Memorias Curso de Cardiología en Perros y Gastos

AMMVEPE 1968 - 2016

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 CARDIOLOGÍA 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) Autonomic‐related; 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, single‐lead 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.

* Contributions of Dr. Wendy A. Ware, DACVIM (Cardiology) to this document are gratefully acknowledged

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 recorders11‐14 – 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 aVF. 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 aVF, in the frontal plane and strongly positive in the lower‐left, precordial leads (V2‐V4). 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 (60o) or lead aVF (90o) 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 & QRS‐T 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‐QRS‐T 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 ST‐T 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 (Q‐T 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) ST‐T changes

Table 2. ECG Reference Ranges for Dogs and Cats ECG Variable Dog 60‐160 beats/min, adults; up to Heart rate 220 beats/min in young puppies Mean electrical axis (frontal plane) +40 to +100 degrees Measurements (lead II)

0.04 sec; to 0.05 sec in large/giant breeds P‐wave height (maximum) 0.4 mV PR interval 0.06–0.13 sec 0.05 sec (small breeds) to 0.06 QRS complex duration (maximum) sec (large breeds) 2.5 mV (small breeds) to 3 mV R‐wave height (maximum) (large breeds)* <0.2 mV depression; <0.15 mV ST segment deviation elevation usually <25% of R wave height; T wave can be positive, negative, or biphasic P‐wave duration (maximum)

QT interval duration *

0.15–0.25 (to 0.27) sec; varies

Cat 120‐240 beats/min 0 to +160 degrees

0.035–0.04 sec 0.2 mV 0.05–0.09 sec 0.04 sec 0.9 mV, any lead; <1.2 mV QRS total excursion, any lead < 0.1 mV deviation maximum 0.3 mV; can be positive (most common), negative, or biphasic 0.12–0.18 (range 0.07–0.2) sec; varies

May be greater in young, thin, deep‐chested 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 base‐apex 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 aVR 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, aVR, aVL, or aVF) with the largest R wave (or more precisely, the greatest net‐ positive 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, aVR, aVL, or aVF) 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 aVF.

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 be included 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 end‐diastolic 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 3rd 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 monitoring1,2,5,16‐19 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 Danes29). 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 T‐wave 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 reflex‐mediated (“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 Cyclic speeding and slowing at normal to slow HR for species. Often Sinus arrhythmia synchronized to ventilation. Wandering atrial pacemaker commonly observed.

Sinus bradycardia Slow sinus rhythm; regular or irregular.

Fast sinus rhythm with subtle variation in P to P (R‐R) intervals; vagal maneuvers might transiently alter the cycle length.

Sinus tachycardia “Fast” sinus tachycardia, over ~240 to 250/min, can result in T‐wave/P‐wave fusion, confusing the rhythm diagnosis.

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

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 Sinus arrest escape activity. Sinus arrest can also occur with inappropriate activation of a baroreceptor reflex (reflex‐mediated syncope).

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.

Sinoatrial block Another variant is SA Wenckebach periodicity; this is considered when the P‐ P interval progressively decreases followed by a relatively‐long pause (this might be a normal, vagally‐induced rhythm).

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 node re‐entry (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 methods41‐49 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 long‐term 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 reflex‐mediated 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 re‐entrant atrial tachycardias,11,57‐59 atrial flutter,57,60‐68 atrial fibrillation (AF),28,69‐91 re‐entrant 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 Ta 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 ST‐T. 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 Must distinguish from sinus arrhythmia Premature atrial complexes Premature P’ often buried in the prior ST‐T Atrial “echoes” (retrograde activity) A longer P‐R interval is common with PACs Retrograde (negative) P’‐waves with atrial echoes Atrial tachycardia Can resemble sinus tachycardia Focal most common in dogs Typically related to atrial dilatation Regular conduction sequences can lead to difficulties in Atrial flutter diagnosis; blocking the AV node (vagal maneuver or diltiazem) usually reveals flutter waves Irregular ventricular response is expected except in cases of Atrial fibrillation concurrent AV conduction disease Presence of ventricular pre‐excitation during sinus rhythm is a Orthodromic supraventricular tip‐off (WPW); however, electrophysiologic study might be tachycardia (accessory pathway) needed for diagnosis. Retrograde P’‐waves in ST‐segment.

Nodal (junctional) rhythms Escape rhythms are secondary to sinus node dysfunction or AV Junctional escapes block Junctional (nodal) tachycardia Nodal tachycardias rare except with digitalis toxicity Most common absence of P‐waves, increased amplitude T‐ Atrial standstill waves (positive OR negative) & widening of QRS complex.

Transient (hyperkalemia) Cats: often misdiagnosed as ventricular tachycardia.

Persistent Sine‐waves with bradycardia = near‐terminal rhythm.

Supraventricular arrhythmias can be transient, recurrent, persistent, or permanent. In most cases, recurrent or permanent atrial arrhythmias are caused by structural heart diseases27,75,78‐81,86,98‐100 associated with congenital, chronic valvular, myocardial, or pericardial disease. These arrhythmias are especially frequent in the giant breeds and other dogs prone to dilated cardiomyopathy (DCM) such as the Irish wolfhound, Newfoundland dog, Saint Bernard, Great Dane and Doberman pinscher. A large atrial mass (size) predisposes to atrial arrhythmias in general and to the perpetuation of atrial fibrillation (AF) in particular; therefore, it is logical that this rhythm is more often observed in larger breeds and when hearts are afflicted by structural disease and atrial dilatation. Atrial fibrillation is relatively uncommon in cats and most (though not all) also have severe structural heart disease.101 Some giant breeds develop chronic atrial arrhythmias without overt structural disease (although this may eventually develop). Thus many dogs with so‐called “lone” AF are likely to manifest cardiomyopathy if followed over a sufficient length of time. Transient atrial arrhythmias often are observed in perioperative situations (often large‐breed dogs), following opioid administration, and with some gastrointestinal diseases (parasympathetic input shortens the atrial refractory period, predisposing to AF). Other causes include intracardiac catheters, cardiac tumors

(especially right atrial hemangiosarcoma), and spontaneous and iatrogenic thyrotoxicosis.64,102 Many atrial arrhythmias are short‐lived and will revert to sinus rhythm; however, in other cases, the arrhythmia is persistent or progressive and might require drug therapy or DC cardioversion.

The ventricular response and regularity during an SVT is determined by the mechanism of the arrhythmia and AV conduction pattern: 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 can 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 with regular SVTs regardless of mechanism, often appearing at the onset of a nonsustained arrhythmia. This finding can 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).

Therapy of supraventricular arrhythmias is often more challenging than for ventricular arrhythmias.

Premature atrial complexes are uncommonly treated other than to manage underlying heart disease. A Holter ECG can be useful in assessing the overall severity of the rhythm disturbance. If PACs are bothersome (to the patient or doctor) or associated with paroxysmal tachycardias, a beta‐blocker such as atenolol or the antiarrhythmic drug sotalol (1‐2 mg/kg PO b.i.d.) can be administered. In the setting of CHF, digoxin (starting at approximately 0.005 mg/kg, PO b.i.d.) can be considered.

When managing focal atrial tachycardia, the clinician should decide if the arrhythmia is more likely of recent onset or chronic in nature. Treatments that can suppress ectopic rhythms, including lidocaine (effective only in acute conditions), sotalol, amiodarone, and flecainide (or propafenone) are more likely to be successful in arrhythmias of recent onset or in the setting of a normal echocardiogram. Many focal atrial tachycardias are relatively resistant to drug suppression and are bested treated with heart rate control.

Drugs that block the AV node – diltiazem, beta‐blockers, and digoxin – are the mainstays, as discussed below for AF. Although rate control can be achieved in some dogs with amiodarone,103 the potential for adverse effects outweigh the benefit. Thus if efforts to suppress an ectopic rhythm fails, or if the arrhythmia is chronic, ventricular rate control is the more logical goal, especially in the setting of structural heart disease.

When atrial tachyarrhythmias are associated with CHF, digoxin is chosen first, but in all other cases, diltiazem or a beta‐blocker alone or in combination will be more effective for rate control, and sometimes these drugs will convert the arrhythmia back to sinus rhythm.

In the management of atrial tachycardia, atrial flutter and atrial fibrillation two general approaches are taken: rhythm control with cardioversion and rate control with drugs. The issue of underlying structural disease is highly relevant in terms of prognosis and treatment. Despite reports of successful cardioversion of AF in dogs with CHF, the general experience is that most dogs revert back to AF in a relatively short time.

Accordingly, accepting some differences of opinion, it is difficult to justify the short‐term benefit of AV synchronization with the risks and costs of the electrocardioversion procedure in a dog with CHF or moderate to severe atrial remodeling. We need more controlled, prospective studies of dogs with CHF who are cardioverted and then maintained with drugs that prevent reversion to AF. Rhythm control in atrial tachyarrhythmias is appropriate for specific cases. Intravenous drug therapy or synchronized DC cardioversion of atrial flutter/fibrillation is reasonable in dogs if the arrhythmia is known to have begun during a perioperative period or is of recent onset. A structurally normal heart should first be assured via echocardiography, and hypokalemia and hyperthyroidism should be excluded as predisposing factors. When the onset of AF (or flutter) is witnessed, spontaneous cardioversion is common within a few hours. Lidocaine (2‐8 mg/kg over 10 minutes) can be tried, especially if AF is vagally mediated,90 and carries the potential for conversion with little down‐side on hemodynamics. Other options for intravenous cardioversion include 1) procainamide (2 mg/kg IV over 2 minutes; up to 20 mg/kg cumulative dosage; with QRS, Q‐T, and BP monitoring); 2) IV amiodarone (use Nexterone® only! Do not use standard IV amiodarone with preservatives; start Nexterone at 2‐3 mg/kg IV infusion over 60 to 120 minutes with BP monitoring and

continue to a cumulative dosage of 5 to 6 mg/kg if tolerated); 3) or diltiazem (start with 0.1 mg/kg over 5 minutes; repeat up to 0.3 to 0.4 mg/kg IV cumulative dosage; with BP monitoring). Diltiazem is used mainly for ventricular rate control when the heart rate is dangerously high (>250/minute) or BP is low; occasionally diltiazem will convert AF to normal sinus rhythm. Biphasic, DC cardioversion is very effective in treating lone AF of recent onset.83,104,105 If the cardioversion is planned, oral amiodarone (loading dose of 4‐6 mg/kg PO b.i.d.) can be given for one week prior to conversion; alternatively intravenous Nexterone® can be administered at 4‐6 mg/kg IV over 2‐3 hours prior to electrocardioversion. Either generic amiodarone (4‐6 mg/kg PO once daily) or sotalol (1 to 2 mg/kg PO twice daily) is prescribed empirically after electrocardioversion to maintain sinus rhythm. These drugs are usually continued for some months to prevent reversion to atrial fibrillation; however, the benefit to risk of such therapy has not been established, and amiodarone carries the risk of hepatotoxicity especially after months of therapy.

For chronic heart rate control of atrial tachyarrhythmias, the goal is blocking AV nodal conduction to reduce the transmission of atrial impulses. A combined treatment with digoxin and diltiazem106 ( a beta‐ blocker) is most often used in dogs with chronic AF associated with CHF. Rate control in cats is typically attained with diltiazem, atenolol, or the combination. In the author’s experience, optimal ventricular rate control in dogs is achieved with a modest dose of digoxin (start with 0.005 mg/kg PO b.i.d.) and aim for a trough blood level of 0.8 to 1.2 ng/ml); moderate dosages of diltiazem (6 to 8 mg/kg/day, PO dividing the total dosage t.i.d. or b.i.d. for standard or long‐acting preparations, respectively); and later adding in a low dose of carvedilol (starting at one 3.125 mg tablet twice daily for a large‐breed dog). Higher dosages of digoxin or diltiazem definitely provide better rate control, but at the expense of anorexia or other adverse effects. The in‐clinic ECG heart rate overestimates the average home heart rate in dogs with AF.91 In the author’s experience, an in‐hospital ECG rate over 60 seconds of 120‐150/minute predicts good control; optimally a Holter ECG should be recorded once the clinic ECG rate seems appropriate. It may take some weeks to achieve optimal rate control.

Genetically predisposed arrhythmias associated with abnormal electrical pathways (bypass tracts)92‐96 are observed in some breeds especially Labrador retrievers. These can predispose to very rapid SVT. Reentrant SVTs employ circuits that develop at the micro (AV nodal/junctional) and macro (by‐pass tract) levels.107 The best‐characterized ones in dogs involve an electrical circuit connecting 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, by premature atrial or ventricular complexes, or by electrophysiologic changes in the electrical pathways constituting the circuit. This permits current to descend down one pathway (typically AV node) and the travel retrograde back to the atria via the accessory pathway, creating a macro‐reentry loop. In most cases the circuit forms an orthodromic SVT: 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, but not all cases, 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 narrow to wide QRS and secondary T‐wave changes. Delta waves can be discrete waves in dogs and cats96,108,109 or more typical of those observed in humans (slurred upstroke of the R‐wave, best seen in precordial leads). 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 is unrelated to the aforementioned atrial arrhythmias. The term indicates that the atrial muscle is unexcitable, and it should not be confused with sinus arrest in which atrial muscle is responsive, but unstimulated. This condition is caused transiently by high serum potassium or persistently by atrial muscle disease or by severe atrial dilation (in cats). In these cases, no P‐waves are evident (atrial standstill) or very tiny, non‐conducted, or low‐amplitude P‐waves are evident. With hyperkalemia the QRS complex becomes widened and the T‐waves large and sometimes tented (especially in V‐leads). A pitfall of diagnosis in cats, where heart rate may not decrease, is that hyperkalemia can be confused with ventricular tachycardia. Persistent atrial standstill caused by atrial myocardial disease and fibrosis is most common in English Springer spaniels, but can also occur in larger retriever breeds and sporadically in others. On

echocardiography one or both atria are markedly dilated and most dogs also develop CHF. In cats apparent atrial standstill can be observed with severe forms of cardiomyopathy and severe atrial dilatation. It is sometimes, but not often, reversible. Treatment involves managing CHF medically and consideration of endocardial ventricular pacemaker implantation, accepting the overall benefit varies widely with survival times ranging from months to years.

Ventricular Arrhythmias Arrhythmias arising in the ventricle parallel those of the atria in terms of nomenclature. Both types of arrhythmias can be hemodynamically destabilizing, but there are important differences: 1) the AV node need not be activated to generate a QRS complex so that heartrate control is generally not an effective strategy; and 2) there is greater potential for sudden death if the rhythm degenerates to ventricular fibrillation or asystole. Unfortunately it is difficult to predict which patients will die suddenly or will benefit from therapy.

In terms of etiology, the aforementioned categories listed in the “Introduction” and the various etiologies mentioned under atrial arrhythmias also apply to ventricular ectopy. Some breeds – especially boxers or English bulldogs (with arrhythmogenic right ventricular cardiomyopathy = ARVC), and many Doberman pinschers with “occult” DCM are prone to ventricular ectopy as part of a genetic/breed predisposition. Another example is Duchenne cardiomyopathy in golden retrievers.110 These arrhythmias can develop within or before the development of overt ventricular dysfunction. Other breeds develop ventricular ectopy as a component of dilated cardiomyopathy. Some of these dogs have relatively normal echocardiograms at the time of first recognition of the arrhythmia and exhibit clinical findings of DCM only further down the road. There are sporadic cases of myocarditis seen in dogs (post‐viral(?); septicemia; Chagas myocarditis), and cats have a well‐recognized endomyocarditis that is difficult to diagnosis antemortem. No doubt there also are many undiscovered, genetically‐programmed channelopathies in dogs that can serve as a substrate for ventricular ectopy but are as yet unrecognized. One well‐characterized example of genetic “electrical disease” is the inherited ventricular ectopy seen in certain lines of German shepherds.111 When ventricular ectopic complexes are recognized in a canine breed that is atypical for a genetic cardiomyopathy, or diagnosed in a dog with no other signs of heart disease, the clinician also must consider a host of potential noncardiac causes, including hypokalemia, autonomic imbalance,112 myocardial ischemia, coronary thrombosis, and other “usual suspects” such as splenic masses, anemia, infections, and drugs. Veterinarians have learned to expect some conditions, such as gastric dilatation‐volvulus, to induce ventricular arrhythmias.

A classification of ventricular rhythms is listed in Table 5. Idioventricular rhythms arise from normally‐ present pacemakers in the His‐Purkinje system. When activated, these escape complexes are rescue mechanisms for sinus node arrest or AV block and should not be suppressed. The typical idioventricular (escape) rhythm in the dog discharges at 20 to 40/minute; however, in the cat the escape rate is much faster (typically 110 to 120/minute) and often approaching 130/minute in cats with chronic complete AV block.113 The so‐called accelerated idioventricular rhythm (AIVR) is thought to indicate normal pacemaker cells hastened by some injury that has altered transmembrane potentials or pacemaker currents. In this regard, sympathetic activity and enhanced calcium transits are relevant factors. These are quite common in dogs following various ischemia‐reperfusion injuries or after general anesthesia. These rhythms are faster than escape rhythms and tend to initiate in late diastole, “warm‐up” for a few beats, then manifest at normal heart rates (typically 60 to 180 per minute). The “slow VTs” often competing with the sinus rhythm such that fusion complexes (from combined ectopic and sinus impulses) are common in AIVR. In general these rhythms are well tolerated and left untreated, in favor of addressing any underlying medical issues.

Table 5. Ventricular Rhythms Rhythm Ventricular escapes Ventricular escape rhythm (idioventricular rhythm)

Comments Secondary to sinus bradycardia, sinus arrest, or AV block; idioventricular rhythm can also be a terminal rhythm from “downward displacement” of the pacemaker.

Timing of PVCs should consider “R on T” and late diastolic PVCs (distinguish from escape complexes) Premature ventricular complexes Distributional patterns include haphazard, bigeminy, trigeminy (two (PVCs, VPCs) variants), couplets, triplets Morphology includes uniform (“unifocal”) & multiform Various categorizations based on rate and morphology Ventricular tachycardia (VT) Accelerated Idioventricular rhythms – generally benign VT – monomorphic, bidirectional, polymorphic, torsade Ventricular flutter Sign‐wave like; cannot distinguish R‐ from T‐wave No consistently formed waveforms; coarse or fine VF Ventricular fibrillation Fine VF can be confused with asystole Absent rhythm Asystole (ventricular standstill) Can occur in DCM or in chronic congestive heart failure

In contrast to idioventricular rhythms, premature ventricular complexes (PVCs, VPCs) and most ventricular tachycardias (VTs) arise early in the cardiac cycle (i.e. compared to the dominant R‐R cycle); these ectopic complexes can be uniform or multiform in morphology. (Note: a fusion complex between a PVC and a sinus impulse also can create intermediate QRS forms and should not be viewed as a multiform complex). In Holter ECG systems, 3 (or more often 4) linked PVCs constitute a “run” of VT. Ventricular tachycardias can be “slow” or “fast”; paroxysmal or sustained; monomorphic or polymorphic; or rapidly varying in orientation (torsade de pointes). The ventricles also can flutter (creating sine waves), or fibrillate (disorganized and lethal activation). In very sick animals or in those with CHF, death can occur from asystole, which is essentially ventricular standstill.

The ECG diagnosis of PVCs or of VT is generally straightforward, although it can be confused by supraventricular tachycardias conducted with aberrancy (bundle branch block) or by hyperkalemia. A full workup includes drug and medical history, consideration of clinical signs (weakness, collapse or syncope), Echo findings, laboratory tests (CBC, chemistries, cardiac troponin‐I), and often abdominal ultrasound. These are obtained to determine the most likely cause and overall clinical significance of the arrhythmia. A Holter ECG can contribute to assessing the severity and complexity of the PVCs, as well as provide a baseline and objective measure of response to therapy. Although some cardiologists always perform a baseline Holter before starting antiarrhythmic therapy, in dogs with syncope or dangerous‐morphology rhythms, there is some risk of delaying therapy (and a single sudden death during that short therapy delay can be enough to modify one’s view about always having a “baseline”!). As discussed earlier, the absolute number of “normal” PVCs per day is controversial, and related in part to classification of some “late” ventricular ectopic complexes (abnormal vs. escapes). Based on some Holter ECG studies, >10/day in cats and >50 to 100/day in dogs would be considered abnormal114 (but these are arbitrary numbers and many cardiologists use lower limits). Spontaneous daily variation24,115 is common (up to ~85%); this should be taken into account when assessing therapy as well. An absolute number of complexes per 24h is not very important when the total count is low. Recall there are 1440 minutes per day so a total of 1000 PVCs, while clearly abnormal, is still <1/minute on average. More critical to consider are: the impact of the underlying cause, the rate and complexity of the arrhythmia (modified “Lown criteria”), and the presence of clinical signs.

The assessment and therapy of ventricular arrhythmias is both controversial and confusing. The patient history (collapse or syncope), signalment, and underlying cause should factor into the assessment. For example, most cats with chronic ventricular ectopy have structural heart disease (cardiomyopathy) or at least an elevated serum troponin suggestive of active myocardial injury, infarction, or myocarditis. A

Doberman pinscher with PVCs on a routine ECG is likely to progress towards overt dilated cardiomyopathy.

