Reading ECGs in veterinary patients: an introduction

January 29, 2020
Meg M. Sleeper, VMD, DACVIM (cardiology)
Meg M. Sleeper, VMD, DACVIM (cardiology)

Section of Cardiology

Volume 51, Issue 2

Understanding the basic electrical principles of the heart is essential for interpreting this valuable diagnostic test.

Electrocardiography is the recording at the body surface of electrical activity in the heart. It is a record of the average electrical potential generated in the heart graphed in voltage and time. Specific waveforms represent stages of myocardial depolarization and repolarization.

The electrocardiogram (ECG) is a valuable diagnostic test in veterinary medicine and is easy to acquire. It is the most important test to perform in animals with an auscultable arrhythmia (other than sinus arrhythmia in dogs). The ECG may also yield useful information regarding chamber dilation and hypertrophy. However, the ECG does not record cardiac mechanical activity, so it does not yield information regarding cardiac contractility. It’s also important to remember that the ECG may be normal even in the face of advanced cardiovascular disease.

The bipolar triaxial lead system we use today was developed by Dutch physiologist Willem Einthoven in the early 20th century, along with the P-QRS-T terminology that describes the ECG waveform complexes. A lead consists of the electrical activity measured between a positive electrode and a negative electrode. The orientation of a lead with respect to the heart is called the lead axis. Electrical impulses with a net direction toward the positive electrode will generate a positive waveform or deflection, and those directed away from the positive electrode will generate a negative waveform or deflection.

As the angle between the lead axis and the direction of the activation wave increases, the ECG deflection in that lead becomes smaller. Electrical impulses with a net direction perpendicular to the positive electrode will not generate a waveform or deflection at all and are said to be isoelectric.

Standard electrocardiographic leads are used to create multiple angles to assess the waveforms that travel through the three-dimensional heart. A single lead would provide information on only one dimension of current flow. For the purposes of this overview, we’ll focus on lead II, a bipolar lead in which the right arm (RA—the right foreleg in veterinary patients) is negative and the left leg (LL—or left hind leg), is positive (Figure 1). We will be discussing primarily rhythm diagnosis.

Figure 1. The three bipolar frontal plane leads (I, II and III) and Einthoven’s triangle (red). In lead I, the right foreleg (RA) is negative and the left foreleg (LA) is positive. In lead II the right foreleg (RA) is negative and the left hind leg (LL) is positive. In lead III the left foreleg (LA) is negative and the left hindleg (LL) is positive. The net depolarization moving through the ventricles (green arrow) is normally oriented toward the left hind leg (the positive pole of lead II) in dogs and cats, and therefore the QRS complex is predominantly positive in lead II. With ECG machines that utilize four electrodes, the electrode placed on the right hind leg is the ground (it is not part of any of the leads).

Recording the ECG

The ECG should be recorded in an area as quiet and distraction-free as possible. Noises from clinical activity and other animals may significantly affect a patient’s heart rate and rhythm. In quadripeds, the magnitude and direction of electrocardiographic vectors determined from limb leads can be vastly altered by changes in the position of muscular attachments of the shoulder girdle to the thorax.

Each pair of limbs should be held in parallel and limbs should not be allowed to contact one another. The animal should be held as still as possible during the ECG, and panting in dogs should be prevented if possible. In some cases, gently holding the animal’s mouth shut or placing a hand on the chest, if trembling is present, may be helpful. Alligator clips or adhesive electrodes may be used, although alligator clip teeth should be blunted and the spring relaxed to minimize discomfort.

Limb electrodes are placed distal to the elbow and stifle joints and wetted with 70% isopropyl alcohol or ECG paste to ensure good electrical contact. If the ECG complexes are too large to fit entirely within the grid of the paper, the calibration should be changed from standard (1 cm = 1 mV) to one-half standard (0.5 cm = 1 mV). The voltage and paper speed calibrations used for the recording must be inscribed during the recording so that this information is part of the permanent record.

