Left Atrium

The LA is the most dorsocaudal chamber of the heart, although its auricular appendage extends to the left and craniad. An enlarged LA bulges dorsally and caudally on lateral view. There is elevation of the left and possibly right mainstem bronchi; compression of the left mainstem bronchus occurs in patients with severe LA enlargement. In cats the caudal heart border is normally quite straight on lateral view; LA enlargement causes subtle to marked convexity of the dorsocaudal heart border, with elevation of the mainstem bronchi. On DV or VD view, the mainstem bronchi are pushed laterally and curve slightly around a markedly enlarged LA (sometimes referred to as the “bowed-legged cowboy sign”). A bulge in the 2- to 3-o’clock position of the cardiac silhouette is common in cats and dogs with concurrent left auricular enlargement. Massive LA enlargement sometimes appears as a large, rounded soft tissue opacity superimposed over the LV apical area on DV (VD) view (Fig. 2-3). LA size is influenced by the pressure or volume load imposed, as well as the length of time the overload has been present. For example, mitral regurgitation of slowly increasing severity may cause massive LA enlargement without pulmonary edema if the chamber has had time to dilate at relatively low pressures. Conversely, rupture of chordae tendinae causes acute valvular regurgitation; there can be pulmonary edema with relatively normal LA size because atrial pressure rises quickly.

FIG 2-3 Lateral (A) and dorsoventral (B) views from a dog with chronic mitral regurgitation. Marked left ventricular and atrial enlargement are evident. Dorsal displacement of the carina is seen in A; the caudal edge of the left atrium (arrows), superimposed over the ventricular shadow, and a prominent left auricular bulge (arrowhead) are seen in B.

Left Ventricle

LV enlargement is manifested on lateral view by a taller cardiac silhouette with elevation of the carina and caudal vena cava. The caudal heart border becomes convex, but cardiac apical sternal contact is maintained. On DV/VD view, rounding and enlargement occur in the 2- to 5-o’clock position. Some cats with hypertrophic cardiomyopathy maintain the apical point; concurrent atrial enlargement creates the classic “valentine-shaped” heart.

Right Atrium

RA enlargement causes a bulge of the cranial heart border and widening of the cardiac silhouette on lateral view. Tracheal elevation may occur over the cranial portion of the heart shadow. Bulging of the cardiac shadow on DV/VD view occurs in the 9- to 11-o’clock position. The RA is largely superimposed over the RV; although differentiation from RV enlargement is difficult, concurrent enlargement of both chambers is common.

Right Ventricle

RV enlargement (dilation or hypertrophy) usually causes increased convexity of the cranioventral heart border and elevation of the trachea over the cranial heart border on lateral view. With severe RV enlargement and relatively normal left heart size, the apex is elevated from the sternum. The carina and caudal vena cava are also elevated. The degree of sternal contact of the heart shadow is not, by itself, a reliable sign of RV enlargement because of breed variation in chest conformation. On DV/VD view, the heart tends to take on a reverse-D configuration, especially without concurrent left-sided enlargement. The apex may be shifted leftward, and the right heart border bulges to the right.

Great Vessels

The aorta and main pulmonary artery dilate in response to chronic arterial hypertension or increased turbulence (poststenotic dilation). Subaortic stenosis causes dilation of the ascending aorta. Because of its location within the mediastinum, dilation here is not easily detected, although widening and increased opacity of the dorsocranial heart shadow may be observed. Patent ductus arteriosus causes a localized dilation in the descending aorta just caudal to the arch, which is where the ductus exits; this “ductus bump” is seen on DV or VD view. A prominent aortic arch is more common in cats than dogs. The thoracic aorta of older cats also may have an undulating appearance. Systemic hypertension is a consideration in these cases.

Severe dilation of the main pulmonary trunk (usually associated with pulmonic stenosis or pulmonary hypertension) can be seen as a bulge superimposed over the trachea on lateral radiograph. On DV view in the dog, main pulmonary trunk enlargement causes a bulge in the 1- to 2-o’clock position. In the cat the main pulmonary trunk is slightly more medial and is usually obscured within the mediastinum.

The caudal vena cava (CaVC) normally angles cranioventrally from diaphragm to heart. The width of the CaVC is approximately that of the descending thoracic aorta, although its size changes with respiration. The CaVC-cardiac junction is pushed dorsally with enlargement of either ventricle. Persistent widening of the CaVC could indicate right ventricular failure, cardiac tamponade, pericardial constriction, or other obstruction to right heart inflow. The following comparative findings suggest abnormal CaVC distention: CaVC/aortic diameter (at same ICS) >1.5; CaVC/length of the thoracic vertebra directly above the tracheal bifurcation >1.3; and CaVC/width of right fourth rib (just ventral to the spine) >3.5. A thin CaVC can indicate hypovolemia, poor venous return, or pulmonary overinflation.

