Chapter 47 - supraventricular tachyarrhythmias Flashcards
List 4 features that help differentiate between V tach and SVT w/ bundle branch block or antegrade conduction over an accessory pathway
- P waves w/ consistent relationship to QRS suggests SVT
- presence of QRS fusion complexes suggests V tach
- response to vagal manoeuvre suggests SVT
- response to lidocaine suggests V tach
which of the following are characteristic of atrial dependent SVT?
- continues despite AV block
- SVT terminated by VPCs
- SVT terminated by vagal maneuver
1.
Other 2 are characteristic of AV node dependent SVT
List 4 most common SVTs in small animals
atrial fibrillation
intraatrial reentrant tachycardia
orthodromic AV reciprocating tachycardia
automatic atrial tachycardia
Predisposing factors for SVT?
acid-base abnormalities
electrolyte disturbances
severe anemia
hypoxemia
describe the most effective vagal manoeuvre in small animals, effectiveness
sustained, gentle compression is applied for 5-10 seconds over the carotid sinus, immediately caudal to the dorsal aspect of the larynx. most often ineffective
initial drug of choice to terminate AV node SVT? MOA?
want negative dromotropy: in dogs diltiazem at 0.125-0.35mg/kg IV slowly over 2-3min, CRI at same dose/hr. calcium channel blocker (class IV)
what contraindication to use of B blockers (class II) such as esmolol may be present?
impaired ventricular systolic function
signs of calcium channel blocker toxicity?
hypotension
negative chronotropy (impaired SA node discharge)
negative dromotropy (impaired AV node conduction)
negative inotropy
impaired insulin release -> BG rises, intracellular Ca2+ drops
signs of B blocker toxicity?
severe bradyarrhythmias
impaired atrial & ventricular contractility
bronchospasm
decreased glycogenolysis, lipolysis, gluconeogenesis
4 effects of B1 stimulation
primarily heart & adipose tissue, coupling of B1 receptors with adenyl cyclase –> cAMP
- increased HR (stimulation of the funny current & L-type calcium current)
- increased myocardial contractility (L type Ca++ current influx stimulating increased sarcoplasmic reticular Ca++ release)
- improved myocardial relaxation (phosphorylation of phospholamban)
- enhanced automaticity of subsidiary pacemakers
list 4 antiarrhythmics effective for SVTs from the SA node, and 1 most common SVT
Class II (B blockers), Class III, Class IV (Ca++ channel blockers), Digitalis SA nodal reentry
list 3 antiarrhythmics effective for SVTs from the atrial myocardium, and 3 most common SVTs
Class IA, Class IC, Class III
a fib, atrial reentry, atrial automaticity
list 6 antiarrhythmics effective for SVTs from the AV node, and 2 most common SVTs
Class IC, Class II (B blockers), Class III, Class IV (calcium channel blockers), Digoxin, Adenosine
AV nodal reentry, junctional automaticity
list 3 antiarrhythmics effective for SVTs from the accessory pathway, and 1 most common SVT
Class IA, Class IC, Class III
AV reciprocating tachycardia
when/why procainamide?
class IA, prolongs effective refractory period, used for atrial and accessory pathway SVTs after another agent slows conduction (i.e. diltiazem)
dogs: 6-8mg/kg IV over 5-10min, 6-20mg/kg IM, CRI 20-40mcg/kg/min
cats: 1-2mg/kg slow IV, 3-8mg/kg IM, CRI 10-20mcg/kg/min
describe how you would perform a precordial thump, likelihood of success?
sharp concussive blow to left precordium w/ animal in R lat –> myocardial depolarisation, may disrupt reentrant tachycardia circuit. low success rate
SVT can be broadly arranged into what two groups?
Atrial and AV node dependent tachyarrhythmias
T/F: Tachycardiomyopathy can be partially or completely reversed.
True
Why can SVTs cause sudden death?
Myocardial ischemia that gives rise to v-tach and v fib
What are some signs that owners might notice with patients with SVT?
Exercise intolerance, weakness, signs of CHF, GI signs (v, inappetance), collapse, noticeable rapid HR, pulsing of the ears, bobbing of the head
T/F PE findings of patients with supraventricular tachyarrhythmias can be normal.
True
T/f: A narrow QRS complex tachyarrhythmia will almost always be an SVT.
True
Up to what percent of wide complex tachyarrhythmias in humans are ventricular in origin?
80%
What can you use to help you distinguish between SVT and v-tach? (4)
a. ID of P waves
b. QRS fusion complexes (v tach)
c. If tachycardia terminates in response to a vagal maneuver
d. If terminates with administration of IV lidocaine, likely v-tach
If an SVT continues despite AV block, where is it’s origin?
Atrial
If an SVT terminates because of a vagal maneuver, where is it’s origin?
AV node dependent
What are the most commonly occurring SVTs in small animals?
A-fib, intra-atrial reentrant tachycardia, orthodromic AV reciprocating tachycardia, automatic atrial tachycardia
What is the most effective vagal maneuver in small animals?
Carotid sinus massage
What are some negative dromotropic classes of drugs that can be used to interrupt a tachyarrhythmic circuit?
B blockers, Ca channel blockers, adenosine
In one study, what was superior in slowing AV nodal conduction while maintaining a favorable hemodynamic profile?
Diltiazem
The effects of B1 receptor stimulation result in what? (4)
- Increased HR 2ndary to stimulation of the funny current and L-type calcium current
- Enhanced myocardial contractility through L-type calcium current influx stimulating increased sarcoplasmic reticular calcium release,
- Improves myocardial relaxation through phosphorylation of phasolamban
- Enhanced automaticity of subsidiary pacemakers
Name three drug classes that slow AV nodal conduction.
- Digitalis glycosides
- Ca channel blockers
- B blockers
This is a relatively B1 selective blocker that competitively inhibits the effects of catecholamines on cardiac B receptors.
Atenolol
What do class I antiarrhythic drugs block?
Fast Na channels
Name 2 Class III antiarrhythmic agents.
Sotalol and amiodarone
