CardioBird

Estimated reading time: 3.54 minutes

 

Welcome back to our series, The ECG Decoded: A Veterinarian’s Guide to the Heart’s Rhythm. We’ve journeyed through primary cardiac arrhythmias, but the heart does not beat in isolation. Its electrical activity is exquisitely sensitive to the body’s metabolic milieu and the drugs we administer. This installment focuses on ECG changes that are secondary to systemic disorders and pharmaceuticals—a critical diagnostic skill that prevents misattributing these findings to primary heart disease.

 

Electrolyte Imbalances: Disrupting the Cellular Spark

The heart’s action potential depends on the precise flow of ions. Imbalances directly alter the ECG, often in predictable ways.

• Hyperkalemia: Elevated potassium is a classic, potentially lethal cause of ECG changes. It progressively suppresses myocardial conduction.
  • ECG Sequence: Tall, peaked T waves → Widened QRS complexes → Loss of P waves → Sine wave pattern → Asystole.
  • Context: Common in urinary obstruction, renal failure, hypoadrenocorticism (Addison’s disease), and iatrogenic causes.
• Hypokalemia: Low potassium increases myocardial cell excitability and delays repolarization.
  • ECG Hallmarks: Flattened or inverted T waves, prominent U waves, ST segment depression. It can predispose to serious arrhythmias, including ventricular tachycardia and Torsades de Pointes.
  • Context: Seen with chronic diuretic use, vomiting, diarrhea, and hyperaldosteronism.
• Hypercalcemia & Hypocalcemia: Calcium primarily affects the plateau phase (Phase 2) of the action potential.
  • Hypercalcemia: Shortens the QT interval.
  • Hypocalcemia: Prolongs the QT interval.
  • Context: Renal disease, parathyroid disorders, critical illness.

 

The Systemic Disease Connection

Many non-cardiac illnesses create a metabolic environment that stresses the heart and conduction system.

• Endocrinopathies:
  • Hypothyroidism: Often associated with sinus bradycardia and, uncommonly, with conduction delays. Resolution with thyroid supplementation supports the link.
  • Hyperthyroidism (Cats): A classic cause of sinus tachycardia. It can also precipitate supraventricular tachycardias (e.g., atrial tachycardia) and lead to secondary cardiac remodeling.
• Critical Systemic Illness: Conditions like sepsis, pancreatitis, gastric dilatation-volvulus (GDV), and severe anemia can induce:
  • Sinus Tachycardia: A compensatory response.
  • Supraventricular and Ventricular Ectopy: Due to catecholamine surge, hypoxia, or myocardial ischemia.
  • Non-Specific ST-Segment Changes: Indicative of generalized myocardial stress or electrolyte shifts.

 

Drug Effects: Therapeutic and Toxic Signatures

Many common veterinary medications have direct electrophysiological effects, which can be therapeutic, incidental, or toxic.

• Anesthetics & Sedatives: Drugs like dexmedetomidine and alpha-2 agonists are potent vagal stimulants, predictably causing a marked sinus bradycardia and first- or second-degree (Mobitz Type I) AV block. These are expected findings but must be monitored.
• Positive Inotropes:
  • Digoxin: Has a narrow therapeutic index. Therapeutic levels can cause PR interval prolongation and sagging ST depression. Toxicity is notorious for causing almost any arrhythmia, with ventricular bigeminy/trigeminy and supraventricular tachycardia with AV block being classic signatures.
• Antiarrhythmics: Ironically, these can be pro-arrhythmic. A drug prescribed for ventricular ectopy (like sotalol) can excessively prolong the QT interval, risking Torsades de Pointes. Monitoring the ECG after initiating such therapy is paramount.
• Chemotherapeutics & Antimicrobials: Some drugs, like doxorubicin, are directly cardiotoxic, leading to irreversible myocardial damage and subsequent arrhythmias or low-voltage complexes. Others may cause electrolyte disturbances that secondarily affect the ECG.

 

A Practical Diagnostic Mindset

When confronted with an ECG abnormality, especially in a patient without historical cardiac disease, always ask: “Could this be secondary?”

1. Review the Patient’s Problem List: Renal values, electrolytes, endocrine status, and active illnesses.
2. Scrutinize the Medication History: Include all recent anesthetics, chronic medications, and supplements.
3. Correlate the ECG Pattern with Known Causes: Peaked T waves should immediately trigger a potassium check. A new bradycardia post-sedation is likely drug-related.
4. Re-evaluate After Treating the Primary Issue: Resolution of an arrhythmia after correcting hypokalemia or treating hyperthyroidism confirms the secondary nature.

At CardioBird, we integrate this systemic perspective into our AI-ECG analysis. Our platform doesn’t just identify an arrhythmia; it flags patterns strongly associated with metabolic disturbances (like hyperkalemia) and considers the patient’s clinical context. We aim to be your expert partner, helping you distinguish between a primary cardiac event and a secondary electrical clue pointing to a critical systemic problem—ensuring you treat the true cause, not just the ECG tracing.

 

This concludes our series on interpreting the ECG. In our final installment, we will synthesize this knowledge by exploring the hemodynamic consequences of arrhythmias and their related clinical signs, completing the journey from electrical signal to patient outcome.

 

The CardioBird Team