When an ECG demonstrates even a few PVCs in a dog of this breed that has collapsed or fainted, the risk of sudden cardiac death is also very high, although that might not be the case for a boxer dog. Thus clinical signs might prompt antiarrhythmic therapy in a Doberman pinscher, recognizing there is no proof treatment will prolong life. Conversely, many asymptomatic boxers have PVCs for years without attendant signs and are best assessed by history and ambulatory (Holter) ECG monitoring before initiating any treatment. When VT or PVCs occur after an acute non‐cardiac disorder, such as gastric dilation or trauma, short‐term therapy might or might not be needed. In contrast, the syncopal boxer or giant breed dog with well‐characterized VT will likely receive life‐long treatment. When ventricular ectopy is identified in the setting of heart failure it is worth having a reasoned discussion with the clients. Many clients opt for no antiarrhythmic therapy even in dogs with runs of VT. This is not unreasonable considering the lack of efficacy data, the potential for drug side effects and negative inotropy, and the simple fact that many pet owners would prefer a “sudden death” to making a “decision for euthanasia”. For these reasons, in dogs with CHF, the authors often ignore PVCs and short runs of VT, especially if these runs are not inducing clinical signs.

Management of ventricular ectopic rhythms involves determining the most likely cause, advancing an educated guess about the clinical significance of the rhythm disturbance (often after a Holter ECG), considering the need for therapy, and possibly choosing one or more drugs. All antiarrhythmic drugs carry the potential for adverse‐effects and worsening of the arrhythmia (proarrhythmia). For acute hospital management in dogs 2% lidocaine remains the drug of choice (2 mg/kg IV bolus over 2 minutes; repeated up to 8 mg/kg over 10 minutes – stop if vomiting or tremors). Lidocaine can also be used at the 1‐2 mg/kg dosage in cats with slow administration to prevent seizures or asystole. Second line drugs include IV procainamide (2 mg/kg IV over 2 minutes; up to 20 mg/kg cumulative dosage in dogs; up to 10 mg/kg cumulative dosage in cats; with QRS, Q‐T, and BP monitoring); esmolol (loading dose of 50 to 100 mcg/kg over 5 minutes; thereafter 25 to 50 mcg/kg/minute, IV; cats without CHF can tolerate loading dosages at the higher range), magnesium salts, and preservative‐free amiodarone (Nexterone®; see dosage under atrial arrhythmias) as back‐up treatments. Premixed (preservative‐free) Nexterone® is an excellent antiarrhythmic drug for dogs in hospital settings, and the drug is underused; in our hospital it is often chosen if lidocaine fails. Electrocardioversion of VT also can be effective116 but requires general anesthesia. For chronic home therapy of PVCs and VT, sotalol (1‐2 mg/kg PO b.i.d.) is generally the best tolerated (beware: negative inotropic effects in CHF), but it is not always as effective as mexiletine (4‐8 mg/kg PO t.i.d.) plus sotalol, mexiletine plus atenolol (0.5 to 1 mg/kg PO bid), or oral amiodarone (4‐6 mg/kg PO b.i.d. for one or two weeks; then 4‐6 mg/kg PO once daily). Amiodarone deserves respect, especially in terms impairing liver function. Flecainide (1 to 2 mg/kg PO b.i.d.) is a potentially useful drug but experience in dogs is low and the drug can lead to “pro‐arrhythmia” in humans (and possibly dogs), especially in settings of a failing heart. We avoid the drug in the setting of CHF or impaired LV function. The addition of a fish oil supplement to the treatment plan resulted in a statistically‐significant reduction in the frequency of PVCs in Boxer dogs117 and is a reasonable add‐in.

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 or Wenckebach type, Mobitz IIA and IIB), and complete (third‐degree block). The finding of second degree block with a concurrent intraventricular conduction disturbance (Type IIB) indicates a high risk for advancement to complete AV block. Treatment of symptomatic AV blocks generally involves referral for permanent pacing and in the authors’ opinion this should be done transvenously in most canine cases. Single or dual chamber pacing systems can be used,45,52,53,117‐130 depending on a variety of patient, technical, and experience factors.

Permanent epicardial pacing has some indications, but these are best discussed with a cardiologist experienced in pacing. Long‐term prognosis depends mainly on etiology of the bradyarrhythmia (with the best prognosis for SSS and AV block without other structural diseases and the worst for persistent atrial

standstill).

Persistent bundle branch block or phasic aberrant ventricular conduction (generally heart rate/cycle length dependent) can be encountered in structurally normal hearts or in those with diseases of the conduction system. These conduction disorders do not require therapy but can inform further diagnostics and when present during a supraventricular tachycardia can be readily confused with VT.

Table 6. Some Strategies for Refractory Ventricular Tachycardia  Reevaluate the ECG ‐ could the rhythm have been incorrectly diagnosed initially? For example, SVT with aberrancy (intraventricular conduction disturbance) can mimic ventricular tachycardia. In these cases, IV diltiazem is usually more effective than lidocaine.  Assess serum K+ (and Mg++) concentration. Hypokalemia reduces the efficacy of class I antiarrhythmic drugs and can predispose to arrhythmia development. o For serum K+ concentration <3 mEq/L, KCl can be infused at 0.5 mEq/kg/hr. o For serum K+ between 3 and 3.5 mEq/L, KCl can be infused at 0.25 mEq/kg/hr. o A serum K+ concentration in the high normal range is the goal. o If the serum Mg++ concentration is <1.0 mg/dl, MgSO4 or MgCl2, diluted in D5W, can be administered at 0.75 to 1.0 mEq/kg/day by CRI.  Try sotalol (PO), or amiodarone (IV or PO loading), or a beta‐blocker in conjunction with a class I drug (e.g., propranolol, esmolol or atenolol with lidocaine, procainamide or quinidine) or a class Ia drug with a Ib drug (e.g., procainamide with lidocaine or mexiletine).  Consider that the antiarrhythmic drug might be exacerbating the rhythm disturbance (proarrhythmia effect). o Polymorphic ventricular tachycardia (or torsade de pointes) has been associated with quinidine, procainamide, and other drug toxicities.  MgSO4 may be effective in animals with ventricular tachyarrhythmias associated with digoxin toxicity or with suspected torsade de pointes. o Administer MgSO4 as a slow IV bolus of 25 to 40 mg/kg, diluted in 5% dextrose in water (D5W), & followed by an infusion of the same dose over 12 to 24 hours o MgSO4 contains 8.13 mEq magnesium per gram, so a similar magnesium dose is provided by calculating 0.15 to 0.3 mEq/kg.  If the animal is tolerating the arrhythmia well, continue supportive care, correct other abnormalities as possible, and continue cardiovascular monitoring alone or with the most effective antiarrhythmic drug.  Consider DC cardioversion, if available.

ANTIARRHYTHMIC DRUGS (this section is courtesy of Dr. Wendy A Ware) Antiarrhythmic drugs can serve to slow a tachycardia’s rate, terminate a reentrant arrhythmia, or prevent abnormal impulse formation or conduction. These effects can occur through modulation of tissue electrophysiologic properties and/or autonomic nervous system effects.

Class I Antiarrhythmic Drugs These agents block membrane Na+ channels and depress action potential upstroke (phase 0). This slows conduction velocity and can interrupt reentrant rhythms. Their membrane‐stabilizing effects also include decreasing excitability and automaticity. They are subclassified according to other electrophysiologic characteristics. Class Ia agents moderately slow conduction, increase action potential duration, and can prolong QRS complex and Q‐T interval durations. Class Ib agents cause little change in conductivity; QRS complex and Q‐T interval durations remain unchanged. Class Ic drugs markedly slow conduction, generally without change in action potential duration.

The electrophysiologic effects of class I drugs are extremely dependent on extracellular K+ concentration; hypokalemia may render these drugs ineffective, whereas hyperkalemia intensifies their

depressant effects on cardiac membranes. All these agents are contraindicated in animals with complete heart block and should be used only cautiously in animals with sinus bradycardia, SSS, and 1 or 2 AV block.

Lidocaine (Class Ib) has little effect on sinus rate, AV conduction rate, and refractoriness at standard doses. It suppresses automaticity in normal Purkinje fibers and diseased myocardium, slows conduction, and reduces the dispersion of refractoriness. Its effects are greater on diseased and hypoxic cardiac cells and at faster stimulation rates. While lidocaine often is effective against VT, it usually is ineffective against supraventricular arrhythmias. However it may induce conversion of SVT and recent onset, vagally‐mediated AF, in some dogs90. Lidocaine produces little or no depression of contractility when given slowly IV at therapeutic doses. Toxic concentrations can cause hypotension. The toxic effects usually relate to the CNS, including agitation, disorientation, mental depression, ataxia, muscle twitches, nystagmus, and generalized seizures (which may require diazepam [0.25–0.5 mg/kg IV] or a short‐acting barbiturate). Nausea can also occur.

Procainamide (Class Ia) prolongs the effective refractory period and slows conduction in the accessory pathway of dogs with orthodromic AV reciprocating tachycardia. Procainamide has both direct and indirect (vagolytic) effects. It is indicated for ventricular (and sometimes supraventricular) tachyarrhythmias, but generally is less effective than quinidine for atrial tachyarrhythmias. Procainamide should be used only cautiously in hypotensive animals. Rapid IV injection of procainamide can produce hypotension and cardiac depression, although to a much lesser degree than quinidine; IM administration does not cause marked hemodynamic effects. Procainamide CRI is useful for arrhythmias responsive to an IV bolus. Toxic effects can include GI upset, QRS or QT prolongation, AV block, and proarrhythmia.

Quinidine (Class Ia) is not often used now, but may be helpful for ventricular and some supraventricular tachyarrhythmias if other strategies are not available or effective. Quinidine must be given with caution to animals with heart failure or abnormal serum K+ concentration. Quinidine depresses automaticity and conduction velocity and prolongs effective refractory period. Corresponding dose‐dependent ECG changes (e.g. prolonged PR, QRS, and QT intervals) result from direct electrophysiologic and vagolytic effects; however, at low doses the drug’s vagolytic effects can offset its direct effects and increase the sinus rate or the ventricular response rate to AF. Because of its propensity to cause vasodilation (via alpha‐receptor blockade), cardiac depression and hypotension, quinidine is not used IV in dogs and cats. Quinidine toxicity extends from the drug’s electrophysiologic and hemodynamic effects. Prolongation of ECG intervals occurs in a dose‐related manner. Marked QT prolongation, right bundle branch block, or QRS widening >25% of pretreatment value suggest toxicity. AV conduction block and and ventricular tachyarrhythmias can result.

Marked QT prolongation implies increased temporal dispersion of myocardial refractoriness, which predisposes to TdP and VF. Other adverse effects include GI signs.

Mexiletine (Class Ib) is similar to lidocaine in its electrophysiologic, hemodynamic, toxic, and antiarrhythmic properties. It is used for ventricular tachyarrhythmias in dogs. It can reduce arrhythmias associated with repolarization abnormalities, by decreasing late Na+ influx during repolarization and thereby decreasing EADs. The combination of a beta‐blocker or class III agent with mexiletine may be more effective and cause fewer adverse effects than mexiletine alone. When used together, mexiletine counteracts the action potential prolongation caused by sotalol. Sotalol, administered with mexiletine, appears to mildly increase mexiletine plasma concentration. Adverse effects of mexiletine can include vomiting, anorexia, tremor, ataxia, disorientation, sinus bradycardia, and thrombocytopenia; administration with food can reduce GI side‐effects.

Class Ic agents slow cardiac conduction velocity markedly but have minimal effect on sinus rate or refractoriness. However, high doses depress automaticity in the sinus node and specialized conducting tissues. Proarrhythmia is a serious potential adverse effect of the class Ic agents. Flecainide prolongs the sinus cycle length and AV nodal conduction time and refractoriness. Flecainide has a blocking effect on the delayed rectifier potassium current (IK) similar to class III agents, but this repolarization prolonging effect is mitgated by its Na+ channel blocking effect, so little change in action potential duration occurs. However, at high plasma concentrations flecainide can prolong QT interval. Adverse effects can include GI signs, hypotension, bradycardia, AV blocks, and sudden death. Propafenone increases AV nodal functional

refractory period, slows intraatrial conduction, and reduces ventricular excitability and triggered activity.

Propafenone also has weak beta‐ and calcium channel blocking activity, and a vagolytic effect. It may be effective for both atrial (including incessant atrial tachycardia) and ventricular tachyarrhythmias.

Propafenone can cause GI side effects, proarrhythmia, and increase concurrent digoxin serum concentration.

Class II Antiarrhythmic Drugs Beta‐blockers act by inhibiting catecholamine effects. These drugs slow HR, reduce myocardial oxygen demand, and increase AV conduction time and refractoriness. They are unlikely to affect repolarization. The antiarrhythmic effect of beta‐blockers relates to beta1‐receptor blockade rather than direct electrophysiologic effects. Most often used are the beta1‐selective agents atenolol, metoprolol, and esmolol.

The non‐selective drug propranolol also is commonly used. Because of possible beta‐receptor upregulation during long‐term beta‐blockade, abrupt discontinuation of therapy could result in serious cardiac arrhythmias; gradual dosage reduction prior to discontinuation is recommended. Beta‐blockers are generally contraindicated with sinus bradycardia, SSS, high‐grade AV block, or severe CHF. Nonselective beta‐blockers may increase peripheral vascular resistance, because of unopposed alpha effects, and promote bronchoconstriction by beta2 antagonism. Lipophilic beta‐blockers, such as propranolol, can cause depressed attitude and disorientation. Other adverse effects of beta‐blockers can include lethargy, fatigue, anorexia, vomiting, diarrhea, hypotension, onset or recurrence of CHF, sinus bradycardia, and AV block.

Beta‐blockers also can mask early signs of acute hypoglycemia in diabetics (e.g. tachycardia and blood pressure changes), and reduce insulin release in response to hyperglycemia.

Class III Antiarrhythmic Drugs These agents prolong action potential duration and effective refractory period without decreasing conduction velocity. They act mainly by inhibiting the repolarizing potassium channel IK (delayed rectifier).

The effects of some drugs in this class (e.g. amiodarone) are greater at higher HRs (‘use‐dependence’), although others exhibit reverse use‐dependence (e.g. sotalol). They are useful for refractory ventricular arrhythmias, especially those caused by reentry. These drugs can have antifibrillatory effects on atrial and ventricular tissues. Currently available agents share some characteristics of other antiarrhythmic drug classes in addition to their class III effects.

Sotalol HCl is a nonselective beta‐blocker with class III effects at higher doses. It has been effective against ventricular tachyarrhythmias in many dogs and some cats. It may be more effective in preventing AF than terminating it because its refractory period prolongation is more pronounced at slower heart rates (reverse use‐dependence). However, its beta‐blocking effect helps control ventricular rate in animals with AF. Sotalol has also been used in cats with severe ventricular tachyarrhythmias. Sotalol (d‐isomer) prolongs the refractory period by selectively blocking the rapid component (IKr) of the delayed rectifier current responsible for repolarization. Sotalol can increase triggered activity (early afterdepolarizations) and can cause TdP at high doses, or with hypokalemia at slow heart rates. Coadministration with mexiletine may reduce sotalol’s proarrhythmic potential. However, sotalol was shown to induce ventricular tachycardia in young German Shepherd Dogs affected with inherited ventricular tachyarrhythmias131, and should be avoided as a sole agent in these animals. Sotalol also is not advised for Boxers with bradycardia‐associated syncope. Adverse effects of sotalol can include reduced myocardial contractility, hypotension, depression, nausea, vomiting, diarrhea, and bradycardia. There are a few anecdotal reports of aggression that resolved after sotalol was discontinued.

Amiodarone is a unique Class III agent. While it prolongs the action potential duration and effective refractory period in both atrial and ventricular tissues, it also shares properties with all three other antiarrhythmic drug classes. Amiodarone is an iodinated benzofuran compound that has effects on Na+, K+, and Ca++ channels, and has noncompetitive alpha1‐ and beta‐blocking properties. Its beta‐blocking and class Ib‐like effects occur soon after administration, but maximal class III effects, with prolongation of action potential and QT interval durations, and reduced Purkinje fiber automaticity, are achieved after weeks of

administration. In contrast to other class III drugs which tend to induce early afterdepolarizations (EADs), amiodarone can abolish EADs. Its Ca++ channel‐blocking effects may contribute to the reduced triggered activity. Amiodarone’s prolongation of action potential duration is more uniform across ventricular tissues than that of other agents, and the occurrence of TdP associated with amiodarone is low. Amiodarone has been effective in converting AF to sinus rhythm in some dogs103. Amiodarone has a delayed onset of action and prolonged time to steady state (>10 weeks). Slow intravenous bolus administration may suppress ventricular arrhythmias in dogs. However, use of the standard (older) IV formulation often precipitates hypotension and anaphylactoid reactions, related to solvents (polysorbate 80 and benzyl alcohol) used to keep the drug in solution. Acute hypersensitivity reaction therapy includes stopping IV amiodarone, and using diphenhydramine (e.g. 1 mg/kg IV), a corticosteroid (e.g. prednisolone 1–2 mg/kg IV), IV fluids and other supportive care as needed. Although antihistamine pretreatment, conservative dosing, and slow injection over 10–20 minutes have been helpful in some cases, use of standard amiodarone IV is not currently recommended. A newer amiodarone formulation (Nexterone) without polysorbate 80 and benzyl alcohol is available and should be safer, but is quite expensive. Many potential side‐effects occur with long‐ term amiodarone use, including depressed appetite, GI upset, pneumonitis leading to pulmonary fibrosis, hepatopathy, thyroid dysfunction, positive Coombs test, thrombocytopenia, and neutropenia. Some of these resolve with drug discontinuation or dosage reduction. Hepatotoxicity appears common and somewhat dose related in Dobermans. Other adverse effects noted with long‐term use in people include corneal microdeposits, photosensitivity, bluish skin discoloration, and peripheral neuropathy; however, amiodarone may have a lesser proarrhythmic effect than other agents and reduce the risk of sudden death.

Amiodarone can increase serum concentrations of digoxin, diltiazem, and, possibly, procainamide and quinidine.

Ibutilide fumarate is used for converting recent onset AF in people, but there is little veterinary experience with it; ibutilide converted only ~50 % of acutely induced AF in a dog study. In dog studies, SA and AV nodal suppression, increased atrial and ventricular refractoriness, QT duration prolongation, increased repolarization dispersion, and induction of EADs were shown. Experimentally, doses effective in terminating AF also increased myocardial refractoriness and QT durations. Ibutilide has caused TdP in dogs with experimental AV block and cardiomyopathy. Dofetilide is another drug that selectively blocks the rapid component of the repolarizing K+ current. It also has been used in people to convert AF and maintain sinus rhythm. However, its efficacy may depend on the duration and underlying mechanism of AF, and it may be more effective in preventing rather than terminating AF. Dofetilide also tends to induce EADs and TdP, especially with cardiac remodeling and increased repolarization variability. Experimentally it appears to have greater effect to prolong QT interval in dogs.

Class IV Antiarrhythmic Drugs This diverse group of drugs reduces cellular Ca++ influx by blocking transmembrane L‐type Ca++ channels. Diltiazem and verapamil (nondihydropyridines) have antiarrhythmic effects, especially on tissues dependent on the slow inward Ca++ current, particularly the sinus and AV nodes. They slow the sinus rate, increase AV nodal refractory period, and can interrupt some arrhythmias caused by abnormal automaticity, triggered mechanisms, and reentry. These agents are most effective against supraventricular tachyarrhythmias, although they might suppress ventricular arrhythmias dependent on abnormal Ca++ fluxes. Verapamil should not be used in animals with heart failure, and is rarely used clinically in other animals. Side‐effects of these agents can include reduced contractility, vasodilation, hypotension, depression, anorexia, lethargy, bradycardia, and AV block. They are usually not prescribed with a beta‐ blocker, but if so, only with caution. Adverse effects of diltiazem are uncommon at therapeutic doses, but anorexia, nausea, bradycardia, and, rarely, other GI, cardiac, or neurologic effects may occur. Cats sporadically develop liver enzyme elevation with anorexia. Anecdotally, some cats become aggressive or show other personality change when treated with diltiazem.

“Class V” Antiarrhythmic Drugs `The designation of Class V is sometimes used to group antiarrhythmic drugs that work by mechanisms other that described in the original four classes. Digoxin, although primarily considered a positive inotropic drug, is useful for slowing the ventricular response rate in AF. Digoxin also may suppress some supraventricular premature depolarizations. These effects are mediated by an increase in parasympathetic tone, which mainly affects the SA and AV nodes and atrial tissue, and direct effects which prolong AV nodal conduction and refractory period. Anticholinergic agents, such as atropine sulfate and glycopyrrolate, increase sinus rate and AV conduction when excessive vagal tone is present. Bradyarrhythmias responsive to parenteral atropine or glycopyrrolate sometimes also respond to oral anticholinergic agents (such as propantheline bromide or hyoscyamine sulfate).

