Chapter 48 - ventricular tachyarrhythmias Flashcards
Firing rate of Purkinje fibres?
30-40 bpm in dogs
60-130 bpm in cats
List three mechanisms of ventricular tachyarrhythmias
reentry
enhanced automaticity
triggered activity
expected rates of idioventricular rhythm, AIVR and VT?
idioventricular = 30-40 (dogs), 60-130 (cats) AIVR = between the two VT = >150-180 (dogs), >220 (cats)
difference between sustained & non sustained VT? significance?
> 30s, <30s
1st usually clinically insignificant
define incessant VT and VT storm
recurrent episodes of sustained VT w/in 24h
ECG features of VT
wide bizarre QRS complexes, >0.06s in dogs, >0.04s in cats, followed by wide T wave in opposite direction
3 most reliable features of VT (cf SVT w/ aberrant ventricular conduction)
AV dissociation
fusion beats
capture beats
why is AV dissociation not a perfectly sensitive feature?
if there is apparent association w/ independent atrial activity or retrograde ventricular conduction to the atrium –> signs of association don’t rule out VT
why do fusion beats and capture beats occur?
two pacemakers competing (overdrive suppression leads to inhibition of slower foci by faster foci)
if unable to differentiate between VT and SVT, what should you use to treat?
treat for VT (lidocaine) as safer - calcium channel blockers, B blockers etc for SVT will be ineffective for VT and worsen hypotension dt vasodilation/negative inotropic effects
four electrolyte imbalances that can contribute to VT
hypokalemia (increases phase 4 depolarisation & prolongs action potential, risk for digoxin tox)
hypomagnesemia (needed for Na-K-ATP pump to maintain K+ conc)
hypocalcemia
hypercalcemia
6 drugs that can prolong QT segment, predisposing to VT
procainamide, sotalol, domperidone, cisapride, chlorpromazine, erythromycin
5 noncardiac causes of VT
hypoxia electrolyte disturbances acid-base disturbances sympathetic stimulation drugs
10 cardiac causes of VT
cardiac tumors (+/- tamponade) myocarditis endocarditis ischemia DCM (esp Dobies) ARVC inherited ventricular arrhythmia of GSDs severe subaortic stenosis pulmonic stenosis cats: HCM, concentric hypertrophy 2ndary to hypertension, hyperthyroidism
expected progression of DCM in dobies
occult stage w/ echo signs of LV dysfxn (30% risk of sudden death) can last 2-4y
overt w/ CHF (30-50% risk of sudden death)
most common origin of ventricular octopus in Dobies with DCM?
left ventricle - leads to right bundle branch block morphology
prevalence of arrhythmias in DCM?
21% all breeds
16% Newfies
92% Dobies
Indicators to treat VT?
symptomatic
>180-200 (hemodynamic compromise)
polymorphic
R-on-T alone may not be enough by itself
Why not just treat anyway?
No evidence it will prevent sudden death
May precipitate it (all antiarrhythmics are proarrhythmic)
First line treatment for VT?
Lidocaine (class IB)
Dogs: 2mg/kg q10-15min up to 4, CRI 25-80mcg/kg/min (beta blockers preferred in cats)
Can follow w/ oral mexiletine (IB) + atenolol (II)
If lidocaine doesn’t work?
Procainamide (class IA) 10-15mg/kg IV over 1-2min, 25-50mcg/kg/min CRI, can follow with orals
When to use B blockers? name 2
if sympathetically driven VT esp pheochromocytoma, thyrotoxic disease in cats - careful with ventricular dysfunction, can cause cardiovascular collapse (negative inotropy)
Esmolol, propranolol
class III drug of choice?
sotalol 1-3mg/kg q12h PO
common side effect of amiodarone? class?
anaphylaxis-like reactions (urticaria, facial edema) Class III (also Ia, II, IV)
The role of magnesium therapy in VT remains to be defined. T/F?
T
Other potential treatments?
sedation/anaesthesia (if high sympathetic output) rapid pacing (overdrive suppression GSDs w/ inherited ventricular arrhythmias) synchronized electrical cardioversion/defib
suggested minimum ECG monitoring period after starting treatment for VT?
min 24h
ECG features of VT
1) wide QRS complex
2) AV dissociation
3) fusion beats
4) capture beats
Most common non-cardiac causes of VT
1) hypoxemia,
2) electrolyte imbalance (hypokalemia, hypomagnesiumemia, hypocalcemia, hypercalcemia)
3) acid-base disorders
4) drugs (increase adrenergic tone)
Most common cardiac disease associated with VT
1) ARVC in Boxers
2) DCM in Dorbie
Other cardiac disease associated with VT (aside from ARVC and DCM)
cardiac tumor, myocarditis, endocarditis, ischemia
cat: idiopathic HCM, concentric hypertrophy secondary to hyperT4 or systemic hypertension
T/F: anti-arrhythmic drugs do NOT prevent sudden death
True
T/F: When the origin of a wide QRS tachycardiac cannot be determined (SVT vs VT), must be managed as if it were VT
True, because drugs used to stop SVT or to slow the ventricular response rate to rapid atrial impulses (i.e., calcium channel blockers and β-blockers) do not interrupt VT and worsen hypotension with their vasodilatory or negative inotropic effects.
Rate of Purkinje fiber’s working as pacemaker?
Dog (30-40 bpm), Cat (60-130 bpm)
Three most reliable diagnostics criteria of VT
1) AV dissociation 2) capture beat 3) fusion beat
T/F: In ARVC, ventricular ectopies typically have a left bundle branch block morphology, indicating their right-sided origin
True
Causes of slower non-sustained VT and AIVR
GDV, HBC, metabolic imbalances
ECG characteristics of VT indicators of risk for sudden death and influence decision of treatment
1) polymorphic VT, continuously changing QRS
2) sustained VT with rates greater than 180-200 bpm
3) R on T- increased risk for VT and sudden death from V-fib
Maximum dose of lidocaine recommendation?
8 mg/kg/hr
What can be used for VTs that do not respond to lidocaine.
Pracanamide
Drug for long-term management of VT, main anti-arrhythmic drug?
Sotalol, (especially in ARVC Boxer), many dogs respond successfully within a few hours of oral administration
What is the common adverse reaction of Sotalol?
Anaphylaxis-like reaction (urticaria, facial edema)
