Cardiology Logo
VETERINARY CLINICAL CARDIOLOGY
CARDIOLOGY CONCEPTS
Electrocardiology
Miscellaneous ECG Abnormalities
1. What are the electrocardiographic signs of hyperkalemia?

Hyperkalemia results in:

  1. Inhibition of atrial myocardial depolarization
  2. Slowing of heart rate
  3. Prolongation of QRS depolarization
  4. And may result in ventricular fibrillation or asystole when very severe

The ECG is a poor substitute for serum potassium levels to determine the degree of abnormality.

ECG Findings:

  1. From reduction of P wave amplitude and prolongation of PR interval to absence of P waves altogether
  2. Increase in QRS duration
  3. Increase of QT duration
  4. Slowing of heart rate
  5. T waves become tall and spiked
  6. Decreased R wave amplitude

Example of Hyperkalemia in a Dog

- Place cursor on the image to see examples of the ECG Findings

Etiology:

  1. Addison’s Disease (hypoadrenocorticism)
  2. Obstructive urinary disease
  3. Oliguric, anuric renal disease
  4. Acidosis
  5. Uncontrolled diabetic ketoacidosis

Treatment:

  1. IV fluids, using 0.9% NaCl (if no urinary obstruction)
  2. Sodium bicarbonate to correct acidosis
  3. Calcium gluconate antagonizes the cardiotoxic effects of potassium
  4. IV glucose and insulin may be needed to drive potassium intracellularly
  5. Treat the underlying disease

Prognosis: Excellent response to prompt therapy

Comments:

  • This disorder must be distinguished from atrial standstill or silent atrium, a diffuse atrial myocardial disorder wherein the atrial tissue is neither capable of initiating an impulse nor being activated (also known as atrioventricular muscular dystrophy). This disorder will not respond to potassium reductive therapy.
  • The most specific ECG feature is the absence of P waves. At times these may be difficult to identify in the frontal plane leads. The V leads are usually the best leads to illustrate P waves.
2. What are the electrocardiographic signs of myocardial hypoxemia/ischemia?

While there are no specific ECG findings that are pathognomonic for hypoxemia, some of the following may be generally suggestive:

  1. Wide QRS complexes
  2. ST segment depression or elevation (≥0.2 mV)
  3. Tall T waves (more than 1/4 total QRS excursion)
  4. Notching of the R wave of the QRS complex (microscopic intramural myocardial infarction or MIMI)
  5. Low amplitude QRS complexes
  6. Conduction disturbances (aberrant conduction) leading to wide and bizarre QRS morphology

Example of ST Segment Depression in a Dog

Example of Microscopic Intramural Myocardial Infarctions (MIMI) in a Dog

3. What is the significance of low amplitude QRS complexes in the dog?

ECG Findings:

  1. Total excursion of the QRS complex is reduced
    • <20 kg dog: <1 mV
    • >20 kg dog: <1.5 mV
  2. Other rhythm disorders may be present

Etiologies may include:

  1. Pleural effusion
  2. Pericardial effusion
  3. Obesity
  4. Hypothyroidism
  5. Pneumothorax
  6. Diffuse myocardial disease
  7. Normal variation

Consequences:

  • There is no hemodynamic significance associated with low amplitude QRS complexes. The underlying problem may have significant hemodynamic impact, however.

Treatment:

  • None required for the ECG finding
  • The underlying disorder should be sought out and treated, if needed
4. What is the significance of wide QRS complexes?

ECG Findings:

  • Dog: >0.06 sec
  • Cat: >0.04 sec
  • Assuming rhythm is sinus in origin (and not ventricular)
  • Example of Wide QRS Complexes in a Dog- Place cursor on the image to see examples of the ECG Findings

    Etiologies:

    1. Aberrant conduction (e.g. bundle branch block) – see below
    2. Myocardial hypoxemia/ischemia
    3. Left ventricular enlargement

    Consequences: As per the underlying etiology

    Treatment: No specific treatment. Address the underlying etiology

    5. What is bundle branch block?

    Bundle branch block is a conduction abnormality whereby an impulse originating from the supraventricular area (sinus node, atria, or AV node) conducts slowly or incompletely (blocks) in one of the two bundle branches (right or left), such that the ventricles are activated non-simultaneously.

    The cause may be a structural or functional lesion of one of the bundle branches, or may be physiologic when a premature beat encroaches on the refractory period of the bundle branches.

    Normal Conduction

    Right bundle branch block

    During right bundle branch block there is a lesion along the right bundle branch which prevents normal conduction down to the right ventricle. As a result, the left ventricle depolarizes normally and then its wave of depolarization spreads to the right ventricle from myocyte to myocyte. The depolarization of the ventricles during takes longer to occur, resulting in wider QRS complexes. ECG characteristics:

    • Supraventricular origin (associated P waves)
    • Wide QRS complexes
    • MEA points to RV

    During left bundle branch block there is a lesion along the left bundle branch which prevents normal conduction down to the left ventricle. As a result, the right ventricle depolarizes normally and then its wave of depolarization spreads to the left ventricle from myocyte to myocyte. The depolarization of the ventricles takes longer to occur, resulting in wider QRS complexes. ECG characteristics:

    • Supraventricular origin (associated P waves)
    • Wide QRS complexes
    • MEA points to LV

    Right Bundle Branch Block in a Dog

    Left Bundle Branch Block in a Dog

    production