Lobar Pulmonary Vessels

Pulmonary arteries are located dorsal and lateral to their accompanying veins and bronchi. On lateral view, the cranial lobar vessels in the nondependent (“up-side”) lung are more ventral and larger than those in the dependent lung. The width of the cranial lobar vessels is measured where they cross the fourth rib in dogs or at the cranial heart border (fourth to fifth rib) in cats. These vessels are normally 0.5 to 1 times the diameter of the proximal one third of the fourth rib. The DV view is best for evaluating the caudal pulmonary vessels. The caudal lobar vessels should be 0.5 to 1 times the width of the ninth (dogs) or tenth (cats) rib at the point of intersection. Four pulmonary vascular patterns are usually described: overcirculation, undercirculation, prominent pulmonary arteries, and prominent pulmonary veins.

An overcirculation pattern occurs when the lungs are hyperperfused, as in left-to-right shunts, overhydration, and other hyperdynamic states. Pulmonary arteries and veins are both prominent; the increased perfusion also generally increases lung opacity. Pulmonary undercirculation is characterized by thin pulmonary arteries and veins, along with increased pulmonary lucency. Severe dehydration, hypovolemia, obstruction to right ventricular inflow, right-sided congestive heart failure, and tetralogy of Fallot can cause this pattern. Some animals with pulmonic stenosis appear to have pulmonary undercirculation. Overinflation of the lungs or overexposure of radiographs also minimizes the appearance of pulmonary vessels.

Pulmonary arteries larger than their accompanying veins indicate pulmonary arterial hypertension. The pulmonary arteries become dilated, tortuous, and blunted, and visualization of the terminal portions is lost. Heartworm disease often causes this pulmonary vascular pattern, as well as patchy to diffuse interstitial pulmonary infiltrates.

Prominent pulmonary veins are a sign of pulmonary venous congestion, usually from left-sided congestive heart failure. On lateral view, the cranial lobar veins are larger and denser than their accompanying arteries and may sag ventrally. Dilated, tortuous pulmonary veins may be seen entering the dorsocaudal aspect of the enlarged LA in dogs and cats with chronic pulmonary venous hypertension. But pulmonary venous dilation is not always visualized in patients with left-sided heart failure. In cats with acute cardiogenic pulmonary edema, enlargement of both pulmonary veins and arteries can be seen.

Supraventricular Premature Complexes

Supraventricular premature complexes are impulses that originate above the atrioventricular (AV) node, either in the atria or the AV junctional area. Because they are conducted into and through the ventricles via the normal conduction pathway, their QRS configuration is normal (unless an intraventricular conduction disturbance is also present). Premature complexes arising within the atria are usually preceded by an abnormal P wave (positive, negative, or biphasic configuration) called a P’ wave. If an ectopic P’ wave occurs before the AV node has completely repolarized, the impulse may not be conducted into the ventricles (an example of physiologic AV block). In some cases, the premature impulse is conducted slowly (prolonged P’Q interval) or with a bundle branch block pattern. Although P’ waves usually do not precede junctional complexes, retrograde conduction into the atria sometimes causes a negative P’ wave to follow, be superimposed on, or even precede the associated QRS complex. If the specific origin of the ectopic complex(es) is unclear, the more general term supraventricular premature complex (or supraventricular tachycardia) is used. Clinically it is usually more important to determine whether an arrhythmia originates from above the AV node (supraventricular) or below it (ventricular) rather than the more specific localization. Supraventricular premature complexes that also depolarize the sinus node reset the sinus rhythm and create a “noncompensatory pause” (i.e., the interval between the sinus complexes preceding and following the premature complex is less than that of three consecutive sinus complexes).

Supraventricular Tachycardias

Tachycardias of supraventricular origin often involve a reentrant pathway using the AV node (either within the AV node or using an accessory pathway). A premature supraventricular or ventricular impulse can initiate reentrant supraventricular tachycardia (SVT). During episodes of reentrant SVT in animals with ventricular preexcitation, the PR interval usually normalizes or is prolonged, and retrograde P’ waves may be evident. The QRS complexes are of normal configuration unless a simultaneous intraventricular conduction disturbance is present.

Atrial tachycardia is caused by rapid discharge of an abnormal atrial focus or by atrial reentry (repetitive activation caused by conduction of the electrical impulse around an abnormal circuit within the atria). In the dog the atrial activation rate per minute is usually between 260 and 380. The P’ waves are often hidden in the QRS-T complexes. Atrial tachycardia can be paroxysmal or sustained. It is usually a regular rhythm unless the rate is too fast for the AV node to conduct every impulse, in which case physiologic AV block and irregular ventricular activation result. A consistent ratio of atrial impulses to ventricular activation (e.g., 2 : 1 or 3 : 1 AV conduction) preserves the regularity of this arrhythmia. Sometimes the impulses traverse the AV node but are delayed within the ventricular conduction system, causing a bundle branch block pattern on the ECG. Differentiation from ventricular tachycardia may be difficult in these cases.

Atrial Flutter

Atrial flutter is caused by a very rapid (usually greater than 400 impulses/min) wave of electrical activation regularly cycling through the atria. The ventricular response may be irregular or regular, depending on the pattern of AV conduction. The ECG baseline consists of “sawtooth” flutter waves that represent the fast, recurrent atrial activation. Atrial flutter is not a stable rhythm; it often degenerates into atrial fibrillation or may convert back to sinus rhythm.

