Ventricular Tachyarrhythmias Flashcards
(56 cards)
What is the pathophysiological mechanism of a ventricular escape rhythm?
Purkinje fibers = surrogate pacemakers when the sinus and AV nodes fail to function appropriately –> ventricular escape rhythm
This rhythm occurs when the heart’s natural pacemaker fails, and the ventricles generate their own rhythm.
What is the ventricular escape rhythm rate in dogs and cats?
dogs: 30-40 bpm
cats: 60-130 bpm
This indicates a slower heart rate, which can be normal in certain conditions.
Define accelerated idioventricular rhythm (AIVR).
- Ventricular rhythm faster than the physiologic idioventricular rhythm but slower than VT
- rate is within 10% the rate of the underlying sinus rhythm
AIVR is a type of ventricular rhythm that occurs under specific conditions.
What is “overdrive suppression”?
- when both rhythms are seen competing on a surface ECG –> faster rhythm inhibits the slower one (= overdrive suppression)
This means the faster AIVR rhythm inhibits the slower sinus rhythm.
Name 5 common causes of AIVR?
- Trauma
- Metabolic imbalances
- GDV
- Splenic mass
- hepatic mass
These conditions can trigger AIVR as a response to systemic disease.
How long does AIVR typically take to resolve?
≤ 4 days
This spontaneous resolution is a characteristic feature of AIVR.
Define ventricular tachycardia (VT).
3 or more consecutive ventricular beats occurring at a rate > 160 to 180/min
Clinical significant VTs typically >250/min
The specific rate threshold may vary based on clinical context.
What important features of VT determine the clinical consequences of arrhythmia?
- Rate
- Duration
Both factors are critical in assessing the severity and potential impact of VT.
List the 3 electrophysiologic mechanisms of ventricular tachycardia
- Reentry
- Enhanced automaticity
- Triggered activity
Please explain the “reenty” mechanism in the context of VT.
- Requires an impulse to leave a point of departure and return to its starting point with a sufficient delay that the cardiac tissue has recovered its excitability
- usually circles around an area of nonconductive tissue (fibrosis, vessel)
- Shortening of the refractory period + slow conduction favor this self-perpetuating mechanism
Layman terms:
- A signal (impulse) starts to run around the track (normal conduction pathway)
- It leaves its starting point and travels in a loop.
- But instead of stopping after one lap, it keeps going around and around, like a car stuck in a loop.
- Each time it circles back, the track (heart tissue) has had enough time to “reset” and is ready to be excited again — so the impulse keeps triggering new heartbeats too quickly.
For reentry to happen, 3 things usually occur:
- A blocked/damaged area in the heart forces the impulse to take a detour
- heart tissue must recover quickly enough (short refractory period) to let the signal excite it again when it comes back around
- impulse must move slowly enough to allow the loop to keep going and not die out
Please explain the “enhanced automaticity” mechanism in the context of VT.
acquisition of spontaneous depolarization due to altered environment
- membrane potential becomes less negative –> can generate an action potential similar to SN
Analogy:
Think of heart muscle cells like workers in a factory. Only one of them (the sinus node) is supposed to ring the bell to start each shift (heartbeat). But if something changes — like a power surge, heat, or damage — other workers (muscle cells) may start ringing the bell themselves, even when they’re not supposed to.
Now, multiple bells are ringing, causing confusion and chaos — ventricular tachycardia.
Please explain the “triggered activity” mechanism in the context of VT.
Results from small membrane depolarizations that appear after and are dependent on the upstroke of the action potential. They trigger an action potential when they reach the threshold potential.
timing:
1. Early afterdepolarizations: occur during the process of repolarization (e.g. hypokalemia, drug-induced QT prolongation)
2. Delayed afterdepolarization: occur after full repolarization (e.g. intracellular Ca++ overload associated with sustained tachycardia and digoxin toxicity)
Layman:
Your heart cells normally fire off one clean, strong electrical signal (called an action potential) to make the heart contract. After that, the cells reset, so they’re ready for the next signal.
But sometimes, after that main signal, extra little blips (called afterdepolarizations) appear. If these blips are strong enough, they can trigger a whole new heartbeat — one that wasn’t supposed to happen.
Name 4 causes for “enhanced automaticity” as an underlying mechanism for the development of VT
- Hypoxaemia
- Catecholamines
- Electrolyte imbalances
- Cardiac disease (e.g., myocardial infarction)
What are the morphologic classifcations of VT?
- Monomorphic = snigle QRS complex morphologgy
- Pleomorphic = ≥ 2 morphologies during the same VT episode
- Polymorphic = variable morphology on beat-to-beat basis (RR variation)
What is the electrophysiologic mechanism of a monomorphic VT?
reentry
= most common type of VT
Does some variation in morphology rule out “reentry” as a electrophyiologic mechanism for the VT?
No
Apart from morphology, what is another classification system for VT?
Sustained vs. non-sustained
How are sustained and non-sustained VT defined?
non-sustained: <30s (usually asymptomatic)
sustained: ≥ 30s
What is an incessant VT/VT storm?
recurrent episodes of sustained VT during 24-hour period
VT storm = life-threatening emergency
What information do we need In order to interpret an ECG?
- animal’s medical history
- clinical presentation
- cardiac function
How do you obtain a valuable ECG for interpretation?
six-lead ECG recording in RL recumbency
What are the criteria for VT?
- broad QRS tachycardia (dogs > 70ms, cats > 40ms)
- Each QRS is followedy by large T wave directed opposite to QRS deflection
- mostly regular, but can be slightly irregular
What is a broad QRS tachycardia with R-R intervals that vary on a beat-to-beat basis, sometimes changing by 100 msec or more classified (until proven otherwise)?
AFib with aberrant ventricular conduction (BBB)
image: Although wide QRS complexes, the rhythm is irregular (RR intervals variable) –> atrial fibrillation. QRS complexes have a positive polarity in lead I, II, III and aVF –> consistent with a left BBB.
What are possible causes of SVTs with wide QRS complexes on an ECG?
- structural BBB
- functional or rate-related BBB
- accessory AV pathway causing preexcitation (rare)
