2.3 Electrocardiogram (ECG) Interpretation & Antiarrhythmic Therapy

ECG Interpretation & Antiarrhythmic Therapy

Core Knowledge: Continuous electrocardiographic (ECG) monitoring is foundational in the veterinary emergency room and intensive care unit. Advanced critical care specialists must rapidly interpret complex dysrhythmias, distinguish life-threatening ventricular ectopy from benign escape rhythms, and choose targeted antiarrhythmic pharmacotherapy based on cellular electrophysiology.

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1. Systematic Lead II ECG Interpretation

ECG interpretation must follow a rigorous 5-step diagnostic sequence to avoid missing subtle conduction abnormalities:

1. What is the Heart Rate? Calculate instantaneous rate (at standard paper speed: $25 \text{ mm/s}$ or $50 \text{ mm/s}$) or mean rate (number of complexes in 30 large boxes at $25 \text{ mm/s} \times 10$). Normal resting canine HR: 60–140 bpm (giant breeds 60–100, toy breeds up to 160); Feline HR: 140–220 bpm.
2. Is the Rhythm Regular or Irregular? Regular, regularly irregular (e.g., normal respiratory sinus arrhythmia in canines), or irregularly irregular (e.g., atrial fibrillation).
3. Are there Distinct P Waves? Are they positive in Lead II? Do they have normal height and duration? (Absence suggests atrial standstill, hyperkalemia, or atrial fibrillation).
4. What is the Relationship Between P Waves and QRS Complexes? Is there a P wave for every QRS? Is there a QRS for every P? Is the PR interval constant or variable?
5. Are the QRS Complexes Narrow/Normal or Wide/Bizarre? Narrow/upright complexes originate above the bundle branches (supraventricular); wide, bizarre complexes originate from ectopic ventricular foci or aberrant ventricular conduction.

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2. Bradyarrhythmias & Conduction Blocks

Bradyarrhythmias compromise cardiac output ($CO = \text{Stroke Volume} \times \text{Heart Rate}$) when compensatory stroke volume increases can no longer offset profound rate drops.

Sinus Bradycardia & Sick Sinus Syndrome (SSS)

• Sinus Bradycardia: Normal sinus rhythm at a rate $<60 \text{ bpm}$ in dogs or $<140 \text{ bpm}$ in cats. Caused by high vagal tone, hypothermia, hyperkalemia, elevated intracranial pressure (Cushing's response), or drugs (opioids, $\alpha_2$-agonists).
• Sick Sinus Syndrome (SSS): Idiopathic degeneration of the SA node and cardiac conduction system, highly prevalent in older Miniature Schnauzers, West Highland White Terriers, and Cocker Spaniels. Characterized by sinus arrest with prolonged pauses (>2–3 seconds), lack of escape rhythms, and alternating bouts of supraventricular tachycardia ("brady-tachy syndrome"). Often refractory to medical management, requiring a permanent transvenous pacemaker.

Atrioventricular (AV) Blocks

VTS Exam Pearl: Atropine works by competitively blocking muscarinic receptors at the SA and AV nodes. In 3rd Degree AV Block with an infranodal ventricular escape rhythm, atropine may increase the P wave (atrial) rate but will not increase the ventricular escape rate because ventricular pacemakers have no functional vagal innervation!

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3. Tachyarrhythmias: Supraventricular vs. Ventricular

                  [Tachyarrhythmia Identified on ECG]
                               │
                  Evaluate QRS Morphology
                               │
        ┌──────────────────────┴──────────────────────┐
   [Narrow & Upright]                            [Wide & Bizarre]
   Supraventricular Origin                       Ventricular Origin
        │                                             │
   ┌────┴────────────────┐                       ┌────┴────────────────┐
 [Regular]           [Irregular]               [Rate > 180 bpm]    [Rate 100–160 bpm]
   SVT                 AFib                      V-Tach               AIVR
 (Diltiazem,        (f-waves,                  (Lidocaine,          (Escape rhythm;
  Vagal Maneuver)    Diltiazem+Digoxin)         Procainamide)        DO NOT SUPPRESS!)

Supraventricular Tachyarrhythmias

1. Supraventricular Tachycardia (SVT): Rapid (often 220–350 bpm), regular rhythm with narrow QRS complexes originating above the AV node. Emergency therapy: Vagal maneuvers (ocular pressure, carotid sinus massage), Diltiazem (0.1–0.25 mg/kg slow IV), or Esmolol (0.25–0.5 mg/kg IV bolus over 5 min).
2. Atrial Fibrillation (AFib): Disorganized, rapid atrial depolarization characterized by absence of P waves, undulating baseline fibrillatory "f" waves, and an irregularly irregular ventricular rhythm with narrow QRS complexes. Rapid ventricular response rates (>220 bpm) cause severe pulse deficits and heart failure. Primary emergency goal: Ventricular Rate Control using Diltiazem $\pm$ Digoxin.

Ventricular Tachyarrhythmias

1. Ventricular Premature Complexes (VPCs): Premature, wide, bizarre QRS complexes not preceded by P waves, with a discordant T wave (T wave deflected in opposite direction of QRS) and a full compensatory pause.
2. Ventricular Tachycardia (VTach): Run of $\ge 3$ consecutive VPCs at a rapid rate ($>160–180 \text{ bpm}$). Classified as monomorphic (identical QRS shape) or polymorphic (varying QRS shapes, including Torsades de Pointes).
   • Criteria for Emergency Antiarrhythmic Treatment of VTach:
     • Sustained ventricular rate $>180 \text{ bpm}$
     • R-on-T phenomenon (VPC falls during vulnerable repolarization phase of preceding T wave, triggering VF)
     • Polymorphic / Multiform complexes
     • Hemodynamic compromise (hypotension with MAP $<60 \text{ mmHg}$, pulse deficits, syncope, weakness)
3. Accelerated Idioventricular Rhythm (AIVR / "Slow VTach"): Ventricular rhythm with wide, bizarre QRS complexes at a rate near the patient's normal sinus rate (100 to 160 bpm in dogs). Commonly seen in critical patients recovering from Gastric Dilatation-Volvulus (GDV), splenic torsion/splenectomy, pancreatitis, or myocardial contusions.

   • VTS Warning: AIVR is an essential escape mechanism and must NOT be suppressed with lidocaine! Suppressing AIVR with antiarrhythmics can eliminate the patient's only functional cardiac pacemaker, resulting in fatal asystole.

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4. Vaughan-Williams Antiarrhythmic Classification

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5. Feline-Specific Arrhythmia Precautions & Lidocaine Toxicity

Cats have distinct hepatic metabolism characterized by deficient glucuronyl transferase activity, making them exquisitely sensitive to lidocaine toxicity.

• Lidocaine Toxicity in Felines: Standard canine IV boluses ($2 \text{ mg/kg}$) administered to cats can trigger profound central nervous system toxicity (tremors, seizures, coma) and cardiovascular collapse (refractory bradycardia, AV block, cardiogenic shock).
• Feline Clinical Rule: Avoid IV lidocaine boluses in cats. If essential for refractory ventricular arrhythmias when other agents fail, use ultra-conservative micro-doses (0.25 to 0.5 mg/kg slow IV over 5 to 10 minutes) under continuous ECG monitoring.