Atropine Response Test: this is used to determine the degree of vagal influence on sinus and AV nodal function. Response to atropine challenge is most consistent with IV administration of 0.04 mg/kg. An ECG is recorded within 5–10 minutes after atropine injection. If the HR has not increased by at least 150%, the ECG is repeated 15 (to 20) minutes after the atropine injection; sometimes, an initial vagomimetic effect on the AV node lasts longer than 5 minutes. The normal sinus node response is a rate increase to 150–160 beats/minute (or >135 beats/minute). A positive response may not predict response to oral anticholinergic therapy.

Sympathomimetic drugs such as terbutaline sulfate, a beta2‐receptor agonist, and the methylxanthine bronchodilators aminophylline and theophylline can increase HR in some animals with bradyarrhythmias when used at higher doses.

Ivabradine is a selective inhibitor of the so‐called “funny current” (If), which is mainly responsible for (initial) slow diastolic depolarization of sinus node cells. By reducing this rate of diastolic depolarization, the drug decreases heart rate; slower heart rates reduce myocardial oxygen requirement and improve coronary perfusion. Ivabradine’s reduction in the sinus rate is dose‐dependent. The drug does not appear to significantly affect conductivity, repolarization, or refractoriness of the AV node, atrial or ventricular myocardium, or His‐Purkinje system. It has recently become available in the US, but is quite expensive; there is little clinical veterinary experience with this agent.

Vagal Maneuver A vagal maneuver is usually tried initially for rapid supraventricular tachycardias (e.g. during preparations for IV catheter placement). It is performed by massaging the carotid sinus region (with gentle continuous pressure over the carotid sinuses, just caudodorsal to the larynx), or by applying firm (but gentle) bilateral ocular pressure, over closed eyelids, for 15–20 seconds; (ocular pressure technique is contraindicated in animals with eye disease). Although a vagal maneuver often is ineffective at first, it may be effective when repeated after antiarrhythmic drug administration if the rhythm disturbance persists. An IV drug that increases vagal or decreases sympathetic tone can potentiate the vagal maneuver in cases where it was initially unsuccessful.

Increasing vagal tone should temporarily slow the rate of sinus tachycardia and allow normal P waves to be seen, although some atrial tachycardias also slow. Reentrant tachycardias involving the AV node are sometimes abruptly terminated by a vagal maneuver, as an increase in AV refractoriness blocks further conduction around the reentry circuit. The vagal maneuver may transiently slow or intermittently block AV conduction to expose abnormal atrial P’ waves from an automatic ectopic atrial focus.

Table 7. Common Dosages of Antiarrhythmic Drugs Drug Dosage Class I

Lidocaine Dog: initial boluses of 2 mg/kg slowly IV (over 2 minutes), up to 8 mg/kg (over 10 min; stop if vomiting or tremors); or rapid IV infusion at 0.8 mg/kg/minute; if effective, then 25‐80 µg/kg/minute CRI; can also be used intratracheally for CPR. Cat: initial bolus of 0.25–0.5 (or 1.0) mg/kg slowly IV; can repeat boluses of 0.15‐0.25 mg/kg, up to total of 4 mg/kg; if effective, 10–40 µg/kg/minute CRI Mexiletine Dog: 4‐6 (‐8) mg/kg PO q8h Cat: * Procainamide Dog: 2 mg/kg IV over 2 minutes; repeat if necessary, up to cumulative dose of 20 mg/kg; 10‐50 µg/kg/minute CRI; 6‐20 (up to 30) mg/kg IM q4‐6h Cat: 1.0‐2.0 mg/kg IV over 2 minutes, repeat if necessary, up to cumulative dose of 10 mg/kg; 10‐20 µg/kg/minute CRI; 7.5‐20 mg/kg IM q(6‐)8h Quinidine Dog: 6‐20 mg/kg IM q6h (loading dose, 14‐20 mg/kg); 6‐16 mg/kg PO q6h; sustained action preparations, 8‐20 mg/kg PO q8h Cat: 6‐16 mg/kg IM or PO q8h Flecainide Dog: 1‐2 (up to 5?) mg/kg PO q12h (not advised if CHF or impaired LV function present) Cat: * Propafenone Dog: 2‐4 (up to 6) mg/kg PO q8h (start low) Cat: * Class II

Atenolol Dog: 0.2‐1.0 mg/kg PO q12 (‐24)h; start low Cat: ?same or 6.25 (‐12.5) mg/cat PO q12 (‐24)h Carvedilol Dog: 0.1‐0.5 mg/kg PO q12h (up to 1.0 mg/kg if normal LV function; start low) Cat: same?

Esmolol Dog: 0.1‐0.5 mg/kg IV over 1 minute (loading dose), followed by infusion of 0.025‐0.2 mg/kg/minute Cat: same Metoprolol Dog: initial dose, 0.1‐0.2 mg/kg PO q24(‐12)h, up to 1 mg/kg q8(‐12)h; start low Cat: 2 up to 15 mg/cat PO q 8(‐12) hr; start low Propranolol Dog: 0.02 mg/kg initial bolus slowly IV (up to maximum of 0.1 mg/kg); initial PO dose, 0.1‐0.2 mg/kg PO q8h, up to 1 mg/kg q8h Cat: Same IV instructions; 2.5 up to 10 mg/cat PO q8‐12h Class III

Amiodarone Dog: 6 (up to 10) mg/kg PO q12h for 7 (to 14) days (loading), then 4‐6 mg/kg PO q24h; For IV administration use Nexterone (not standard amiodarone – see text): 2‐3 mg/kg slow IV infusion over 1‐2 hours and monitor BP; (can continue to cumulative dose of 5 to 6 mg/kg, if tolerated).

Cat: * Sotalol Dog: 1‐2.5 (‐5?) mg/kg PO q12h Cat: 10‐20 mg/cat PO q12 h (or 2‐4 mg/kg PO q12h)

Class IV Diltiazem

Verapamil (note: diltiazem is preferred)

Anticholinergic Atropine Glycopyrrolate

Hyoscyamine Propantheline

Sympathomimetic Dobutamine Isoproterenol

Theophylline (ext. release) Terbutaline Other Agents Digoxin

Dog: Acute IV for rapid rate control of AF: 0.05‐0.15 mg/kg IV over 2‐3 minutes, can repeat if needed. Acute IV for SVT: 0.1(‐0.2) mg/kg over (3‐)5 minutes IV, can repeat to cumulative IV dose of 0.3‐0.4 (‐0.7) mg/kg; monitor BP. CRI: 0.02‐0.08 mg/kg/min. Oral loading dose: 0.5 mg/kg PO followed by 0.25 mg/kg PO q1h to a total of 1.5(‐2.0) mg/kg or conversion. Oral maintenance: (standard formulation) initial 0.5‐1 mg/kg (up to 2‐3 mg/kg) PO q8h. Extended release (diltiazem ER): 1.5‐4 (up to 6) mg/kg PO q 12h Cat: Same?; oral maintenance: 1.5‐2.5 mg/kg (or 7.5‐10 mg/cat) PO q8h; Extended release (diltiazem ER), 30 mg/cat/day (one half of a 60 mg internal tablet within the 240 mg capsule), can increase to 60 mg/day in some cats if necessary Dog: initial dose, 0.02‐0.05 mg/kg slowly IV, can repeat q5min up to a total of 0.15(‐0.2) mg/kg; 0.5‐2 mg/kg PO q8h (diltiazem preferred) Cat: initial dose, 0.025 mg/kg slowly IV, can repeat every 5 minutes up to a total of 0.15(‐0.2) mg/kg; 0.5‐1 mg/kg PO q8h

Dog: 0.02‐0.04 mg/kg IV, IM, SC; 0.04 mg/kg PO q6‐8h Cat: same Dog: 0.005‐0.01 mg/kg IV or IM; 0.01‐0.02 mg/kg SC Cat: same Dog: 0.003–0.006 mg/kg PO q8h Cat: * Dog: 0.25‐0.5 mg/kg, or 3.73‐7.5 mg/dog, PO q8‐12h Cat: *

Dog: 2.5 to 5 mcg/kg/min, initial (up to 20 mcg/kg/min) CRI Cat: 2.5 to 5 mcg/kg/min CRI, start low Dog: 0.04‐0.08 µg/kg/minute CRI Cat: same Dog: 10 mg/kg PO q12h Cat: 10‐15 mg/kg q24h Dog: 0.14 mg/kg, or 2.5‐5 mg/dog, PO q8‐12h Cat: 0.1‐0.2 mg/kg, or 0.625‐1.25 mg/cat, PO q12h

Dog: Maintenance dose for dogs <22 kg, 0.005‐0.008 mg/kg PO q12h; dogs >22 kg, 0.003‐0.005 mg/kg (or 0.22 mg/m2) PO q12h.

Cat: 0.007 mg/kg (or 1/4 of 0.125 mg tab) PO q48h.

Table compiled by Drs. Wendy A Ware (Iowa State Univ) and John Bonagura (Ohio State University) * = effective dosage not known; BP = blood pressure; CHF = congestive heart failure; CRI = constant rate infusion; CPR = cardiopulmonary resuscitation; LV =left ventricular.

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CARDIAC AUSCULTATION John D Bonagura DVM, MS, DACVIM (Cardiology, Internal Medicine) Veterinary Clinical Sciences, Ohio State University College of Veterinary Medicine

CARDIAC AUSCULTATION – INTRODUCTION The stethoscope (and its clinical use) was first described by the French physician, Laennec in 1816. He used a rolled tube of paper to transmit sounds from thorax to ear and subsequently described the relationships between these sounds and underlying thoracic diseases in his treatise De l'Auscultation Mediate. His observations, along with those of other clinical investigators, continue to influence clinical decision-making. Auscultation of the heart and lungs remains an important examination technique for the detection of thoracic disease. This presentation reviews some of the key features of auscultation in dogs and cats, including examination techniques and the interpretation of auscultatory findings relative to acquired and congenital cardiac disorders.

The auscultatory exam is expedient and cost effective. When completed by an experienced clinician, auscultation carries a high predictive value for identification of certain serious heart diseases. Some diagnoses can be attained with high sensitivity and specificity through auscultation. Two examples include the diagnosis of a patent ductus arteriosus (PDA) in a puppy with a continuous murmur and the identification mitral regurgitation (MR) in the older dog with a typical holosystolic, left apical murmur. Auscultation also carries high sensitivity, but lower specificity, for the diagnosis of outflow tract obstructions, septal defects, and sustained or recurrent cardiac arrhythmias. Often the results of auscultation, combined with the signalment, clinical history, and findings on physical diagnosis point to a tentative cardiac or respiratory diagnosis. This presumptive diagnosis is then confirmed, refined, or refuted through Doppler echocardiography, radiography, or electrocardiography. It is emphasized that auscultation is less sensitive for the recognition of patients with cardiomyopathies, pericardial diseases, pulmonary hypertension, trivial valve lesions, or infrequent or sporadic arrhythmias. These are challenging conditions to recognize or confirm without ancillary studies such as cardiac ultrasound or ambulatory electrocardiography.

The essential abnormalities of cardiac auscultation include the following: abnormal heart rate or irregular rhythm (arrhythmia); abnormal intensity of heart sounds (loud, soft, or variable); extra sounds (gallops and clicks); split sounds; cardiac murmurs; and pericardial friction rubs.

Different classification systems for heart sounds and murmurs are designed to foster communication among clinicians and carry clinical relevance. This subject is addressed below. A respiratory examination is also performed using the stethoscope, and the breath sounds detected should be classified and assessed as well (these are summarized at the end).

METHODS Heart sounds are generally too low in frequency or amplitude to be detected by the human ear. Accordingly, careful auscultation is necessary to identify the limited vibrations that fall within our audible frequency-amplitude spectrum. This requires a stethoscope to transfer (not amplify) the sounds from the patient to the examiner.

The choice of a stethoscope is one of personal preference, and there is no ‘best’ model for everyone. Some reasonable stethoscope choices advocated by the author are included in this section. The traditional stethoscope design has a diaphragm and shallow bell (selected by twisting the chest piece head). Many of these instruments permit an exchange to a differentsized (pediatric) diaphragm or (deep) bell (Tycos Harvey Elite®; MDF Procardial C3®). Newer stethoscope models carry one or two tunable diaphragms. A single tunable diaphragm is found

on some instruments (3M Littman® Master Classic II and Master Cardiology models); this chest piece is acoustically superior in many ways. However, it is designed for adults and is somewhat large for cats and smaller dogs so the examiner must learn to place it carefully. Another popular stethoscope (3M Littman Cardiology III®) uses both “adult” and “pediatric” sized tunable diaphragms in a single rotating head. For clinicians preferring a light pediatric stethoscope with a small footprint there are very good and economical models available (e.g. 3M Littman Classic II® Pediatric Stethoscope; MDF® Pediatric Stainless Steel Dual Head Stethoscope). These pediatric scopes are especially good for small dogs, cats, ferrets, and birds. While amplified stethoscopes generally are not recommended because of the potential for artifacts and distortion, they can be useful for those hard of hearing or for recording documenting sounds (3M Littman Electronic® 3000 series). Ultimately, the most important part of the stethoscope are the “bits between the earpieces”! A practiced and knowledgeable examiner will succeed with any number of stethoscope models.

Stethoscope designs have improved the acoustics of the instrument, but it must be used properly to obtain optimal clinical results. Of importance are acquiring an instrument of acceptable quality and tube length (typically 22 to 28 inches; longer tubes are not better); directing the binaurals rostrally (towards the nose) and aligning these to the ear canals by gently adjusting the headset; inserting comfortable earpieces snugly to obtain an airtight seal; and applying the chest pieces with proper technique. The stethoscope chest pieces include two general types: traditional and “tunable”. A traditional flat diaphragm is applied gently but firmly to the chest to accentuate higher frequency sounds such as normal heart and breath sounds. This chest piece is used for 90% of the examination. The traditional shallow or deep bell chest pieces are applied lightly to achieve an airtight seal and enhance auscultation of lower pitched sounds.

Examples of the latter include the third and fourth heart sounds and some diastolic murmurs.

Combination chest pieces (“tunable diaphragms”) change their frequency response with varying pressure such that flattening the chest piece accentuates higher-pitched sounds (like a typical diaphragm) while gentle pressure brings out the lower pitched sounds like a traditional bell.

There are also intermediate levels of pressure that can optimize certain sounds and murmurs; however, careful attention must be directed to subtle pressure changes to optimize the chest piece functionality.

The conditions for auscultation exert a substantial influence on the results of the examination. The room must be quiet, the patient gently restrained by an assistant, and the examiner relaxed. It is preferable for the dog to stand in order to locate the valve areas accurately. A cat can be gently restrained with one hand under the caudal abdomen; this encourages the cat to rest on the forelimbs. The patient must be calm and ventilation and purring controlled if possible. Ventilation (especially panting) that is synchronous to the heart rhythm can mimic cardiac murmurs. Gently holding the mouth closed, whistling, or briefly obstructing the nares are effective maneuvers for reducing ventilation artifacts in dogs. Showing a cat water dripping in a sink, holding the cat, or gently pressing the larynx might reduce the degree of purring. Sound artifacts can be misinterpreted as abnormal heart or lung sounds.

These include ventilation and panting (mimics murmurs); twitching (sounds like an extra heart sounds or premature beats); and friction from rubbing the chest piece across hair (sounds like pulmonary crackles or rales). Excessive pressure on the chest can distort the thorax of small animals and create abnormal flow patterns and murmurs.

The clinical examination method involves integration of auscultation with palpation of the precordium and examination of the pulses. Auscultation is preceded by palpation of the arterial pulse to estimate heart rate, regularly, and pulse strength and character. Ideally, the jugular venous pulse should also be inspected, but practically this is rarely done in healthy patients because of the need to clip neck hair. The thoracic wall over the heart (precordium) is palpated on both sides in order to assess the apical beats. The prominent left apical impulse occurs coincident with opening of the semilunar valves (a systolic thrust). The impact is normally

strongest at the left fifth intercostal space near the costochondral junction. A weaker impulse is normally palpable on the right hemithorax at approximately the right third to fourth ICS. Dilatation of the left ventricle displaces the apex beat caudoventrally. Hypertrophy of the left or the right ventricle can produce an impulse more prominent than normal; this is termed a precordial heave. Interpretation of these changes requires considerable experience and practice. Of great value is the identification of a precordial vibration or ‘thrill’. A precordial thrill is the palpable manifestation of a loud murmur and it typically indicates the point of maximal murmur intensity, a descriptor that informs the differential diagnosis.

The entire precordium is examined, with particular attention directed to the cardiac valve areas and the first and second heart sounds, which indicate the onset of systole and diastole, respectively. While the exact anatomic location of the valve areas depends on the species, breed, chest conformation, and size of the heart, a common relative location can be identified.

From caudal to cranial are the mitral–tricuspid–pulmonic–aortic with the tricuspid valve on the right side and other valves areas on the left. The author approaches the patient from the caudal perspective, allowing the stethoscope to follow the natural curve of the arm; if one can learn to be ambidextrous in holding the chest piece, the examination can be very efficient. A useful approach in dogs begins with palpation of the left apical impulse where mitral sounds radiate well and the lower-pitched, first heart sound is best heard. The mitral listening area is there and immediately dorsal to the apex. Other valve areas are found from this point. The aortic valve area is located one or two intercostal spaces craniodorsal to the mitral area, and the sharper, higher-pitched second heart sound is usually loudest at that location. Once the aortic second sound is identified, the stethoscope can be moved one interspace cranial and slightly ventral (over the pulmonary valve area). The tricuspid valve area is over the right hemithorax, cranial to the mitral area, and covers a relatively wide area. The pulmonary artery extends dorsally from the pulmonic valve. The left ventricular outflow tract (LVOT) is located near the center of the heart and aortic sounds and aortic ejection murmurs usually radiate to each hemithorax, although these are usually loudest over the aortic area and craniodorsal to the valve.

Cardiac “apex” and cardiac “base” are commonly used expressions to designate the region ventral (ventricles) and dorsal to the atrioventricular groove but are not specific for any cardiac valve. Mitral and tricuspid valve sounds and murmurs generally project ventrally to the apical regions. Ventricular septal defects are also louder ventrally (along the sternal edges) in most patients. In contrast, murmurs originating at the semilunar valves or the great arteries are detected best over the base, generally over the left, craniodorsal cardiac base. Murmurs that originate in the subvalvular regions of the outflow tracts are often heard both ventrally and craniodorsally. For example, it is common for a loud murmur of subvalvular aortic stenosis (SAS) in dogs to radiate to be well detected at aortic valve area, the mitral valve area, and in the ascending aorta on both left and right sides of the chest.

Valve areas in cats are less distinct and the edges of the chest piece usually cover multiple valves. Consequently, most clinicians do not identify specific feline valve areas but instead use descriptors such as “apical”, “caudal”, “cranial”, and “sternal”. In many cats, the apical impulse is located close to the midline and most auscultation is conducted along the left and the right sternal borders. The first sound is loudest along the left apical (caudal) sternal border. The normal second sound is louder over the left cranial sternal border. A typical murmur of mitral regurgitation is loudest over the caudal left sternal border (apex) whereas typical ejection and functional murmurs are loudest along the left or right cranial sternal borders. However, these are generalizations and distinguishing the source and cause of feline heart murmurs is quite challenging.

TRANSIENT CARDIOVASCULAR SOUNDS Transient sounds are vibrations of short duration because their genesis depends on abrupt changes in pressure and blood flow. The transient sounds, as well as cardiac murmurs, are

timed relative to the first (S1) and second (S2) heart sounds. Following initial activation of the ventricles and the rapid development of ventricular pressure, the first sound is heard indicating the onset of systole for the clinician. At the end of ventricular ejection, the second sound is generated, heralding the onset of diastole to the clinician. Any transient sounds detected during systole or diastole are considered abnormal in small animals.

Both S1 and S2 are relatively high-frequency sounds. The first sound is associated with vibrations of the cardiac structures and blood pool near the time of atrioventricular (AV) valve closure, while the second sound is caused by vibrations occurring at the time of closure of the aortic and pulmonic valves. The first sound is lower-pitched (duller), longer, and more obvious over the left apex. The relatively sharper and shorter second sound is more prominent over the aortic and pulmonic valve areas and in some normal dogs is closely split during inspiration.

These two transient sounds can become abnormal in certain conditions. Pericardial or pleural effusions and myocardial failure (as with dilated cardiomyopathy) decrease the intensity of the heart sounds. Conversely, both heart sounds tend to be relatively loud in healthy animals under high sympathetic drive or those with thin body conformation.