Atrial Fibrillation

This common arrhythmia is characterized by rapid and chaotic electrical activation within the atria. There are no P waves on the ECG because there is no uniform atrial depolarization wave. Rather, the baseline usually shows irregular undulations (fibrillation waves). Lack of organized electrical activity prevents meaningful atrial contraction. The AV node, being bombarded by chaotic electrical impulses, conducts as many as possible to the ventricles. Ultimately the (ventricular) heart rate is determined by AV conduction velocity and recovery time, which are influenced by prevailing autonomic tone. Atrial fibrillation (AF) causes an irregular heart rhythm that is often quite rapid (Fig. 2-11). The QRS complexes are usually normal in configuration because intraventricular conduction pathway is usually normal. Minor variation in QRS complex amplitude is common, however, and intermittent or sustained bundle branch blocks can occur. AF tends to be a consequence of severe atrial disease and enlargement in dogs and cats; it is usually preceded by intermittent atrial tachyarrhythmias and perhaps atrial flutter. AF sometimes occurs spontaneously in giant breed dogs without evidence of underlying heart disease (“lone” AF). The heart rate can be normal in these dogs.

FIG 2-11 Atrial fibrillation. A, Uncontrolled atrial fibrillation (heart rate 220 beats/min) in a Doberman Pinscher with dilated cardiomyopathy (lead II, 25 mm/sec). B, Slower ventricular response rate after therapy in a different Doberman Pinscher with dilated cardiomyopathy showing baseline fibrillation waves. Note lack of P waves and irregular RR intervals. Eighth complex from left superimposed on calibration mark. Lead II, 25 mm/sec.

Ventricular Premature Complexes

Ventricular premature complexes (VPCs or PVCs) originate below the AV node and do not activate ventricular muscle via the normal ventricular conduction pathway. Therefore their QRS configuration differs from the animal’s sinus complexes. Ventricular ectopic complexes are usually wider than sinus-origin complexes because of slower intramuscular conduction. Because VPCs usually are not conducted backward through the AV node into the atria, the sinus rate continues undisturbed; thus the VPC is followed by a “compensatory pause” in the sinus rhythm. When the configuration of multiple VPCs or ventricular tachycardia is consistent in an animal, the complexes are described as being uniform, unifocal, or monomorphic. When the VPCs occurring in an individual have differing configurations, they are said to be multiform or polymorphic. Increased electrical instability may accompany multiform VPCs or tachycardia.

Ventricular Tachycardia

Ventricular tachycardia consists of a series of VPCs (usually at a rate greater than 100 beats/min). The RR interval is most often regular, although some variation can occur. Nonconducted sinus P waves may be superimposed on or between the ventricular complexes, although they are unrelated to the VPCs because the AV node and/or ventricles are in the refractory period (physiologic AV dissociation). The term capture beat refers to the successful conduction of a sinus P wave into the ventricles uninterrupted by another VPC (i.e., the sinus node has “recaptured” the ventricles). If the normal ventricular activation sequence is interrupted by a VPC, a “fusion” complex can result. A fusion complex represents a melding of the normal QRS configuration and that of the VPC (see Fig. 2-10, E). Fusion complexes are often observed at the onset or end of a paroxysm of ventricular tachycardia; they are preceded by a P wave and shortened PR interval. Identification of P waves (whether conducted or not) or fusion complexes helps in differentiating ventricular tachycardia from SVT with abnormal (aberrant) intraventricular conduction.

Polymorphic ventricular tachycardia is characterized by QRS complexes that vary in size, polarity, and often rate; sometimes the QRS configuration appears as if it were rotating around the isoelectric baseline. Torsades de pointes is a specific form of polymorphic ventricular tachycardia associated with Q-T interval prolongation.

Accelerated Ventricular Rhythm

Also called idioventricular tachycardia, accelerated ventricular rhythm is a ventricular-origin rhythm with a rate of about 60 to 100 beats/min in the dog (perhaps somewhat faster in the cat). Because the rate is slower than true ventricular tachycardia, it is usually a less serious rhythm disturbance. An accelerated ventricular rhythm may appear intermittently during sinus arrhythmia, as the sinus rate decreases; the ventricular rhythm is often suppressed as the sinus rate increases. This is common in dogs recovering from motor vehicle trauma. Often this rhythm disturbance has no deleterious effects, although it could progress to ventricular tachycardia, especially in clinically unstable patients.

Ventricular Fibrillation

Ventricular fibrillation is a lethal rhythm that is characterized by multiple reentrant circuits causing chaotic electrical activity in the ventricles; the ECG consists of an irregularly undulating baseline (Fig. 2-12). The ventricles cannot function as a pump because coordinated mechanical activity cannot occur in the presence of incoordinated electrical activation. Ventricular flutter, which appears as rapid sine-wave activity on the ECG, may precede fibrillation. “Course” ventricular fibrillation (VF) has larger ECG oscillations than “fine” VF.