Evaluation of the ECG

Areas of artifact should be identified as the ECG is being recorded so they can be addressed if possible. Electric (60-cycle) noise may be due to poor electric grounding (of the subject, the electrocardiograph or the table on which the ECG is being performed) or adjacent equipment such as lights or other electrical equipment. Electric noise appears on the ECG as regular fine, sharp, vertical oscillations. As mentioned earlier, placing a hand on the animal’s thorax may aid in reducing trembling or respiratory artifacts.

It’s important that artifacts not be misinterpreted during ECG evaluation. The heart rate (atrial and ventricular) should be calculated and waveform amplitudes and interval durations measured on a section of the ECG (lead II) that is run at a paper speed of 50 mm/sec. On a normal ECG, each P wave is followed by a QRS complex at a species-specific normal interval. Specific measurements to obtain for thorough ECG interpretation include:

  • P wave amplitude and duration
  • P-R interval duration
  • QRS complex duration
  • R-wave amplitude
  • QT segment duration.

Additionally, the mean electrical axis and the cardiac rhythm should be determined. Rhythm analysis will be discussed below.

Electrophysiology principles

Several principles are important to remember when undertaking ECG rhythm assessment. All normal cardiac cells are capable of depolarizing when stimulated by a neighboring cell (excitability) and subsequently stimulate discharge of their neighboring cells. This capability is termed conductivity. However, only certain cells are capable of automaticity (beating on their own). These pacemaker cells undergo spontaneous depolarization (the resting potential becomes less negative) during diastole until the threshold potential is reached. Changes in the speed of spontaneous depolarization occur gradually over several heart cycles. Therefore, tachycardia associated with pacemaker cells (for example, sinus tachycardia) speeds up gradually over several seconds, unlike tachycardia originating from ectopic foci, which often accelerates abruptly.

Specialized cells in the sinus node, atrioventricular (AV) node, and His-Purkinje system are capable of automaticity. However, under normal circumstances, pacemaker cells outside the sinoatrial (SA) node do not reach threshold because the depolarization wavefront from the sinus node discharges them before they automatically depolarize. This is because pacemaker cells distal to the sinus node, called subsidiary pacemaker cells, have a slower depolarization rate than the sinus node. Immediately after depolarizing, cardiac cells are refractory. Once the cell has returned to its resting potential it is again excitable (it can be activated again).

Evaluation of waveforms

The P wave is generated by atrial depolarization. P waves may be absent in several dysrhythmias, including atrial fibrillation and atrial standstill. Alternatively, P waves may be buried in other waveforms (and therefore not visible), which commonly occurs in supraventricular tachycardia (Figure 2). P wave enlargement (taller or wider than normal) is recognized as an indicator of atrial enlargement.

Figure 2. Lead II ECG from a dog (25 mm/sec; 10 mm/mV).

Heart rate: 150 bpm in early and late portion of strip; heart rate in middle section is 300 bpm; tachycardia.

R-R regularity: Regularly irregular in early and late portion of strip; regular in middle section.

QRS morphology: Narrow, normal-looking QRS shape; supraventricular origin.

P waves: There is a P wave for every QRS complex and a QRS complex for every P wave, except in the region of tachycardia.

Rhythm diagnosis: Sinus rhythm with supraventricular tachycardia or atrial tachycardia. (Because of the abrupt transition to and from sinus rhythm and the rapid rate, sinus tachycardia can be ruled out.)

The P-R interval represents atrial depolarization and conduction through the AV node. Prolongation of the P-R interval is termed first-degree AV block. Depolarization that originates in the ventricle (either a ventricular premature complex [VPC; Figure 3] or an escape beat) will not spread through the rapid conduction pathway but will instead spread cell to cell in a slower fashion, resulting in a widened, abnormal QRS complex. The resultant T wave will also be abnormal and usually discordant (in the opposite direction of the QRS complex).

Figure 3. Lead II ECG from a dog (25 mm/sec; 5 mm/mV).

Heart rate: 170 bpm; normal to mildly elevated.

R-R regularity: Regularly irregular (the heart speeds up and then slows down gradually in a regular rhythm); one complex is earlier than the others.

QRS morphology: Narrow, normal-looking QRS shape except for the one complex that is earlier than the others; predominantly supraventricular rhythm with one wide QRS complex that is premature.

