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1968 - 2016 MEMORIAS DE LAS PONENCIAS EN EL CURSO DE CARDIOLOGÍA EN PERROS Y
1968 - 2016 MEMORIAS DE LAS PONENCIAS EN EL CURSO DE CARDIOLOGÍA EN PERROS Y

1968 - 2016

MEMORIAS DE LAS PONENCIAS EN EL CURSO DE CARDIOLOGÍA EN PERROS Y GATOS MÉXICO, D.
MEMORIAS DE LAS PONENCIAS
EN EL CURSO DE CARDIOLOGÍA
EN PERROS Y GATOS
MÉXICO, D. F., DICIEMBRE 8 Y 9 DE 2016

Asociación Mexicana de Médicos Veterinarios Especialistas en Pequeñas Especies, S. C. www.ammvepe.com.mx

PONENCIAS DEL CURSO DE CARDIOLOGÍ A EN PERROS Y GATOS

AMMVEPE

Diciembre 8 y 9 de 2016

MANAGEMENT OF CARDIAC ARRHYTHMIAS John D. Bonagura DVM, MS, DACVIM

CARDIAC AUSCULTATION John D. Bonagura DVM, MS, DACVIM

CONGENITAL HEART DISEASE John D. Bonagura DVM, MS, DACVIM

PERICARDIAL DISEASES IN DOGS: DIAGNOSIS & MANAGEMENT John D. Bonagura DVM, MS, DACVIM

RADIOGRAPHIC DIFFERENTIAL DIAGNOSIS OF CARDIOPULMONARY DISORDERS John D. Bonagura DVM, MS DACVIM

Asociación Mexicana de Médicos Veterinarios Especialistas en Pequeñas Especies, S. C. www.ammvepe.com.mx

MANAGEMENT OF CARDIAC ARRHYTHMIAS REFERENCE NOTES

John D. Bonagura DVM, DACVIM Veterinary Clinical Sciences, Ohio State University *

Heart rhythm disturbances (arrhythmias, dysrhythmias) can be classified following ECG analysis based on the heart rate (normal, bradyarrhythmia, tachyarrhythmia); anatomic origin of the rhythm disturbance (sinoatrial node, atrial, atrioventricular node or junction, or ventricle); and electrophysiological mechanism if evident (enhanced automaticity, reentry, myocardial fibrillation). The underlying basis for abnormal cardiac rhythms include a number of possible factors. Even without overt cardiac disease, structural or physiologic abnormalities that alter normal cardiac cellular conduction properties or excitability (automaticity) can predispose to arrhythmias. Such changes can occur during cardiac remodeling in patients with heart disease and failure, or can result from genetic or environmental factors. Myocyte hypertrophy, abnormal ion channel structure or function, tissue inflammation or fibrosis, or other derangements may be involved. For example, in cardiomyopathy increasing heterogeneity of repolarization and conduction velocity across the ventricular wall, from endocardium to epicardium, increases the propensity for ventricular arrhythmia development. Yet even with such underlying abnormalities, an arrhythmia may not occur unless provoked by some triggering event. For example, an abrupt change in cardiac cycle length (heart rate) or a premature stimulus can trigger a sustained arrhythmia when the underlying conditions are favorable. Additional modulating factors further influence whether an arrhythmia occurs or is sustained. These factors might include changes in cardiac sympathetic or vagal tone, circulating catecholamine concentrations, electrolyte disturbances, and ischemia. The clinical association of most arrhythmias can be grouped into one of five general categories: 1) Primary cardiac disease (structural or electrical diseases; often genetically predisposed); 2) Metabolic & endocrine disorders; 3) Autonomicrelated; 4) Drugs & toxins; and 5) the “Usual suspects”. The last group refers to a large number of noncardiac disorders that induce arrhythmias by causing ischemia reperfusion, release of cytokines, altered autonomic traffic, or unknown mechanisms. Examples include gastric dilatation, sepsis, anemia, and splenic disease in dogs. Understanding the likely clinical association of an arrhythmia can facilitate specific treatments and guide the duration of therapy and prognosis. Clinical evaluation in most cases involves a complete physical examination including careful cardiovascular (CV) evaluation, ECG, diagnostic imaging, and selected laboratory tests. When structural or genetically predisposed cardiac disease is the likely cause, the workup can focus on echocardiography and thoracic radiographs. If an acute insult or myocarditis is suspected, a cardiac troponin (cTnI) is recommended, accepting that severe arrhythmias can lead to ischemia and secondary elevations in this biomarker. When a noncardiac disorder is suspected or there is no clear evidence of primary heart disease, the ECG, CBC, routine serum chemistries with electrolytes (especially potassium and magnesium), cTnI, and at least a screening 2D Echo is advised. Abdominal ultrasound often focused on the spleen – is another useful test. In some locations and clinical settings, tests for infectious disease agents are also appropriate. Not to be overlooked in the quest for an etiology is the importance of correctly diagnosing the heart rhythm disturbance. There are certainly challenges (as illustrated under specific rhythm disturbances). ECG recordings for rhythm analysis can be acquired from simple, singlelead recordings (typically lead II or a thoracic lead from the ICU or a phone app), or multiple lead (6 or 9 lead) recordings. Multiple lead recordings can be recorded sequentially or simultaneously. Multiple leads, as well as special leads systems, can be helpful when P waves are difficult to identify, as often occurs in cats or during narrow QRS tachycardias in dogs. Sometimes just moving the forelimb electrodes to the thorax (left arm to left apex and right arm to the craniodorsal right cardiac base and selecting lead I) and increasing the sensitivity of the recording to 20 mm/mV can be helpful for identifying P waves.