FIG 2-12 Ventricular fibrillation. Note chaotic baseline motion and absence of organized waveforms. A, Coarse fibrillation; B, fine fibrillation. Lead II, 25 mm/sec, dog.

Escape Complexes

Ventricular asystole is the absence of ventricular electrical (and mechanical) activity. Escape complexes and escape rhythms are a protective mechanism. An escape complex occurs after a pause in the dominant (usually sinus) rhythm. If the dominant rhythm does not resume, the escape focus continues to discharge at its own intrinsic rate. Escape rhythms are usually regular. Escape activity originates from automatic cells within the atria, the AV junction, or the ventricles (see Fig. 2-10, G). Ventricular escape rhythms (idioventricular rhythms) usually have an intrinsic rate less than 40 to 50 beats/min in the dog and 100 beats/min in the cat, although higher ventricular escape rates can occur. Junctional escape rhythms usually range from 40 to 60 beats/min in the dog, with a faster rate expected in the cat. It is important to differentiate escape from premature complexes. Escape activity should never be suppressed with antiarrhythmic drugs.

Conduction Disturbances Within the AV Node

Abnormalities of AV conduction can occur from excessive vagal tone, drugs (e.g., digoxin, xylazine, medetomidine, verapamil, and anesthetic agents), and organic disease of the AV node and/or intraventricular conduction system. Three categories of AV conduction disturbances are commonly described (Fig. 2-13). First-degree AV block, the mildest, occurs when conduction from the atria into the ventricles is prolonged. All impulses are conducted, but the PR interval is longer than normal. Second-degree AV block is characterized by intermittent AV conduction; some P waves are not followed by a QRS complex. When many P waves are not conducted, the patient has high-grade second-degree heart block. There are two subtypes of second-degree AV block. Mobitz type I (Wenckebach) is characterized by progressive prolongation of the PR interval until a nonconducted P wave occurs; it is frequently associated with disorders within the AV node itself and/or high vagal tone. Mobitz type II is characterized by uniform PR intervals preceding the blocked impulse and is thought to be more often associated with disease lower in the AV conduction system (e.g., bundle of His or major bundle branches). An alternative classification of second-degree AV block based on QRS configuration has been described. Patients with type A second-degree block have a normal, narrow QRS configuration; those with type B second-degree block have a wide or abnormal QRS configuration, which suggests diffuse disease lower in the ventricular conduction system. Mobitz type I AV block usually is type A, whereas Mobitz type II frequently is type B. Supraventricular or ventricular escape complexes are common during long pauses in ventricular activation. Third-degree or complete AV block is complete failure of AV conduction; no sinus (or supraventricular) impulses are conducted into the ventricles. Although a regular sinus rhythm or sinus arrhythmia is often evident, the P waves are not related to the QRS complexes, which result from a (usually) regular ventricular escape rhythm.

FIG 2-13 AV conduction abnormalities. A, First-degree AV block in a dog with digoxin toxicity (lead aVF, 25 mm/sec). B, Second-degree AV block (Wenckebach) in an old cat under anesthesia. Note gradually prolonged PR interval with failed conduction of third (and seventh) P wave(s) followed by an escape complex. The fourth and eighth P waves (arrows) are not conducted because the ventricles are refractory (lead II, 25 mm/sec). C, Second-degree AV block in a comatose old dog with brainstem signs and seizures. Note the changing configuration of the P waves (wandering pacemaker) (lead II, 25 mm/sec). D, Complete (third-degree) heart block in a Poodle. There is underlying sinus arrhythmia, but no P waves are conducted; a slow ventricular escape rhythm has resulted. Two calibration marks (half-standard, 0.5 cm = 1 mV) are seen. Lead II, 25 mm/sec.

Intraventricular Conduction Disturbances

Abnormal (aberrant) ventricular conduction occurs in association with slowed or blocked impulse transmission in a major bundle branch or ventricular region. The right bundle branch or the left anterior or posterior fascicles of the left bundle branch can be affected singly or in combination. A block in all three major branches results in third-degree (complete) heart block. Activation of the myocardium served by the blocked pathway occurs relatively slowly, from myo-cyte to myocyte; therefore the QRS complexes appear wide and abnormal (Fig. 2-14). Right bundle branch block (RBBB) is sometimes identified in otherwise normal dogs and cats, although it can occur from disease or distention of the right ventricle. Left bundle branch block (LBBB) is usually related to clinically relevant underlying left ventricular disease. The left anterior fascicular block (LAFB) pattern is common in cats with hypertrophic cardiomyopathy.

FIG 2-14 ECG from a dog that developed right bundle branch block and first-degree AV block after doxorubicin therapy. Sinus arrhythmia, Leads I and II, 25 mm/sec, 1 cm = 1 mV.