Diastolic sounds or gallops are abnormal in dogs and in cats. These are audible manifestations of filling sounds (that would be considered normal sounds in larger animal species). Gallops are lower-frequency sounds and associated with vibrations surrounding either sudden termination of early ventricular filling (S3) or atrial contraction and end-diastolic ventricular filling (S4). These sounds indicate diastolic dysfunction when detected in dogs or cats. A third sound is typical of a very diseased ventricle, reduced diastolic chamber compliance with ventricular filling occurring under high venous pressures. Hence, a ventricular gallop is sometimes considered a heart failure sound. An atrial gallop is typically associated with impaired ventricular relaxation (as occurs with feline hypertrophic cardiomyopathy or hypertensive heart disease) and probably stems from the brief, compensatory increase in atrial pressure needed to fill the ventricle at end-diastole. This enhancement of end-diastolic filling leads to an audible sound timed between the P-wave and QRS-complex of the ECG (it is called S4 because it was the last sound discovered). If both filling sounds are present and the heart rate is rapid, the gallops can be superimposed producing a summation gallop. In general, an atrial gallop (S4) indicates less severe disease than an S3 gallop. Some otherwise healthy older cats have this sound in the hospital when stressed; this is likely due to normal aging changes in ventricular relaxation. However, in many cases, gallop sounds are the only auscultatory abnormality of cardiomyopathy or hypertensive heart disease and these sounds will vary with both heart rate and venous filling pressures. Thus in most cases a gallop sound prompts further investigation with echocardiography.

Systolic clicks are extra systolic transient sounds. Mid-systolic clicks are common in dogs with mitral or tricuspid valve disease and are probably indicative of prolapse from abnormal chordae tendineae or valve redundancy. These high-pitched sounds can be fixed or labile within the systolic period; single or multiple; louder of the left or right apex depending on the valve source; and often come and go with changes in heart rate or ventricular volume. Isolated clicks in a mature dog suggest early or mild degenerative disease. Systolic clicks become superimposed with murmurs in dogs with advanced mitral regurgitation and can be difficult to hear in that setting. Systolic clicks are also detected in some cats with hypertrophic cardiomyopathy, but without a phonocardiograph recording, the distinction between an S4 and early systolic click in a cat can be very challenging. These are also detected in some dogs and cats with mitral valve dysplasia. Ejection clicks are infrequently detected in dogs affected by valvular pulmonic stenosis or pulmonary hypertension; these tend to be loudest over the pulmonic valve or pulmonary artery (left craniodorsal).

In many patients, the first recognition of a cardiac arrhythmia occurs during auscultation and palpation of the femoral arterial pulse. Auscultatory findings in arrhythmias and conduction disturbances include abnormal heart rate (bradycardia or tachycardia), irregular cadence to the

rhythm, variable intensity of the heart sounds, extra or absent heart sounds, or splitting of S1 or S2. These findings indicate the need for an ECG. A cyclically irregular rhythm is very normal in dogs and usually indicates (respiratory-related) sinus arrhythmia. In cats, sinus arrhythmia is uncommon in hospital settings and represents another indication for an ECG. Many arrhythmias lead to variable intensity of the first and second heart sounds caused by beat-to-beat variations in ventricular preload. This affects the development of ventricular pressure and arterial pulse pressure and therefore the loudness of the heart sounds and character of the following pulse. In cases of premature ventricular activation, the ventricular pressure might be insufficient to open the aortic valve and a single early sound along with a pulse deficit (S1 with a pulse) occurs. This is often confused with an S3 gallop sound (the S1-—S2—prematureS1 is confused with an S1— S2—S3). Most premature beats are followed by a pause. This is explained by penetration (resetting) of the sinus node by the ectopic focus or to physiologic atrioventricular block of the next sinus impulse by the premature ventricular activation. In cats, it may be more common to recognize the post-extrasystolic pause rather than the actual premature heart sound. Pauses also can be caused by sinus node disorders (sinus arrest) and by atrioventricular (AV) block.

A subtle sign of some arrhythmias is splitting of the heart sounds. This is usually due to asynchronous ventricular activation as occurs with ventricular ectopia or bundle branch blocks (splits are challenging to identify). Ventricular tachycardia for example, can lead to a series of less distinct heart sounds when compared to those heard during normal sinus rhythm. Severe pulmonary hypertension increases the intensity of S2 (by increasing the closing pressure on the pulmonary root and eliminating physiologic splitting of the second sound). In advanced cases audible splitting of the second sound can be detected should left and right ventricular ejection times become widely disparate.

Although a cardiac murmur is often considered the hallmark auscultatory finding in heart disease, as indicated above, some cardiovascular diseases might not be associated with this finding. However, transient cardiac sounds can be abnormal in these patients and the clinician should be vigilant for these abnormalities. Moreover, in the differential diagnosis for “extra sounds” the clinician should consider true gallops (S3 and S4), clicks, widely split sounds, and premature beats. An ECG can usually rule out an arrhythmia if the extra sounds are persistent.

CARDIAC MURMURS Cardiac murmurs are prolonged audible vibrations. Although murmurs are a hallmark of many cardiac diseases, very often murmurs are innocent or functional (i.e., the heart is structurally normal). Murmurs are associated with high velocity blood flow (typically >1.6 m/sec) and vibrations that develop about disturbed or turbulent flow; these generate changes in the flow stream capable of generating audible sound waves. Turbulence and wake fluctuations are more common when flow velocity increases, viscosity of the blood decreases, or when flow moves through a larger blood vessel.

Clinically the causes of cardiac murmurs relate to a number of common conditions.

Adrenergic stimulation, secondary to anxiety, fear, exercise, fever, drugs, or hyperthyroidism, is a common denominator underlying many functional heart murmurs. Both sympathomimetic activation (by increasing contractility) and peripheral vasodilation (by reducing afterload) can increase ventricular systolic function. This can lead to higher ejection velocity into the great vessels, dynamic obstruction in either ventricle and foster high-velocity or turbulent blood flow.

Anemia decreases viscosity of blood and like hyperthyroidism is associated with increased sympathetic activity and peripheral vasodilation. Increased ventricular stroke volume can cause mild-to-moderate increases in ejection velocities and result in an ejection murmur in the absence of any valvular obstruction. Examples include bradycardias (pronounced sinus arrhythmia, AV block, and athletic heart) and atrial septal defect. Structural heart lesions offer pathways for blood to flow from high to low-pressure zones; this pathophysiology represents the most common explanation for pathologic (organic) murmurs. Examples include flow across a

restrictive ventricular septal defect (VSD), a stenotic valve, an incompetent valve, or through an aortic to pulmonary shunt (as with PDA). A common reason for heart murmurs in cats are the primary or secondary cardiomyopathies; murmurs stem from either secondary mitral regurgitation or dynamic ventricular obstruction. Another common cause of murmurs in older cats is aortic dilatation (aortoannular ectasia) with discrete upper septal thickening (in the subaortic ventricular septum).

Cardiac murmurs should be described based on timing and shape, intensity (loudness), and point of maximal intensity (PMI). Additional qualifiers include the murmur radiation, pitch and quality. The general timing of the murmur is designated as systolic, diastolic, continuous, or to-and-fro (systolic – diastolic with a pause a S2). The adjectives “proto”, “meso”, and “tele” are sometimes used to indicate early, middle, and late. Within this timing are descriptions qualifying the onset/end and relative loudness of the murmur as characterized by a phonocardiographic recording. This creates an impression of the murmur’s “shape”. For example, ejection murmurs cannot begin until after S1 and must end by S2 and peak in early to mid-systole unless caused by a severe obstruction to flow. The shape of ejection murmurs is crescendo-decrescendo (diamond-shaped). In contrast, loud holosystolic murmurs of mitral regurgitation (MR) and tricuspid regurgitation (TR) usually obliterate the first and second sounds and are plateaushaped. The intensity or loudness of the murmur is arbitrarily graded on a 1-6 scale; we use the following convention in our practice: Grade 1 Very soft, localized murmur detected only in a quiet room after intense listening.

Grade 2 Soft murmur, heard immediately but relatively localized to a single area.

Grade 3 Moderate intensity murmur that is evident at more than one location.

Grade 4 Moderate intensity to loud murmur that radiates well but without a consistent precordial thrill Grade 5 Loud, widely radiating heart murmur with a precordial thrill.

Grade 6 Loud murmur with a precordial thrill, audible with stethoscope off the thorax The point of maximal intensity is communicated by indicating the location, valve area, or intercostal space where the murmur is loudest. A murmur usually projects from the PMI in the direction of abnormal blood flow. Murmurs can also radiate through solid structures to the chest wall, as often occurs with MR radiating to the left apex. The radiation of a loud cardiac murmur can be extensive and can off some clues about the genesis of the murmur. However, very loud murmurs tend to radiate widely and can sometimes be confusing. Pitch and quality pertain to the frequency and subjective assessment of the murmur by the examiner. Murmurs consisting of one fundamental frequency with overtones are described as “musical”, whereas murmurs of mixed frequencies are typically noted to be “harsh.” Most murmurs are of mixed frequency.

Functional Murmurs are those unassociated with obvious cardiac pathology. These murmurs arise from physiologic changes (see above) or undefined causes (so-called innocent murmurs).

In small animals, nearly all functional murmurs are systolic and the murmur is typically ejection in shape, meaning it begins after S1 and ends prior to S2. The PMI of the functional ejection murmur is at or adjacent to the aortic or the pulmonary valve and the murmur radiates craniodorsally into the aorta or pulmonary artery. In general, functional murmurs are soft, grade 1-2/6, and relatively brief with both heart sounds evident. In puppies, most innocent murmurs become softer during the vaccination sequence and eventually disappear (at about 4 months of age). A classical innocent murmur has a humming or musical character likely related to a vibrating intracardiac structure. Functional ejection murmurs in larger canine breeds can persist throughout life. In many of these dogs, the murmur is protomesosystolic, grade 2 to 3/6 in intensity, and transiently accentuates following exercise to a grade 3 to 4/6 intensity. These ejection murmurs are evident without any accompanying structural lesions on 2D echocardiography. In fact echocardiographic correlates to a functional murmur are inconsistent with the most frequent being mildly increased aortic ejection velocity on spectral Doppler

imaging (1.7 to 2.4 m/s). It is nearly impossible to distinguish functional ejection murmurs from those due to trivial LVOT stenosis based on velocity alone. Some breeds, such as boxers and bull terriers, have a relatively narrow aorta, and ejection murmurs in some of these dogs could represent the effect of ventricular-annular disproportion as opposed to true subvalvular aortic stenosis (SAS). This issue is controversial and largely unresolved. It should be noted, however, that in breeds rarely affected by SAS (such as greyhounds), functional ejection murmurs are also associated with mildly elevated aortic ejection velocities. Systolic murmurs over the cranial sternal borders are common in cats without echocardiographic evidence of significant heart disease. Many of these murmurs arise from flow across the LVOT (often in to a dilated aorta).

Others are caused by dynamic intra-ventricular obstruction (see next section).

Dynamic mid-ventricular and outflow tract obstructions are another potential cause of systolic murmurs in dogs and cats. The classic auscultatory feature is a mid-to-late systolic murmur associated with emptying of ventricular blood and physical contract between cardiac walls, papillary muscle, or mitral valve elements. The Doppler signal is dagger-shaped, typical of obstruction that begins dynamically, as ejection progresses and ventricular volume decreases.

The heart can be structurally normal or hypertrophied in these cases. Mid-ventricular obstruction of the left ventricle (LV) is often from dehydration or concentric hypertrophy of the chamber.

When the murmur arises in the right ventricle (RV), the obstruction is often between the freewall and the supraventricular crest and is often explained by high sympathetic tone, ventricular septal thickening, or right ventricular hypertrophy. Dynamic RV obstruction is especially common in stressed and dehydrated cats.

Whether these murmurs should be considered functional or a consequence of pathology depends largely on the findings on 2D echocardiography. Some cats with hypertrophic cardiomyopathy (HCM) have prominent mid-ventricular obstruction. The finding is also common in cats with hypertrophy thickening from systemic hypertension and hyperthyroidism. Midventricular obstruction differs from dynamic LVOT obstruction caused by systolic anterior motion of the mitral valve associated with HCM in cats and mitral valve malformations in cats and dogs.

In that situation, elements of the anterior (septal) mitral leaflet are pulled towards the ventricular septum creating both dynamic obstruction and an eccentric jet of MR. Aortic Stenosis Obstruction in the LVOT is most often causes by subvalvular aortic stenosis (SAS) in dogs and by HCM in cats. The lesions of SAS include a congenital, subvalvular, fibrous obstruction below the aortic valve that can be discrete or envelop the outflow tract to the base of the aortic valve proper. Other causes of LVOT obstruction are valvular aortic stenosis (AS), mitral valve malformations, and chronic infective endocarditis of the aortic valve. Depending on the lesion, aortic regurgitation (AR) will occur to varying degrees. In most cases, AR is a Doppler diagnosis and the regurgitation is silent to auscultation.

The murmur of (S)AS is systolic, flow dependent, and crescendo-decrescendo in configuration. As with most ejection murmurs, the murmur intensifies following exercise, inotropic stimulation, a ventricular premature beat, a long pause in sinus arrhythmia, or with increases in venous return and stroke volume. The typical PMI of SAS is over the left thorax at the aortic/subaortic region with strong radiation of the murmur apically towards the mitral area and craniodorsally into the ascending aorta. The murmur tends to project into the carotids and even radiate to the skull. The murmur of SAS can be loudest over the right dorsal cardiac base owing to radiation into a dilated ascending aorta. In pure valvular or rare supravalvular AS, the murmur can be loudest on either side of the thorax. With moderate to severe (S)AS the murmur peaks later in systole â&#x20AC;&#x201C; sounding more holosystolic than ejection in configuration; at the same time the arterial pulses are hypokinetic and late-rising. If a diastolic murmur of aortic regurgitation develops with (S)AS, both a systolic and a decrescendo diastolic murmur are evident. This leads to the to-and-fro murmur of AS/AR and to bounding arterial pulses.

Pulmonic Valve Stenosis (PS) is a congenital malformation of the pulmonary valve characterized by varying degrees of valve thickening, leaflet fusion and tethering, and hypoplasia of the annulus or along the base of the valve. It is most common in dogs and relatively rare in cats (and more likely to be infundibular in this species). The resultant murmur is systolic, crescendoâ&#x20AC;&#x201C;decrescendo, and loudest over the pulmonary valve (at the left second to third ICS) with strong radiation dorsally into the post-stenotic dilatation of the main pulmonary.

Thus, the murmur tends to be heard very well over the left, cranial to dorsal cardiac base and is sometimes confused with a PDA for this reason. An early systolic ejection click might be detected with careful auscultation (from a fused but mobile valve). A concurrent murmur of tricuspid regurgitation (TR) is often heard over the tricuspid valve area caused by secondary right ventricular enlargement or tricuspid dysplasia. Pulmonary regurgitation is invariably present on Doppler studies but rarely audible. However, following successful balloon catheter valvuloplasty, there is often moderate to severe pulmonary insufficiency creating an early to middiastolic decrescendo murmur of pulmonary regurgitation. Rarely severe pulmonary regurgitation is present with native valvular dysplasia and the associated to-and-fro murmur of PS/PR is easily confused with a PDA. Congenital PS is often associated with a prominent jugular pulse (giant A-wave). In contrast to dogs with SAS, the arterial pulses should be normal in character unless there is heart failure.

Mitral Regurgitation is one of the most common and important flow disturbances responsible for a pathologic systolic heart murmur. MR develops secondary to malfunction of any portion of the mitral apparatus. Causes include congenital mitral dysplasia, myxomatous degeneration of the valve (endocardiosis) in the dog, infective endocarditis, redundancy or rupture of a chordae tendineae (in the dog), and causes of left ventricular dilatation or hypertrophy, such as cardiomyopathy, hyperthyroidism, systemic hypertension, and PDA. This murmur is loudest over the mitral valve area or the palpable left apex where it is projects well (or near the left sternal edge in cats). MR murmurs radiate both dorsally and to the right (usually one grade softer on the right hemithorax). The MR murmur can be decrescendo in peracute leakage (from equilibration of LV-LA pressures) or in mild cases (as the regurgitant orifice closes in late systole). The murmur is soft in hypotensive patients; alternatively, systemic hypertension can amplify the intensity. The musical systolic â&#x20AC;&#x153;whoopâ&#x20AC;? is a striking frequency phenomenon in some dogs. Progressive increase in the intensity of the first heart sound is a unique feature of MR in dogs with valvular endocardiosis and probably indicates cardiac dilatation with maintenance of left ventricular systolic function. Additionally, the intensity of the MR murmur usually increases with the degree of valvular incompetency (assuming normal ABP) in dogs with myxomatous disease. The intensity of a MR murmur in other causes of MR is not as reliably correlated to the severity. Cats with hypertrophic cardiomyopathy often have a labile murmur of MR related to dynamic left ventricular outflow tract obstruction and systolic anterior motion of the mitral valve.

Tricuspid regurgitation is another common cardiac murmur and in many ways is similar to mitral regurgitation. Causes include valve malformation, degenerative valve disease (endocardiosis), right ventricular enlargement (from pulmonic valve stenosis, right sided cardiomyopathy, chronic bradycardia, or pulmonary hypertension), dirofilariasis, transvenous pacing leads, and (very rarely) tricuspid endocarditis. The PMI of this murmur is the tricuspid valve area on the right, and dorsal radiation is typical. In young puppies with TV dysplasia (e.g., Labrador retrievers), the murmur can be very soft and readily missed. It can be difficult to distinguish TR from the radiating murmur of MR. The following support concurrent TR in the this setting: a prominent jugular pulse, right precordial thrill, different frequency murmur than that heard at the left side, louder right than left-sided murmur, or right-sided CHF. The murmur of TR is often very loud in the setting of pulmonary hypertension. Eccentric jets of TR from

degenerative TV prolapse can also lead to very prominent murmurs of TR along with a right sided thrill.

Ventricular Septal Defect is the most common congenital heart malformation of cats, and also occurs with some frequency in dogs. A large nonrestrictive VSD (i.e., no substantial pressure difference between the ventricles) is also part of the tetralogy of Fallot. When the defect communicates the left ventricular outlet with the perimembranous ventricular septum, the murmur is loudest just below the tricuspid valve, along the right sternal border. When the defect is subarterial, communicating the subaortic septum with the subpulmonary septum, the murmur may is most prominent over the craniodorsal left cardiac base (similar to PS). If the aortic valve has prolapsed into the ventricular septal defect, there may be a diastolic murmur of aortic regurgitation as well.

Aortic Regurgitation is the most important diastolic cardiac murmur. Causes include infective endocarditis, congenital aortic valve disease, prolapse of an aortic valve cusp into a subaortic ventricular septal defect, and aortic root dilatation in aged cats. This murmur is a long, diastolic, decrescendo murmur heard best over the aortic valve at the left hemithorax. The murmur is also well heard at the right cardiac base.

Diastolic murmurs are otherwise rare in dogs and cats. Differential diagnosis includes the soft, low-pitched rumble of congenital mitral or tricuspid stenosis but these are very rare conditions. There is often concurrent atrioventricular valvular regurgitation, which may lead to a systolic murmur.

Patent Ductus Arteriosus is the most important cause of a continuous murmur and is described as “distant” and “machinery” (like a machine shop) in quality. The murmur must be carefully located dorsally on the cranial left base, over the main pulmonary artery (which is the sink for the shunt). Although it is continuous, the murmur does vary and loudness peaks around the time of S2. Often there is concurrent mitral regurgitation (due to left ventricular dilatation) which can be responsible for a systolic murmur over the left apex. The stethoscope should be “inched” up and back from the left apex to the PMI of the continuous murmur at the left base. In terms of differential diagnosis, continuous murmurs (bruits) can be detected over congenital or acquired arteriovenous fistulas, including those associated with thyroid carcinomas or limb injuries. Within the thorax, coronary artery to pulmonary artery fistulas and systemic arterial to pulmonary artery vascular malformations can result in a continuous cardiac murmur. Rare cases of reversed PDA usually have no murmur or a soft ejection murmur with a tympanic and sometimes split second heart sound.

AUSCULTATION – RESPIRATORY (BREATH) SOUNDS Normal respiratory sounds include vesicular and bronchovesicular sounds, bronchial breathing, and tracheal sounds (panting). Normal sounds can become accentuated or decreased in diseases of the thorax or with left sided congestive heart failure (CHF). An increase in bronchial sounds is often detected as a nonspecific finding of pulmonary disease including pulmonary edema. Decreased sounds can indicate pleural fluid (ventral fluid line) or air. Displaced sounds can occur with a mass lesion or diaphragmatic hernia. Normal sounds and abnormal (adventitious) sounds might only become evident after enforcing deeper breathing, which can be encouraged by closing the mouth and holding off one nostril or by occluding both nostrils for a brief period to encourage deep breaths or sighs.

Abnormal upper airway sounds include: 1) tracheal snaps (tracheal collapse); 2) stertor (inspiratory snoring) typical of pharyngeal or nasopharyngeal diseases, and 3) stridor, an

inspiratory wheeze loudest over the larynx. Stridor or altered inspiratory pitch is typical of upper airway obstruction. Low-pitched inspiratory noise can also indicate upper airway obstruction.

While upper airway obstruction is classically inspiratory, fixed obstructions can lead to airway noise during both phases of ventilation.

