Electrocardiography - The Merck Veterinary Manual

Electrocardiography

Electrocardiography is the recording of cardiac electrical activity from the body surface. It can be used not only to identify cardiac arrhythmias and conduction disturbances, but also chamber enlargement.

Waveform Abnormalities:

Chamber enlargement can be indicated by waveform abnormalities. In lead II in dogs and cats, wide P waves are suggestive of left atrial enlargement, tall P waves of right atrial enlargement, tall R waves of left ventricular enlargement, and deep S waves of right ventricular enlargement. Wide QRS complexes can occur in patients with ventricular enlargement; however, they can also be due to conduction disturbances (see below). While the ECG may suggest chamber enlargement, thoracic radiographs and echocardiography are more sensitive.

Sinus Rhythm:

The sinus node initiates each cardiac contraction in a normal animal, sets the normal rate and rhythm, and is called the pacemaker of the heart. Normal sinus rhythm is a rhythm that is regular and originates at the sinus node. Sinus bradycardia is a regular sinus rhythm that is slower than expected. Clearly, expected heart rate will vary by species or by situation (eg, exercise, anesthetized, resting). Sinus bradycardia may be noted in patients that are overdosed with anesthesia or agents that can result in elevated vagal tone or reduction of sympathetic tone (eg, xylazine, digoxin), hypothermic patients, hypothyroid patients, patients with sick sinus syndrome, or in patients with elevated vagal tone secondary to systemic disease such as respiratory, neurologic, ocular, GI, or urinary tract disease. Treatment for sinus bradycardia is typically not needed unless clinical signs associated with the bradycardia, such as weakness or collapse, are noted. In dogs and cats, atropine (0.04 mg/kg, IV, IM, or SC) may be considered for treatment of bradycardia. The initiating cause should also be corrected.

Sinus tachycardia is the finding of a regular sinus rhythm at an excessive rate. Causes include stress (resulting in high sympathetic drive), hyperthyroidism, fever, hypovolemia, cardiac tamponade, heart failure, or administration of agents that can increase the rate of sinus node discharge (eg, catecholamines). Treatment involves resolving the underlying cause. Sinus arrhythmia occurs as a result of irregular discharge of the sinus node. The site of impulse formation remains the sinus node; however, the frequency of the discharge varies. Sinus arrhythmia is a normal finding in dogs and horses; it is abnormal in cats. Heart rate usually increases with inspiration and decreases with expiration. The rhythm is irregular, with >10% variation in the RR interval. The variation in heart rhythm is associated with variation in the intensity of vagal tone. It is abolished by reduced vagal tone or increased heart rate resulting from excitement, exercise, or administration of atropine. It may be associated with a wandering pacemaker (P waves vary in shape) within the sinoatrial (SA) node and a varying PR interval. Sinoatrial block occurs when the impulse from the SA node fails to be conducted through the surrounding tissue to the atria and ventricles. Thus, no P waves or QRS complexes are noted on the ECG. In second-degree SA block (which is most common), some of the SA impulses fail to conduct, resulting in a pause that is an exact integer multiple of the normal PP interval.

Sinus arrest is the failure of the SA node to discharge for a short period of time, resulting in a pause between complexes on the ECG (typically accepted as a pause exceeding twice the normal RR interval). Atrial standstill (sinoventricular rhythm) occurs as a result of the atria being unable to depolarize. There are no P waves present on the ECG and no atrial fibrillation. The heart rate is typically 40-60 bpm in dogs affected by this condition, depending on the precise etiology. Causes include hyperkalemia (where the atrial myocardium is poisoned), myocarditis, and specific forms of cardiomyopathy where the atrial myocardium is replaced by fibrous tissue. Treatment for hyperkalemia-induced atrial standstill requires treatment of the underlying hyperkalemia. Sick sinus syndrome involves the sinus node; however, other portions of the specialized conduction tissue of the myocardium, including the AV node, can be affected. This disease is commonly noted in geriatric dogs such as Miniature Schnauzers and can result in periods of bradycardia caused by sinus arrest or sinoatrial block, tachycardia, or conduction disturbances such as second degree AV block (see below). Initial treatment usually involves sympathomimetics to increase heart rate (eg, extended-release theophylline, 10 mg/kg, PO, bid; or terbutaline, 0.14 mg/kg, PO, bid-tid in dogs). In patients that do not respond to oral therapy, pacemaker implantation may be warranted.

