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8. ECG > Conduction abn > Flashcards

Conduction abn Flashcards

1
Q

What is a fascicular block

A
  • 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
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2
Q

What type of conduction disturbance HCM cats

A

L anterior fascicular block

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3
Q

L anterior fascicular block is common in

A

in cats with HCM → turbulent flow in LVOT, myocardial fibrosis

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4
Q

Why is anterior LBB fascicle in more vulnerable

A

o Different blood supply
o Longer/thinner
o Located in turbulent LVOT

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5
Q

What vector is affected in ventricular depol by L anterior fascicular block

A
  • 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)
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6
Q

ECG characteristics of LAFB

A

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

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7
Q

ECG characteristics for RBBB + LAFB

A

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

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8
Q

L posterior fascicular block

A

Less common: anatomic organization makes L posterior fascicle ↓ risk to be damaged

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9
Q

Which vector is affected by LPFB

A
  • 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
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10
Q

ECG characteristics LPFB

A

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

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11
Q

What are the 3 types of bifascicular blocks

A

Complete LBBB
RBBB w/ LAFB
RBBB w/ LPFB

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12
Q

What does LBBB usually indicates and consequences

A

severe myocardial damage

o Deteriorated LV systolic fct → worsens intra/interventricular dyssynchrony

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13
Q

ECG characteristics complete LBBB

A

 Normal MEA
 ↑QRS duration from wide R wave
 Q wave can remain present → early electrical activation from lateral RV wall

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14
Q

ECG characteristics RBBB + LAFB

A

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

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15
Q

ECG characteristics RBBB + LPFB

A

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

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16
Q

Trifascicular block

A
  • 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
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17
Q

Causes of SA block

A

impaired automaticity, conduction or both

18
Q

1st degree SA block

A
  • Cannot be recognized on surface ECG
  • Prolongation of interval btw sinus impulse and P wave
19
Q

2nd degree SA block

A
  • 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
20
Q

3rd degree SA block

A
  • Escape rhythm
21
Q

Demonstrate why the distal chamber (i.e., the atria) accelerates in “classic” Wenckebach periodicity. SA block

A

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

22
Q

2AVB mobitz 1

A
  • 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
23
Q

Max change in PR w/ 2AVB

A

2nd beat after blocked P

24
Q

Characteristic of RR interval w/ 2AVB mobitzI

A

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
25
Q

Atypical Wenckebach 2AVB

A
  • Frequent with ratio of AV conduction >7:6
  • Variable PR, maximum prolongation is NOT 2nd beat after block
  • No ↓RR before block
26
Q

Advanced 2AVB

A
  • 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
27
Q

Define “ventriculophasic sinus arrhythmia”

A
  • 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
28
Q

ALTERNATING WENCKEBACH

A
  • 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
29
Q

Define AV dissociation

A

Atria and ventricles are independent → asynchronous activation

30
Q

Causes of AV dossication

A

o Slowing of dominant PM → allow independent ventricular PM (junctional or ventricular escape rhythm)
o Acceleration of latent PM (↑ automaticity)
o Complete heart block

31
Q

DDX

A

o HypoK+
o Vtach
o 3AVB
o Focal junctional tachycardia
o AIVR

32
Q

Focal junctional tachycardia

A
  • ↑ automaticity or triggered activity in junctional area
    o Proximal to apex of Koch’s triangle
    o Posterior to distal AV bundle
33
Q

FJT most common in

A

Young labs

34
Q

ECG FJT

A

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

35
Q

IAVD

A
  • 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
36
Q

What is accrochage

A

same rate for short or long periods

37
Q

IAVD: types of synchronization

A

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

38
Q

IAVD: effect of retrograde activation

A

d/c of junctional PM > SA node → suppress SA node PM

39
Q

Mechanism of ventriculo phasic arrhythmia

A

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

40
Q

Paradoxical ventriculo-phasic sinus arrhythmia

A
  • PP interval including QRS are longer than PP w/o QRS
41
Q

Mechanism of paradoxical ventriculo-phasic sinus arrhythmia

A
  • 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

8. ECG (19 decks)

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