Abnormal lower airway (adventitious) sounds include rhonchi, wheezes, and crackles. A sonorous rhonchus is an inspiratory or expiratory noise (r/o transmission of upper respiratory stertor) which suggests the presence of fluid or exudate in larger airways, as with bronchitis or pneumonia. Wheezes (sibilant rhonchi) are high-pitched expiratory sounds typical of bronchial narrowing. The usual associations are bronchial disease (bronchitis, asthma) or attenuation of a main bronchus caused by left atrial dilation, hilar lymphadenopathy, primary bronchial collapse, or a pulmonary mass lesion. Crackles (“rales”) are discontinuous sounds similar to radio static or the sound of Velcro pulled apart. These sounds are caused by the explosive opening of collapsed small airways. Though there is a tendency to relate these to “fluid in the lungs,” there is not a consistent correlation as crackles might be detected with pulmonary edema, pneumonia, bronchitis, or pulmonary fibrosis. The loudest crackles are typically detected in primary lung diseases. Subtle crackles are evident only after a deep breath.

References 1. Detweiler DK, Patterson DF. A phonograph record of heart sounds and murmurs of the dog. Ann N Y Acad Sci. 1965;127(1):322-40 2. Vörös K, Nolte I, Hungerbühler S, et al.: Sound recording and digital phonocardiography of cardiac murmurs in dogs by using a sensor-based electronic stethoscope. Acta Vet Hung. 2011; 59(1):23-35.

3. Wagner T, Fuentes VL, Payne JR, McDermott N, Brodbelt D. Comparison of auscultatory and echocardiographic findings in healthy adult cats. J Vet Cardiol. 2010; 12(3):171-82.

4. Little CJ, Ferasin L, Ferasin H, Holmes MA. Purring in cats during auscultation: how common is it, and can we stop it? J Small Anim Pract. 2014;55(1):33-8. 5. Blass KA, Schober KE, Bonagura JD, Scansen BA, et al.: Clinical evaluation of the 3M Littmann Electronic Stethoscope Model 3200 in 150 cats. J Feline Med Surg. 2013 Oct;15(10):893-900. 6. anagement of incidentally detected heart murmurs in dogs and cats.

Côté E, Edwards NJ, Ettinger SJ, et al.: Working Group of the American College of Veterinary Internal Medicine Specialty of Cardiology on Incidentally Detected Heart Murmurs. J Am Vet Med Assoc. 2015 May 15;246(10):1076-88.

CONGENITAL HEART DISEASE John D. Bonagura, DVM, MS, DACVIM (Cardiology, Internal Medicine) Veterinary Clinical Sciences, The Ohio State University

Principles Cardiac malformations are developmental lesions of the heart or great vessels present at birth.

CHD can be caused by genetic, environmental, chromosomal, infective, toxicologic, or nutritional factors or develop from teratogenic effects of drugs. Most defects are considered genetic in origin, but the precise mode of inheritance often is unknown. There are numerous examples of breedrelated predispositions to specific cardiac malformations (see Tables at the end of these reference notes). Penetrance of a lesion can be incomplete, making clinical recognition difficult or impossible.

The pathophysiology of CHD can be classified arbitrarily as: left-to-right shunts, right-to-left shunts, outflow tract stenosis, atrioventricular valve malformations, and complex malformations.

Left-to-right shunts, outflow tract stenosis, and valvular malformations are likely to cause congestive heart failure (CHF), arrhythmias, syncope, or sudden cardiac death. Right-to-left shunts and complex malformations create hypoxemia and secondary polycythemia with clinical complications related to tissue hypoxia and blood hyperviscosity. A number of uncommon complications also can develop, including hypertrophic osteopathy.

The first step in the management of congenital heart disease involves recognition of a congenital malformation of the heart. This must be done by the family veterinarian, so emphasis here is placed on honing auscultation skills, distinguishing functional murmurs from those caused

by CHD, and developing a general understanding of the cardiac malformations affecting dogs and cats. Unless the family veterinarian identifies and refers the patient (or accurately diagnoses the situation in the practice), appropriate management can never be accomplished. Since thoracic surgery and cardiac catheterization/intervention are not part of routine veterinary practice, most patients are referred to a cardiology specialist for management.

The actual therapy of heart malformation can involve surgical, catheter-based, or medical treatments. Some disorders are relatively mild and require no treatment, but many are severe and life-shortening. Prior to any therapy, a definitive diagnosis must be established. This requires a complete echocardiographic study with Doppler and an advanced knowledge of the different variations of heart and vascular malformations. Many cases of CHD are complicated by multiple issues that must be considered before an accurate diagnosis, prognosis, and therapy plan and be advanced. Heart surgery is difficult as it may require cardiopulmonary bypass (making treatment impractical in many cases, even in referral situations). Thus, definitive surgical repair of CHD is rarely accomplished except for extracadiac procedures like closure of patent ductus arteriosus (PDA) or reduction of a congenital peritoneopericdardial diaphragmatic hernia.

Similary, catheter-based interventions need sufficient equipment for quality angiography and intervention. Catheter-based treatments for PDA or pulmonary stensois (PS) can end badly if the operating clinician is inexperienced. Thus it is strongly recommended that surgical or interventional management of cardiac defects be undertaken only by those with appropriate training.

Symptomatic medical therapy also can be needed for complications of CHD, namely control of CHF, cardiac arrhythmias, PH, or secondary polycythemia. Such treatment can be directed by the general practitioner provided the disorder is well characterized and the complications and management issues understood.

Congestive heart failure is a consequence of progressive volume or pressure overload of the affected ventricle. With time, diastolic and systolic ventricular function decline and cardiac output

becomes limited. This situation is worsened by development of mitral or tricuspid valvular regurgitation or atrial fibrillation. The end-result is development of left- or right-sided CHF. Initial management of left sided CHF involves treatment with furosemide (2-4 mg/kg IV, IM, or SQ), oxygen, and possibly 2% nitroglycerine ointment. Sedation with butorphanol (0.1 to 0.25 mg/kg IM or SQ) can be added if necessary. Pimobendan (0.25 to 0.3 mg/kg PO q12h) is often included in therapy of CHF due to CHD. If this approach fails to control the CHF, and the cause is a left to right shunt, sodium nitroprusside (0.5 to 2.5 micrograms/kg/min infusion) can be used to reduce the arterial blood pressure and magnitude of shunting. Alternatively, hydralazine (0.5 to 2 mg/kg PO q12h) or enalapril (0.25 to 0.5 mg/kg PO q12h) or other angiotensin converting-enzyme (ACE) inhibitor can be initiated to reduce afterload and reduce left-to-right shunting. Care must be taken to maintain systolic blood pressure in the 80 to 120 mm Hg range, particularly in cases of aortic stenosis where hypotension can reduce coronary perfusion.

Chronic medical therapy of CHF includes furosemide, an ACE-inhibitor, spironolactone, and pimobendan (see elsewhere in this Program).. The use of beta-blockers in treatment of dogs with CHF due to CHD is unresolved, and care must be used to avoid bradycardia, especially in dogs with fixed obstructions such as SAS and PS, as cardiac output in these conditions is relatively heart rate dependent. For dogs already taking beta-blockers as cardioprotection, once CHF develops, the beta blocker should be continued, the dosage reduced if needed to obtain a target examination heart rate in the 100 to 140/minute range. In some cases, medical therapy for CHF can be discontinued if definitive repair of the defect can be successfully performed. This is particularly true in young animals with PDA. Controlling arrhythmias in the setting of severe CHD can help to maintain a compensated state and can prevent sudden death. Atrial fibrillation is particularly destabilizing to dogs with CHD and established heart failure. Heart rate control can be achieved with digoxin, diltiazem, and a betablocker. Electrical cardioversion is another option to restore sinus rhythm, unless atrial enlargement is severe, in which case it is not likely to yield long-term success. Re-entrant SVT due to an accessory pathway can be encountered and radiofrequency catheter ablation of the anomalous pathway can eliminate the arrhythmia substrate. In the interim, diltiazem (to block the AV node) and flecainide or another antiarrhythmic drug given to block the accessory pathway.

Ventricular arrhythmias are often recognized in canine SAS and PS. Holter ECG monitoring can be indicated to screen for rhythm disturbances, especially in dogs with exertional symptoms.

Chronic therapy of important ventricular tachycardia can include sotalol, mexiletine plus a beta blocker (including sotalol), amiodarone, or procainamide.

Management of pulmonary hypertension due to high pulmonary vascular resistance is difficult as the anatomic vascular changes responsible often are irreversible. The evaluation of PH usually requires referral to a specialist experienced in CHD. PH usually develops rapidly in dogs with large left-to-right shunts (prior to six months of age). In cats development is more gradual, and if caught in time, can be arrested by closure of the defect or management of a stenotic mitral valve.

When a reactive component of vasoconstriction is identified, drugs that reduce pulmonary vascular resistance such as sildenafil at initial doses of 1 to 2 mg/kg q12h PO can be beneficial.

Currently this therapy is very expensive. Arterial blood pressure must be monitored as reduced systemic resistance will lead to greater right-to-left shunting. Controlled exercise is important to prevent exertional collapse or dyspnea. This can be difficult to achieve in puppies or kittens.

Management of polycythemia can be required. This condition is usually a consequence of complex malformations (double outlet right ventricle; tricuspid or pulmonary atresia) or of right-toleft shunting across a PDA or septal defect related to an obstructive lesion of the right heart (PS, double-chambered right ventricle, tricuspid stenosis) or pulmonary hypertension. Balloon valvuloplasty or surgery can decrease right-sided pressures and reduce shunting in the case of an anatomic obstruction; drugs can be tried to reduce pulmonary vascular resistance (see above).

Care must be exercised in the setting of a large VSD as florid left-to-right shunting can develop if RV pressures approach normal. Phlebotomy can be required in patients with right-to-left shunting

and secondary polycythemia. While a PCV of 62 to 65% often is well tolerated, values exceeding 68 to 70% are likely to cause exercise difficulties or predispose to thrombotic stroke or sudden death. Periodic phlebotomy with replacement by IV or subcutaneous crystalloid fluid. When the need for phlebotomy becomes too frequent, bone marrow suppression can be attempted using hydroxyurea (10 to 20 mg/kg PO daily). Treatment can not work, and anorexia, GI disturbances, and skin rash can limit tolerability of the drug. A CBC and platelet count should be performed regularly.

Patent Ductus Arteriosus (PDA) Overview – PDA is a persistent patency of the fetal ductus arteriosus. The ductus connects the descending aorta and the main or adjacent left pulmonary artery. This defect is reported to be present in approximately 2.5 of 1000 live canine births. Left to right shunting leads to pulmonary overcirculation, volume overload of the left heart, and progressive LV dysfunction. Left sided CHF can develop. Cardiomyopathy of chronic volume overload and atrial fibrillation are common in larger breeds with untreated PDA. In a small percent of cases, reversed shunting is caused by pulmonary vascular injury (Eisenmenger’s physiology). Most puppies are apparently asymptomatic. Once tachypnea and exercise intolerance develop, left-sided CHF is likely.

Exertional rear limb weakness is typical of “reversed” PDA. PDA is a genetic disorder in many breeds, including: Bichon frise, Chihuahua, Cocker spaniel, Collie, English Springer spaniel, German shepherd, Irish and Gordon setters, Poodles, Maltese, Kerry blue terrier, Keeshond, Labrador retriever, Newfoundland, Pomeranian, Shetland sheepdog, and Yorkshire terrier. The precise mode of inheritance is undetermined, likely related to multiple or modifying genes. Females are predisposed, but both sexes are affected. PDA is rare in cats.

Diagnosis –The most striking diagnostic finding during physical examination is a continuous cardiac murmur loudest over the left craniodorsal cardiac base. The diastolic component of the murmur is less prominent or absent in very young puppies, in cats, or in cases of progressive pulmonary hypertension. Arterial pulses are typically hyperkinetic as the arterial pulse pressure is wide. This is explained by the large LV stroke volume and low diastoic pressure associated with pressure run off across the ductus. The LV can be palpably enlarged with caudoventral apical displacement. Pelvic limb weakness that improves with rest, differential cyanosis, loss of the continuous murmur, and a loud second heart sound are typical of reversed PDA. Radiographs and 2D echocardiography demonstrate dilation of the left atrium, LV, ascending aorta, descending aorta (“ductus bump”), and main pulmonary artery. Radiographs identify pulmonary overcirculation in left to right shunting PDA. Doppler studies reveal continuous blood flow in the main pulmonary artery. Mitral regurgitation and pulmonic insufficiency are commonly found due to chamber dilatation. Echocardiography can document reduced LV systolic function. The typical ECG findings are enlargement of the LV and possibly the left atrium. In reversed PDA, the diagnostic studies demonstrate mainly right heart enlargement, dilation of the main pulmonary artery, and reduced pulmonary blood flow. Contrast echocardiography following cephalic vein injection will demonstrate contrast in the descending aorta.

The differential diagnoses includes aortopulmonary window, a congenital connection between the ascending aorta and pulmonary artery; ventricular septal defect with aortic regurgitation; and aortic stenosis/regurgitation. Multiple bronchial artery to pulmonary fistulas can create a PDA like situation in terms of lung circulation and left-sided volume overload; however, a continuous murmur may not be evident mandating, angiography for diagnosis. The signs of reversed PDA can mimic those of neuromuscular diseases, particularly myasthenia gravis.

Therapy – Closure or occlusion is strongly recommended in left-to-right shunting defects as the one-year mortality for untreated dogs probably exceeds 60%. In the reversed (right-to-left) shunting PDA, closure of the defect is contraindicated. Thoracotomy and surgical ligation of the

ductus is a very successful with a perioperative mortality that should be <5% at experienced surgical centers, and is <2% in the best hands. Closure generally results in complete resolution of signs. A post-operative murmur of mitral regurgitation is common due to LV stretch, but is generally gone by the time of suture removal. Less-invasive transcatheter techniques for closure of PDA have gained significant popularity and have superseded surgery at many hospitals. As with surgery, success is highest in the hands of experienced operators. Embolization coils (Gianturco) are best suited for small diameter defects with a gradually tapering diameter; the various Amplatzer occluding devices has been modified for both small and larger diameter (>5 mm) defects. The current Amplatz Canine Ductal Occluder is highly effective and only limited by the size of the patient in terms of vascular access (more challenging in dogs <3 kg). When CHF complicates PDA, medical management is needed (discussed previously). Reversed PDA has a poor prognosis though with vigilant therapy some patients live beyond 5 years of age, affected mainly by rear limb weakness during exercise. Management of pulmonary hypertension and polycythemia were discussed previously.

Early therapeutic intervention can slow or eliminate irreversible myocardial damage and prevent heart failure. For example, after successful closure of a PDA, most dogs will live a normal life without need for cardiac follow-up. The prognosis following isolated closure of a PDA is excellent.

A normal life-span can be anticipated, and most cases do not require any cardiac follow-up.

Exceptions to this rule include dogs with marked LV systolic dysfunction (by Echo), dogs with prior CHF, or dogs with atrial fibrillation. Such patients should be referred to a cardiologist for evaluation. Follow reversed PDA dogs by monitoring clinical signs and the PCV.

Ventricular Septal Defect (VSD) Overview – A VSD is a communication between the left and right ventricles. Unless there is a reason for elevated right ventricular pressure, shunting proceeds from LV to RV. The location of a VSD determines the classification of the defect. This is generally defined by 2D echocardiographic and color coded Doppler studies studies as paramembranous (perimembranous), inlet, muscular (trabecular), or subarterial (subpulmonic, supracristal, doublycommitted). Large defects are sometimes associated with malalignment of the aorta. These lesions are likely to cause aortic root prolapse and permit aortic valvular regurgitation. A large VSD also forms one component of the tetralogy of Fallot. VSD shows a genetic predisposition in some breeds, including English bulldogs and Springer spaniels.

The shunting physiology of VSD is similar that of PDA, representing a left to right shunt with pulmonary overcirculation and volume overload of the left atrium and LV. Large septal defects usually progress to left-sided CHF. This is particularly true when there is complicating aortic regurgitation. The degree of RV overload depends on the size of the defect, the presence of RV outflow tract obstruction, the location of the defect, and pulmonary vascular resistance.

Concurrent PS, a double-chambered RV (a midventricular fibromuscular obstruction), or development of Eisenmenger’s physiology can lead to reversed shunting. Most dogs and cats are asymptomatic. Occasional cases show signs of CHF or pulmonary hypertension. Cyanosis indicates a complicated VSD. Experimentally, VSD in various species can be associated with a number of drugs, infections, or environmental factors. Most cases of uncomplicated VSD in dogs are well tolerated so long as the defect is “restrictive”. Defects <50% of the aortic root area are restrictive in nature. Very large defects are likely to cause CHF and death at approximately one to two months of age as pulmonary vascular resistance drops; puppies and kittens are uncommonly presented to veterinarians at this age.

Diagnosis – A systolic murmur, generally loudest over the cranial right sternal edge, is typical of the membranous VSD. However, if the defect is located elsewhere in the septum, or if fibrous tissue proliferation partially occludes the defect, the jet of flow can be diverted resulting in a

systolic murmur that is apical or loudest over the left sternal edge. In the setting of concurrent aortic regurgitation, a diastolic murmur may be audible, and this usually indicates a clinicallyrelevant complication that will shorten lifespan. Results of radiography are quite variable, but overcirculation of the lungs is common. Various combinations of left and right heart enlargement are typical. The main pulmonary artery can be dilated from increased flow or PH. The ECG can be normal, LV enlargement or wide or splintered Q-wave in leads I, II, and aVF may be observed.

Echocardiography is diagnostic with 2D imaging and Doppler studies delineating the location, direction and velocity of shunting. Restrictive defects are characterized by high velocity (>4 m/s) shunting, indicating maintenance of left-to-right ventricular pressure gradient. It is important to scrutinize the right ventricle for obstructive lesions and the LV outflow tract for aortic root for malalignment or aortic regurgitation.

The differential diagnosis includes other causes of systolic murmurs, particularly tricuspid valve dysplasia, aortic stenosis and some cases of double-chambered right ventricle. Mitral regurgitation can create a similar murmur in terms of timing. Subpulmonic defects create left basilar murmurs that can be confused with pulmonic or aortic stenosis.

Therapy – Most dogs and cats with an isolated, uncomplicated VSD (without severe aortic regurgitation or other lesions) that survive to 4 months of age will not require any treatment.

Surgical closure of septal defects is the definitive treatment but requires cardiopulmonary by-pass and open heart surgery. While this has been successfully performed in dogs and cats, it is not a common practice in veterinary medicine. Palliative pulmonary arterial banding is available to create a supravalvular PS and reduce the magnitude of left-to-right shunting. This procedure is recommended only for those animals with rapidly progressive cardiomegaly and with overt or impending CHF. Simple cardiomegaly is not an indication for banding. A cardiologist should be consulted. Transcatheter and perventricular occlusion devices (“hybrid surgery”) can be applied to dogs.

If CHF does develop, medical management is indicated (discussed previously). Right to left shunting can develop in dogs or cats with VSD due to PH, valvular or subvalvular PS, or progressive, midventricular fibromuscular obstruction (so called double-chambered RV). Exercise intolerance and polycythemia can develop. Treatment is as described above for polycythemia.

A small, restrictive VSD carries an excellent prognosis for longevity. CHF associated with VSD is actually uncommon in most small animals with VSD as they are “naturally-selected” and rarely require intervention. CHF should be anticipated in the dog with a VSD and aortic root prolapse and audible aortic regurgitation. In these cases, CHF can develop in middle-age from LV volume overload. The author empirically treats these patients with ACE-inhibitors. CHF also develops in some cats with VSD, especially when the defect is non-restrictive. Not infrequently a VSD will be observed to close from fibrous tissue proliferation or adherence of the septal leaflet of the tricuspid valve. This can lead to a septal aneurysm but without significant shunting. These lesions are essentially closed.

Atrial Septal Defect (ASD) Overview – An ASD is a communication between the left and right atria. Unless there is a reason for elevated right ventricular pressure, shunting generally proceeds from left to right. The location of an ASD determines the classification of the defect. These are generally defined by detailed 2D echocardiographic and color Doppler studies as a secundum, primum, or sinus venosus defect. A defect in the ventrally-located atrioventricular septum, or of the embryonic endocardial cushions, can lead to a complicated situation of a primum (ventral) ASD, inlet septal VSD, and malformation of the septal leaflets of the atrioventricular valves with atrioventricular valvular regurgitation. This latter situation is terms (a complete) atrioventricular septal defect. A patent foramen ovale is created when the two atrial septal membranes (I and II) are either pulled or pushed apart. Patency can be maintained by either severe left atrial stretch or from a higher

than normal right atrial pressures that push the membranes apart. The latter is caused by some other form of right-sided disease. ASD is sometimes recognized in dogs with advanced mitral regurgition and probably represents an atrial tear in the thin-walled fossa ovalis.

The pathophysiology of ASD is that of a left to right shunt with volume overload of the right atrium and right ventricle. There is also pulmonary overcirculation, but the left atrium typically decompresses to the right atrium and can be normal in size (except with an endocardial cushion defect). A large ASD can cause right-sided CHF or lead to pulmonary vascular injury with pulmonary hypertension. An endocardial cushion defect can cause left-sided or biventricular CHF. Right to left shunting can occur across an ASD (or PFO) in the setting of PH, or from obstructive lesions on the right side of the heart. Severe tricuspid regurgitation also can cause cyanosis by raising right atrial pressure.

