The primary indication for obtaining an electrocardiogram (ECG) is to evaluate an arrhythmia.
The primary indication for obtaining an electrocardiogram (ECG) is to evaluate an arrhythmia. Patients with a history of syncope, episodic weakness, or collapse should be evaluated with an ECG. An ECG is an insensitive test for assessment of specific cardiac chamber enlargement, and interpretation of structural heart disease is best done using radiography and echocardiography. In order to simplify and standardize the process of ECG analysis, the interpreter should evaluate ECG's in a specified order, which aids in interpretation of difficult arrhythmias. The first step is to calculate the heart rate, either an average or an instantaneous rate. Average heart rate is the number of beats in 6 seconds x 10, or the number of beats in 3 seconds x 20. The instantaneous rate obtained by measuring the R-R interval (in seconds) of the particular beat (preceeding beat is the first R to the beat of interest R), and dividing it into 60 s. The second step of ECG analysis is to assess whether the rhythm is regular or irregular, and if there is a pattern of the irregularity. Next, and most importantly, the rhythm is classified as either supraventricular or ventricular in origin. Supraventricular rhythms typically have narrow, upright QRS complexes in lead I, II, AVF, III, unless there is a bundle branch block. Ventricular arrhythmias have wide, tall or deep (negative) S waves, and have wide and bizarre T waves, and are not associated with a P wave. Assessment of the relationship of P waves to the QRS complexes is critical for determining many supraventricular and ventricular arrhythmias. At 50 mm/s and typically standard amplitude of 10 mm/mv, complex morphology (height and width of complexes, PR interval) should be measured. Lastly, the mean electrical axis is calculated, which can indicate whether there is a marked left or right axis deviation (normal MEA is 40-100 in dogs, 0-160 in cats). Right axis deviation is seen with right ventricular hypertrophy (normal QRS duration) or right bundle branch block (prolonged QRS duration).
Bradyarrhythmias are classified if the heart rate is < 80 bpm in small dogs, <70 bpm in medium-large dogs, and < 60 bpm in giant breed dogs, and < 120 bpm in cats. Sinus bradycardia is seen in animals with high vagal tone, sedation, hypothermia, sinus nodal disease, or increased intracranial disease (i.e. Cushings reflex). Sinus arrhythmia is a common normal variant, and often occurs in a pattern associated with respirations, where the heart rate increases during inspiration and decreases on exhalation. Often there is a wandering pacemaker, with changes in the P wave amplitude following the pattern of irregular rhythm (often there are taller P waves during inspiration when the heart rate increases) and is due to a shift in the location of sinus nodal depolarization associated with high vagal tone. Sinus arrhythmia is often caused by high vagal tone, but some animals with early sick sinus syndrome may have what appears to be a pronounced sinus arrhythmia, which must be differentiated using an atropine challenge test. Sick sinus syndrome (SSS) is the most common arrhythmia in Schnauzers and Cocker Spaniels, and may also occur in other dogs. SSS is composed of several arrhythmias, with sinus arrest (pause > 2 x RR interval) the signature of the disease. Other abnormalities include: sinus bradycardia, sinus arrhythmia, first and second degree atrioventricular block (2DAVB). Supraventricular tachycardia (SVT) may preceed sinus arrest (i.e. tachy-brady syndrome). Syncope usually occurs when there is a pause of sinus arrest of > 6 seconds. An atropine challenge test is necessary to help differentiate sinus bradycardia or sinus arrhythmia due to high vagal tone from SSS. High dose atropine (0.04 mg/kg SC) is given and the ECG repeated 30 minutes later. Dogs with high vagal tone have regular sinus tachycardia, with HR > 140, and no pauses of sinus arrest or AV block. Dogs with SSS often have pauses of sinus arrest or suboptimal increase in rate (<130 bpm). If there is a significant atropine response and the resting rate is slow (<65), terbutaline, a nonselective beta agonist, can be given. If there is no clinical improvement, other anticolinergic agents such as propantheline could be given. Asymptomatic dogs with SSS have a significant risk of sudden death during general anesthesia, and require either a temporary pacemaker or isoproterenol constant rate infusion (CRI). A permanent pacemaker is the treatment of choice for symptomatic dogs with SSS. Atrial standstill is a rare bradyarrhythmia, caused by severe hyperkalemia (reversible atrial standstill) or a serious atrial myopathy (permanent atrial standstill). ECG consists of lack of P waves and a nodal or less commonly purkinge escape. Electrolytes should be measured if this arrhythmia is seen, and atropine should be given. The prognosis for patients with atrial standstill and myopathy is very poor, and they are not ideal pacemaker candidates because they often quickly progress to develop severe right heart failure.
