Philip R. Fox, DVM, MSc, DACVIM, DECVIM (Cardiology), ACVECC
ELECTROCARDIOGRAPHY--CLINICAL IMPORTANCE
Electrocardiography is clinically useful 1) to diagnose cardiac arrhythmias, 2) as an adjunct to detect cardiac enlargement (dilation or hypertrophy), and (3) indicate certain electrolyte, acid-base, systemic, or metabolic disorders.
Effective management of arrhythmias, heart failure, and a variety of systemic and metabolic disorders requires accurate ECG assessment. The ECG may be useful in evaluating animals with metabolic diseases such as endocrinopathies (e.g., hypoadrenocorticism, thyrotoxicosis, pheochromocytoma) or systemic disorders (e.g., shock, neoplasia). Severe electrolyte disorders, acid-base disturbances, or metabolic changes may affect myocyte electrochemical gradients altering depolarization or repolarization with associated ECG abnormalities. Electrocardiographic alterations in such cases may reflect systemic and not organic heart disease. Thus, it is essential to correlate the ECG with other diagnostic tests.
CLINICAL TECHNIQUE
I. Recording the ECG
Eupneic animal-- Record the ECG with the animal in right lateral recumbency.
Dyspneic animal-- To reduce stress, record the ECG with pet standing or sternal. Alcohol or conducting paste is applied to the skin and electrodes.
II. Placement of ECG Electrodes
A. Bipolar standard limb leads I, II, and III, unipolar limb leads aVR, aVL, and aVF:
Place electrodes just above the olecranon and over the patellar ligaments.
B. Unipolar precordial (thoracic) leads are often helpful in confirming cardiac chamber enlargement; emphasizing deflections of the standard limb leads (particularly if P waves are not clearly visible); and confirming data recorded on other limb leads.
Left chest leads placed at 6th intercostal space at the edge of the sternum (CV6LL (r2), and at the costochondral junction (CV6LU (v4)
Right chest lead at 5th ICS at the edge of the sternum (CV5RL (rv2)
At dorsal spinous process of the 7th thoracic vertebra, V10
III. The P-QRS-T Complex
P wave reflects atrial depolarization and precedes the QRS complex.
Q wave is the first negative wave in the ventricular depolarization complex.
R wave is the first positive wave.
S wave is the first negative wave following the R wave.
T wave represents ventricular recovery (repolarization).
IV. Interpreting Heart Rate and Rhythm (from lead II rhythm strip)
Heart Rate
Varies widely between canine breeds but is relatively similar amongst feline breeds. In dogs the typical rhythm is sinus arrhythmia or sinus rhythm. Large and giant breeds may have resting heart rates between 60 to 120 beats per minute. Small and toy breeds may vary from 55 to 60 (with pronounced respiratory sinus arrhythmia) to 180. In cats sinus rhythm is the norm and heart rate varies from about 150 to 220. With increased sympathetic tone (fright or excitement, pain, systemic or metabolic disease), resting heart rates may increase dramatically. Bradycardia is generally <60bpm for adult dogs (breed variations) and <140bpm in adult cats at the veterinary office. Some normal animals have very slow rates at home or during sleep.
Both atrial and ventricular rates are calculated since they may vary. When the basic rhythm is irregular, the ventricular rate can be estimated by counting the number of cycles (R-R intervals) within 3 seconds and multiplying by 20 (paper speed 50mm/sec). When rhythm is regular, heat rate may be calculated as follows:
1. At a paper speed of 50 mm/sec, the width of one small calibration box = 0.02 sec. Therefore, the number of small boxes equaling 1 minute is determined by dividing 0.02 sec into 60 seconds, or 3,000. Thus, heart rate/minute may be calculated by dividing the number of small boxes within one R-R interval into 3,000. At paper speed of 25mm/sec, one small calibration box = 0.04 sec and heart rate is calculated by dividing the number of small boxes within one R-R interval into 1500.