ASD is genetic predisposed in some breeds and family lines (e.g., standard poodles in North America). Most dogs and cats with an isolated ASD appear asymptomatic. There are no specific signs of an ASD. The pressure difference across an ASD is relatively small; therefore, the defect does not cause a murmur aside from that of increased flow across the pulmonary valve (“relative” PS). Classically the second heart sound will be split, owing to a longer duration of right ventricular ejection. Occasional cases show signs of CHF or of pulmonary hypertension. Cyanosis indicates a complicated ASD. Diagnosis – The identification of a systolic murmur creates suspicion for CHD. Careful auscultation should reveal a splitting of the second heart sound owing to delayed pulmonary valve relative to aortic valve closure. Radiography of a secundum ASD demonstrates right heart enlargement, dilation of the pulmonary artery, and overcirculation of the lungs. Left atrial size is variable. With a complete endocardial cushion defect (atrioventricular septal defect), significant mitral or AV valve regurgitation can occur. This can lead to left atrial enlargement and eventually signs of left-sided or biventricular CHF. The ECG generally shows RV and usually right atrial enlargement with right axis deviation. A left cranial frontal axis is more typical of a primum ASD or an endocardial cushion defect. Echocardiography is diagnostic with 2D imaging demonstrating the septal defect and Doppler studies delineating the direction of shunting, which is often bidirectional. It is important to scrutinize the right ventricle for obstructive lesions and the atrioventricular valves for malformation and valvular regurgitation. Differential diagnosis includes other causes of systolic murmurs in young dogs including functional murmur, valvular pulmonic stenosis, and aortic stenosis. Anomalous pulmonary venous drainage can create a similar physiology but appears rare in animals. This lesion can be associated with a sinus venosus type ASD. Therapy – There is little experience in the management of ASD in dogs and cats as this defect is relatively uncommon. In the case of patent foramen ovale, treatment of the related lesion can cause the defect to functionally close. Transcatheter atrial septal occlusion devices have been developed for closure of septal defects in children and have been applied to dogs. Open-heart surgery has been used for successful closure of ASDs, but is not readily available. If CHF does develop, medical management is indicated (discussed previously). Right to left shunting ASD will likely create exercise intolerance and polycythemia. Treatment is as described above for polycythemia. A yearly cardiologist examination with an echocardiogram is recommended for most dogs and cats with an ASD. Late-onset pulmonary vascular disease with PH can occur.

Tetralogy of Fallot Overview – The tetralogy of Fallot is defined by the following anatomical defects: pulmonic stenosis (PS), large (unrestrictive) VSD, dextropositioned aorta, and right ventricular hypertrophy.

This condition represents one of the most common causes of cyanotic CHD. The presence of PS increases RV systolic pressure and allows shunting of blood from right to left. Depending on the severity of RV outflow obstruction and the systemic vascular resistance, blood will shunt from

right to left, left to right, or (most commonly) in a bi-directional manner. Right to left shunting leads to hypoxemia, cyanosis, and secondary polycythemia. There is a genetic basis for tetralogy of Fallot in some breeds including the English bulldog and Keeshond. The history can include exercise intolerance, syncope, or tachypnea. When the PS is not severe, the condition can be well tolerated and shunting is predominately left to right (“pink tetralogy”).

Diagnosis – A systolic murmur of PS is typically detected over the left base. Cyanosis is typical, especially after exercise. Pulse oximetry can identify clinically significant desaturation (<90%).

Blood gas analysis reveals hypoxemia, often with pO2 < 65 mm Hg. Right ventricular hypertrophy is evident by ECG and imaging studies. Radiographs demonstrate right ventricular rounding, a small and straight left heart border on the VD projection, and pulmonary under-circulation. The ascending aorta can be widened ventrally on the lateral projection (over-riding aorta). 2D echocardiography is diagnostic and demonstrates the four components of the malformation.

Doppler studies show low velocity (bidirectional) shunting across the VSD over the cardiac cycle, while high velocity flow of PS (typically 4 to 5 m/s) is evident across the proximal pulmonary artery.

The PCV may indicate polycythemia; pulse oximetry can show desaturation of hemoglobin.

Cardiac catheterization is rarely needed to establish the diagnosis.

The differential diagnosis for the various signs of tetralogy includes tricuspid atresia, pulmonary atresia (pseudotruncus arteriosus), and PS with a VSD or an ASD (or patent foramen ovale).

Complex malformations such as double outlet RV can lead to cyanotic heart disease.

Therapy – Animals with a sedentary lifestyle will often tolerate this disease well, especially if the PS is not too severe. Some will live for 5 or more years. Exercise creates vasodilation in skeletal muscle and increases tissue oxygen demands; accordingly, most affected animals have signs of tachypnea and exercise intolerance with exertion. Sudden death is common consequent to progressive hypoxemia, polycythemia and cardiac arrhythmias. Drugs that cause systemic vasodilation should be avoided in these patients as right-to-left shunting can be exacerbated.

Beta-blockage with the nonspecific beta-blocker propranolol (starting at 0.25 mg/kg PO q8h and up-titrating over 4 weeks to 1 mg/kg PO q8h) can be beneficial by reducing exercise-induced RV hyper-contractility, an event that can add a dynamic component to RV outflow obstruction. The beta2 blocking effect should theoretically benefit by preventing some exercise induced peripheral vasodilation. Definitive surgical treatment for tetralogy of Fallot includes closure of the VSD and removal or bypass of the stenosis under cardiopulmonary by-pass. Palliative surgery involves creation of an extra-cardiac shunt between the systemic and pulmonary circulations (e.g., BlalockTausig shunt). Such shunts increase pulmonary flow, improve arterial saturation, and can produce significant clinical improvement. The major limitation is the extent to which these shunts will remain patent. Aspirin or another drug that inhibits platelet activation (such as clopidogrel) is indicated. Balloon valvuloplasty of a stenotic pulmonary valve can reduce RV pressures, but complete resolution of the PS will generally allow for marked left to right shunting. Polycythemia should be managed as described previously.

Follow-up evaluation should emphasize clinical signs, PCV, and arterial oxygen saturation.

Yearly reevaluation is indicated. If a palliative shunt has been created, Doppler evaluation of shunt patency should be undertaken.

Pulmonic Stenosis (PS) Overview – PS is a congenital narrowing of the pulmonic valve, subpulmonic region, or immediate supravalvular tissues. The components of valvular PS include valve thickening, fusion along the valvular commissures, and varying degrees of hypoplasia of the valve. Subvalvular obstruction can be fixed (fibrous) or related to dynamic obstruction due to muscular hypertrophy.

An unusual type of subvalvular PS is associated with a single origin of the coronary arteries (R2A); this is most common in English bulldogs. The left coronary artery is located adjacent to a subvalvular obstruction in this condition.

Pressure overload of the RV is created with increased systolic pressure needed to eject blood across the stenotic valve. This pressure is generated by concentric hypertrophy of the ventricle.

High velocity ejection is needed to pump the RV stroke volume. This is associated with significant post-stenotic turbulence in the great vessel. If there is a concurrent patent foramen ovale, ASD, or VSD, right to left shunting can develop. Cardiac output is limited. Right-sided CHF can occur from combinations of diastolic and systolic RV dysfunction, tricuspid regurgitation, and possibly atrial fibrillation.

A genetic basis is responsible for most cases of canine PS, with higher prevalence in the following breeds: terriers (multiple breeds), Beagle, Boykin spaniel, Boxer, Chihuahua, Cocker spaniel, English bulldog, Mastiff, Samoyed, and schnauzers. PS is rare in cats. Most affected dogs are asymptomatic, but tiring, exercise intolerance, and syncope can be observed in severe cases. If CHF occurs, there will be abdominal distension from ascites.

Diagnosis â&#x20AC;&#x201C; The typical ejection murmur of PS is systolic and loudest over the pulmonary valve and craniodorsal left base. The more severe the defect, the louder and later peaking the murmur.

An ejection sound can be detected in valvular PS. A loud holosystolic murmur on the right is suggestive of tricuspid regurgitation from either right ventricular hypertrophy or concurrent tricuspid valve malformation. Membranes should be pink unless there is a right-to-left shunt across a PFO, ASD or VSD. A prominent jugular pulse can be identified. Right-sided CHF with hepatomegaly and ascites will be found in a small percentage of cases. Rarely, pleural effusion or chylothorax are identified in dogs with CHF. The ECG, thoracic radiographs, and 2D echocardiogram will demonstrate RV enlargement and often dilation of the right atrium. Imaging should reveal post-stenotic dilation of the pulmonary artery in severe cases. The pulmonary circulation is normal to reduced. Doppler echocardiography maps high-velocity, turbulent flow in the RV outflow tract and into the pulmonary artery. Provided RV systolic function is normal (and the patient is not heavily sedated or anesthetized), the peak velocity of ejection correlates with the severity of obstruction. Peak velocities exceeding 5 m/s are considered severe (100 mm Hg peak pressure gradient), and carry a guarded to poor prognosis. Velocities of <3.5 m/s indicate a relatively mild stenosis. Careful examination of the atrial septum and ventricular septum with color Doppler is needed to exclude a right to left shunt. A contrast echocardiogram is an efficient way to screen for a defect. Cardiac catheterization is rarely needed to establish the diagnosis.

The differential diagnsosis includes other causes of CHD that create a systolic murmur or right sided enlargement such as tetralogy of Fallot and ASD. Trivial PS may be difficult to distinguish from a functional ejection murmur.

Therapy â&#x20AC;&#x201C; Mild PS (peak pressure gradients measured by Doppler studies of <50 mm Hg) generally carries a good prognosis (survival of 8 years or more). Some dogs in the 50 to 100 mm Hg range (moderate stenosis) do benefit from valvuloplasty in terms of exercise capacity, but many of these dogs do well without intervention. Comparatively, severe disease (Doppler echocardiographic gradient > 100 mmHg) increases the likelihood of sudden death or CHF. Transcatheter balloon valvuloplasty is the treatment of choice for these dogs, especially when the lesion is characterized by valvular thickening with commissural fusion. In experienced hands the procedure mortality is <5% and the dilation results in a 50% or greater reduction of RV systolic pressures. If the cases are chosen carefully, most treated dog will benefit. Therapy should not be delayed as gradients and muscular hypertrophy can progress with time and growth. This approach is generally unsafe in dogs with single origin of the coronary artery associated with subvalvular stenosis. When PS is complicated by severe RV hypertrophy or subvalvular fibromuscular obstruction, balloon valvuloplasty combined with propranolol or atenolol therapy (1 mg/kg PO, q12h). In some cases the dynamic muscular obstruction resolves over time; otherwise, atenolol can be continued for life. Surgical techniques including patch grafting, pulmonary valve repair or resection, or surgical dilation may help cases of severe (fibro-) muscular RV obstruction, broad subvalvular fibrous ring, or when PS is complicated by marked pulmonary valvular

hypoplasia. Cutting balloons and catheter delivered stents have also been used in dogs with subvalvular PS, but a limited annulus size usually limits this success. High pressure balloons can sometimes be effective and are also useful for more typical valvular stenoses in some dogs. An RV to pulmonary artery conduit can be placed surgically to bypass a hypoplastic valve or stenosis due to an anomalous coronary artery, but surgical mortality is high. Instead we use a balloon procedure but do not overize past the annulus. In cases that cannot be treated more definitively, atenolol provides cardiac protection and is well tolerated. PS with patent foramen ovale, ASD, or VSD can progress to right-to-left shunting with polycythemia, and is treated as described previously.

In cases of mild stable PS, re-evaluation can not be necessary. The dog with moderate to severe PS should have an annual examination and echocardiogram with Doppler study performed by a cardiologist. This is especially true in large breed dogs where growth during the first year may lead to a relative increase in severity of the obstruction. The pressure gradient, competency of the tricuspid valve, and RV systolic and diastolic heart function should be followed.

Aortic Stenosis (AS) Overview â&#x20AC;&#x201C; AS is typically related to developmental narrowing of the left ventricular outflow tract. The most common location for obstruction is the subvalvular portion of the outflow tract (subaortic stenosis or SAS), related to a fixed (fibrous) obstruction. The condition is common in dogs and rare in cats. Valvular AS is observed in some dogs and is characterized by thick or fused aortic valve leaflets, or by the presence of fused bicuspid leaflets. Dynamic obstruction of the outflow tract also can occur due to malformation of the mitral valve allowing systolic anterior motion of the mitral valve. This unusual form of SAS is labile and worsens with high sympathetic tone (and benefits from beta-blockade). Additional features of AS include LV hypertrophy and narrowing of the intramural coronary arteries, which reduces myocardial perfusion. Dogs with AS are at a higher risk for infective endocarditis. The aorta is often abnormal with what has been termed postâ&#x20AC;?stenotic dilation, but a primary aortopathy might also be pertinent to the further development of this defect. For example, abnormal ventricular septal to aortic angles have been identified in Boxers and in golden retrievers, even in very young dogs.

Pressure overload of the LV is created with increased systolic pressure needed to eject blood across the stenotic zone. This pressure is generated by concentric hypertrophy of the LV. High velocity ejection is needed to pump the LV stroke volume. This is associated with significant poststenotic turbulence in the great vessel. Coronary arterial insufficiency can lead to subendocardial ischemia. This predisposes to exercise intolerance and cardiac rhythm disturbances. Cardiac output is limited. Left-sided CHF can occur from combinations of diastolic and systolic LV dysfunction, mitral regurgitation, and possibly atrial fibrillation. Syncope or sudden death can be triggered by exertion. Ventricular arrhythmias or stimulation of ventricular mechanoreceptors (cardiac baroreceptor reflex) can be responsible.

SAS is a genetic disorder in many canine breeds including the Golden retriever, Newfoundland, Bull terrier, German shepherd, Boxer, English bulldog, among many. Most affected dogs are asymptomatic, but tiring, exercise intolerance, and syncope can be observed in severe cases.

Should CHF develop, there will be tachypnea and other respiratory signs related mainly to pulmonary edema.

Diagnosis â&#x20AC;&#x201C; The typical ejection murmur of AS is systolic and loudest over the aortic valve and subaortic areas. In SAS, the more severe the defect, the louder and later peaking the murmur and the more likely a prominent right-sided component will be evident (true valvular AS is often loudest over the right dorsal base). A loud holosystolic murmur over the apex may be indicative of concurrent mitral regurgitation. The femoral pulse is late-rising and weak in cases of moderate to severe AS. Overt left-sided CHF will be found in a small percentage of cases.

The ECG, thoracic radiographs, and 2D echocardiogram will demonstrate LV enlargement and

less often dilation of the left atrium. Radiography shows a normal pulmonary circulation in most cases. Imaging often reveals post-stenotic dilation of the ascending aorta (on the right of the midline). The Echo finding of hyperechogenicity of the subendocardial myocardium and papillary muscles indicates severe stenosis with ischemic fibrosis of muscle. The finding of left atrial dilation is also a poor prognostic sign and stems from left ventricular failure; mitral valve disease; or an (often overlooked) left-to-right shunt. Doppler echocardiography maps high-velocity, turbulent flow in the LV outflow tract and into the ascending aorta. Generally the most accurate velocities are obtained from a subcostal transducer position. Provided LV systolic function is normal (and the patient is not heavily sedated or anesthetized), the peak velocity of ejection correlates with the severity of obstruction. Peak velocities exceeding 4.5 to 5 m/s are considered severe (>80 to 100 mm Hg peak pressure gradient), and carry a guarded to poor prognosis. Cardiac catheterization is rarely needed to establish the diagnosis.

The differential diagnosis includes other causes of CHD that create a systolic murmur or leftsided enlargement, including VSD and mitral valve malformation. Pulmonic stenosis, atrial septal defect, and functional murmurs are additional causes of left sided ejection murmurs. .

Therapy – Transcatheter balloon dilation of the stenotic orifice has been performed and successfully reduces LV pressure gradients by approximately 40 to 50%. However, this benefit however becomes attenuated over time and the procedure has largely been abandoned, though it can be a consideration for severe cases of SAS and is certainly beneficial in the patient with valvular AS due to mobile, but fused valve leaflets. Recently clinicians have been using a combination of a cutting balloon followed by a high-pressure balloon with the intent of “scoring” the subvalvular lesion and then dilating it. It remains to be seen if this will be any more effective.

Open surgical resection of the stenotic lesion provides the best long term success in terms of reduction of gradients, but it requires cardiopulmonary bypass, and long-term survival has been disappointing. Beta-blockade with atenolol (1-2 mg/kg PO bid) seems to improve survival over historical controls and a median survival of > 4 years has been observed in dogs from our hospital with even severe SAS (gradients >120 mm Hg). Atenolol is recommended for all dogs with a peak gradient >50 mm Hg. Beta-blockade is particularly helpful in the specific situation of dynamic SAS caused by mitral valve malformation wherein beta-blockade can completely alleviate the obstruction and allow regression of LV hypertrophy.

Unfortunately, severe SAS carries a discouraging prognosis owing to premature death. Sudden arrhythmic cardiac death and progressive LV dysfunction with development of CHF are typical outcomes. Mature dogs with mild SAS are more likely to live normal lives, though some still experience sudden death. Dogs with even mild disease are at higher risk for development of bacterial endocarditis. Therefore, prophylactic antibiotics should be administered during elective surgical procedures or whenever wound contamination is an issue.

In cases of mild stable SAS, re-evaluation may not be necessary. The dog with moderate to severe SAS should have an annual examination and echocardiogram with Doppler study performed by a cardiologist. The pressure gradient, competency of the aortic and mitral valves, and LV systolic and diastolic heart function should be followed. Giant breed dogs should be evaluated just prior to full maturity, as the severity of the obstruction can increase dramatically following rapid growth.

Atrioventricular Valvular Dysplasia Overview – Dysplasia or malformation of the mitral or tricuspid valves includes a number of morphologic abnormalities of the atrioventricular valve apparatus including combinations of: malformed papillary muscles; excessively short or long chordae tendineae; abnormal development of the valve leaflets and cusps; and fusion along valve commissures. The functional outcome of mitral or tricuspid dysplasia is either valvular regurgitation (most common) or valvular stenosis with obstruction to ventricular filling. Both disorders can occur. Severity can range from

trivial to life-threatening. There can be concurrent defects such as atrial septal defect or patent foramen ovale.

Dysplasia of the tricuspid valve is relatively common malformation of larger breeds of dogs and especially of the Labrador retriever. In fully‐formed tricuspid valve dysplasia the lesions are dramatic. These can include: malformed and thickened leaflets; excessively long or short chordae tendineae; either normal or ventral displacement (Ebstein’s anomaly) of the annulus with leaflets inserting beyond the normal apical offset; and prominent bridging between the medial and lateral papillary muscles near the apex). In most cases the septal leaflet appears to be adhered to the septum for a longer distance (failure to delaminate) and this is the cause of apical coaptation of the valves. In severe cases massive RA dilation is expected along with significant RV eccentric hypertrophy. Depending on the leaflet and chordal arrangements there may also be stenosis or rarely atresia of the tricuspid valve. These lesions have also been observed in cats. In contrast, mild tricuspid valve malformations are associated with subtler abnormalities in the valve apparatus structure and motion and there is more controversy about these diagnoses because some “dysplastic” valves might simply be variations on normal.

Both atrioventricular valvular regurgitation and valvular stenosis lead to atrial dilation on the affected side and predispose to CHF and to atrial arrhythmias, including atrial fibrillation. If the stenotic valve is competent, ventricular function is relatively normal. In cases of mitral stenosis, reactive changes in the pulmonary vascular tree can lead to significant pulmonary hypertension with right ventricular hypertrophy and limited exercise capacity; this is most common in cats. In tricuspid stenosis (or severe regurgitation) there is a high potential for continued patency of the foramen ovale. This can lead to right to left shunting, arterial hypoxemia, and create a form of cyanotic heart disease.

Atrioventricular valve dysplasia is most likely a genetic disorder in a variety of breeds particularly the Labrador retriever (tricuspid valve) and Bull terrier and Great Dane (mitral valve).

The precise mode of inheritance across various breeds has not been determined. Tricuspid dysplasia in Labrador retrievers can be associated with anomalous conduction pathways predisposing to reentrant supraventricular tachycardias. Clinical signs can be absent until the onset of CHF or atrial fibrillation. Observant owners generally recognize some exercise intolerance. In the case of trivial or mild malformation, the dog is normal. In the case of tricuspid dysplasia with a patent foramen ovale, there can be tiring and obvious cyanosis.

Diagnosis – The most common clinical sign is a systolic murmur of atrioventricular valvular regurgitation over the affected valve area. Diastolic murmurs of atrioventricular valve stenosis are usually very soft and easily missed. Membranes should be pink unless there is a right-to-left shunt.

Definitive diagnosis of mitral or tricuspid dysplasia requires careful 2D echo imaging of the affected valve combined with Doppler studies that record transvalvular flow and identify valvular regurgitation. There are characteristic Doppler flow patterns for valvular stenosis and regurgitation, and severity of the disease can be gauged by an experienced examiner using noninvasive ultrasound studies.

In mitral valve dysplasia signs are mainly left-sided, and with mitral regurgitation radiography, ECG, and 2D echocardiography will demonstrate LV and left atrial dilatation. Marked left atrial dilation is evident with mitral stenosis. Atrial fibrillation is common and can precipitate clinical signs. CHF with Pulmonary edema is a common finding. In mitral stenosis there can be Doppler echocardiographic evidence of pulmonary hypertension with secondary right ventricular hypertrophy.

