ECG reading session-cardiac arrhythmias (Proceedings)


Arrhythmias can be classified based on ECG analysis based on the heart rate (normal, bradyarrhythmias, tachyarrhythmias); anatomic origin of the rhythm disturbance (SA, atrial, atrioventricular, or ventricular); or electrophysiologic mechanism when evident.

Arrhythmias can be classified based on ECG analysis based on the heart rate (normal, bradyarrhythmias, tachyarrhythmias); anatomic origin of the rhythm disturbance (SA, atrial, atrioventricular, or ventricular); or electrophysiologic mechanism when evident. Keys to recognizing cardiac arrhythmias include an analysis of rate, regularity, patterns, P-QRS relationship, waveform morphology, and conduction intervals. In terms of a methodological approach to rhythm diagnosis, it is recommended that one begin as follows: 1) Identify the patient, lead(s), paper speed, calibration signals, and artefacts; 2) Decide if the rate is slow, normal, or fast for the species; 3) Identify regularity or lack thereof and search for repetitive patterns in irregular rhythms; 4) Identify P and QRS complexes and the relationship between these waveforms; 5) Scrutinize the morphology and consistency of the P-waves and the QRS complexes; 6) Consider the conduction intervals across the atria (P-wave duration), atrioventricular conduction system (P-R interval), ventricles (QRS duration), and overall repolarization time (Q-T interval); 7) Identify the frontal axis as normal, left, or right; 8) Evaluate the QRS morphology for conduction disturbances, obvious bundle branch or fascicular blocks, and for cardiomegaly pattern(s); 9) Assess the ST-T for repolarization abnormalities; and 10) interpret the ECG with consideration of the entire clinical and laboratory picture.

Sinus rhythms

Physiologic rhythms during routine exam include normal (regular) sinus rhythm and sinus arrhythmia. Sinus rhythm disorders are often due to high vagal or sympathetic tone; any patient with sinus bradycardia or tachycardia should be evaluated with this in mind. Additionally, drugs, anesthetics, temperature, and endocrine status (thyroid or adrenal) can affect sinus node rate. Dogs with respiratory disease can show pronounced sinus arrhythmia with wandering pacemaker; the short cycles can resemble premature atrial complexes. Management of sinus rhythm disturbances is focused first on treating any underlying conditions. Occasionally inappropriate sinus tachycardia is treated with a beta-blocker. Sinus bradycardia can be treated in the hospital with atropine or glycopyrrolate. Chronic, progressive, sinus node dysfunction is common in miniature Schnauzers, West Highland white terriers, and cocker spaniels. Insufficient escape activity may result in collapse or syncope ("sick sinus syndrome"). The best long-term therapy for this syndrome is not drugs like anticholinergics or terbutaline but permanent transvenous pacing. Pacemaker programming is critical for optimal system performance (e.g. VVIR mode) and long-term outcomes are generally excellent.

Supraventricular arrhythmias

Supraventricular rhythm disturbances are among the most common and difficult of all ECG diagnoses. These arrhythmias include premature atrial complexes, atrial tachycardia, atrial flutter, atrial fibrillation (AF), re-entrant supraventricular tachycardia (SVT), and atrial standstill. Supraventricular arrhythmias can be transient, recurrent, or permanent. In most cases, recurrent or permanent arrhythmias are caused by structural heart diseases associated with congenital, chronic valvular, myocardial, or pericardial disease. Some giant canine breeds develop chronic atrial arrhythmias without overt structural disease. Lone AF in Irish wolfhounds is an example.

The ventricular rate response in a SVT is determined by the type of arrhythmia and AV conduction: the ventricular response can be slow or fast; regular or irregular. In high-sympathetic states, AV conduction of supraventricular arrhythmias can be very rapid, as with AF in the setting of congestive heart failure (CHF). Organized, regular SVT associated with atrial tachycardia, atrial flutter or re-entrant SVT often induce ventricular responses of 300 to 400 per minute! In 2:1 AV conduction of atrial tachycardia or flutter, the rate may suddenly double or half as the conduction ratio (P':QRS) changes. Subtle electrical alternans is a common finding in regular SVTs regardless of mechanism. This finding may help to separate a pathologic SVT from a "fast" sinus tachycardia (wherein alternans is uncommon). Supraventricular tachyarrhythmias also can be conducted with bundle branch block, and the resultant QRS complexes can be confused with PVCs or ventricular tachycardia (VT).