2. A large calibration box comprises five small boxes. At a paper speed of 50mm/sec, it is = 0.02 sec times 5, or 0.1 sec; at paper speed of 25mm/sec, it = 0.2 sec. Thus, the number of large boxes equaling 1 minute is determined by dividing 0.1 sec into 60 seconds, or 600. Therefore, the number of large boxes within one R-R interval divided into 600 gives the heart rate per minute at 50 mm/sec paper speed. At 25mm/sec paper speed, heart rate is calculated by dividing the number of large boxes within one R-R interval into 300.
V. Measuring the P-QRS-T Complex
P-wave--duration measured from its beginning to the end; amplitude is measured from the isoelectric base line to the maximum height of the P wave.
P-R interval--measured from the beginning if the P wave to the beginning of the QRS complex.
QRS complex duration--measured from the beginning of the Q wave (if present) or R wave (if no Q wave), to the end of the S wave (if present) or to where the R wave deflection crosses the baseline.
QRS amplitude (represents the sum of excursions from the positive R wave and negative S wave). Amplitudes of the Q, R, and S waves are measured from the baseline to the point of their maximal excursion.
S-T interval--segment between end of the QRS complex and beginning of T wave.
Q-T interval--distance between the beginning of the Q wave and end of the T wave.
Cardiac Rhythm (calipers are helpful for making interval measurements).
All recorded leads must be examined for arrhythmias.
1. General inspection will show whether the tracing shows characteristic of an arrhythmia or represents normal sinus rhythm.
2. Identify P waves. Is there a P wave for every QRS? Determine whether the P waves are uniform, multiform, regular, irregular, associated with the QRS complex, or absent.
3. Measure the P-R interval.
4. Evaluate QRS complexes. Evaluate their configuration, uniformity, and regularity.
5. Analyze the P-QRS-T relationships. Doubling the ECG sensitivity may help. Precordial chest leads may help demonstrate P waves.
C. Limitations
Electric 60-cycle "noise" may be due to poor electric grounding (of the electrocardiograph, the animal, or table on which the animal is positioned) or adjacent lights or electrical equipment. It is recognized on the ECG tracing as a regular sequence of fine, sharp, vertical oscillations.
Muscular tremor and respiratory motion are common and cause the electrode clips to vibrate and produce spurious recording artifacts. The placement of a hand on the animal's thorax or blowing into the animal's face may help reduce these artifacts.
Movement artifact may be reduced by positioning the electrode clips correctly, using appropriate conductive gel, and by manually preventing the electrodes or wires from moving during respiration.
Cardiac lesions do not always cause or correlate with ECG abnormalities. The ECG may be normal even in face of advanced cardiovascular disease or heart failure, or a morphologically normal heart may develop lethal arrhythmias.
Major shortcoming of ECG--low sensitivity for inferring chamber enlargement or hypertrophy.
DECIDING WHETHER TO TREAT
A number of clinical issues must be weighed when considering whether to repress or abolish tachyarrhythmias. Tachycardia shortens diastolic filling, decreases coronary blood flow, reduces myocardial oxygen supply, causes ischemia and results in more serious arrhythmias. Certain tachyarrhythmias may deteriorate by becoming electrically unstable. Tachyarrhythmias may depress cardiac output and contribute to hemodynamic impairment or hypotension. Hemodynamic impact of tachyarrhythmias are influenced by factors related to underlying cardiac disease and the particular type of arrhythmia. These include 1) loss of synchronized atrial systole, 2) altered ventricular activation sequence, 3) rapidity of ventricular rate, 4) timing of ectopic beats relative to preceding P-QRS-T complexes, 5) background vasomotor tone, 6) cardiac effects of antiarrhythmic drugs, and 7) underlying cardiac function or health. Cardiac output is the product of heart rate x stroke volume. With sustained paroxysmal atrial tachycardia (i.e., >300/sec), stroke volume decreases and arterial pressure may rapidly decline.
Electrical instability is increased by rapid ventricular rates and multifocal impulse origination. Additional factors include timing of the ectopic impulse (i.e., the earlier the premature complex relative to the preceding T wave, the greater electrical liability). Depolarizations occurring within the preceding T wave are extremely dangerous. The underlying state of ventricular function, systemic and metabolic alterations, and concurrent drug or anesthetic agents influence electrical stability.