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8. ECG > SVT > Flashcards

SVT Flashcards

1
Q

DDX wide complex tachycardia

A

o Vtach
o SVT with aberrancy
 L or R BBB: anatomical or functional
* Functional → recovery time in RBB longer
o Bradycardia depend ent (phase 4)
o Tachycardia dependent (Ashman’s, phase 3)
 L or R heart enlargement
 Accessory pathway

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2
Q

Chung’s phenomenon

A

wider, ↓ amplitude P wave results from aberrant atrial conduction from the previous premature complex

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3
Q

Mechanism of vagal maneuver

A

↑ vagal tone → ↓ sinus rate
o Mechanisms
 Hyperpolarization → IKAch channel activation
 Inhibition of If (which promotes depol during hyperpol)
o Slows AV node conduction: hyperpol + ↓AP amplitude
o Carotid massage → stimulate carotid baroR → branch of 9th Cr nerve (nerve of Hering) → vasomotor center of medulla → ↑ efferent p∑ to heart

If ∑ tone is elevated, may not terminate arrhythmia

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4
Q

SVT

A

A flutter
Afib
AVNRT
Automatic junctional tachycardia
OAVRT

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5
Q

Atrial flutter vs other SVT

A

2:1 conduction can be difficult to distinguish from other SVT
o Bix rule: when T wave equally spaced btw 3 R waves → suspect atrial flutter

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6
Q

Afib predisposing factors

A

Critical mass
Autonomic influence
Atrial stretch
Number of wavelets
Electrical remodeling

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7
Q

Afib: critical mass

A

 Needs myocardial area of adequate size

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8
Q

Afib: vagal tone

A

 ∑ and p∑ ↓ refractory period → potentiate re-entry
 Vagal stimulation → unequal shortening of atrial refractoriness → heterogeneity
 Simultaneous stim of both = ↑ vulnerability

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9
Q

Afib: atrial stretch

A

 Effective refractory period ↑ in thinner areas → dispersion of refractoriness

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10
Q

Afib: # of wavelets

A

 Multiple re-entrant circuits
 To be perpetuated: >6 wavelets must be propagating at the same time
* # of wavelets → correlation to coarse vs fine Afib
* Coarse Afib: more organized pattern of re-entry
 Propensity determined by size of atria, size of conduction block, wavelength
 Atrial refractory period: ↑ with body size
 Longer wavelength = fewer wavelets
* 8cm = critical length
* ↑ ∑ and p∑ shorten wavelength → ↑ likelihood for Afib

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11
Q

Afib: electrical remodeling

A

 Physiologic adaptation of ↑HR
 Atrial refractory period shorten → change in composition of ion channels responsible for repol
 Not instantly reverse with conversion → ↑ likelihood to return in Afib following conversion

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12
Q

Afib pathology changes

A

 Transmission electron micrographs of atrial myocardium showed:
* Mitochondrial swelling
* ↓density and organization of cristae
* Cytosolic Ca2+ overload
* Fibrosis
* Myocytolysis
* Cellular hypertrophy
* Alteration in gap junctions

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13
Q

Afib: influence of AV nodal conduction

A

 Determine ventricular response rate
* Many penetrate only partially → varying degree of AV nodal block
* Concealed conduction

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14
Q

AVNRT

A

Triggered by APC
Dual AV node pathway: fast and slow

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15
Q

Automatic junctional tachycardia

A

o Negative P waves in superior leads II, III, aVF
 Before (high junctional) or after (low junctional) QRS
o Rare to have normal to long P-R → more likely coronary sinus rhythm

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16
Q

OAVRT

A
  • Orthodromic (bypass tract-mediated) macro-re-entrant tachycardia: accessory pathway
    o Depend on location/direction of conduction in AP
    o May cause short P-R and delta waves
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17
Q

Substrate for arrhythmia

A

structural or physiologic abnormality
o Region of damage tissue → slowed conduction
o Abnormality in depol/repol channels → prolong AP duration

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18
Q

Triggers for arrhythmia onset

A

o Premature beat
o Change in HR → can allow EADs (bradycardia) or DADs (tachycardia)

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19
Q

Modulators of arrhythmias

A

o Catecholamines
o Ischemia
o Electrolyte changes
o Alterations in autonomic tone

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20
Q

Decision for tx

A

depend on c/s and hemodynamic compromise
o Hemodynamic compromise
 Occasional premature complexes, short bursts → no clinical importance
 Sustained SVT or >8-10s → ↓CO, BP, CA perfusion
* ↓ coronary flow from ↓ diastolic interval + ↓AoP
 Chronic ↑HR >250bpm for >3-4weeks → tachycardiomyopathy
* Reversible if HR controlled
 Afib = loss of atrial systole → ↓ SV of 20%