Specialized recordings using trans esophageal or intracardiac electrode catheters also provide insight regarding atrial activity, but these are rarely used. Ambulatory ECG recorders Holter monitors, 1 8 event monitors, 1,9,10 and implantable loop recorders 11 14 – all have their place in diagnosis, assessment and management of arrhythmias and clinical signs such as exertional collapse and syncope. Some uses of these specialized recording devices are discussed below under specific rhythm disturbances. For certain complex heart rhythm disturbances, multipolar intracardiac electrode catheters are needed for diagnosis; this requires a cardiac electrophysiologist and specialized equipment and training. Advanced analyses including signal averaged ECG and heart rate variability (HRV) are considered research tools.

NORMAL ELECTRICAL ACTIVITY The normal cardiac rhythm begins in the SA node in the right atrium and the subsequent depolarization proceeds from right to left and cranial to caudal generating positive P waves of <40 ms duration in most dogs and cats in Leads I, II, and aV F . Assuming conduction across the AV node and His Purkinje system is normal, the PR interval will be <130 ms for (non giant) canine breeds and <100 ms for most cats. The normal canine and typical feline QRS complexes are also positive in leads I, II aV F , in the frontal plane and strongly positive in the lower left, precordial leads (V 2 V 4 ). Ventricular depolarization is dominated and least cancelled as it flows towards the left apex in dogs; accordingly, the largest, positive QRS complexes in the limb leads are found in either lead II (60 o ) or lead aV F (90 o ) This frontal axis is less consistent in normal cats, especially those with small QRS complexes. The normal QRS complex is relatively compact (or “narrow”) and typically 50 ms in dogs (<60 ms in giant breeds) and 40 ms in cats. The ST segment usually falls within 0.1 to .15 mm from the baseline at standard calibration (with the baseline reference being the segment in front of the P wave). However, if there is PR segment depression from a prominent Ta (atrial repolarization) wave, the reference baseline becomes the PR segment (from the end of P wave to the onset of the QRS). Prominent Ta waves are often observed in dogs with atrial dilatation, during sinus tachycardia (when the PR abbreviates), and in complete AV block. 15

APPROACH TO ECG INTERPRETATION A consistent approach to ECG interpretation is recommended. The recording/paper speed, lead(s) used, calibration, as well as the tracing quality (i.e. all complexes within the grid, minimal artifact), should first be identified. Then the heart rate (HR) and heart rhythm are determined. If multiple frontal plane leads are available, an estimate of mean electrical axis (MEA) can be obtained. Finally, individual waveform duration and amplitude (in Lead II, by convention) should be measured. Because variation in HR is common, especially in dogs, estimating the average heart rate over several seconds is usually more accurate and practical than calculating an instantaneous heart rate. Simply count the number of QRS complexes within a 3 or 6 second period and then multiply by 20 or 10, respectively. If the heart rhythm is regular, 3000 divided by the number of small boxes (at paper speed 50 mm/sec) between the onset (or R wave peak) of successive QRS complexes equals the approximate heart rate.

The heart rhythm is evaluated by scanning the ECG for patterns or irregularities and identifying individual waveforms. Common rhythm abnormalities are described below. Calipers are useful for assessing the regularity and interrelationships of the waveforms. Ectopic complexes are described by their general site of origin (supraventricular [atrial, AV junctional] or ventricular) and their timing (premature [earlier than the next expected sinus impulse] or escape [late; after a longer pause]). The frequency and complexity of ectopic complexes are also evaluated, e.g. whether they occur occasionally or frequently; as singles, pairs, triplets, or a tachycardia [paroxysmal or sustained]; and whether they appear uniform [monomorphic] or of variable configuration [polymorphic, multiform]. The absence of normal P waves may indicate atrial fibrillation, sinus arrest, or failure of intraatrial conduction (atrial standstill or the effects of hyperkalemia [silent atrium]). Disturbances of the AV nodal and infranodal conduction system are common, and can cause various degrees of AV block, or just abnormal intraventricular conduction (major bundle branch block or a nonspecific intraventricular conduction