In tricuspid valve dysplasia with regurgitation, diagnostic examinations point to problems on the right side of the heart including atrial and ventricular enlargement. Right-sided CHF with hepatomegaly and ascites will be found in advanced cases. Atrial fibrillation is common. Rarely, pleural effusion or chylothorax are identified in dogs with CHF due to tricuspid valve malformation.

A prominent jugular pulse can be identified. Notched or “splintered” R-waves can be observed in dogs with tricuspid malformation. Re-entrant supraventricular tachycardias or ventricular pre-

excitation are occasionally observed on the ECG. Cyanosis, arterial hypoxemia, and polycythemia are expected when severe tricuspid dysplasia is complicated by an atrial septal defect.

Dogs can survive for many years with atrioventricular valvular malformation, and therefore acquired disorders such as valvular endocardiosis, dilated cardiomyopathy, and infective endocarditis are considerations in the differential diagnosis of mitral dysplasia. Endocardiosis, pulmonary hypertension, and right-sided cardiomyopathies can lead to tricuspid regurgitation and must be distinguished from tricuspid dysplasia.In the setting of cyanotic heart disease, the differential diagnosis is similar to that indicated above for tetralogy of Fallot. Atrioventricular stenosis also can stem from an obstructive fibrous or fibromuscular ring situated above the mitral or tricuspid valve (“supravalvular mitral/tricuspid ring”). Tricuspid stenosis can be confused with (or occur along with) an obstructive partitioning of the right atrium termed “cor triatriatum dexter”.

In this malformation, the caudal right atrium is separated from the tricuspid orifice by a persistent membrane with a small orifice. This situation obstructs caudal vena caval blood flow and leads to hepatomegaly and ascites. A similar condition (though more rare) can occur in the left atrium (cor triatriatum sinister), leading to pulmonary venous obstruction.

Therapy – Balloon valvuloplasty has been performed with variable success in dogs with tricuspid and mitral valvular or supravalvular stenosis. Surgical repair or annular support of affected valves can be attempted. Replacement of dysplastic valves has been performed successfully with cardiopulmonary by-pass. Most cases are treated medically when signs of CHF or atrial fibrillation develop. Consideration should be given to ACE-inhibitor (enalapril) and to betablocker therapy (carvedilol or metoprolol) for establishing cardioprotection in dogs with severe mitral regurgitation and associated cardiomegaly. The benefit of such therapy in tricuspid dysplasia is more uncertain.

Tricuspid malformation, associated with an ASD, can lead to right-to-left shunting; secondary polycythemia should be managed (discussed above).

Mild mitral or tricuspid valvular dysplasia is often well-tolerated; however, severe lesions lead to CHF and arrhythmias such as atrial fibrillation. Dogs with severe mitral disease usually develop CHF in early to middle age, particularly when the valve is both stenotic and incompetent. Many dogs with relatively severe tricuspid regurgitation survive for 7 or 8 years before CHF ensues.

It is more common for dogs with severe mitral valve dysplasia to develop left-sided CHF during the first five years of life. Critical atrioventricular valvular stenosis is likely to cause signs within the first one or two years of life. Asymptomatic dogs and cats with moderate to severe disease should have a cardiology evaluation and echocardiogram yearly, or more often if warranted by clinical findings.

Reference 1. Oyama MA, Sisson DD, Thomas WP, Bonagura JD: Congenital heart disease. In: Ettinger SJ, Feldman EC (eds): Textbook of Veterinary Internal Medicine, 6th ed. St Louis: Elsevier Saunders, 2005; and 2009.

Some Canine Breed Predilections to Congenital Heart Disease Basset Hound Beagle Bichon Frisé Boxer Boykin Spaniel Bull Terrier Chihuahua Chow Chow Cocker Spaniel Collie Doberman Pinscher English Bulldog English Springer Spaniel German Shepherd Dog German Shorthaired Pointer Golden Retriever Great Dane Keeshond Labrador Retriever Maltese Mastiff Newfoundland Pomeranian Poodle Rottweiler Samoyed Schnauzer Shetland Sheepdog Terrier breeds Weimaraner Welsh Corgi West Highland White Terrier Yorkshire Terrier

PS PS PDA SAS, PS, ASD PS MVD, AS PDA, PS PS, CTD PDA, PS PDA ASD PS, VSD, ToF PDA, VSD SAS, PDA, TVD, MVD SAS SAS, TVD, MVD TVD, MVD, SAS ToF, PDA TVD, PDA, PS PDA PS, MVD SAS, MVD, PS PDA PDA SAS PS, SAS, ASD PS PDA PS TVD, PPDH PDA PS, VSD PDA

AS, Aortic stenosis; ASD, atrial septal defect; CTD, cor triatriatum dexter; MVD, mitral valve dysplasia; PDA, patent ductus arteriosus; PPDH, peritoneopericardial diaphragmatic hernia; PS, pulmonic stenosis; SAS, subaortic stenosis; ToF, tetralogy of Fallot; TVD, tricuspid valve dysplasia; VSD, ventricular septal defect.

Congenital Heart Disease in Dogs â&#x20AC;&#x201C; Data from Combined Studies Defect Patent ductus arteriosus (PDA) Subaortic stenosis (SAS) Pulmonic valve stenosis (PS) Ventricular septal defect (VSD) Tricuspid valve dysplasia (TVD) Mitral valve dysplasia (MVD) Other defects Persistent right aortic arch or other vascular ring anomaly (PRAA) Tetralogy of Fallot (ToF) Atrial septal defect (ASD) Total

Numbe r 1207 1102 1039 413 216 204 160

Percentag e 25.7 23.5 22.1 8.8 4.6 4.3 3.4

155 110 89 4694

3.3 2.3 1.9 100

Reprinted from Scansen BA, Cober RE, Bonagura JD. Congenital heart disease. In: Bonagura JD, Twedt DC, editors. Kirk's Current Veterinary Therapy XV (15th ed). St. Louis, Elsevier/Saunders; 2014. p. 756-761.

Congenital Heart Disease in Cats â&#x20AC;&#x201C; Data from Combined Studies Ventricular septal defect (VSD) Patent ductus arteriosus (PDA) Tricuspid valve dysplasia (TVD) Mitral valve dysplasia (MVD) Atrioventricular septal defects (AVSD) Aortic stenosis (AS) Tetralogy of Fallot (ToF) Atrial septal defect (ASD) Persistent right aortic arch (PRAA) Endocardial fibroelastosis (EFE) Pulmonic stenosis (PS) Other malformation Double outlet right ventricle (DORV) Cor triatriatum sinister

80 49 47 44 42 31 30 26 23 21 17 11 7 7

18.4 11.3 10.8 10.1 9.7 7.1 6.9 6.0 5.3 4.8 3.9 2.5 1.6 1.6

Total

435

100%

Pericardial Diseases in Dogs: Diagnosis & Management John D Bonagura DVM, DACVIM (Cardiology, Internal Medicine) Veterinary Clinical Sciences, Ohio State University Congenital peritoneopericardial diaphragmatic hernia (PPDH) and acquired pericardial effusions represent the most important disorders affecting the pericardium of dogs. Pericardial effusion (PE) refers to the accumulation of an excessive volume or abnormal type of fluid within the space bordered by the epicardium and parietal pericardium. Pericardial diseases impair diastolic ventricular function. When the heart is compressed by a PE to the point that intrapericardial pressures rise and cardiac filling is impaired, a state of cardiac tamponade is present.

Important congenital forms of pericardial disease in dogs include congenital PPDH and the rare cysts. Careful radiographic evaluation leads one to suspect the diagnosis. Findings include altered radiographic density in the caudoventral portion of the pericardial space, often with cranial displacement of the carina. A linear shadow ventral to the caudal vena cava represents the persistent mesothelial remnant delineating the dorsal border of the communication.

Ultrasonography is diagnostic. The condition is treated surgically, but may be an incidental finding in mature animals and not warrant intervention.

Etiology Acquired pericardial effusions are common in dogs. The pericardial fluid is typically classified using clinicopathologic methods. Causes of transudates include right-sided CHF, PPDH, cysts, and hypoalbuminemia. Exudates are caused by pericarditis, including that associated with perforating foreign bodies. Sterile (inflammatory) pericarditis can complicate recurrent, idiopathic intrapericardial hemorrhage. Hemorrhagic pericardial effusions are the most common fluid type collected from dogs. In patients <6 years, idiopathic pericardial hemorrhage predominates. In older dogs, hemangiosarcoma of the right atrium, aortic body tumor (chemodectoma), ectopic thyroid carcinoma, and pericardial mesothelioma are major causes. The latter is a difficult and sometimes controversial histopathological diagnosis. Metastatic pericardial neoplasia is recognized at necropsy but is an uncommon antemortem diagnosis. Uncommon causes of pericardial hemorrhage include left atrial tearing from mitral regurgitation; blunt trauma; coagulopathy, and complicated thoracocentesis. Chyle is a very rare fluid type.

Pathophysiology Pericardial effusion leads to clinical signs by compressing the heart. Cardiac tamponade refers to "the decompensated phase of cardiac compression resulting from an unchecked rise in the intrapericardial fluid pressure." The normally negative intra-pericardial pressure becomes positive relative to atmosphere and pressures rise quickly once elastic limits of the pericardium are reached. Tamponade can develop quickly with sudden hemorrhage into the space, as with a bleeding tumor. In chronic cases, larger volumes can be accommodated before intrapericardial pressures rise. The pathophysiology can be summarized as: Increased (positive) intrapericardial pressure  diastolic collapse of the thinner-walled right atrium and ventricle along with compression of the proximal vena cava  reduced right ventricular filling  decreased preload  decreased stroke volume and cardiac output  and arterial hypotension if compensatory mechanisms (heightened sympathetic activity, vasoconstriction, and renal retention of sodium and water) are insufficient.

Clinical signs The clinical consequences of tamponade are straightforward. Syncope, collapse or even

sudden death can occur if hypotension is acute and severe. Given sufficient time, compensatory measures are activated to maintain arterial blood pressure (BP). Congestive heart failure, with a predominately right-sided component is the most common consequence of chronic cardiac tamponade. Dogs become exercise intolerant, develop abdominal distension, lose muscle mass, and might become tachypneic if pleural effusion supervenes.

Breed predispositions to specific neoplasm types are relevant in the differential diagnosis, as with golden retrievers (idiopathic hemorrhage, hemangiosarcoma), St. Bernard dogs (idiopathic hemorrhage) and brachycephalic breeds (chemodectoma). Fever or thoracic pain could indicate inflammatory pericarditis; occasionally other signs of systemic disease such splenomegaly might be noted. Overt right-sided CHF is characterized by elevated jugular venous pressure, muffled (distant) heart sounds, ascites, and possibly signs of pleural effusion. If superficial venous distension is missed, a diagnosis of liver disease or abdominal neoplasia might be erroneously entertained. Arterial hypotension or pulsus paradoxicus, a marked inspiratory fall in BP is often detected; this is caused by respiratory variation in ventricular filling that becomes exaggerated within an encased heart. Pulsus paradoxicus is identified using a Doppler flow detector or by careful palpation/observation. Breath sounds are muffled with tachypnea or respiratory distress if there is moderate to large pleural effusion.

Electrocardiogram (EKG) The EKG can be normal, but any of the following might be observed: decreased amplitude QRS complexes; electrical alternans with large effusates and swinging of the heart; ST-segment elevation from epicardial injury (indicating pericarditis); sinus tachycardia; vagal reflexes that induce sinus arrhythmia or sinus bradycardia; or heart rhythm disturbances. The latter include atrial and ventricular premature complexes secondary to epicarditis, invasive cardiac neoplasia, ischemia from tamponade, concurrent heart disease, or splenic disease.

Diagnostic Imaging As the cardiac silhouette enlarges, thoracic radiographs will be suggestive of the diagnosis but have relatively low sensitivity and specificity. The size increases and cardiac borders lose their angles and waists, eventually becoming globular in shape. The cardiac outline might be especially â&#x20AC;&#x153;sharpâ&#x20AC;?, presumably from diminished motion of the distracted pericardium. The left atrial border on the lateral view may become rounded. This and the common finding of diminished pulmonary vascularity help to distinguish cardiac tamponade from cardiomegaly due to cardiomyopathy or chronic valvular disease. If CHF has developed, there may be increased pulmonary interstitial densities, distension of the caudal vena cava, hepatomegaly, or pleural effusion. Heart base tumors can deviate the trachea. Metallic densities (such as a shotgun pellet) should be taken as risk factors for pericarditis. Fluoroscopy reveals reduced cardiac motion.

Echocardiography is a highly sensitive test for detecting pericardial effusion and most cardiac mass lesions. Abnormal fluid accumulation is evident as a sonolucent (generally black) space between the epicardium and pericardium, extending from apex to base. A mixed echogenic fluid suggests cellular exudate or recent hemorrhage. The effusion can be loculated (localized) in inflammatory diseases or following a surgical pericardial window. A tumor of the right atrium or along the right atrioventricular groove is suggestive of hemangiosarcoma. A heart base mass around the aorta is typical of chemodectoma or ectopic thyroid carcinoma. Thickened pericardium with tumors on the parietal surface may suggest mesothelioma, but these are difficult to discern.

False positives for mass lesions can stem from clot formation and the fat pad normally present between the pulmonary artery and aorta. Pleural effusions, ascites, dilated caudal vena cava, and distended hepatic veins also may be observed. Diastolic collapse of the right atrium or right ventricular wall is supportive of increased intrapericardial pressure and corresponds to effusion with tamponade. Inversion of the atrial wall and protracted collapse of the ventricular wall are more specific signs. However, both false positives (from massive pleural effusions) and false

2Â

negatives (from concurrent elevated CVP expanding the cardiac chambers) do occur. The distinction between idiopathic hemorrhagic pericardial effusion and bleeding from a tumor is crucial in terms of prognosis and might require a high-resolution, technically-proficient, echocardiogram recorded from each side of the thorax using multiple views. In some cases, exploratory surgery or advanced imaging (CT, MRI) will be needed to exclude a mass lesion.

Clinical Laboratory Serum biochemistries usually reflect the heart failure; cardiac troponins can increase from myocardial ischemia. The CBC may suggest inflammation, hemorrhage, or hemangiosarcoma (nucleated RBC’s). Pleural and peritoneal effusions are obstructive (transudate, modified transudate). Pericardial effusions are typically hemorrhagic; reactive mesothelial cells are common (but not diagnostic of mesothelioma). Most heart base tumors exfoliate poorly so cytological diagnosis in unreliable. Flow cytometry has been positive in some cases. Cultures are usually negative.

Pericardiocentesis Needle or catheter drainage of the pericardial space is the initial treatment for cardiac tamponade. Intrapericardial pressures fall rapidly with removal of ~1/2 of the volume. The steps can be summarized as follows and are demonstrated in the lecture.  Prepare patient: o Left-lateral recumbency (spine elevated) o IV catheter o BP cuff o ECG electrodes o ± Sedation (butorphanol 0.1 to 0.2 mg/kg). o Identify puncture site over right thorax o Clip/prepare target area o Infiltrate ~3 ml of 2% lidocaine, skin to pleura  Glove and prepare catheter (14 to 20 gauge Angiocath®) with extra side holes  Perform centesis o Insert catheter in a controlled motion into the pericardial space o Once fluid exits freely, advance catheter over needle o Connect tubing & aspirate o Collect clot and EDTA tubes o Monitor for extrasystoles & hypotension o Recheck ultrasound Follow-up Care Other medical therapies are rarely administered. Judicious doses of furosemide (postpericardiocentesis) will hasten mobilization of ascites. Chemotherapy is recommended for optimal palliation of hemangiosarcoma. Treatments involving corticosteroids or colchicine require study.

Surgical procedures A number of different procedures can be performed in carefully selected cases. Right auriculectomy is performed rarely for isolated hemangiosarcoma. Major thoracic surgery with subtotal pericardiectomy is indicated for recurrent idiopathic pericardial hemorrhage and for infective pericarditis (to prevent constrictive pericarditis). Less-invasive procedures (via balloon pericardiotomy, thoracoscopy, or mini-thoracotomy) involve creation of “windows” for palliation of heart base masses along with visualization and pericardial biopsy in older dogs with recurrent effusions. These have also been used for recurrent idiopathic hemorrhage but substantial long-

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term follow up on these cases is still needed to gauge the risk of constriction.

References: Atencia S1, Doyle RS, Whitley NT. Thoracoscopic pericardial window for management of pericardial effusion in 15 dogs. J Small Anim Pract. 2013 54(11):564-9 Case JB, Maxwell M, Aman A, Monnet EL. Outcome evaluation of a thoracoscopic pericardial window procedure or subtotal pericardectomy via thoracotomy for the treatment of pericardial effusion in dogs. J Am Vet Med Assoc. 2013 Feb 15;242(4):493-8 Côté E1, Schwarz LA, Sithole F. Thoracic radiographic findings for dogs with cardiac tamponade attributable to pericardial effusion. J Am Vet Med Assoc. 2013 Jul 15;243(2):232-5..

Nelson OL, Ware WW: Pericardial Effusion, in Bonagura JD and Twedt DC (eds): Current Veterinary Therapy XV, St. Louis, Elsevier/Saunders, 2014.

MacDonald KA, Cagney O, Magne ML. Echocardiographic and Clinicopathologic Characterization of Pericardial Effusion in Dogs: 107 cases (1985-2006). J Am Vet Med Assoc. 2009; 15;235(12):1456-61.

Stafford Johnson M, Martin M, Binns S, Day MJ. A retrospective study of clinical findings, treatment and outcome in 143 dogs with pericardial effusion. J Small Anim Pract. 2004; 45(11):546-52.

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RADIOGRAPHIC DIFFERENTIAL DIAGNOSIS OF CARDIOPULMONARY DISORDERS John D Bonagura DVM, MS, DACVIM (Cardiology, Internal Medicine) Veterinary Clinical Sciences, The Ohio State University Columbus, Ohio, USA

The clinical signs of cardiac and respiratory diseases are similar and the clinician must be adept at distinguishing heart from respiratory diseases. Knowledge of common (and less common) diagnoses, skill in orchestrating a logical workup, and ability to interpret thoracic radiographs are keys to success.

Most bronchopulmonary disorders, as well as problems within the mediastinum and pleural space, are identified because of the initial signs of cough, tachypnea, or respiratory distress (dyspnea). The clinician must have an appreciation of the numerous causes of these clinical signs and the resources to evaluate these problems. The clinical “work-up” is summarized in Table 1. In addition to the history and physical examination, radiographic examination of the thorax is critical, and the clinician must learn to identify common patterns of thoracic disease.

The causes of acute and chronic respiratory disease can be classified simply, as follows:  Mechanical or obstructive lesions causing major-airway obstruction or compression  Cardiac diseases  Pulmonary vascular diseases  Bronchial diseases including bronchitis and asthma  Infectious and noninfectious pulmonary parenchymal diseases including edema, hemorrhage, and pneumonia  Tumors and mass lesions of the bronchopulmonary tree  Mediastinal diseases  Pleural space disorders (causing respiratory distress) – see Table 2 Initial Management: Dyspneic patients must be stabilized before radiography Sedatives should be administered if restraint is difficult or the patient is distressed.  For cats: acepromazine (0.05 to 0.1 mg/kg) mixed with butorphanol (0.25 mg/kg) and administered IM provides mild to moderate sedation. ACP should not be used in hypotensive or hypothermic cats.  For dogs: one of the following protocols is usually effective: 1) butorphanol (0.25 to 0.5 mg/kg, IM); or 2) acepromazine (0.025 mg/kg) mixed with butorphanol 0.25 mg/kg IV or IM; or 3) acepromazine (0.025 mg/kg) plus buprenorphine (0.0075 mg/kg), IV or IM.  Oxygen should be given by cage, tent, or mask (if tolerated). At a minimum, a fan should be directed to the face to help relieve dyspnea and dissipate heat.  The clinical staff should be ready to perform tracheal intubation and positive pressure ventilation should life-threatening dyspnea be evident and respiratory arrest imminent.

Obvious laryngeal or tracheal stridor may indicate airway obstruction that can be temporarily managed by tracheal intubation.  Thoracocentesis should be performed if pleural effusion or pneumothorax is suspected.  For suspected pulmonary edema (when the patient cannot be examined by radiography) administer parenteral furosemide (2 - 4 mg/kg IV or IM), oxygen, and nitroglycerine paste (¼ inch of 2% ointment for cats or small dogs; ½ to 1-inch for large dogs).  For suspected feline asthma, use a pediatric spacer and a standard albuterol inhaler; administer two “puffs” of albuterol into the spacer and allow the cat to breath through the mask for 10 to 15 seconds. A positive response should provide a presumptive diagnosis of reactive bronchospasm. If positive, administer short-acting glucocorticoids and oral airway dilators (or continue using inhaled albuterol twice daily). Typical doses include: dexamethasone Na phosphate - 0.5 to 1 mg/kg IV or IM; sustained release oral theophylline 25 mg/kg once daily; terbutaline sulfate (0.1 mg dose SQ or IV; or ¼ to ½ of a 2.5 mg terbutaline tablet PO 12h).