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21
Q

Risk of sudden death

A

 ↑ catecholamines → ↑ ischemia
 Myocardial failure
 Degeneration to Vfib

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22
Q

Goals/criteria for tx

A

 Return hemodynamic stability
 Conversion of the arrhythmia
* Most dogs → sinus rhythm not obtainable
o From cardiac pathology + anlarged atria
o Longer arrhythmia persist → less likely to convert
o ↑ vagal tone: ↓ atrial refractory period + ↑ dispersion of refractoriness

  • Drugs may ↑ or ↓ # of wavelets → determine if drugs stabilizes or convert arrhythmia
    o Effect on wavelength
    o ↑ excitable gap can abolish re-entrant circuit (area of recovered and excitable myocardium)
    o Converting drugs may initially ↑ ventricular response rate

 Control ventricular response rate

  • Vary depending on type of arrhythmia, concealed conduction, AV node integrity, level of autonomic tone
     If ∑ tone is elevated, may not terminate arrhythmia
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23
Q

Use-dependency

A

antiarrhythmic action depends on HR
o Reverse use-dependency: ↑HR → ↓ anti arrhythmic action
 If drug has an effect on AP duration: ex. Sotalol will ↑ AP duration, but ↓ effect at ↑HR because of shortening of AP

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24
Q

Afib: multiple wavelet model

A

o Multiple chaotic wavefront through atrial myocardium
o Self sustained Afib → needs critical # wavefront coexisting
o Occurs when trigger (APC, rapidly firing focus, small re-entry site) + substrate to maintain are present

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25
Q

Afib: predisposing factors

A

o High vagal tone
 Ach: ↓ refractory period non uniformly → heterogeneity of refractoriness
o Short effective refractory period
o Dispersion of refractoriness = heterogeneity of atrial myocardium → electrical or physical
o Large atrial myocardial size
 Intense exercise w ↑ LAP → lead to ↑ atrial stretch and related APCs
 Activation pathways are ↑ length → ↑ chances of circus mvt
o Slowed conduction velocity
o Structural obstacles/lesions (ie. Fibrosis)
o Transient K+ depletion

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26
Q

Afib: initiation

A

o Rapid atrial stimulation
o APC → start a circus mvt of depol around the atria
 Require large mass of tissue suitable for refractory and excitable cell

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27
Q

Afib: consequences days to weeks

A

Loss of atrial contractile function
 20% of ventricular filling → not attributed to c/s at rest (passive filling is sufficient)
* More important contribution during exercise can affect performance
* ↑ ∑ tone: ↑AV node conduction → disproportionate tachycardia

28
Q

Afib: surface mapping of atrial activity

A

o Sinus rhythm: wavefront is conducted → surrounding tissue is refractory
o Afib: wavefront has adjacent excitable tissue that can conduct depol

29
Q

Most common arrhythmia in cattles/ predisposing factors

A
  • Afib = most common arrhythmia in cattle
    o Associated w GI disorders → ↑ vagal tone
    o Functional → no structural cardiac dz
    o Maintained by large atrial mass → permit re-entry if
     Short refractory period
     Slowed conduction
  • APCs: may occur as commonly as Afib in cattle w GI dz
    o May precede/predispose to Afib
30
Q

Afib in cattles reported w/ which med

A
  • Neostigmine: anticholinesterase agent → prolong Ach effect at synapse
    o Facilitate transmission of nerve impulse in autonomic ganglia → ↑ vagal activity
     Not cross blood brain barrier (unlike physostigmine)
     Locally ↑ [Ach]: used for tx of postsx ileus, myasthenia gravis, neuromuscular blockade
    o Most common cardiovascular side effect: bradycardia → ↑ vagal tone at SA node
    o Report 3 cattles w GI dz developed Afib w neostigmine administration
     2 converted back to sinus rhythm after neostigmine was stopped
31
Q

Electrolyte abn in cattles and Afib

A
  • HypoK+ and hypoCa2+ documented in cattle w Afib → role unclear
    o Can lead to slowed conduction of AP → ↑ potential of re-entrant arrhythmias
    o Seem to be major risk factor to development of Afib and APCs
32
Q