disturbance). Marked bradycardia can occur from 3 and high grade 2 AV block. Because AV nodal conduction velocity normally is relatively slow, conditions that enhance vagal tone or otherwise further reduce nodal conduction velocity tend to promote conduction failure. However, the AV block that occurs when a supraventricular tachyarrhythmia such as atrial fibrillation or atrial tachycardia stimulates the AV node at a rate faster than it can normally conduct is considered physiologic, not pathologic. Keys to diagnosing a cardiac arrhythmia include an analysis of ventricular and atrial rates, regularity of the rhythm, patterns of arrhythmias, P QRS relationship, ECG waveform morphology, and conduction intervals. The most important aspect of rhythm diagnosis involves identification of P waves and their relationship to the QRS complexes. In terms of a methodological approach to rhythm diagnosis, it is recommended that one include the “10 steps” shown in Table 1. After completing your analysis, interpret the ECG tracing in light of the clinical, imaging and laboratory findings.

Table 1. An Approach to ECG Rhythm Analysis

1. Identify the patient, lead(s), paper speed, calibration signals, and artifacts

2. Decide if the ventricular rate is slow, normal, or fast (for the species; Table 2)

3. Identify if the rhythm is regular (R to R intervals evenly spaced) or irregular

 

a.

If irregular, search for any recurring patterns

4. Identify P waves & QRST complexes and the relationship between these waveforms (P R and R

P)

 

a. Is sinus rhythm present (with or without other abnormalities), or are there no consistent P QRST relationships?

 

b. Are all P waves followed by a QRS and all QRS complexes preceded by a P wave?

5. Scrutinize the morphology and consistency of the P waves, QRS complexes, and STT

 

a. If premature (early) complexes are present, do they look the same as sinus QRS complexes, implying atrial or junctional (supraventricular) origin, or are they wide and of different configuration than sinus complexes, implying a ventricular origin or, possibly, abnormal (aberrant) ventricular conduction of a supraventricular complex (e.g. bundle branch block pattern)?

 

b. Are premature QRS complexes preceded by an abnormal P wave (suggesting atrial origin)?

 

c. Are there baseline undulations instead of clear and consistent P waves, with a rapid, irregular QRS occurrence (compatible with atrial fibrillation)?

 

d. Are there long pauses in the underlying rhythm before an abnormal complex occurs (escape complex or rhythm)?

6. Consider conduction intervals across the atria (P wave duration), atrioventricular conduction system (P R interval), ventricles (QRS duration), and overall repolarization time (QT interval, in light of the heart rate)

 

a. Is an intermittent AV conduction disturbance present?

 

b. Is consistent relation between P waves and QRS complexes totally lacking, with a slow and regular QRS occurrence (implying complete AV block with ventricular escape rhythm)?

7. For sinus and supraventricular complexes, estimate the mean electrical (frontal) axis (if multiple limb leads available; Figure 1).

 

a.

Note the orientation of terminal electrical activity of the ventricle (last 50% of QRS)

8. Evaluate the QRS morphology for patterns typical of intra ventricular conduction disturbances including bundle branch and fascicular blocks

9. Evaluate the P waves and QRS complexes for patterns consistent with cardiomegaly

10. Assess the ST T for repolarization abnormalities; classify as primary or secondary (from abnormal QRS complex) STT changes

Table 2. ECG Reference Ranges for Dogs and Cats

ECG Variable

Dog

Cat

Heart rate

60 160 beats/min, adults; up to 220 beats/min in young puppies

120 240 beats/min

Mean electrical axis (frontal plane)

+40 to +100 degrees

0 to +160 degrees

Measurements (lead II)

   
 

0.04

sec; to 0.05 sec in

 

P wave duration (maximum)

large/giant breeds

0.035–0.04 sec

P wave height (maximum)

0.4 mV

0.2

mV

PR interval

0.06–0.13 sec

0.05–0.09 sec

QRS complex duration (maximum)

0.05

sec (small breeds) to 0.06

 

sec (large breeds)

0.04 sec

 

wave height (maximum)

2.5 mV (small breeds) to 3 mV (large breeds)*

0.9

mV, any lead; <1.2 mV QRS

R

total excursion, any lead

ST segment deviation

<0.2 mV depression; <0.15 mV elevation

< 0.1 mV deviation

T

wave

usually <25% of R wave height; can be positive, negative, or biphasic

maximum 0.3 mV; can be positive (most common), negative, or biphasic

QT interval duration

0.15–0.25 (to 0.27) sec; varies

0.12–0.18 (range 0.07–0.2) sec; varies

* May be greater in young, thin, deepchested dogs Table compiled by Drs. Wendy A Ware and John D Bonagura.