Conduction Disturbances:

Atrioventricular (AV) block refers to alteration of impulse conduction from the atria to the ventricles. In first-degree AV block (prolonged conduction), the conduction time is increased and is recognized on an ECG as an increased PR interval. In second-degree AV block (intermittent conduction), occasional impulses fail to be conducted through the AV junction, and atrial contraction is not followed by ventricular contraction. The block may occur at regular intervals or at random. During the block, there is no S₁ or S₂ and no arterial pulse. In horses, the sound associated with atrial contraction (S₄) is commonly heard, and the occurrence of S₄ not followed by other heart sounds is diagnostic for second- or third-degree heart block. S₄ may also be audible in dogs with second-degree AV block. In all species, an atrial jugular wave may be seen during the block. When the PR intervals preceding the dropped beat progressively lengthen, the condition is known as the Wenckebach or Mobitz type I second-degree AV block. If the PR intervals do not change, the condition is known as a Mobitz type II second-degree AV block.

In third-degree AV block or complete heart block, none of the impulses are conducted from the atria to the ventricles. The ventricular rhythm is established from an ectopic nodal or ventricular pacemaker that discharges at a slower rate than the SA node, and the atria and ventricles beat independently of each other. The heart and pulse rates are regular, but there is a pronounced bradycardia that is relatively unresponsive to factors that usually increase heart rate (eg, exercise or excitement). The difference in timing between atrial and ventricular contractions results in variation in ventricular filling and consequent variation in intensity of S₁ and arterial pulse pressure. Periodically, the atria contract when the ventricle is in systole, which results in large pulsations in the jugular vein (cannon A waves). In some animals, the faster atrial contractions can be detected with a stethoscope.

The significance of the AV block varies by species. Both first- and second-degree AV block may be present without outward evidence of cardiac disease. First-degree AV block may result from excessive vagal tone and generally is not considered significant in dogs or horses unless other evidence of heart disease is present. In all species, second-degree AV block may be indicative of heart disease. However, in horses, it is more commonly the result of high vagal tone. It is detected at resting heart rates of <40 bpm and, as in SA block, may be induced or abolished by situations that decrease vagal tone. Complete AV block is always abnormal in dogs and cats.

AV block may be caused by fibrosis, neoplasia, other injuries to the AV node, hypoxia, agents that increase vagal tone, or electrolyte abnormalities. Treatment is aimed primarily at correcting the underlying cause. It is frequently associated with syncope, especially during exercise or excitement. Oral therapy, such as extended-release theophylline (10 mg/kg, PO, bid) or terbutaline (0.14 mg/kg, PO, bid-tid in dogs), may be useful in animals with second-degree AV block that are symptomatic (syncope, weakness). Complete heart block is usually associated with irreversible lesions; pharmaceuticals are typically ineffective at resolving the conduction disturbance, and cardiac pacemaker implantation is warranted.

Arrhythmias:

Arrhythmias can be divided into bradyarrhythmias, in which the heart rate is excessively slow, and tachyarrhythmias, in which the heart rate is excessively rapid. The former includes sinus bradycardia, sinus arrest, SA block, AV block, and atrial standstill (see above). Tachyarrhythmias can be divided into supraventricular and ventricular based on their site of origin. Supraventricular premature depolarizations are premature depolarizations that originate from a site outside the sinus node and above the ventricles. They are also called atrial or nodal premature complexes/depolarizations/beats. Possible sites for ectopic depolarizations include the atrial myocardium and junction (proximal AV node, AV node, and bundle of His). Electrocardiographically, supraventricular premature depolarizations include a QRS complex that appears normal but occurs prematurely. A P wave of variable morphology may be noted preceding the supraventricular premature depolarization or may be hidden in the preceding sinus complex. Supraventricular premature depolarizations are most commonly a result of chronic mitral regurgitation in dogs, but may be caused by any heart disease that can result in atrial enlargement, as well as other underlying causes such as myocarditis, sick sinus syndrome, stress, or other causes for increased sympathetic drive. Supraventricular tachycardia is a series of supraventricular premature depolarizations occurring consecutively. Accessory pathways are congenital abnormalities that allow an electrical connection between the atria and ventricles outside the normal connection (AV node/bundle of His). These pathways or bypass tracts have been recognized in dogs and cats and can result in supraventricular tachyarrhythmias. Treatment may involve radiofrequency catheter ablation of the bypass tract; oral medications such as diltiazem and digoxin (not the drug of choice) have also been tried.

