Supraventricular Tachycardias Flashcards
(33 cards)
What are SVTs?
rapid cardiac rhythms that require atrial or AV nodal tissue or both for their initiation and maintenance
Nme 8 causes of SVTs
- Sepsis
- Pancreatitis
- splenic torsion
- GDV
- end-stage congenital heart disease
- cardiac neoplasia
- Myocarditis
- Endocarditis
What breeds can have lone atrial fib without underlying disease?
Irish Wolfhound, Great Dane
On what do the clinical symptoms of SVTs depend on?
- rate
- frequency of the arrhythmia
- severity of any organic cardiac dysfunction or other noncardiac diseases
What is a sequaela of sustained + uncontrolled SVT?
tachycardia-induced cardiomyopathy
Name 3 proposed pathomechanism of tachycardia-induced cardiomyopathy
- myocardial energy depletion + impaired energy utilization –> reduced myocardial energy stores
- myocardial ischemia due to persistent supra-physiologic HR resulting in impaired coronary blood flow
- abnormal Ca++ handling at persistent high HR
What is Atrioventricular accessory pathway (Wolff-Parkinson-White-Syndrome)?
congenital muscular bundles penetrate the normal fibrous skeleton between the atria and ventricles –> alternate route of conduction between atria + ventricles
Dogs: often conduct retrograde
Discuss pathomechanisms of sepsis-associated myocardial dysfunction
- myocardial ischemia
- abnormal Ca++ handling effects of tachycardia
- excessive SNS activation –> catecholamine induced toxic effects on cardiomyocytes –> inflammation, oxidative stress, apoptosis, necrosis
- diminished ventricular filling
–> conservative lowering of HR (E.g. esmolol) –> improved mortality in people
How are SVTs classified?
–> based on their site of origin and dependence of the AV node
- Atrial tachyarrhythmias
- sinus tachycardia
- snius nodal reentrant tachycardia
- atrial tachycardia
- multifocal atrial tachycardia
- atrial flutter
- atrial fibrillation - AV nodal tachyarrhythmias
- AV nodal reentrant tachycardia
- AV reentrant tachycardia (accessory pathway)
- junctional tachycardias
What are the ECG changes seen with Afib?
- no P-waves
- “f” waves (fibrillation waves - representing atrial activity)
- fast ventricular response rate (dog: >160/min; cat: >220/min)
- irregularly irregular (chaotic) rhythm
- normal QRS morphology with varying height
Causes: often advanced haeart disease (exception lone AFib)
What are the ECG changes seen with Atrial flutter?
- no P-waves
- “F” waves (flutter waves - saw-tooth atrial activity with slower rate)
- fast ventricular response rate
- RR regular or irregular depending on AV conductino (1:1 to 6:1; often 2:1)
–> unstable rhythm - will degenerate into AFib
Causes: Structural cardiac disease, noncardiac disease
What are the ECG changes seen with Multifocal atrial tachycardia?
- rapid irregular RR
- usually intermittent
- P-wave present but with variable conformation (several atrial ectopic foci)
- variable PR interval
Causes: Pulmonary disease, Cardiac disease, electrolyte disorders, metabolic disorders
–> can degenerate in AFib
What are the ECG changes seen with focal atrial tachycardia? What are common causes?
- regular RR
- sustained or paroxysmal P’’
- P-wave present with retrograde conduction (negative in lead II)
Causes: Hyperthyroidism, Hypokalemia, Digoxin toxicity
What are the ECG changes seen with Atriventricular reentry tachycardia mediated by accessory pathway? What are common causes?
- regular RR
- sustained or paroxysmal
- P’ present with retrograde conduction (negative in lead II)
Caueses: cardiac disease, incidental finding
How is an ECG interpreted?
- Narrow QRS tachycardia?
○ Dogs: <70ms
○ Cats: <40ms
○ Exeption: high septal or fascicular ventricular tachycardias
○ Comparing the QRS complexes during the tachycardia in question with those QRS complexes from either a previous ECG or to sinus complexes - Normal QRS duration
- Normal QRS polarity (mean electrial axis)
- Regular RR interval?
○ Irregular
* atrial fibrillation
* Atrial flutter with varying block
* Multifocal atrial tachycardia
○ Regular
* All others
CAVE: SVTs can uncommonly conduct with either a right, or less commonly a left, BBB = wide and altered QRS morphology
How can you differentiate VT from SVT?
How to approach Tachycardia (decision tree)
Name 10 causes of sinus tachycardia
- Hypovolemia
- Hypotension
- Sepsis
- Anaemia
- Hypoxemia
- CHF
- Pain
- Fear
- Sympathomimetic toxicity
○ Chocolate
○ Albuterol - Disease with accentuated SNS
○ Hyperthyroidism
○ Pheochromocytoma
How to differentiate sinus tachycarida from SVTs
- Intermittent
○ Yes: SVT
○ No: ST - PR interval
○ Short with widening of initial QRS upstroke –> preexcitation –> SVT - P wave morphology
○ Normal: ST
○ Abnormal: SVT - Rate
○ Very fast: SVT (up to 300 bpm)
○ ST: usually <220 bpm - Response to vagal maneuver?
○ Yes: SVT
○ No: ST - Response to IV fluid bolus?
○ Yes: ST - Response to short-acting drug (e.g. diltiazem IV, esmolol)
○ Yes: SVT
What are indications for a vagal maneuver, how is it performed and what is the underlying pathophysiological mechanism?
- therapeutic: initial management of a narrow-complex tachycardia
- diagnostic: Differentiation of SVT from VT/ST
- Application of pressure to
- carotid sinuses (10s)
- Ocular/periorbital region
- Nasal planum
increases parasympathetic output to heart via vagus nerve –> slowing of AV nodal conduction
What is the success rate in people for termination of SVT via vagal maneuvers?
19-54%
What drug classes can be used for the treatment of SVTs? Name examples.
- Beta-blockers (Atenolol, Esmolol, Propanolol)
- Sodium channel blockers (Lidocaine, Procainamide)
- Potassium channel blockers (Sotalal, Amiodarone)
- Calcium channel blockers (Diltiazem, Cardizem)
- Others: Digoxin, Magnesium chloride
What is the initial approach to SVTs?
hemodynamic, respiratory, metanolic and electrolyte support first
–> short and infrequent runs of SVTs without hemodynamic compromise do not require antiarrhythmic therapy
What is the mechanis of drugs like calcium channel blockers and beta blockers, used in the treatment of SVTs?
Slow AV conduction