Mean electrical axis The MEA describes the average direction of the ventricular depolarization process in the frontal plane. It represents the summation of the instantaneous depolarization boundaries during ventricular activation (QRS complex). Estimation of the MEA helps the clinician identify major intraventricular conduction disturbances or – with less sensitivity ventricular enlargement patterns that shift the average direction of ventricular activation. Since the MEA is determined in the frontal plane, only the six frontal leads are used (not chest or baseapex leads). By convention, the leads’ reference positions are defined by degrees (from 0 ˚ to ±180 ˚ ) around a circle (see figure below). The positive pole (electrode) of most leads lies on the ‘positive’ side of the circle; however, it is important to note that the positive pole of leads aV R and aVL lie on the ‘negative’ side of the circle. The MEA can be estimated by either of the following methods:

Find the lead (I, II, III, aV R , aV L , or aV F ) with the largest R wave (or more precisely, the greatest netpositive QRS area)). The location of the positive electrode of this lead along the frontal axis is the approximate MEA.

Find the lead (I, II, III, aV R , aV L , or aV F ) with the most isoelectric QRS (positive and negative deflections are about equal). Then identify the lead perpendicular to this lead on the hexaxial lead diagram. If the QRS in this perpendicular lead is mostly positive, the MEA is toward the positive pole of this lead. If the QRS in the perpendicular lead is mostly negative, the MEA is oriented toward the negative pole. If all leads appear isoelectric, the frontal axis is indeterminate. Normal MEA ranges for dogs and cats generally orient towards leads II and aV F .

ECG complex measurement Abnormal complex measurements may indicate specific chamber enlargement or hypertrophy, as well as conduction or repolarization abnormality. Waveform amplitudes are recorded in millivolts (mV) and durations in seconds. Only one thickness of the inscribed pen line should beincluded for each measurement. At a trace speed of 25 mm/sec, each small (1 mm) box on the ECG grid is 0.04 seconds in duration from left

to right. At a paper speed of 50 mm/sec, each small box equals 0.02 seconds. At standard calibration, a deflection up or down of 10 small boxes (1 cm) equals 1 mV.

COMMON ECG ARTIFACTS Artifacts complicate ECG interpretation and can mimic arrhythmias. Common ECG artifacts include intermittent shivering or muscle tremor artefact, purring in cats, respiratory motion or limb movement artifacts, and 60Hz electrical interference. ECG artifacts are sometimes confused with arrhythmias, but artifacts do not disturb the underlying cardiac rhythm. In contrast, ectopic complexes often disrupt the underlying rhythm and are followed by a T wave. Identifying whether the ECG deflection in question changes the underlying rhythm and also is followed by a T wave usually allows differentiation between intermittent artifacts and arrhythmias. Evaluating more than one simultaneously recorded lead is also helpful.

HEMODYNAMIC CONSEQUENCES OF ARRHYTHMIAS The hemodynamic effects of an arrhythmia depend on a number of factors. These include whether underlying disease is present and the effect it might have on cardiac function, the ventricular activation rate, the duration of the arrhythmia, the temporal relation between atrial and ventricular activation, the sequence or coordination of ventricular activation, drug therapy, and the animal’s activity level. Arrhythmias that compromise cardiac output and coronary perfusion promote hypotension, myocardial ischemia, impaired pump function, and, sometimes, sudden death. These arrhythmias tend to be either very rapid (e.g. sustained ventricular or supraventricular tachycardias) or very slow (e.g. advanced AV block with a slow or unstable ventricular escape rhythm). Rapid tachycardias promote myocardial ischemia because they reduce coronary perfusion pressure and shorten diastole (when most coronary blood flow occurs). Rapid ventricular tachycardia can quickly degenerate into fibrillation. Supraventricular tachycardia could promote secondary ventricular arrhythmias related to poor myocardial perfusion, ischemia, and increased sympathetic stimulation. Persistent tachycardia of either supraventricular or ventricular origin (e.g. ventricular rates of 180–200 beats/minute) will cause myocardial failure within a few weeks. The resulting cardiac enlargement, functional changes, and neurohormonal activation that occur mimic spontaneous cardiomyopathy. This tachycardia induced cardiomyopathy is reversible if heart rate is controlled within a few weeks of onset. AF and atrial standstill cause loss of effective atrial contraction (the “atrial kick”). This can negatively affect ventricular filling (preload). At slower heart rates, the relative importance of atrial contraction to total ventricular filling is small, so any negative effect on cardiac output is likely to be clinically inconsequential at rest. However, as heart rate increases, the importance of atrial contraction increases; the atrial kick can contribute up to 30% of total ventricular enddiastolic volume at high heart rates. During exercise or with heart failure, the loss of atrial contraction can have a pronounced negative effect on cardiac output. Cardiac output also can be impaired by loss of AV synchronization, as well as by ventricular dyssynchrony. AV synchrony is lost when the atria and ventricles beat at different rates, as occurs with various premature beats and abnormal tachycardias, during 3 rd degree AV block (with ventricular escape rhythm), and also with accelerated ventricular origin rhythms, including an artificially paced ventricular rhythm. Ventricular dyssynchrony involves delayed or uncoordinated activation and contraction of one ventricle compared to the other, or septum compared to free wall. Ventricular tachyarrhythmias typically cause some degree of ventricular dyssynchrony, which can exacerbate the arrhythmia’s negative impact on cardiac output at any given HR. Major bundle branch blocks also cause dyssynchronous ventricular contraction that could reduce cardiac output depending on HR and myocardial function. Especially in animals with underlying myocardial disease, ventricular dyssynchrony can contribute to deteriorating cardiac function, even without overt intraventricular conduction delay or ventricular tachyarrhythmias.