Ventricular Preexcitation

Early activation (preexcitation) of part of the ventricular myocardium can occur when there is an accessory conduction pathway that bypasses the normal slow-conducting AV nodal pathway. Several types of preexcitation and accessory pathways have been described. Most cause a shortened PR interval. Wolff-Parkinson-White (WPW) preexcitation is also characterized by early widening and slurring of the QRS by a so-called delta wave (Fig. 2-15). This pattern occurs because the accessory pathway (Kent’s bundle) lies outside the AV node (extranodal) and allows early depolarization (represented by the delta wave) of a part of the ventricle distant to where normal ventricular activation begins. Other accessory pathways connect the atria or dorsal areas of the AV node directly to the bundle of His. These cause a short PR interval without early QRS widening. Preexcitation can be intermittent or concealed (not evident on ECG). The danger with preexcitation is that a reentrant supraventricular tachycardia can occur using the accessory pathway and AV node (also called AV reciprocating tachycardia). Usually the tachycardia impulses travel into the ventricles via the AV node (antegrade or orthodromic conduction) and then back to the atria via the accessory pathway, but sometimes the direction is reversed. Rapid AV reciprocating tachycardia can cause weakness, syncope, congestive heart failure, and death. The presence of the WPW pattern on ECG in conjunction with reentrant supraventricular tachycardia that causes clinical signs characterizes the WPW syndrome.

FIG 2-15 Ventricular preexcitation in a cat. Note slowed QRS upstroke (delta wave; arrows) immediately following each P wave. Lead II, 50 mm/sec, 1 cm = 1 mV.

Other QRS Abnormalities

Small-voltage QRS complexes sometimes occur. Causes of reduced QRS amplitude include pleural or pericardial effusions, obesity, intrathoracic mass lesions, hypovolemia, and hypothyroidism. Small complexes are occasionally seen in dogs without identifiable abnormalities.

Electrical alternans is an every-other-beat recurring alteration in QRS complex size or configuration. This is most often seen with large volume pericardial effusions (see Chapter 9).

QT Interval

The QT interval represents the total time of ventricular activation and repolarization. This interval varies inversely with average heart rate; faster rates have a shorter QT interval. Autonomic nervous tone, various drugs, and electrolyte disorders influence the duration of the QT interval (see Box 2-6). Inappropriate prolongation of the QT interval may facilitate development of serious reentrant arrhythmias when underlying nonuniformity in ventricular repolariza tion exists. Prediction equations for expected QT duration have been derived for normal dogs and cats.

Holter Monitoring

Holter monitoring allows the continuous recording of cardiac electrical activity during normal daily activities (except swimming), strenuous exercise, and sleep. This is useful for detecting and quantifying intermittent cardiac arrhythmias and therefore helps identify cardiac causes of syncope and episodic weakness. Holter monitoring is also used to assess the efficacy of antiarrhythmic drug therapy and to screen for arrhythmias associated with cardiomyopathy or other diseases. The Holter monitor is a small battery-powered digital or analog tape recorder worn by the patient, typically for 24 hours. Two or three ECG channels are recorded from modified chest leads using adhesive patch electrodes. During the recording period, the animal’s activities are noted in a patient diary for later correlation with simultaneous ECG events. An event button on the Holter recorder can be pressed to mark the time a syncopal or other episode is witnessed.

The digitized recording is analyzed using computer algorithms that classify the recorded complexes. Evaluation and editing by a trained Holter technician experienced with veterinary recordings are important for accurate analysis. Fully automated computer analysis can result in significant misclassification of QRS complexes and artifacts from dog and cat recordings. A summary report and selected portions of the recording are enlarged and printed for examination by the clinician. Evaluation of a full disclosure print-out of the entire recording is also helpful when compared with the selected ECG strips and the times of clinical signs and/or activities noted in the patient diary (see Suggested Readings for more information). A Holter monitor, hook-up supplies, and analysis can be obtained from some commercial human Holter scanning services, as well as many veterinary teaching hospitals and cardiology referral centers.

Wide variation in heart rate is seen throughout the day in normal animals. In dogs maximum heart rates of up to 300 beats/min have been recorded with excitement or activity. Episodes of bradycardia (<50 beats/min) are common, especially during quiet periods and sleep. Sinus arrhythmia, sinus pauses (sometimes for more than 5 seconds), and occasional second-degree AV block are apparently common in dogs, especially at times when mean heart rate is lower. In normal cats heart rates also vary widely over 24 hours (e.g. from ∼70 to ∼290 beats/minute. Regular sinus rhythm predominates in normal cats, and sinus arrhythmia is evident at slower heart rates. Ventricular premature complexes occur only sporadically in normal dogs and cats; their prevalence likely increases only slightly with age.

Event Recording

Cardiac event recorders are smaller than typical Holter units and contain a microprocessor with a memory loop that can store a brief period of a single modified chest lead ECG. The event recorder can be worn for periods of a week or so, but it cannot store prolonged, continuous ECG activity. Event recorders are used most often to determine whether episodic weakness or syncope is caused by a cardiac arrhythmia. When an episode is observed, the owner activates the recorder, which then stores the ECG from a predetermined time frame (e.g., from 30 seconds before activation to 30 seconds after) for later retrieval and analysis. Implantable (subcutaneous) recording devices have also been used in some veterinary patients and can allow intermittent ECG monitoring over an extended time frame.