What are accessory pathways

A

congenital muscular bundle (Kent bundle) remaining after formation of fibrous skeleton
o Penetrate fibrous skeleton → direct connection btw atria and ventricles
 2nd conduction pathway + AV node
o Isolated or multiple, most commonly around TV annulus

33
Q

AP are most common in

A

young Labradors <2y/o, Boxers, American Short hairs with HCM

34
Q

AP classified based on

A

anatomical site
o L and R lateral
o L and R anterior
o Antero-septal
o Mid-septal

35
Q

Characteristics of electrical conduction in AP

A

: bi/unidirectional, antegrade or retrograde
o Bidirectional in 1/3 of cases
o Unidirectional, retrograde in 2/3 of cases

36
Q

What is ventricular pre-excitation and when do we see it

A

with antegrade conduction through accessory pathway
o Early activation of ventricles from accessory pathway
o Conduction through accessory pathway
 All or none rule → conduct impulse w/o delay or block
 No decremental conduction

37
Q

ECG ventricular pre-excitation

A

short PR, delta wave, wide QRS complex
 Overt ventricular pre-excitation
 Wide QRS represent fusion beat btw wavefront from accessory pathway and AV node

38
Q

ventricular pre-excitation no sign on ECG = name?

A

non manifest

39
Q

ventricular pre-excitation: Degree of PR interval shortening depend on

A
  • Conduction time through accessory pathway and antegrade refractory period
  • Antegrade conduction time through AV node and refractory period
  • Influence of autonomic nervous system
  • Distance from atrial insertion site, accessory pathway and normal conduction system
  • Intra-atrial conduction time
  • Refractory period of atrial myocardium
40
Q

o 3 mechanisms for normal PR with pre-excitation

A

 Intra-atrial conduction delay → prolongs initial portion of PR
 Long distance btw atrial insertion of accessory pathway and SA node
 Slow conduction in accessory pathway

41
Q

Intermittent pre-excitation/pre-excitation alternans mechanisms

A

 Phase 3 or 4 block in accessory pathway
 Concealed conduction through accessory pathway from ectopic complexes
 Supernormal conduction
 Regular antegrade block of accessory pathway with longer refractory period
 Impedance mismatch at point of insertion of accessory pathway to ventricular muscle
 ↑vagal tone during respiration → greater effect on accessory pathway vs AV node

42
Q

What is necessary for formation of re-entry circuit

A

retrograde conduction is mandatory for formation of macro re-entrant circuit
o Orthodromic AV reciprocating tachycardia
o Permanent junctional reciprocating tachycardia

43
Q

OAVRT circuit

A
  • Activation always results from normal conduction down AV node
  • Eccentric retrograde atrial activation → starts away from AV node
    o Sequential activation of both atria
44
Q

Trigger/mechanism OAVRT

A

: triggered by APC/VPC
o APC blocked antegrade in accessory pathway → conducted in AV node → ventricular depolarization
 Accessory pathway recovered → conduct impulse retrograde to atria → atrial depol
 AV node recovered → conduct impulse again → macro re-entrant circuit
o VPC blocked retrograde in AV node → conducted in accessory pathway → atrial depolarization
 AV node recovered → conduct impulse retrograde to ventricles → ventricular depol
 Accessory pathway recovered → conduct impulse again → macro re-entrant circuit
o Can also be terminated by a premature beat entering the circuit

45
Q

ECG features OAVRT

A

o Sudden initiation (APC)/termination
o Narrow QRS: normal duration/morphology → conduction along AV node
o Regular RR, rapid
 Alternation of cycle length in rare cases
* Simultaneous presence of multiple accessory pathways with different conduction time
* Alternation of conduction through fast and slow AV nodal pathways
o Electrical alternans: beat to beat variation in R wave amplitude >0.1mV
o Ventriculo atrial conduction with 1:1 ratio → negative P’ wave in ST segment
o Short R-P’ interval → <50% R-R interval
 RP’/P’R ratio <0.7

46
Q

Permanent junctional reciprocating tachycardia circuit

A
  • Form of reciprocating tachycardia
    o Antegrade limb: AV node
    o Retrograde limb: R postero-septal accessory pathway
     Unidirectional retrograde conduction
     Decremental properties
47
Q

ECG features permanent junctional reciprocating tachycardia

A

o Narrow QRS
o Ventricular rate 230-250bpm
o Regular RR with cycle length irregularity → variation of ventriculo-atrial conduction along accessory pathway (decremental conduction)
o Electrical alternans
o Ventriculo atrial conduction with 1:1 ratio
o Long/variable RP’ with RP’/P’R ratio >0.7

