CardioBird

Estimated reading time: 3.93 minutes

 

Welcome back to our series, The ECG Decoded: A Veterinarian’s Guide to the Heart’s Rhythm. We now arrive at one of the most critical topics in veterinary cardiology: Ventricular Arrhythmias. These rhythms originate in the ventricles themselves, bypassing the heart’s coordinated conduction system. They range from occasional, benign “blips” to immediate, life-threatening emergencies. This guide will equip you with a clear, practical framework for recognizing, classifying, and responding to these potent cardiac alarms.

 

The Hallmark of Danger: The Wide QRS Complex

The single most important ECG feature of a ventricular arrhythmia is a wide and bizarre QRS complex (typically > 70 ms in dogs). This occurs because the electrical impulse does not travel via the fast His-Purkinje network. Instead, it spreads slowly from cell to cell through the ventricular muscle, resulting in a prolonged, often notched, and abnormally shaped QRS. Recognizing this pattern is the first and most crucial step.

 

A Spectrum of Severity: From PVCs to VF

Ventricular arrhythmias are not a single entity but a spectrum defined by their frequency, morphology, and hemodynamic impact.

1. Premature Ventricular Complexes (PVCs)
   A PVC is a single, early beat arising from an irritable ventricular focus.
   • ECG Hallmarks: It appears as a premature, wide, and bizarre QRS complex that is not preceded by a P wave. It is typically followed by a compensatory pause—a longer-than-normal interval before the next normal beat, as the SA node’s rhythm is reset.
   • Clinical Significance: Occasional PVCs can be normal in some patients. However, increasing frequency (> 20-30/hr), multiform morphology (different shapes), or runs of consecutive PVCs signal more significant underlying heart disease, electrolyte imbalance, or systemic illness.
2. Ventricular Tachycardia (VT)
   VT is defined as three or more consecutive PVCs at a rapid rate (>160 bpm in dogs). This is where clinical urgency escalates.
   • ECG Hallmarks: A run of rapid, regular or irregular, wide QRS complexes. P waves are usually absent or dissociated (marching independently at a slower rate).
   • Types & Urgency:
     • Non-Sustained VT: Short bursts (< 30 seconds) that terminate on their own.
     • Sustained VT: Lasts > 30 seconds or requires intervention to stop. This is a true medical emergency.
     • Monomorphic VT: All QRS complexes look identical, often suggesting a single irritable focus.
     • Polymorphic VT: QRS complexes vary in shape, indicating electrical instability. Torsades de Pointes, a specific type associated with a long QT interval, falls into this category.
3. Ventricular Flutter & Fibrillation (VF)
   These are terminal, chaotic rhythms where the ventricles quiver rather than contract, producing no effective cardiac output.
   • Ventricular Flutter: Appears as a rapid, sinusoidal waveform without distinct QRS complexes.
   • Ventricular Fibrillation: A completely chaotic, irregular baseline with no identifiable waves. This is the rhythm of cardiac arrest, requiring immediate CPR and defibrillation.

 

The Critical Distinction: VT vs. SVT with Aberrancy

One of the most challenging and vital tasks is distinguishing VT from a Supraventricular Tachycardia (SVT) with a wide QRS complex (due to a bundle branch block). Misdiagnosis can lead to fatal therapeutic errors. While a full discussion of differentiating criteria (Brugada criteria, etc.) is beyond this summary, key principles include:

• AV Dissociation: The presence of independent P waves (marching through the wide QRS rhythm) is virtually diagnostic of VT.
• Extreme Axis: A QRS axis that is “northwest” or wildly different from normal sinus beats strongly suggests VT.
• History: A patient with known structural heart disease (e.g., DCM, ARVC) is far more likely to have VT.

When in doubt, treat a regular, wide-complex tachycardia as VT. It is the safer assumption.

 

Causes and Clinical Approach

Ventricular arrhythmias are often a symptom, not the primary disease. Common triggers include:

• Structural Heart Disease: Myocardial failure (DCM), infiltration, or infarction.
• Breed-Specific Cardiomyopathies: e.g., Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC) in Boxers.
• Systemic Illness: Severe metabolic derangements (e.g., hypokalemia, hypoxia), gastric dilatation-volvulus (GDV), pancreatitis, or sepsis.
• Drugs/Toxins: Certain anesthetics, sympathomimetics, or cardiac glycosides.

Your clinical approach must be two-pronged: 1) Assess the immediate hemodynamic stability of the patient (weak, collapsed, pale?), and 2) Investigate the underlying cause. Treatment ranges from monitoring occasional PVCs to emergency intravenous antiarrhythmics (e.g., lidocaine) and electrical cardioversion for unstable VT.

At CardioBird, we understand the gravity of these rhythms. Our AI-ECG analysis is meticulously calibrated to identify not just the presence of a ventricular arrhythmia, but to classify its type, quantify its burden, and flag concerning patterns like R-on-T phenomenon or polymorphic VT. We provide this analysis with clarity and speed, giving you the confidence to make urgent, life-saving decisions and to monitor the efficacy of treatment over time.

In our next issue, we will explore how systemic conditions and medications can leave their signature on the ECG, often mimicking primary heart disease.

 

The CardioBird Team