ARRHYTHMIAS: WHEN TO TREAT? The arrhythmias of greatest concern are those that cause hemodynamic compromise such as hypotension during anesthesia or clinical signs like syncope. Some arrhythmias associated with breed related dilated cardiomyopathy are known to be associated with sudden death; this is an issue in Doberman pinschers. Conversely, especially in asymptomatic animals with a structurally normal heart, the risk of an arrhythmia might be very low. Such arrhythmias can include isolated premature beats, accelerated idioventricular rhythm, brief episodes of paroxysmal tachycardia, and intermittent low grade AV block. The question of whether to use antiarrhythmic drug therapy for arrhythmias that cause no clinical signs is controversial and influenced by individual circumstances. Nevertheless, in all cases a search for underlying abnormalities potentially associated with the arrhythmia, as well as monitoring of the patient’s rhythm and clinical status are warranted. Arrhythmias causing acute clinical signs should be treated, as should persistent tachycardias, because of their negative long term effect on myocardial function. Successful therapy often means reduction in frequency or repetitive rate of ectopic beats to restore normal hemodynamic status and eliminate clinical signs. Some antiarrhythmic therapies are thought to reduce the risk for sudden death; however, there is no clinical trial evidence that reduction of arrhythmia frequency will translate to improved survival or reduction in the risk for sudden cardiac death. Besides their expense, antiarrhythmic drugs have multiple adverse effects that can include provoking new arrhythmias (proarrhythmia). Exercise restriction and stress avoidance are important to reduce sympathetic nervous activation (which can exacerbate arrhythmias) and as well as cardiac workload. Treatment for concurrent cardiac or extracardiac disease is the best management for some arrhythmias. For example, in the setting of congestive heart failure (CHF) isolated arrhythmias are usually ignored and the heart failure managed medically.

NORMAL AND ABNORMAL CARDIAC RHYTHMS The predominant rhythm in most healthy dogs evaluated by ambulatory monitoring 1,2,5,16 19 is sinus arrhythmia with a daily average heart rate of about 70 to 85/minute, seemingly varying with breed. Wandering atrial pacemaker is commonly observed in dogs and transient second degree AV block is sometimes present; these are manifestations of vagotonia in dogs. For cats the daily average heart rate is typically 150 to 170 per minute on 24h Holter recordings with significant variation in average heartrate among cats. 6,8,20,21 Although sinus arrhythmia is uncommon in hospitalized cats, those monitored at home often exhibit periods of this rhythm. The number of ventricular and atrial ectopic complexes considered normal is a source of some controversy in both dogs and in cats. Multiple studies show very small numbers in most healthy dogs – typically <10 PACs and <10 PVCs in 24h in healthy subjects – but again, there is individual variation. The assessment of “normal” with respect to ectopy is complicated by the frequent occurrence of escape complexes during sleep and our inability to compare Holter data to a true “gold standard” of (genetic) normalcy. Echocardiography is typically used but is an inferior method for deciding if the heart is electrically or genetically normal. This issue becomes especially obvious in canine breeds prone to heart rhythm disturbances associated with cardiomyopathies (including Doberman pinschers 3,22,23 , Boxers, 24,25 English bulldogs, 26 Irish wolfhounds, 27,28 and great Danes 29 ). A similar concern arises in cats owing to the high degree of occult hypertrophic cardiomyopathy (HCM) in this species. 30

