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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
Afib: predisposing factors
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
26
Afib: initiation
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
27
Afib: consequences days to weeks
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
Afib: surface mapping of atrial activity
o Sinus rhythm: wavefront is conducted → surrounding tissue is refractory o Afib: wavefront has adjacent excitable tissue that can conduct depol
29
Most common arrhythmia in cattles/ predisposing factors
* 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
Afib in cattles reported w/ which med
* 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
Electrolyte abn in cattles and Afib
* 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
What are accessory pathways
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
AP are most common in
young Labradors <2y/o, Boxers, American Short hairs with HCM
34
AP classified based on
anatomical site o L and R lateral o L and R anterior o Antero-septal o Mid-septal
35
Characteristics of electrical conduction in AP
: bi/unidirectional, antegrade or retrograde o Bidirectional in 1/3 of cases o Unidirectional, retrograde in 2/3 of cases
36
What is ventricular pre-excitation and when do we see it
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
ECG ventricular pre-excitation
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
ventricular pre-excitation no sign on ECG = name?
non manifest
39
ventricular pre-excitation: Degree of PR interval shortening depend on
* 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
o 3 mechanisms for normal PR with pre-excitation
 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
Intermittent pre-excitation/pre-excitation alternans mechanisms
 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
What is necessary for formation of re-entry circuit
retrograde conduction is mandatory for formation of macro re-entrant circuit o Orthodromic AV reciprocating tachycardia o Permanent junctional reciprocating tachycardia
43
OAVRT circuit
* 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
Trigger/mechanism OAVRT
: 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
ECG features OAVRT
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
Permanent junctional reciprocating tachycardia circuit
* Form of reciprocating tachycardia o Antegrade limb: AV node o Retrograde limb: R postero-septal accessory pathway  Unidirectional retrograde conduction  Decremental properties
47
ECG features permanent junctional reciprocating tachycardia
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
Pre-excited tachycardias
* 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
ECG features of preexcited tachycardias
* 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
Antidromic AV reciprocating tachycardia
* Same anatomical circuit as OAVRT but opposite impulse direction o Ventricles activated by accessory pathway o Atria activated by AV node
51
ECG features of antidromic AVRT
o Wide QRS o Regular RR o P’ wave w/i QRS complex * Not described yet in dogs/cats
52
What is meant by longitudinal dissociation of the AV node?
* 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
Differences OAVRT vs AVNRT
* 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
Types of AP
* Bundle of Kent → direct AV connections * James’ fibers → atrionodal tracts (atrium to low AV node) * Mahaim’s fibers → nodoventricular tracts
55
Wolff-Parkinson-White syndrome
* 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
ECG features WPW
o Short PR, delta wave o Delta wave: slurred and broad QRS
57
Lown-Ganong-Levine syndrome
* Pre-excitation in sinus rhythm via James’ fibers accessory pathway
58
ECG features LGL
o Short PR o No delta wave or slurring of R wave → normal ventricular activation Narrow QRS
59
What is the Concertina effect relative to the WPW type syndrome?
* 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
How does the term “fusion” have relevance in WPW pre-excitation?
* 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
What drugs are likely to break a re-entrant SVT associated with WPW syndrome? Why?
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
AV nodal reciprocating tachycardia mechanism
* 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
Forms of AVNRT
o Slow-fast → common  Antegrade through slow pathway, retrograde through fast pathway o Fast-slow → uncommon o Intermediate Not documented in dogs
64
ECG features AVNRT
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
What is an echo beat
single impulse conducted retrogradely

8. ECG (21 decks)

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