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Evaluation of Thoracic Radiographs – Principles and Suggestions Thoracic radiographs are essential in all cases of dyspnea or chronic cough. Good-quality VD/DV and lateral films are needed to evaluate the trachea, bronchial tree, the lungs, mediastinum, lymph nodes, and pleural space. A systematic approach should be taken as suggested in Table 3. Interpret the radiographic findings in two ways: 1) Independently – what “story” can you make from the signalment and the radiographs? 2) Within the clinical context – how do the radiographic findings relate to known clinical problems & clinical examination findings?

Cardiac Evaluation – Assessment of the cardiac silhouette, great vessels, pulmonary circulation, and veins is particularly important if heart failure, heartworm disease, or pulmonary vascular disease is suspected. However, over-interpretation of cardiac size frequently misleads the clinician to an erroneous diagnosis of heart failure, as with obese cats with intrapericardial fat, toy breed dogs, and films exposed during expiration. A vertebral heart score may be instructive when heart enlargement is in doubt (see Table). Cardiomegaly (left ventricular dilation/hypertrophy) in cats is often manifested as elongation of the heart. A bulge in the 1 to 3 o'clock positions on the VD view is typical of left auricular dilation, and often suggests an advanced form of feline cardiomyopathy. Apex shifting to the midline is also common in cats with cardiomegaly. Cardiomegaly is also common with moderate to severe anemia, with hyperthyroidism, with systemic hypertension, and with chronic respiratory disease. Pulmonary edema in CHF is often more ventral than one might expect. Dilation of both lobar arteries and veins is typical of left-sided CHF with pulmonary hypertension. The aorta is often dilated and tortuous in older cats. Heartworm disease can lead to dilation of the lobar pulmonary arteries (especially the right). Peracute heartworm death can cause a "white lung" with severe alveolar infiltration.

Mediastinal Lesions – Mediastinal widening is typical of fluid accumulation or mass lesions.

Pneumomediastinum suggests tracheal perforation (e.g. from trauma) or a lesion in the esophagus. Lymphoma and thymoma are common mediastinal neoplasms in cats. It should also be noted that benign mediastinal lesions can be encountered including mediastinal cysts in young and older animals and mediastinal (thymic) hemorrhage in young dogs.

Pulmonary Densities – If thoracic radiographs indicate abnormal thoracic densities, characterize these as either increased or decreased thoracic density. If lung density is decreased (air density) rule out an over-exposure problem, pneumothorax or pneumomediastinum, or intrapulmonary gas trapping. The latter is typical of "asthma" in cats. If lung density is increased, rule out expiratory film, (under-)exposure problem, motion, prominent vessel margins, or true increase in fluid density within the thorax. If there is increased fluid density, determine if it is within the pleural space, lung, or mediastinum.

If there are increased pulmonary densities, determine the distribution of densities (e.g., cranioventral, multifocal, right lobar, perihilar, accessory lobe [surrounds caudal vena cava], or disseminated). Indicate the precise pattern of increased lung density (i.e., alveolar, interstitial linear/unstructured or nodular, peribronchial, or mixed). Characteristic patterns may be suggestive of specific diseases (for example, chronic bronchitis causes bronchial patterns; atelectasis and pneumonia are common in the right middle lobe). Determine the presence or absence of airway collapse or obstruction. Examine the thorax for mediastinal widening or density changes. Inspect the film for hilar or mediastinal lymphadenopathy (typical of fungal diseases, lymphoma, and pulmonary granulomatous diseases which are rare in cats). Mixed pulmonary densities in multiple lobes are common with lungworms, atypical pneumonia, disseminated neoplasia, fungal diseases, and Mycoplasma infection.

Pleural effusion typically obscures the borders of the heart and diaphragm (border effacement), produces fissure lines, fills the costophrenic angles, and moves with gravity. Pleural effusion is more obvious on the DV view, but the lungs will be better visualized in cases of pleural effusion on the VD view. There are numerous causes of pleural effusion in cats (Table 2).

Additional Diagnostic Studies Following physical diagnosis and radiography, a number of additional diagnostic studies can be helpful in determining the underlying reason for respiratory signs.

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Routine laboratory tests are often obtained in animals with signs of thoracic disease (Table 1).

CBC abnormalities may be present to suggest infection, inflammation, or necrosis; however, the neutrophil count can be very misleading and nearly normal in cases of significant pulmonary infiltration. Eosinophilia, in the absence of intestinal or ectoparasitism, suggest the possibility of heartworm disease, lungworms, allergic bronchitis, lymphoma, granulomatous disease, or pulmonary infiltrates with eosinophils. Obtain a heartworm antigen test in areas where heartworm is endemic (or an antibody/antigen test in cats, if indicated). Knowledge of the FeLV and FIV status is always useful. Serologic testing for toxoplasmosis, systemic fungi, and feline infectious peritonitis (FIP) is indicated in selected cases. If radiographs are compatible with lungworm infection (e.g., paragonimiasis), use direct fecal studies including smears, routine flotation, and sedimentation methods (Baermann) may be helpful in screening for lungworms.

Consider additional diagnostic tests (if indicated from the examination, prior test results, or lack of response to prior treatment).

Alternative imaging can be quite helpful in some cases. Fluoroscopy is useful for identifying dynamic collapse of the larger airways (trachea and main bronchi). Ultrasonography of the thorax is indicated in cases of suspected heart disease, pericardial effusion, heart base or mediastinal mass, diaphragmatic hernia, consolidated lung, or large pleural effusion. Pleural effusion - in the absence of enlarged jugular veins, cardiomegaly, or distended hepatic veins usually indicates a noncardiac condition.

Computerized tomography (CT) can be very helpful in assessing the lung for metastasis, pulmonary infiltrates, bronchial lesions, and pulmonary vascular lesions that cannot be seen radiographically. The method is also helpful for identifying mediastinal masses or hilar lymphadenopathy. This examination is made less useful when there is pleural effusion or pulmonary atelectasis. Some studies (with fast imagers) can be done with sedation.

Esophagoscopy is helpful in diagnosing esophageal-tracheal fistula or causes of aspiration pneumonia.

The electrocardiogram (ECG) and echocardiogram are appropriate for assessing patients with suspected heart failure or pericardial disease.

Endoscopy provides for direct visualization of the upper airways, trachea, and proximal bronchi and is indicted when intraluminal masses, foreign body, or other causes of unexplained airway obstruction or inflammation is suspected. Endoscopes must be appropriate size for cats and small dogs, and often these are unavailable. Following initial visual inspection, airway culture is performed, generally with a guarded culture swab designed for endoscopes or airway cultures.

This is followed by a detailed examination of the trachea and bronchial tree followed by bronchial washing, brush cytology, mucosal biopsy, or bronchoalveolar lavage.

Airway cytology is a helpful examination in many noncardiac thoracic diseases. If clinical signs and prior laboratory test results inadequately explain cough or dyspnea, or the reason for increased pulmonary density, the clinician should obtain a lower airway tissue sample for culture and cytology or cytology of pleural fluid should that be present. The method of choice for obtaining airway samples depends on experience, availability of equipment, and the nature of pulmonary infiltration. Endotracheal â&#x20AC;&#x153;washesâ&#x20AC;? and brush cytology are should be evaluated by a clinical pathologist for predominant cell type, presence or absence of microorganisms, and other cytologic features which can contribute to the diagnosis. A bronchoalveolar lavage is treated in a similar qualitative manner, but it is also important to request a quantitative cell count. The wash sample is divided for culture, requesting aerobic culture and sensitivity, +/- anaerobic culture, and special culture media for Mycoplasma (especially in cats). In general, any upper airway inflammation (e.g. mucous from bronchitis) will contaminate lower airway samples of a BAL, and this should be appreciated when interpreting a BAL. A modified approach for obtaining respiratory cytology in cats and very small dogs is to first Page-3

intubate with a sterile tube (2.3 to 3 Fr), place the patient in right or left lateral recumbency, hyperoxygenate, give two puffs of albuterol from an inhaler, then remove the adaptor from the tube and obtain a culture through the endotracheal tube using a guarded brush). Next, use a 3way stopcock as an adaptor in the end of the inflated endotracheal tube to obtain a â&#x20AC;&#x153;tracheobronchialâ&#x20AC;? wash. Sterile saline (5-6 cc) is quickly flushed into the side port, and then aspirated back preferably with suction and a mucous trap. The cat is turned to the other side, the wash procedure is repeated, and the fluid samples pooled. If a second stopcock is attached to the first one, the cat can be ventilated with oxygen between the two washes. This approach seems to represent a hybrid of a tracheal wash and a BAL, but clearly samples the most distal airways.

Fine needle lung aspirate (FNA) is another alternative for assessment of the dyspneic or coughing patient with multifocal, diffuse, or lobar infiltrates. This method, like the BAL, may be especially helpful if the cat is not coughing and producing bronchial exudate or if pulmonary infiltrate is limited to the interstitial space. Pneumothorax is a common complication.

Inspection of the thorax and biopsy of the lung or pleura by thoracotomy or thoracoscopy is sometimes the only method for attaining a diagnosis in disseminated pulmonary disease (e.g., neoplasia, granulomatous disease). Thoracoscopy is particularly useful in experienced hands and avoids the morbidity of traditional thoracotomy (which is also problematic in terms of approach and degree of invasiveness needed for suitable exploration). Lung biopsy is especially helpful in diseases characterized by marked interstitial infiltration or disorders unexplained by prior, less-invasive tests. When a singular localized lung lesion is evident from radiographs, and either a foreign body or tumor is suspected, consider surgical removal and biopsy of the affected lobe. Optimally, exploratory procedures for solitary lung masses should be preceded by detailed noninvasive imaging, including CT of the chest.

Notes:

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Table 1. Diagnosis of Respiratory Disease Bronchopulmonary Diseases  History and physical examination (observation, auscultation, percussion of the thorax)  Thoracic radiography  Complete blood count  Heartworm tests (ELISA antigen tests, HW antibody test for cats)  Fecal examinations (flotation and Baermann sedimentation to detect lung parasites)  Serologic testing when appropriate (e.g., immunodiffusion or urinary antigen tests for systemic mycoses, IgM ELISA for Toxoplasmosis, etc.)  Arterial blood gas | Pulse oximetry  Culture of tracheobronchial secretions (transtracheal, endotracheal using a guarded swab, or aspiration through sterile tubing placed down a sterilized endoscope port)  Endotracheal aspiration cytology  Bronchoscopy (visual examination and cytology)  Bronchial brushing  Bronchial aspiration cytology  Bronchoalveolar lavage with a wedged bronchoscope  Ultrasound examination of the heart and mediastinum or of consolidated lung tissue  Fine needle aspiration (FNA) of the lung or mass lesion  Lung biopsy  Pulmonary function testing

Diseases of the Pleural Space History and physical examination (observation, auscultation, percussion of the thorax)  Thoracic radiography (pre- and post-thoracocentesis)  Thoracocentesis with cytology of pleural effusate +/- culture and sensitivity of pleural effusate  Serological testing when appropriate (FIV, FIP)  Biochemical tests (e.g. serum/pleural effusion triglyceride concentration for chylothorax)  Ultrasound examination of pleural space, lungs, and mediastinum  CT or MRI of thorax  Lymphangiography

Diseases of the mediastinum  History and physical examination (observation, auscultation, percussion of the thorax)  Thoracic radiography  Ultrasound examination  CT or MRI of mediastinum  FNA of mediastinal masses  Esophageal contrast studies  Bronchoscopy

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Table 2. Differential Diagnosis of Pleural Effusion Cardiac Causes  Congenital Heart Disease  Valvular heart disease  Pericardial Diseases  Canine Cardiomyopathy (dilated in the dog)  Feline Cardiomyopathies (hypertrophic, restrictive, dilated, right ventricular)  Silent atrium  Chronic bradycardia  Chronic severe tachycardia  Advanced thyrotoxic Heart Disease  Moderate To Severe Anemia Leading To High Output Failure  Obstruction of Venous Return From The Cranial Vena Cava

Pulmonary Causes  Lung Lobe Torsion  Pulmonary neoplasia  Pleuropneumonia (uncommon in cats)  Atypical Pneumonia (Nocardiosis)  Pulmonary Thrombosis And Embolism

Chylous Effusion  Idiopathic  Obstructed or Traumatized Thoracic Duct or cranial vena cava  Primary Lymphatic Disorder  Congestive Heart Failure  Pericardial Disease  Heart Base Tumor or Mass  Mediastinal Mass  Feline Heartworm Disease

Hemothorax  Bleeding Disorders, including Rodenticide Toxicity  Trauma  Neoplasia

Infectious Causes  Feline Infectious Peritonitis  Pyothorax (Bacterial, Nocardia, Actinomycosis, Anaerobic Infections)  Blastomycosis  Penetrating trauma

Neoplastic Causes  Mediastinal Mass  Heart Based Tumors  Primary Lung Tumors  Disseminated Neoplasia Other Causes  Marked Hypoproteinemia  Overinfusion of Fluids  Diaphragmatic Hernia  Thoracic Trauma  Central Venous Catheters (Perforation or Thrombosis)  Thrombosis or Obstruction of The Cranial Vena Cava  Abdominal Surgery  Pancreatitis  Idiopathic

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Table 3. Thoracic Radiography: Some Guidelines for Evaluation of Thoracic Radiographs Initial Steps  Identify the films, case number and date  If analog films, place the films on the view box correctly (if digital, insure proper labels): Cranial is oriented to your left side on the lateral X-ray film; the patient’s right side is oriented to your left side on the VD or the DV view  Remember there is substantial variation among species and breeds.  For example, cats have more horizontally oriented hearts on the lateral view and the heart takes up less space in the thorax.  Deep-chested dogs, such as the Doberman pinscher, have a more upright-oriented cardiac axis.  There are also differences between left and right lateral projections and VD and DV films.

This is useful to remember when evaluating serial studies.  Start with a system…….try P-E-P  Positioning – is the patient straight (sternum on spine on the VD/DV; not excessively rotated on the lateral). Is the beam properly centered over the thorax?  Exposure – is the exposure sufficient to allow you to follow vascular structures and does the technique penetrate (but still allow you to see) the ribs? Remember: underexposure makes the lung parenchyma appear too dense; overexposure burns out subtle pulmonary densities.  Phase of Ventilation – were the films exposed during inspiration? Expiratory films cause the pulmonary parenchyma to appear more dense leading one to over-diagnose “interstititial” patterns. Furthermore, the heart may appear more enlarged if the thorax is not sufficiently expanded.  Examine the extrathoracic structures and bones for disease, organomegaly, rib destruction, and other lesions. Remember that dyspnea or vigorous coughing can lead to rib fractures or movement of the stomach into the esophagus (hiatal hernia or G-E intussusception) . Do not mistake calcification of the costochondral junction for disease. Pectus excavatum may be identified in cats and dogs and will often lead to a mediastinal shift on the VD/DV projections.

Examine the mediastinum  Identify widening cranially or caudally suggests mass lesions (ddx: thymus in young animal).  Identify mediastinal shifts that may suggest atelectesis.  Look for free air, especially in cases of pneumothorax.  Identify the trachea and follow its course to the carina. Recall breed variations (bulldogs – hypoplasia; basset hounds – large)  Try to identify the main left and right bronchus; these bifurcate just cranial to the left atrium.  Identify any bronchial collapse or compression (as with enlarged left atrium or hilar lymphadenopathy).  Identify tracheal deviation – as might occur with cardiomegaly (dorsal deviation), persistent right 4th aortic arch, mediastinal masses, or chemodectoma. Remember that tracheal position depends greatly on head positioning and that in some breeds (bulldogs!) some rightward deviation is normal on the VD projection.  Evaluate the tracheal lumen for narrowing, collapse, or abnormal densities (as with Oslerus osleri nodules at the carina or the rare intraluminal neoplasm)  Examine the esophagus – is it air-filled, dilated, or containing a foreign body or soft tissue (as with gastroesophageal intussusception)  In cats especially remember to consider peritoneopericardial diaphragmatic hernia in the differential diagnosis of cardiomegaly.

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Identify Cardiomegaly  Obtain an overall opinion of cardiac size on both views. Enlarged or not? If so, is the cardiomegaly mild, moderate or severe? Measure the Vertebral Heart Score – if you are uncertain about the presence of cardiomegaly. A VHS that exceeds 8.0 in a cat is suspicious for cardiomegaly (average value is 7.5 vertebral bodies). A VHS that exceeds 10.5 to 11 in a dog is likely to indicate cardiomegaly; even more useful are serial evaluations in a dog. There are some breed variations in VHS nicely summarized on Dr. Jim Buchanan’s web site, see: http://www.vin.com/library/general/JB111VHS.htm  Measure the apical-basilar length from the ventral border of right bronchus at level of circular carina to the apex of the heart. This is the major axis measurement.  Then draw a line perpendicular to your first measurement, extending from the cranial to caudal heart border. This is the minor cardiac axis. Select the greatest length but do not extend the measurement into the caudal vena cava or left atrium.  Identify the 4th thoracic vertebral body – inspect the dorsal spinous processes (the fourth TV is the 4th one with a “tall” dorsal spinous process; you can also count the ribs as they insert on the spine)  Measure the VHS from the cranial edge of T4 caudally.  Count the number of vertebral bodies encompassed in the major + minor axis lengths.

Extrapolate to the nearest decimal point.  Cardiac elongation on the lateral or DV views is typically due to LV enlargement.  Widening: Either RV or LV enlargement can cause cardiac widening.  Note if there are any distinctive bulges or rounded borders that suggest specific chamber enlargements?  Be familiar with the location of the cardiac chambers around the perimeter of the heart.  One species difference: on the VD/DV view the 1-3 o’clock border in cats is usually the left auricle; in dogs 1-2 o’clock is the main PA and 2-3 o’clock represents the left auricle.  Key to the diagnosis of left sided CHF is assessment of the left atrium. Estimate left atrial enlargement as mild, moderate or severe. Mild is a slight separation of the bronchi or prominence of the LA. Moderate is prominence with moderate separation or a distinct auricular bulge and/or squaring of the caudal atrial border. Severe is caudal bulging of the left atrium on the lateral view and prominent rounding on the VD projection. The left auricle in cats is often quite prominent on the VD view, but on the lateral the left atrium is more difficult to assess.

Great Vessels and Pulmonary Vessels  Examine the great vessels. Inspect the aortic arch and descending aorta; examine the main pulmonary artery and the lobar pulmonary artery branches. Identify any bulges or dilations that might suggest congenital or acquired disease. Identify lobar vascular abnormalities.  Dilated aorta – subaortic stenosis (ascending/arch), PDA (descending), generalized dilation (hypertension), dilation/redundant (senile change in cats; idiopathic in dogs).  Dilated main PA – pulmonic stenosis (post-stenotic dilation), left to right shunt (ASD, VSD, PDA), or pulmonary hypertension (heartworm disease, idiopathic PH). Remember that an oblique VD film will make the PA appear dilated.  Identify abnormal vascular patterns  Dilated pulmonary veins – r/o left sided CHF; beware that superimposition of an artery and vein can make the vessel appear large.  Dilated pulmonary arteries – r/o pulmonary hypertension (heartworms, thromboembolism)  Dilated arteries and veins – r/o normal variation or magnification on the DV view (farther from the cassette), high cardiac output (hyperthyroidism), left to right shunt, or combination of left sided CHF + pulmonary hypertension.

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Pleural Space  Inspect the pleural surface for mass lesions, especially if there is rib destruction.  Evaluate the thorax for pleural effusion, a sign of right sided, left sided, or biventricular CHF (as well as many noncardiac conditions). Remember that the DV will show the effusion more readily but also obscure the lung to a greater degree.  Diagnostic criteria for pleural effusion include: increased fluid density, blunting of costophrenic angles, identification of two or more fissure lines, border effacement (silhouetting or obscuring) of the diaphragm or cardiac borders, and widening of the mediastinal recesses. A horizontal beam may be helpful in selected cases.  Don’t be confused by ventral subcutaneous fat on the lateral view – verify the diagnosis on the VD view (fissure lines, blunted angles)  Rounding of the lung borders suggests chronicity of the effusion of inflammatory response (as with chylothorax in cats).  Pneumothorax often occurs from trauma (including iatrogenic barotraumas from ventilation), needle puncture during diagnostic procedures, consequent to pneumomediastinum, and following rupture of lung cysts or bullae.

Pulmonary Parenchyma  Identify abnormal pulmonary densities. If increased, note the distribution. Classify when possible as:  Interstitial – nodular or linear (obscures blood vessels). Linear interstitial density is overinterpreted. If you can see vessel walls clearly, the lung is probably normal.  Alveolar – generally a very dense infiltrate that will silhouette or efface part of the heart or diaphragm. Air bronchograms are classic findings.  Bronchial – The bronchial walls are evident from thickening or infiltration.  Note: Pulmonary edema can cause a mixed pulmonary pattern including interstitial fluid accumulation around blood vessels and airways and later progressing to an alveolar infiltrate – classically bilateral (may be slightly worse on right), caudal, and perihilar.

Notes:

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