Sinus Rhythms The normal sinus node can discharge regularly (normal sinus rhythm), and irregularly due to autonomic influence (sinus arrhythmia). Sinoatrial discharge rate also can be slower or faster than normal for the species (sinus bradycardia and sinus tachycardia, respectively). Each of these rhythms is characterized by a normal P wave preceding the QRS complex. Under some conditions sinus bradycardia and sinus tachycardia are physiological, as with sleep or exercise; however, these rhythms can also arise from number of influences and medical disorders as indicated below. Sinoatrial exit block, sinus arrest, and sinus node re

entry are considered abnormal rhythms involving the sinus node (see Table 3). Physiologic sinus rhythms during routine clinical (hospital) examinations include normal (regular) sinus rhythm and sinus arrhythmia in dogs. Sinus arrhythmia does occur in unstressed cats but is uncommon in the clinic due to sympathetic dominance in that setting. It also should be noted that sinus node activity usually persists in the presence of functional or anatomical impairment of atrioventricular (AV) conduction. This is a useful diagnostic feature especially when atrial activity is driven by the sinus node during periods of AV block, nodal (junctional) rhythm, ventricular tachycardia (VT) or ventricular pacing. These rhythms often lead to so called AV dissociation , which is simply a description of two independent pacemaker foci – one driving the atria and one depolarizing the ventricles. AV dissociation it is not a rhythm diagnosis per se but a consequence of another rhythm disturbance. Although retrograde atrial activation can occur during AV dissociation, 31 leading to “capture” (depolarization or suppression) of the SA node, this is relatively uncommon in dogs and cats. In the clinical setting normal sinus rhythm in dogs occurs at relatively higher rates of approximately 60 to 180 per minute when recorded by ECG and with the dog in lateral recumbency. The heart rate for cats in normal sinus rhythm is usually 160 to 240 per minute, again, with the recording done in lateral recumbency (and undoubtedly inducing stress). Sinus arrhythmia in dogs is characterized by similar rates but with cyclic variation in the atrial rate and often a wandering atrial pacemaker (with P waves becoming taller during the shorter cycles in the left caudal leads). Although most sinus arrhythmias tend to develop at relatively slow heart rates in dogs, concurrent sympathetic and parasympathetic surges can occur resulting in a relatively fast, but irregular rhythm. Most sinus arrhythmias in dogs are ventilation related, with heart rate accelerating through inspiration; however, this relationship is not always obvious, especially in panting dogs or when the overall sinus rate is relatively high. In these cases, other factors, such as baroreceptor reflexes, might also be operational. Dogs with respiratory disease often show pronounced sinus arrhythmia with a wandering pacemaker. The short cycles in these cases can resemble premature atrial complexes (PACs) although the earlier P waves are rarely summated on the prior Twave during sinus arrhythmia (in contrast to PACs). As a general rule, vagally induced arrhythmias should abate or become more regular with exercise or other causes of sympathetic tone. Failure of sinus node discharge leads to a transient absence of P waves and the rhythm is called sinus arrest when the ensuing pause exceeds at two normal P P intervals. Brief pauses are sometimes referred to as sinus pause and this might represent a variant of sinus arrhythmia, sinoatrial block, or sinus arrest. In cases of recurrent sinus arrest the heart will usually be rescued by pacemaker cells located in the atrial tissues, AV junction, or His Purkinje system. These subsidiary pacemakers can initiate escape complexes or an escape rhythm. Chronic, progressive, sinus node dysfunction is especially prevalent in miniature schnauzers, West Highland white terriers, and Cocker spaniels, but also observed in other breeds. With sufficient escape activity most dogs are asymptomatic, but failure of subsidiary pacemakers – a sign of more diffuse conduction system disease can result in collapse or syncope creating the sick sinus syndrome. 32 40 Additionally some dogs with sinus node disease experience atrial or other types of paroxysmal supraventricular tachycardias that can overdrive the sinus node and promote periods of sinus arrest. This is the so called bradycardia tachycardia syndrome of sick sinus syndrome. Most of these cases are easily diagnosed from a standard 2 to 5 minute ECG, especially in cases of symptomatic sinus node dysfunction. Sinus arrest is often confused (and might overlap with) the vagally mediated sinus bradycardia and arrest associated with an exaggerated baroreceptor reflex. This reflexmediated (“vasovagal”, “neurocardiogenic”) syncope generally stems from a combination of vagally induced cardiac depression and the simultaneous withdrawal of sympathetic stimulation to blood vessels. Classically, weakness or collapse is induced by sudden sympathetic stimulation of the heart associated with a stressor. This reflex involves activation of cardiac mechanoreceptors (C fibers) leading to (inappropriate) activation of the baroreceptor reflex. The reflex is most often preceded by a period of sinus tachycardia followed quickly by sudden sinus node slowing, transient AV block, sinus arrest, and junctional or ventricular escape activity. These can be readily observed on an event monitor. In humans, vasodepressor effects (vasodilation) can persist even after recovery of the heart rate; thus, the diagnosis can be elusive without an excellent history and event monitor

recording. (Frequently, recordings taken just after the fainting are normal). Although this condition is barely mentioned in veterinary literature, it is likely the diagnosis in many cases of so called “sick sinus syndrome” when sinus arrest is recorded during exercise/excitement induced syncope.

Table 3. Sinus Rhythms

Rhythm

 

Comments

Normal sinus rhythm

P

to P intervals vary by <10%; normal HR for species

Sinus arrhythmia

Cyclic speeding and slowing at normal to slow HR for species. Often synchronized to ventilation. Wandering atrial pacemaker commonly observed.