Heart Rate Variability (HRV)

Phasic fluctuations in vagal and sympathetic tone during the respiratory cycle, and also during slower periodic oscillations of arterial blood pressure, influence the variation in time between consecutive heartbeats. HRV refers to the fluctuation of beat-to-beat time intervals around their mean value. HRV is influenced by baroreceptor function as well as by the respiratory cycle and sympathetic/parasympathetic balance. The degree of HRV decreases with severe myocardial dysfunction and heart failure, as well as other causes of increased sympathetic tone. The variation in instantaneous heart rate (R-to-R intervals) can be evaluated as a function of time (time-domain analysis) as well as in terms of the frequency and amplitude of its summed oscillatory components (frequency-domain or power spectral analysis). Frequency-domain analysis allows assessment of the balance between sympathetic and vagal modulation of the cardiovascular system. The potential clinical usefulness of HRV as an indicator of autonomic function, and possibly of prognosis, for veterinary patients is being explored (see Suggested Readings).

Signal-Averaged Electrocardiography (SAECG)

Digital signal averaging of the ECG provides a means of enhancing ECG signal resolution by discarding random components (noise) so that small-voltage potentials that may occur at the end of the QRS complex and into the early ST segment can be detected. These so-called ventricular late potentials can be found in patients with injured myocardium; they indicate the presence of conditions that predispose to reentrant ventricular tachyarrhythmias. The presence of late potentials on SAECG has been identified in some Doberman Pinschers with ventricular tachycardia and significant ventricular dysfunction, but the sensitivity for predicting risk of ventricular tachycardia is unclear (see Suggested Readings).

Common 2-D Echocardiographic Views

A variety of planes can be imaged from several chest wall locations. Most standard views are obtained from either the right or left parasternal positions (directly over the heart and close to the sternum). Images are occasionally obtained from subxiphoid (subcostal) or thoracic inlet (suprasternal) positions. Long-axis views are obtained with the imaging plane parallel to the long axis of the heart; short-axis views are perpendicular to this plane (Figs. 2-20 to 2-25). Images are described by the location of the transducer and the imaging plane used (e.g., right parasternal short-axis view, left cranial parasternal long-axis view). 2-D imaging allows an overall assessment of cardiac chamber orientation, size and wall thickness. The RV wall is usually about one third of the thickness of the LV free wall and should be no greater than half its thickness. The size of the right atrial and ventricular chambers is subjectively compared with that of the left atrium and ventricle; the right parasternal long axis and left apical 4 chamber views are useful for this. All valves and related structures as well as the great vessels are systematically examined. Any suspected abnormality is scanned in multiple planes to further verify and delineate it.

FIG 2-20 Two-dimensional short-axis echocardiographic views from the right parasternal position. The center diagram indicates the orientation of the ultrasound beam used to image cardiac structures at the six levels shown. Several of these positions guide M-mode beam placement as well as Doppler evaluation of tricuspid and pulmonary flows. Corresponding echo images are shown clockwise from the bottom. A, Apex. B, Papillary muscle. C, Chordae tendineae. D, Mitral valve. E, Aortic valve. F, Pulmonary artery. AMV, Anterior (septal) mitral valve cusp; AO, aorta; APM, anterior papillary muscle; CaVC, caudal vena cava; CH, chordae tendineae; LA, left atrium; LPA, left pulmonary artery; LV, left ventricle; LVO, left ventricular outflow tract; PA, pulmonary artery; PM, papillary muscle; PMV, posterior mitral valve cusp; PPM, posterior papillary muscle; PV, pulmonary valve; RA, right atrium; RAu, right auricle; RC, LC, NC, right, left, and noncoronary cusps of aortic valve; RPA, right pulmonary artery; RV, right ventricle; RVO, right ventricular outflow tract; TV, tricuspid valve.

(From Thomas WP et al: Recommendations for standards in transthoracic 2-dimensional echocardiography in the dog and cat, J Vet Intern Med 7:247, 1993.)

FIG 2-21 Two-dimensional long-axis echocardiographic views from right parasternal position. Each diagram on the left indicates the location of the ultrasound beam as it transects the heart from the right side, resulting in the corresponding echo image on the right. Long-axis four-chamber (left ventricular inflow) view is above. Long-axis view of the left ventricular outflow region is below. AO, Aorta; CH, chordae tendinae; LA, left atrium; LC, left coronary cusp of aortic valve; LV, left ventricle; LVW, left ventricular wall; MV, mitral valve; PM, papillary muscle; RA, right atrium; RPA, right pulmonary artery; RV, right ventricle; TV, tricuspid valve; VS, interventricular septum.

(From Thomas WP et al: Recommendations for standards in transthoracic 2-dimensional echocardiography in the dog and cat, J Vet Intern Med 7:247, 1993.)

FIG 2-22 Left caudal (apical) parasternal position. Four-chamber view optimized for ventricular inflow is above. Five-chamber view optimized for left ventricular outflow is below. These views provide good Doppler velocity signals from mitral and aortic valve regions. AO, Aorta; AS, interatrial septum; LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

(From Thomas WP et al: Recommendations for standards in transthoracic 2-dimensional echocardiography in the dog and cat, J Vet Intern Med 7:247, 1993.)