Recurrent atrial premature complexes or atrial tachycardia are often treated with drugs that suppress ectopic rhythms, including lidocaine (acutely), sotalol, and amiodarone. When efforts to suppress these ectopics fail, ventricular rate control is the goal. When atrial tachyarrhythmias are associated with CHF, digoxin is chosen first, but otherwise, diltiazem or a beta-blocker are more effective for rate control, and sometimes these drugs will convert the rhythm back to sinus. Combined therapy with digoxin and diltiazem is often used in chronic AF associated with CHF. Synchronized DC cardioversion of atrial flutter/fibrillation is another approach, particularly in dogs with lone atrial fibrillation. Amiodarone or sotalol are often prescribed after cardioversion to maintain sinus rhythm. These drugs should be continued for at least three months if possible to prevent reversion to atrial fibrillation; however, amiodarone therapy can lead to severe hepatotoxicity in dogs.

Reentrant SVTs employ circuits that develop at the micro and macro levels. The best characterized in dogs use a circuit involving the atria, AV node, and an accessory AV pathway that bypasses (or longitudinally separates) the AV conduction system. The tachycardia is often triggered by a sudden change in sinus cycle length, a premature atrial or ventricular complex. In most cases the circuit is "orthodromic"; down the AV node with an associated normal (narrow) QRS. Retrograde P'-waves may be identified in the ST segment (an R–P'). In some dogs periods of sinus rhythm are associated with ventricular pre-excitation, a helpful clue to the presence of an accessory pathway. Pre-excitation is characterized by a short PR interval and early ventricular activation (the delta wave) with wide QRS and T-waves. Management of reentrant SVT is done with drugs initially (diltiazem and procainamide can be tried), but referral to a specialist for catheter ablation of the accessory path is the best treatment.

Atrial standstill indicates that the atrial muscle is inexcitable. This condition is caused transiently by high serum potassium or persistently by atrial muscle disease or severe atrial dilation (in cats). In these cases, no P-waves are evident (atrial standstill) or very tiny, non-conducted or broad-low amplitude P waves are evident. Persistent standstill is most common in English Springer spaniels, but can also occur in larger retriever breeds. In cats apparent atrial standstill can be observed with severe forms of cardiomyopathy.

Ventricular arrhythmias

Arrhythmias arising in the ventricle parallel those of the atria in terms of nomenclature. But there are important differences: 1) the AV node need not be activated to generate a QRS complex, and 2) there is greater potential for sudden death if the rhythm degenerates to ventricular fibrillation or asystole.

Idioventricular "escape" complexes are rescue mechanisms for sinus node arrest or AV block and should not be suppressed. The typical idioventricular rhythm in the dog discharges at 20 to 40/minute, but in the cat the rate is much faster, approaching 130/minute in many cats with complete AV block. Premature ventricular complexes (PVCs, VPCs) arise early, and can be uniform or multiform in morphology. A fusion complex between a PVC and a sinus impulse also can create intermediate QRS forms and are less serious. Ventricular tachycardia (VT) can be "slow" or "fast"; paroxysmal or sustained (>30 secs); monomorphic or polymorphic; or rapidly varying in orientation (torsade de pointes). The ventricles also can flutter (producing sine waves), or fibrillate (a disorganized and lethal activation). In very sick animals or in those with CHF, death can occur from asystole, which is essentially ventricular standstill.

Clearly PVCs are among the most common rhythm disturbances. Causes include primary electrical or structural heart diseases, electrolyte and metabolic disturbances, autonomic imbalance, drugs, toxins, and the "usual suspects", such as splenic masses and gastric dilatation. It can be difficult to decide if PVCs are "clinically significant" or not, but the issue is important. For example, most cats with chronic ventricular ectopy have structural heart disease (cardiomyopathy) or an elevated serum troponin suggestive of active myocardial injury or myocarditis. A Doberman pinscher (at least one from North America) with PVCs on a routine ECG is likely to progress towards overt dilated cardiomyopathy. Furthermore, when an ECG demonstrates even a few PVCs in a Doberman pinscher that has collapsed or fainted, the risk of sudden cardiac death within the year is very high. Such information may prompt antiarrhythmic therapy, recognizing that there is no proof treatment will prolong life. Conversely, some boxers have PVCs for years without signs and are best assessed by history and ambulatory (Holter) ECG monitoring.

ECG diagnosis of PVCs or of VT is generally straightforward. In many cases a full workup including drug history, history of clinical signs (weakness, collapse or syncope), Echo findings, laboratory tests (CBC, chemistries, serum troponin-I), and abdominal ultrasound may be needed to determine the likely cause and significance. The Holter ECG can help assess the severity of ventricular arrhythmias, complexity of the complexes, and response to therapy. The absolute number of "normal" PVCs (not simply ectopics) per day is controversial, but in the author's (arbitrary) opinion >10/day in cats and >50/day in dogs should be considered abnormal. Day to day variation is common (up to ~85%) and this must be taken into account when considering both severity and "response" to any treatment.