Sinus bradycardia

Slow sinus rhythm; regular or irregular.

Sinus tachycardia

Fast sinus rhythm with subtle variation in P to P (RR) intervals; vagal maneuvers might transiently alter the cycle length. “Fast” sinus tachycardia, over ~240 to 250/min, can result in Twave/P wave fusion, confusing the rhythm diagnosis.

Sinus pause

Long pauses during sinus arrhythmia; can be normal (vagal) or early sign of sinus node dysfunction.

Sinus arrest

Termed “sick sinus syndrome” (SSS) when associated with clinical signs and not triggered only by excitement. Signs in SSS usually depend on a lack of escape activity. Sinus arrest can also occur with inappropriate activation of a baroreceptor reflex (reflex mediated syncope).

Sinoatrial block

Rare in dogs and only tenable as a diagnosis when the inter atrial (P wave) interval bounding a long pause is “exactly” twice to three times the normal P P interval. Nearly impossible to diagnose in the setting of sinus arrhythmia. Another variant is SA Wenckebach periodicity; this is considered when the P

interval progressively decreases followed by a relatively long pause (this might be a normal, vagally induced rhythm).

P

Sinus node re entry

Difficult to diagnosis with certainty; the coupled P waves should be nearly identical. Can be confused with sinus arrhythmia occurring in paired complexes followed by a pause. Also can be confused with atrial bigeminy (sinus complex followed by an ectopic atrial complex) if the ectopy originates near the crista terminalis (i.e., close to the SA node).

In considering the differential diagnosis of sinus rhythm disturbances, it is emphasized that most are caused by either exaggerated vagal or sympathetic tone. For example, an athletic dog is likely to have a very low resting heart rate, often falling into the 40’s or lower, a physiologic sinus bradycardia. Patients with elevated CSF pressure can develop sinus bradycardia through activation of the baroreceptor reflex (“Cushing’s reflex”) and secondary increases in vagal tone. Paradoxically, many causes of shock in cats are associated with sinus bradycardia. Conversely, predictable causes of reflex sinus tachycardia include pain, anxiety, hypotension, and heart failure. Additionally, drugs such as anesthetics, digoxin, dexmedetomidine, phenylephrine, theophylline, and catecholamines (acting directly or via autonomic effects); plant, animal, prescription and illicit drug toxicities body temperature; and endocrine status (especially thyroid and adrenal) can positively or negatively modify sinus node discharge rate. Thus the management of sinus rhythm disturbances is focused initially on identifying and treating any underlying conditions. In most situations sinus tachycardia means activation of the sympathetic nervous system. A rapid volume or colloid infusion will slow the heart rate in many cases of reflex sinus tachycardia due to hypovolemia or another cause of reduced ventricular preload. This is often a first treatment in critical care and perioperative settings (for patients not in congestive heart failure or CHF). Pain control or relief from anxiety often reduces a physiological sinus tachycardia, and successful therapy of heart failure usually reduces sinus node rate as well. Occasionally, inappropriate sinus tachycardia is treated with a beta blocker

such as esmolol (IV) or atenolol (PO). This is especially relevant when the sinus rate persistently exceeds ~240/minute in dogs or ~280/minute in cats and no definable etiology has been found. Although atenolol therapy can be administered to blunt the sinus tachycardia of cats with thyrotoxicosis, in most cats the heart rate slows with methimazole therapy. Drug therapy of sinus tachycardia might also be appropriate when a sympathomimetic toxin (e.g. Baker’s chocolate) has been ingested and the heart rate does not slow with volume infusion and sedation. Sinus bradycardia can be treated and sometimes prevented in the hospital with atropine or glycopyrrolate. Cats with cardiogenic shock rarely respond to atropine and are best treated with an inotropic drug with sympathomimetic properties (for example, dobutamine at 2.5 to 5 mcg/kg/min for initial therapy). With increased cardiac output and passive warming the heart rate will increase in cats that survive and often P waves will become more obvious. Short term management of sinus bradycardia that is refractory to drugs can involve temporary pacing by transvenous, transesophageal, or transcutaneous methods 41 49 provided the sedation or anesthesia needed to make these procedures tolerable and humane is given. The best long term therapy for sick sinus syndrome (SSS) is permanent transvenous pacing. In bradycardia tachycardia syndrome, antiarrhythmic drugs that either suppress atrial ectopy or block the AV node can also be given once pacing has commenced (see next section on atrial arrhythmias). Pacemaker programming is critical for optimal system performance (e.g. VVIR or rate responsive demand mode) 50 56 and longterm outcomes are generally very good with single chamber atrial or ventricular pacing (the latter is less complicated). Although often prescribed (and anecdotally appear to reduce lethargy and weakness in some dogs with early stage SSS), anticholinergic drugs such as hyoscyamine (Levsin®) or sympathomimetic drugs such as terbutaline and theophylline long acting are rarely effective in preventing recurrent bouts of sinoatrial syncope. These drugs generally are only used if pacing cannot be performed for some reason. Importantly, pacemaker therapy shouldn’t be delayed for drug trials unless the diagnosis is uncertain or the symptoms infrequent. Optimal treatment for sinus node depression related to documented reflexmediated syncope is unknown. For those with predominately cardiodepressor activity (sinus slowing/AV block) cardiac pacing with hysteresis might help; however, if there is a prominent vasodilator component, pacing could be insufficient to prevent collapse or syncope. This has not been studied in veterinary medicine. In these patients treatment is directed initially to controlling circumstances that precipitate syncope and managing any identified comorbidity (such as heart failure, pulmonary hypertension or respiratory disease). Beta blockade – given to prevent the initial cardiac triggering of the reflex – has been disappointing, often makes things worse. Medical therapy with hyoscyamine, theophylline long acting, or terbutaline can be tried as 2 4 week trials.