FIG 2-23 Left caudal (apical) parasternal 2-dimensional views optimized for left ventricular inflow and left auricle (above) and left ventricular outflow (below). AMV, Anterior (septal) mitral valve cusp; AO, aorta; LA, left atrium; LAu, left auricle; LV, left ventricle; PMV, posterior mitral valve cusp; RC, NC, right and noncoronary cusps of aortic valve; RVO, right ventricular outflow tract.

(From Thomas WP et al: Recommendations for standards in transthoracic 2-dimensional echocardiography in the dog and cat, J Vet Intern Med 7:247, 1993.)

FIG 2-24 Left cranial parasternal short-axis view optimized for right ventricular inflow and outflow. This view is useful for Doppler interrogation of tricuspid and pulmonary artery flows. PA, Pulmonary artery; PV, pulmonary valve; RA, right atrium; RC, LC, NC, right, left, and noncoronary cusps of aortic valve; RV, right ventricle; TV, tricuspid valve.

(From Thomas WP et al: Recommendations for standards in transthoracic 2-dimensional echocardiography in the dog and cat, J Vet Intern Med 7:247, 1993.)

FIG 2-25 Left cranial parasternal long-axis views optimized for aortic root (above), right atrium and auricle (middle), and right ventricular outflow and main pulmonary artery (below). These views are used to evaluate the heart base and can provide good Doppler signals for tricuspid and pulmonary flows. AO, Aorta; CaVC, caudal vena cava; LA, left atrium; LV, left ventricle; PA, pulmonary artery; PV, pulmonary valve; RA, right atrium; RAu, right auricle; RC, NC, right and noncoronary cusps of aortic valve; RV, right ventricle; RVO, right ventricular outflow tract.

(From Thomas WP et al: Recommendations for standards in transthoracic 2-dimensional echocardiography in the dog and cat, J Vet Intern Med 7:247, 1993.)

End diastolic and systolic LV internal dimensions and wall thickness are usually obtained using M-mode, but appropriately timed 2-D frames can also be used. Several methods can be used to estimate LV volume and wall mass. LA size is better assessed using 2-D rather than M-mode. Several methods for measuring LA size have been described. One is to measure the cranial-caudal diameter (top-to-bottom on screen) at end-systole using a right parasternal long axis four-chamber view. In cats this LA dimension normally is <16 mm; a diameter >19 mm may indicate greater risk for thromboembolism. Because of greater body size variation in dogs, LA dimension is usually compared with the 2-D aortic root diameter measured across the sinuses of Valsalva. A 2-D maximal LA diameter : aortic root ratio between 1.7 to 1.9 is considered normal.

M-Mode Views

Standard M-mode views are obtained from the right parasternal transducer position. The M-mode cursor is positioned with 2-D guidance using the right parasternal short-axis view. Precise positioning of the ultrasound beam within the heart (perpendicular to the structures to be measured) and clear endocardial images are essential for accurate M-mode measurements and calculations. For example, papillary muscles within the left ventricle must be avoided when measuring free-wall thickness. Fig. 2-26 illustrates standard M-mode views. In cases in which the M-mode cursor cannot be optimally aligned (e.g., in animals with focal or asymmetric hypertrophy), wall thickness measurements from 2-D images are preferred.

FIG 2-26 Common M-mode views. The diagram (A) indicates the approximate orientation of the one-dimensional ultrasound beam through the heart to achieve the corresponding M-mode images. A lead II ECG is recorded with the echo images for timing within the cardiac cycle. End diastole occurs at the onset of the QRS complex (yellow measure lines); end systole (pink measure lines) is the time when the dimension between the interventricular septum (IVS) and left ventricular free wall (LVW) is smallest. B, Image at the level of the chordae tendineae within the left ventricular lumen (LV), corresponding to cursor line “1” in A. Internal dimensions of the LV are measured from the leading (anterior) edge of the left endocardial wall of the IVS to the leading edge (luminal surface) of the posterior LVW. The thickness of the IVS is measured from the right endocardial surface of the IVS to the leading edge of the left endocardial septal wall at end diastole and end systole; the posterior LVW is measured at the same times from the endocardial surface to (but not including) the leading edge of the epicardial echoes. C, Image at the mitral valve level, cursor line “2” in A. The motion of the anterior (AM) and posterior (PM) mitral leaflets is described by the letters shown. Diastolic opening of the valve occurs at point D and systolic closing occurs at point C (see text for more information). D, Image at the aortic root (Ao) level “3” (where valve cusps are seen). Diameter is measured at end diastole from the leading (anterior) edge of the anterior aortic wall to the leading edge of the posterior wall. The left atrium (LA; usually the auricular region) is measured at the time of peak anterior aortic movement. RV, Right ventricular lumen; RVW, right ventricular wall.