Atrioventricular blocks are another group of bradyarrhythmias. First degree AV block is defined by a prolonged PR interval, and all P waves are conducted and associated with QRS complexes. It does not cause a clinical problem, and is often caused by high vagal tone or cardiac antiarrhythmic medications. Second degree atrioventricular block (2DAVB) is divided into Mobitz type I (i.e. Wenkebach) where there are progressively prolonging PR intervals preceeding the dropped P wave, Mobitz type II where the PR interval does not prolong prior to the dropped P wave, and high grade 2DAVB where there are never 2 consecutively conducted P waves (can describe the ratio of P's to QRS, such as 2:1, 3:1). High vagal tone may cause Mobitz type I 2DAVB. AV nodal disease can cause Mobitz type I, II, and always causes high grade 2DAVB. An atropine challenge test should be done for any animal with 2DAVB to assess the role of high vagal tone in the arrhythmia. Third degree AV block (3DAVB) is evidenced by lack of any association of P waves with QRS complexes, and is caused by severe AV nodal disease. Nodal escape beats have a supraventricular morphology and typically a rate of 40-60 bpm in dogs, and 80-100 in cats. Purkinge escape beats are wide and bizarre, ventricular beats occurring at a slower rate of 20-40 bpm in dogs, and 60-80 bpm in cats. Patients with high grade 2DAVB and 3DAVB often present for lethargy, collapse, or syncope. Lidocaine or other ventricular antiarrhythmic therapy (beta blockers, mexilitene, sotalol) is contraindicated for treatment of 3DAVB, even if there are ventricular premature beats, as it will likely eliminate the life-saving purkinge escape beats. Dogs with high grade 2DAVB have equal risk to dogs with 3DAVB for sudden death, and have a 30% risk of dieing suddenly within 6 months of diagnosis regardless of whether clinical signs are present. Dogs with high grade 2DAVB and 3DAVB should be treated with a permanent pacemaker. 3DAVB is much better tolerated in cats than in dogs, because their escape rates are often quite fast (often 80-140 bpm). In a recent study, median survival of cats with 3DAVB was 386 days, and most died of non-cardiac causes. Only 1 cat received a permanent pacemaker, and no cats died suddenly.
Supraventricular tachyarrhythmias are a broad category of arrhythmias arising from the AV node or atria. Sinus tachycardia consists of heart rate >160 bpm, with narrow upright QRS complexes and associated P waves. The tachycardia gradually increases and decreases without an abrupt onset or break. It is often an important physiologic compensation for hypovolemia, anemia, fever, hypoxia, sepsis, hyperthyroidism, and many other systemic abnormalities, and does not require antiarrhythmic treatment. On the contrary, supraventricular tachycardia (SVT) is caused by an ectopic atrial focus or a re-entrant pathway involving the AV node or an accessory pathway. SVT may be initiated by a P wave that appears different from the sinus nodal P wave, and may be negative or buried in the preceeding T wave. PR interval may be different than the sinus derived PR interval. Often SVT has a rapid rate of 200-300 bpm, and typically has an abrupt onset and termination. SVT in cats is often 300-400 bpm. SVT often causes syncope, and requires emergency treatment with intravenous antiarrhythmics including IV diltiazem (0.125-0.25 mg/kg slow IV over 1-2 minutes, repeating dose if ineffective), esmolol (0.25-0.5 mg/kg IV over 1-2 minutes), or adenosine. Cardioversion may be another option for refractory SVT. Ideally, an echocardiogram is done to assess myocardial function, since beta blockers should not be given if there is severe myocardial failure. Choices, in order of preference, for chronic therapy include diltiazem (1-4 mg/kg PO TID, often high doses are needed), atenolol (1-2 mg/kg PO BID) and sotalol (1-3 mg/kg PO BID). Chronic tachycardia >180 bpm for longer than a couple of weeks may lead to pacing induced myocardial failure, which is indistinguishable from idiopathic dilated cardiomyopathy (DCM) on echocardiography. Tachycardiomyopathy, however, is rapidly reversible once rate control has been established. Atrial flutter is an irregularly irregular supraventricular arrhythmia with narrow upright QRS complexes and saw-toothed flutter (F) waves with rate of 250-350 bpm. The ventricular rate is variable and depends on amount of vagal tone at the AV node, but is often very fast if heart failure is present. Atrial fibrillation appears similar to atrial flutter, except there are less distinct fibrillatory waves or undulating baseline. Both atrial flutter and atrial fibrillation are often associated with severe underlying cardiac disease, and heart failure is often present. Antiarrhythmic therapy is aimed at decreasing the AV nodal conduction by prolonging AV nodal conduction time and refractory period, which decreases the number of wavelets that depolarize the ventricles. Chronic oral therapy is used to maintain the heart rate <140 bpm, and choices include: diltiazem (0.5- 3 mg/kg PO TID, starting at low dose), atenolol (0.5-2 mg/kg PO BID), or sotalol (1-3 mg/kg PO BID). Digoxin increases vagal tone and may aid in slowing the ventricular response rate, but is not usually adequate to maintain adequate rate control in severely tachycardic cases. Some cardiologist prefer electrical cardioversion to regain sinus rhythm, but there may be high recurrence rates in patients with significant cardiac disease and cardiomegaly. Giant breed dogs may develop "lone" atrial fibrillation in the absence of structural heart disease, and may not require antiarrhythmic therapy if heart rates are in the normal range. "Lone" atrial fibrillation often forshadows development of DCM in Irish Wolf hounds, so serial echocardiograms are needed over time.