Management of ventricular ectopic rhythms involves determining the most likely cause, advancing an educated guess about the clinical significance, considering the need for therapy, and possibly choosing one or more drugs. All antiarrhythmic drugs carry the potential for side-effects and worsening of the arrhythmia (proarrhythmia). Lidocaine remains the drug of choice for acute management, with IV procainamide, esmolol, magnesium salts, and amiodarone as back up treatments. For chronic therapy, sotalol is generally the best tolerated (except for negative inotropic effects in CHF), but it not always as effective as mexiletine plus sotalol, mexiletine plus atenolol, or amiodarone. Amiodarone deserves respect, especially in terms impairing liver function. Flecainide may be another potentially useful drug but overall experience in dogs is low and the drug can lead to "pro-arrhythmia" in humans and in experimental canine arrhythmias.

Conduction disturbances

In addition to sick sinus syndrome, persistent atrial standstill, and ventricular pre-excitation (each discussed above), conduction disturbances include the AV blocks; bundle branch blocks, and intraventricular conduction disturbances. The AV blocks are classified as first, second (Mobitz I, Mobitz IIA and IIB), and complete (third-degree block). Treatment of symptomatic AV blocks generally involves referral for permanent pacing. Single or dual chamber pacing systems can be used, depending on a variety of patient and technical factors. Long-term prognosis depends mainly on etiology of the bradyarrhythmia (best prognosis for SSS and AV block without other structural diseases and worst for persistent atrial standstill). Persistent bundle branch block or phasic aberrant ventricular conduction can be encountered in structurally normal hearts or in those with disease of the bundle branches.

Antiarrhythmic therapy – overview

Drugs, electrolytes, pacing, direct current shock, and radiofrequency energy can be used to treat disorders of heart rhythm. Antiarrhythmic drug dosing varies and drug safety is highly dependent on ventricular function and proarrhythmic effects. General canine dosing guidelines are indicated below:

  • Amiodarone (5 mg/kg IV as a slow infusion with caution (may want to pretreat with benadryl and dexamethosone to reduce risk of anaphylactoid reaction); 8 to 10 mg/kg PO daily x 2 weeks; thereafter 4–6 mg/kg PO daily); beware: cholestatic liver injury with related anorexia, vomiting and weight loss; thyroid dysfunction

  • Atenolol (0.5–1 mg/kg PO q12h; reduce dosage at least 50% in congestive heart failure)

  • Diltiazem (0.1 mg/kg slow IV boluses repeated to 0.4 to 0.5 mg/kg cumulative dose with BP monitoring; 3–6 mg/kg PO, total daily dose, divided b.i.d. or t.i.d. depending on the preparation. Initial doses in congestive heart failure should be lower – 1.5 mg/kg total daily dose – and then can be rapidly uptitrated)

  • Esmolol (50–200 micrograms/kg/minute IV infusion); use care with anesthesia or LV dysfunction.

  • Flecainide (1–2 mg/kg b.i.d. to t.i.d. – preliminary dose); negative inotrope so use with care in CHF; may widen QRS complex leading to proarrhythmia.

  • Lidocaine (2 mg/kg boluses IV to 8 mg/kg cumulative dose; thereafter, 25–75 micrograms/kg/min constant rate infusion); beware: vomiting and neurotoxicity

  • Mexiletine (5–8 mg/kg PO q8h) – can be combined with a beta blocker or sotalol; beware: anorexia and neurotoxicity; rarely acute hepatic injury; some oral preparations can no longer be obtained in USA.

  • Procainamide (2 mg/kg slow IV boluses to 20 mg/kg cumulative dose; 10–20 mg/kg PO q8h of long-acting preparation); beware: hypotension; oral preparations have been discontinued in USA.

  • Sotalol (1–2 mg/kg PO q12h); higher dosages may be tolerated in some dogs; beware: bradycardia

Effective use of any antiarrhythmic drug depends on clinical response and experience. Hypokalemia and hypomagnesemia can nullify the beneficial effects of class I agents while exacerbating pro-arrhythmic effects of Class III agents. Some drugs are more effective at particular heart rates (use dependence) and may worsen an arrhythmia by changing the rate. Every drug used to treat arrhythmias is considered an extralabel drug use in veterinary practice and treatment recommendations are based mainly on clinical experience; specific recommendations have been included above. Additional effects from activation/block of the autonomic nervous system and depression of myocardial contractility may occur. Most antiarrhythmic drugs demonstrate a proarrhythmic effects in a percentage of patients. Even beta-blockers can be proarrhythmic indirectly by slowing heart rate and prolonging cell cycle length. Thus antiarrhythmic therapy a true risk: benefit proposition.

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