Atrial flutter is a rare arrhythmia that, if present, typically precedes the development of atrial fibrillation. It is in essence a rapid supraventricular tachycardia where P waves commonly appear as a “saw-toothed” baseline. The atrial rate of discharge is so rapid (usually >400 bpm) that only intermittent impulses are conducted because of intermittent AV nodal refractoriness. The ventricular rate may be regular and rapid or irregular and rapid.

Atrial fibrillation is an irregular rhythm that is typically rapid and caused by disorganized depolarization of the atria. Stimulation of the AV node occurs frequently but in a random fashion, resulting in a rapid and irregular rhythm. The irregularity results in variation in the diastolic filling period between contractions and, consequently, variation in intensity of the heart sounds and amplitude of the arterial pulses. With exceptionally short diastolic periods, there is insufficient filling of the ventricles to produce an arterial pulse after ventricular contraction. At rapid heart rates, this produces a pulse rate that is considerably lower than the heart rate (pulse deficit). Electrocardiography demonstrates an absence of P waves, the presence of rapid F waves, and an absolute irregularity in the RR intervals. In dogs and cats, atrial fibrillation with high heart rates usually indicates severe cardiovascular disease. Causes include any heart disease resulting in atrial enlargement (eg, cardiomyopathy, degenerative valve disease), myocarditis, or noncardiac disease such as neoplasia or (less commonly) gastric dilation and volvulus syndrome in dogs. In ruminants, atrial fibrillation is sometimes paroxysmal in association with GI tract disorders, but it also may occur as a sequela for cor pulmonale or with cardiac disease. In horses, atrial fibrillation may occur in conjunction with other cardiac disease such as mitral insufficiency. It also can occur in the apparent absence of serious underlying cardiac disease and, in horses with high vagal tone, may occur with a bradycardia. There is significant irregularity of heart rhythm and variation in heart sound intensity and pulse amplitude but no pulse deficits in these patients. When the resting rate is 26-48 bpm, there may be few signs of cardiac disability except with heavy exercise. The heart rate increases in response to moderate exercise. At very slow rates, several seconds may elapse between some contractions, and syncope may occur. Atrial fibrillation occurs more commonly in draft and other large horses. It occurs in racehorses in association with poor racing performance and may be paroxysmal. Atrial fibrillation with a low, resting heart rate is not incompatible with long life, but affected horses should not be used for riding. Conversion to a sinus rhythm with quinidine at a dosage of 22 mg/kg, PO, every 2 hr is sometimes attempted in horses and is often followed by a return to successful performance in racing animals. The chance for success is greatest when conversion is attempted shortly after the initial onset.

Ventricular premature depolarizations arise from a site within the ventricular myocardium. On an ECG, the complex appears wide and bizarre and is premature relative to the preceding sinus complex. There is no associated P wave. Causes include primary myocardial disease, electrolyte imbalance, acute toxicities, noncardiac disease such as neoplasia (eg, splenic hemangiosarcoma in dogs), gastric distention (such as seen with gastric dilation and volvulus syndrome in dogs), or trauma. Ventricular tachycardia is the presence of 3 or more ventricular premature depolarizations consecutively. Ventricular fibrillation is a result of microreentrant circuits within the ventricular myocardium resulting in the absence of effective ventricular contractions and is thus a terminal rhythm. An idioventricular rhythm is the presence of only ventricular escape complexes on an ECG and is also typically a terminal rhythm. Accelerated idioventricular rhythm is a slow form of ventricular tachycardia where the ventricular tachycardia rate is less than ~120 bpm in dogs. This is considered a benign arrhythmia in most animals. While the underlying cause should be sought and treated as necessary, the arrhythmia itself typically results in no clinical signs and requires no specific therapy.