Ventricular arrhythmias may occur due to abnormal automaticity of non-excitatory ventricular myocardial cells, enhanced automaticity of purkinge cells, or most commonly re-entrant circuits involving diseased ventricular myocardium. Ventricular premature complexes (VPC's) are premature beats, with wide and bizarre QRS and T waves and no P wave. VPC morphologies include tall and wide QRS complexes (left bundle branch block morphology) that likely arise from the right ventricle or basilar interventricular septum, or deep (negative) S waves that likely arise from the left ventricle. R on T phenomenon, couplets, and triplets are a higher grade of malignancy. Although VPC's may not be hemodynamically deleterious, they may identify patients with significant structural or functional heart disease that require an echocardiogram. Ventricular arrhythmias are also common with other systemic dieases, after trauma, in post-surgical splenectomy or gastric dilation volulus patients, and often improve with treatment of the underlying problem and tincture of time. Greater than 3 VPC's in a row (instantaneous ventricular rate > 160 bpm) is considered non-sustained ventricular tachycardia, and signifies a highly malignant arrhythmia grade and risk of sudden death. Sustained ventricular tachycardia lasts longer than 30 seconds, and often requires emergency treatment. Accelerated idioventricular rhythm consists of a ventricular derived rhythm with a rate of 80-160 bpm, and is most often seen in systemically ill dogs or post-operative splenectomy or GDV patients, and does not typically require therapy. Holter monitors are necessary to help quantify the severity of ventricular arrhythmias, and are especially useful in Doberman Pinschers and Boxer dogs. Normal dogs have < 50 VPC's in 24 hours and there is a grey zone of 100-500 VPC's/24 hours (for Boxer dogs). > 50 VPC's in 24 hrs, 1 couplet or triplet in overtly normal Doberman Pinshers with normal echocardiographic studies was highly predictive of development of DCM. Couplets, triplets, and non-sustained ventricular tachycardia are abnormal and require antiarrhythmic treatment. Sustained ventricular tachycardia requires acute antiarrhythmic therapy and hospitalization. Lidocaine is the drug of choice (2-4 mg/kg IV, repeated to 6 mg/kg total cumulative dose followed by CRI 30-90 mcg/kg/min). Intravenous procainamide, esmolol, or amiodarone are other choices for refractory ventricular arrhythmias. Chronic antiarrhythmic treatment choices include sotalol (1- 3 mg/kg PO BID), atenolol (1-2 mg/kg PO BID), mexilitene (5-7 mg/kg PO TID), and amiodarone (10-15 mg/kg PO BID x 7 days then 5-7 mg/kg PO q24 hr). If there is severe decompensated DCM, atenolol and possibly sotalol should be avoided as they will further decrease contractility. Sotalol or the combination of atenolol and mexilitene effectively decreases the severity of arrhythmia and reduces syncopal episodes in Boxer dogs with arrhythmogenic right ventricular cardiomyopathy. Follow-up ECG and ideally holter monitoring is important after starting antiarrhythmic medication. Often combination antiarrhythmic therapy is needed, such as sotalol and mexilitene, or amiodarone and low dose atenolol or mexilitene. Amiodarone is typically reserved for refractory ventricular arrhythmias or for treatment of severe ventricular arrhythmias in dogs with severe DCM.
Terminal arrhythmias include asystole, where there is lack of any electrical cardiac activity, and ventricular fibrillation. Both should be treated aggressively with immediate cardiac defibrillation (5-10 joules/kg extrathoracic), as well as emergency drugs including atropine and epinephrine. Asystole has very little chance of cardioversion, given the lack of electrical activity. If there is refractory ventricular fibrillation, bretylium may be a last resort.
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