SVT Flashcards
DDX wide complex tachycardia
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
Chung’s phenomenon
wider, ↓ amplitude P wave results from aberrant atrial conduction from the previous premature complex
Mechanism of vagal maneuver
↑ 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
SVT
A flutter
Afib
AVNRT
Automatic junctional tachycardia
OAVRT
Atrial flutter vs other SVT
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
Afib predisposing factors
Critical mass
Autonomic influence
Atrial stretch
Number of wavelets
Electrical remodeling
Afib: critical mass
Needs myocardial area of adequate size
Afib: vagal tone
∑ and p∑ ↓ refractory period → potentiate re-entry
Vagal stimulation → unequal shortening of atrial refractoriness → heterogeneity
Simultaneous stim of both = ↑ vulnerability
Afib: atrial stretch
Effective refractory period ↑ in thinner areas → dispersion of refractoriness
Afib: # of wavelets
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
Afib: electrical remodeling
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
Afib pathology changes
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
Afib: influence of AV nodal conduction
Determine ventricular response rate
* Many penetrate only partially → varying degree of AV nodal block
* Concealed conduction
AVNRT
Triggered by APC
Dual AV node pathway: fast and slow
Automatic junctional tachycardia
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
OAVRT
- 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
Substrate for arrhythmia
structural or physiologic abnormality
o Region of damage tissue → slowed conduction
o Abnormality in depol/repol channels → prolong AP duration
Triggers for arrhythmia onset
o Premature beat
o Change in HR → can allow EADs (bradycardia) or DADs (tachycardia)
Modulators of arrhythmias
o Catecholamines
o Ischemia
o Electrolyte changes
o Alterations in autonomic tone
Decision for tx
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%
Risk of sudden death
↑ catecholamines → ↑ ischemia
Myocardial failure
Degeneration to Vfib
Goals/criteria for tx
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
Use-dependency
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
Afib: multiple wavelet model
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
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
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
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
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
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
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
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
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
AP are most common in
young Labradors <2y/o, Boxers, American Short hairs with HCM
AP classified based on
anatomical site
o L and R lateral
o L and R anterior
o Antero-septal
o Mid-septal
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
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
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
ventricular pre-excitation no sign on ECG = name?
non manifest
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
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
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
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
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
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
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
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
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
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
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
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
ECG features of antidromic AVRT
o Wide QRS
o Regular RR
o P’ wave w/i QRS complex
* Not described yet in dogs/cats
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
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
Types of AP
- Bundle of Kent → direct AV connections
- James’ fibers → atrionodal tracts (atrium to low AV node)
- Mahaim’s fibers → nodoventricular tracts
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
ECG features WPW
o Short PR, delta wave
o Delta wave: slurred and broad QRS
Lown-Ganong-Levine syndrome
- Pre-excitation in sinus rhythm via James’ fibers accessory pathway
ECG features LGL
o Short PR
o No delta wave or slurring of R wave → normal ventricular activation
Narrow QRS
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
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
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
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
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
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
What is an echo beat
single impulse conducted retrogradely