Supraventricular Arrhythmias Atrial and other supraventricular rhythm disturbances are among the most common and difficult to treat of all ECG diagnoses These supraventricular arrhythmias include the following: premature atrial complexes (PACs or APCs), focal and reentrant atrial tachycardias, 11,57 59 atrial flutter, 57,60 68 atrial fibrillation (AF), 28,69 91 reentrant supraventricular tachycardia (SVT) using an accessory bypass tract, 92 96 nodal (junctional) rhythms, 31 and atrial standstill (Table 4). The authors have excluded sinus rhythm disturbances in this classification although others include sinus tachycardia as a form of SVT. Conceptually it is helpful to consider the most common atrial arrhythmias as inter related. These include recurrent PACs, focal and micro reentrant atrial tachycardias, 97 atrial flutter, 63,65 and AF. Some patients exhibit all of these rhythm disturbances at one point or another. The diagnosis of PACs and nonsustained (paroxysmal) atrial tachycardia is relatively straightforward (see Table 4), but the differences between sustained atrial tachycardia and atrial flutter can be subtle; without electrophysiological studies, is sometimes difficult to tell one from the other and we do not yet have firm criteria for these diagnoses in small animals. In general, atrial flutter is observed in dogs with dilated right atrial chambers and is characterized by saw toothed flutter waves in the baseline and the lack of an isoelectric shelf. Atrial tachycardias in dogs often fit the human criteria for focal atrial tachycardia and many exhibit positive P

waves in the caudal limb leads creating some diagnostic confusion with sinus tachycardia. Furthermore, large T a waves in atrial tachycardia can mimic flutter waves. The atrial rate in atrial tachycardia is often in the 250 to 300 per minute range (or faster) and physiological AV block is common. 97 With atrial flutter the atrial rate is usually in the 260 360/minute range but the macro reentry loop in the right atrium can result in slower or faster cycle lengths. 63 The recognition of atrial tachycardia or flutter can be challenging if there is a regular conduction sequence, especially with 1:1 atrioventricular conduction, as ectopic P’ waves or F waves are buried in the QRS complexes or STT. In cases of regular, narrow QRS tachycardia, the ECG differential diagnosis is usually one of four SVTs: (1) sinus tachycardia (typically <300/min); 2) focal atrial tachycardia; 3) atrial flutter; or 4) AV nodal dependent, orthodromic reentrant SVT using an accessory pathway or longitudinal dissociation of the AV node. Blocking the AV node is especially helpful in confirming the diagnosis and can be attempted with a vagal maneuver, diltiazem, or esmolol (see below).

Table 4. Atrial & Supraventricular Rhythms

Rhythm

Comments

Premature atrial complexes Atrial “echoes” (retrograde activity)

Must distinguish from sinus arrhythmia Premature P’ often buried in the prior ST T A longer P R interval is common with PACs Retrograde (negative) P’ waves with atrial echoes

Atrial tachycardia Focal most common in dogs

Can resemble sinus tachycardia Typically related to atrial dilatation

Atrial flutter

Regular conduction sequences can lead to difficulties in diagnosis; blocking the AV node (vagal maneuver or diltiazem) usually reveals flutter waves

Atrial fibrillation

Irregular ventricular response is expected except in cases of concurrent AV conduction disease

Orthodromic supraventricular tachycardia (accessory pathway)

Presence of ventricular pre excitation during sinus rhythm is a tip off (WPW); however, electrophysiologic study might be needed for diagnosis. Retrograde P’ waves in STsegment.

Nodal (junctional) rhythms Junctional escapes Junctional (nodal) tachycardia

Escape rhythms are secondary to sinus node dysfunction or AV block Nodal tachycardias rare except with digitalis toxicity

Atrial standstill