P waves: There is a P wave for every QRS complex and a QRS complex for every P wave, except for the wide complex.

Rhythm diagnosis: Mild sinus tachycardia with one ventricular premature contraction.

Ventricular enlargement may alter QRS deflections, duration or amplitude. Aberrant conduction, such as through right or left bundle branch, can also alter the QRS duration and morphology (shape) for a similar reason. If conduction through a ventricular bundle branch is blocked, the depolarization wavefront cannot spread along the rapid conduction pathway in the affected ventricle. Conduction still spreads from cell to cell, but it is much slower (hence the widened QRS). Other causes of wide QRS complexes include electrolyte abnormalities such as hyperkalemia and certain medications (i.e. some antiarrhythmic agents).

Assessing the rhythm

When evaluating the heart rhythm on an ECG, using a stepwise approach simplifies the process.

1. Count the heart rate and determine if it is normal or abnormal (bradycardia or tachycardia). In cases of AV dissociation, there may be different atrialand ventricular rates.

2. Look at R-R regularity. Rhythms originating from a single site in the ventricles or atria are often regular, whereas rhythms originating from the sinus node are often irregular due to variations in adrenergic activity (Figure 4).

Figure 4. Lead II ECG from a dog (25 mm/sec; 10 mm/mV).

Heart rate: 90 bpm; normal.

R-R regularity: Regularly irregular (the heart speeds up and then slows down gradually in a regular rhythm).

QRS morphology: Narrow, normal-looking QRS shape; supraventricular origin.

P waves: There is a P wave for every QRS complex and a QRS complex for every P wave; P-wave shape looks normal.

Rhythm diagnosis: Sinus arrhythmia.

3. Evaluate the shape or morphology of the QRS complex. Does it appear normal or wide? Causes of wider-than-normal QRS complexes include ventricular origin (Figure 5), electrolyte abnormalities (hyperkalemia), aberrant conduction (bundle branch block), ventricular hypertrophy or certain medications. Is there a P wave for every QRS complex and a QRS complex for every P wave? If so, sinus rhythm is likely. If there are P waves without QRS complexes, AV block is present.

Figure 5. Lead II ECG from a dog (25 mm/sec; 5 mm/mV).

Heart rate: 300 bpm; tachycardia.

R-R regularity: Regular.

QRS morphology: Wide complex; ventricular (always keep in mind other possible causes of wide complex tachycardia, especially if rhythm doesn’t respond to therapy as expected).

P waves: Not visible.

Rhythm diagnosis: Ventricular tachycardia, sustained.

4. Determine the degree of AV block. In first-degree AV block, every P wave produces a QRS complex but the AV conduction is slow and the P-R interval is therefore prolonged. If only some P waves block (i.e. do not result in a QRS complex), the rhythm is second-degree AV block (Figure 6). Second-degree AV block is further broken down into Mobitz type 1 (Wenkebach type), in which there is gradual lengthening of the P-R interval until a P wave blocks, or Mobitz type 2, in which the P-R intervals are constant. Complete dissociation (there are P waves and QRS complexes but no connection between them) is present with third-degree or complete heart block

Figure 6. Lead II ECG from a dog (25 mm/sec; 5 mm/mV).

Heart rate: 130 bpm; normal.

R-R regularity: Regularly irregular (the heart speeds up and then slows down gradually in a regular rhythm).

QRS morphology: Narrow, normal-looking QRS shape; supraventricular origin.

P waves: Several P waves occur without a following QRS complex (after the second, sixth and ninth QRS complexes).

Rhythm diagnosis: Second-degree AV block (P-R interval is fixed; therefore, second-degree AV block type 2).

As with any clinical skill, becoming adept at ECG interpretation requires practice. Understanding the basic electrical principles of the heart is helpful for reading all ECGs, and it is essential for interpretation of more complex arrhythmias.

Dr. Sleeper is a clinical professor of cardiology at the University of Florida College of Veterinary Medicine who has published more than 75 peer-reviewed original articles, 50 review articles or case reports, and four books.

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