48
Q

Pre-excited tachycardias

A
  • Accessory pathway with short antegrade refractory period
    o Ability to conduct fast HR caused by SVTs
    o Short refractory period → ability to create fast ventricular rates
49
Q

ECG features of preexcited tachycardias

A
  • ECG characteristics
    o Wide QRS
    o Regular RR
    o Fast HR
  • Afib with intermittent conduction through AP → only pre-excited SVT described in dogs
50
Q

Antidromic AV reciprocating tachycardia

A
  • Same anatomical circuit as OAVRT but opposite impulse direction
    o Ventricles activated by accessory pathway
    o Atria activated by AV node
51
Q

ECG features of antidromic AVRT

A

o Wide QRS
o Regular RR
o P’ wave w/i QRS complex
* Not described yet in dogs/cats

52
Q

What is meant by longitudinal dissociation of the AV node?

A
  • AV node is divided into fast and slow pathway
    o Slow pathway: inferior to main body of AV node
     Fast recovery period
    o Fast pathway: anterosuperior to main body of AV node
     Slow recovery period
53
Q

Differences OAVRT vs AVNRT

A
  • Mechanism of re-entry:
    o OAVRT/AAVRT/WPW are characterized by the presence of an AP (Kent’s Bundle) bypassing the AV node
    o AVNRT: the re-entry circuit is in the AV node
  • Pre-excitation: only seen w/ AP
    o Not present in AVNRT: PR is normal or prolonged
54
Q

Types of AP

A
  • Bundle of Kent → direct AV connections
  • James’ fibers → atrionodal tracts (atrium to low AV node)
  • Mahaim’s fibers → nodoventricular tracts
55
Q

Wolff-Parkinson-White syndrome

A
  • Ventricular pre-excitation with c/s related to episodes of paroxysmal SVT
  • Pre-excitation in sinus rhythm via Bundle of Kent accessory pathway
    o Equivalent of OAVRT
56
Q

ECG features WPW

A

o Short PR, delta wave
o Delta wave: slurred and broad QRS

57
Q

Lown-Ganong-Levine syndrome

A
  • Pre-excitation in sinus rhythm via James’ fibers accessory pathway
58
Q

ECG features LGL

A

o Short PR
o No delta wave or slurring of R wave → normal ventricular activation
Narrow QRS

59
Q

What is the Concertina effect relative to the WPW type syndrome?

A
  • Cyclic pattern of PR interval and QRS duration
  • Progressively more prominent preexcitation of QRS followed by gradual diminution
    o Constant HR
    o Progressive ↓PR with ↑ QRS width
  • Predictor of long refractory period → ↓ risk of sudden death
60
Q

How does the term “fusion” have relevance in WPW pre-excitation?

A
  • Refer to anterograde conduction through accessory pathway and AV node
  • Fusion of waveforms
    o Short PR, slurred R wave, delta wave → wide QRS
    o Slow activation myocyte→ myocyte through accessory pathway fusing with normal His Purkinje activation
61
Q

What drugs are likely to break a re-entrant SVT associated with WPW syndrome? Why?

A

Class IC and III will slow conduction
* Procainamide, lidocaine most effective

  • Directed at the accessory pathway of AV node
    o Both important components of re-entry circuit
    o Accessory pathway conduction:
     Na+ dependent fast inward current for impulse transmission

o AV node conduction: Ca2+ slow inward current
* Electrical cardioversion or radiofrequency ablation

62
Q

AV nodal reciprocating tachycardia mechanism

A
  • Anatomical re-entry circuit including AV node and surrounding atria
  • AV node is divided into fast and slow pathway → LONGITUDINAL DISSOCIATION
    o Slow pathway: inferior to main body of AV node
     Fast recovery period
    o Fast pathway : anterosuperior to main body of AV node
     Slow recovery period
  • Mechanism
    o Premature beat → refractory fast pathway → antegrade conduction through slow pathway
    o Slower conduction velocity → reach distal AV node after fast pathway has recovered
    o Retrograde conduction through fast pathway
63
Q

Forms of AVNRT

A

o Slow-fast → common
 Antegrade through slow pathway, retrograde through fast pathway
o Fast-slow → uncommon
o Intermediate

Not documented in dogs

64
Q

ECG features AVNRT

A

o No P waves → retrograde depol of atria occurs at same time of QRS
 If P waves, negative in lead II, III, aVF
o Regular RR
o Paroxysmal

65
Q

What is an echo beat

A

single impulse conducted retrogradely

8. ECG (19 decks)

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