“P” wave (Fig. 6.1)

Broad (duration >0.04 s and/or notched)

Left atrium enlargement (P-mitrale)

Tall (amplitude >0.4 mV)

Right atrium enlargement (P-pulmonale)

Tall and broad (>0.4 mV and >0.04 s)

Biatrial enlargement

Variable amplitude of P wave

Wandering pace maker

Absence of P wave

Atrial standstill or silent atrium

Ta wave (increased height of descending arm of “P”)

Right atrium enlargement

“QRS” complex (Fig. 6.2)

Tall “R” (amplitude >2.5 mV in small breeds >3.0 mV in large breeds)

Left ventricular enlargement (LVE) or left bundle branch block (LBBB)

Wide “QRS” (duration >0.05 s small breeds, >0.06 s large breeds)

LVE or LBBB

Deep “S” (amplitude >0.35 mV in leads II, III, aVF; >0.8 mV in lead CV5RL)

Right ventricular enlargement (RVE) or right bundle branch block (RBBB)

Deep “Q” wave (amplitude >0.5 mV in leads II, aVF)

RVE

Low-voltage “QRS” complexes (amplitude <0.5 mV in leads I, II, III, aVF)

Pericardial effusions

Pleural effusions

Pneumothorax

Obesity

Cardiomyopathy

Hypothyroidism

Loose lead contact with skin

Notched “QRS” with normal duration

Normal or minor atrioventricular defect

“R”-alternans (varying amplitude)

Pericardial effusion

Alternating bundle branch block

Supraventricular tachycardia

“J” wave (Fig. 6.3)

Deflection at “R” ST junction

Hypothermic dogs

Normal dogs

S-T segment/J point (Fig. 6.4)

Elevation (>0.15 mV), i.e., above the baseline

Hypoxia

Pericarditis

Infarction

Secondary change (ventricular hypertrophy, VCPs, conduction disturbance)

Left ventricular epicardial injury.

Transmural myocardial infarction

Digoxin toxicity

Depression (>0.2 mV), i.e., below the baseline

Infarction, ischemia

Conduction disturbance

Cardiac trauma

Hyper- or hypokalemia

Secondary change (VCPs, ventricular hypertrophy, conduction disturbance)

Digitalization

Myocardial infarction/injury

False depression

Slurring or coving

Left ventricular hypertrophy

P-R interval (Fig. 6.5)

P-R interval is inversely proportional to heart rate

Increase (>0.13 s)

First-degree heart block

Q-T interval (Fig. 6.6)

Increased (>0.25 s)

Hypocalcemia

Hypothermia

Hypokalemia

CNS disorders

Ventricular hypertrophy

Conduction disorders

Strenuous exercise

Quinidine toxicity

Ethylene glycol poisoning

Secondary to prolonged QRS duration

Short (<0.15 s)

Hypercalcemia

Hyperkalemia

Digitalis toxicity

“T” wave (Fig. 6.7)

“T” wave changes are mostly nonspecific

Sudden change in polarity

Hypoxia

Abnormal conduction

Ventricular enlargement

Metabolic disorders

Height >25% of “R”

Hyperkalemia

Small biphasic

Hypokalaemia

Large T wave

Myocardial hypoxia

Ventricular enlargement

Intraventricular conduction abnormalities

Hyperkalemia

Metabolic diseases

Respiratory diseases

Normal variation

Tented T wave

Hyperkalemia

T-alternans (amplitude varying)

Pericardial effusion

Alternating bundle branch block

Supraventricular tachycardia

“U” wave (Fig. 6.8)

Small rounded deflection after T wave.

It was first described by Einthoven (1906).

Represents last phase of ventricular repolarization.

Usually monophasic, positive, or negative.

Characteristic of hypokalemia in dogs (Tai Fu et al. 1984).

U wave with same polarity of T has also been seen in normal human beings (Goesing et al. 2009).

“R-R” interval (Figs. 6.9, 6.10, and 6.11)

Variable

Arrhythmia

Pause between R-R <twice of normal R-R interval

Sinus block

Pause between R-R >twice of normal R-R interval

Sinus arrest