arrhythmia
- 2 phase chronotropic effect
o Positive chronotropic effect (acceleration) → early appearance of P after QRS → ↓PP interval with QRS
Atrial stretch by mechanical effects: may impact d/c of normal SA node impulse
Ventricular contraction may ↑ SA node blood supply → earlier SA node d/c after QRS
o Negative chronotropic effect (deceleration) → longer PP w/o QRS
BaroR changes in vagal tone → ↑BP → vagal reflex → ↓ SA node d/c → ↑PP w/o QRS