Common Measurements and Normal Values

The standard dimensions measured with M-mode and their timing are also indicated in Fig. 2-26. The leading edge technique is used when possible (i.e., from the edge closest to the transducer [leading edge] of one side of the dimension to the leading edge of the other). In this way, only one endocardial surface is included in the measurement. LV wall and interventricular septal thicknesses, as well as LV chamber dimensions, should be determined at the level of the chordae tendineae, rather than the apex or mitral valve level. Measurements may also be taken from 2-D images if they are of high resolution and frames from the appropriate times in the cardiac cycle are used. Somatotype, breed, and body size greatly influence echo measurements in dogs. Endurance training also affects measured parameters, reflecting the increased cardiac mass and volume associated with frequent and sustained strenuous exercise. Some guidelines for approximate normal canine values are found in Table 2-3. Normal measurements in cats are more uniform but are also influenced by body size (Table 2-4). Chamber volume and ejection fraction are better estimated from optimized 2-D frames using the modified Simpsons’ method rather than M-mode images because of greater potential for inaccurate geometric assumptions from one dimensional measurements (see Supplemental Readings for further information). The right parasternal long axis view is usually better for assessing LV size than the left apical view.

TABLE 2-4 Echocardiographic Measurement Guidelines for Cats^*

Diastolic measurements are made at the onset of the QRS complex of a simultaneously recorded ECG. Systolic measurements of the LV are made from the point of peak downward motion of the septum to the leading edge of the LV free-wall endocardium at the same instant. The septum and LV wall normally move toward each other in systole, although their peak movement may not coincide if electrical activation is not simultaneous. Paradoxic septal motion, in which the septum seems to move away from the LV wall and toward the transducer in systole, occurs in some cases of RV volume and/or pressure overload. This abnormal septal motion can also be visualized on 2-D images; it precludes accurate assessment of LV function using fractional shortening.

The fractional shortening (FS; % delta D) is commonly used to estimate LV function. FS is the percent change in LV dimension from diastole to systole ([LVIDd - LVIDs]/LVIDd × 100). Most normal dogs have an FS between 25% to 27% and 40%; in most cats FS is 35% to 65%, although there is some variability. It is important to note that this index, like others taken during cardiac ejection, has the significant limitation of being dependent on ventricular loading conditions. For example, reduced LV afterload (as occurs from mitral insufficiency, ventricular septal defect, or peripheral vasodilation) facilitates ejection of blood and permits greater FS, although intrinsic myocardial contractility is not increased. The exaggerated FS in patients with severe mitral regurgitation causes the appearance of increased contractility in those with normal myocardial function and can mask deteriorating contractile function. Regional wall motion abnormalities as well as arrhythmias can affect the FS.

The use of the calculated end-systolic volume index (ESVI) has been suggested as a more accurate way to assess myocardial contractility in the presence of mitral regurgitation. This index (ESV/m² body surface area) compares ventricular size after ejection with body size rather than with the volume-overloaded end-diastolic ventricular size. LV volume estimation from 2-D rather than M-mode images is recommended. Extrapolation from human studies suggests an ESVI <30 ml/m² is normal, 30 to 60 ml/m² indicates mild LV systolic dysfunction, 60 to 90 ml/m² represents moderate LV dysfunction, and >90 ml/m² indicates severe LV dysfunction. A number of other methods can also be used to assess LV function.

Mitral valve motion is also evaluated with M-mode. The anterior (septal) leaflet is most prominent and has an “M” configuration. The posterior (parietal) leaflet is smaller; its motion mirrors the anterior leaflet, appearing as a “W.” Tricuspid valve motion is similar. The mitral valve motion pattern is identified by letters (see Figure 2-26). Point E occurs at maximal opening of the valve during the rapid ventricular filling phase. The valve drifts into a more closed position (point F) at the end of rapid ventricular filling. Atrial contraction causes the valve to open again (point A). At rapid heart rates the E and A points can merge. The mitral valve closes (point C) at the onset of ventricular systole. In normal animals the mitral E point is close to the interventricular septum. Increased E point-to-septal separation is usually associated with reduced myocardial contractility, but aortic insufficiency can also cause this. In animals with LV outflow obstruction, hemodynamic forces during ejection can pull the anterior mitral leaflet toward the septum. This is called systolic anterior motion (SAM), and it causes the normally straight mitral echos (between points C and D) to bend toward the septum during systole (see Figure 8-4). Diastolic flutter of the anterior mitral leaflet can sometimes be seen when an aortic insufficiency jet causes the leaflet to vibrate (Figures 2-27 and 2-28).

FIG 2-27 Color flow Doppler image of an aortic regurgitation jet angled toward and along the anterior leaflet of the mitral valve in a 2-year-old Rottweiler with aortic valve endocarditis. The regurgitant jet causes the mitral leaflet to flutter in diastole as seen in Fig. 2-28. Imaged from the right parasternal long axis position. Ao, Aorta; LA, left atrium; LV, left ventricle; RV, right ventricle.

FIG 2-28 Color M-mode (A) and standard M-mode (B) images of the mitral valve from the dog in Fig. 2-27. The disturbed flow from aortic regurgitation is seen as the colors along the anterior leaflet in the left ventricular outflow region. Fine fluttering of the anterior mitral leaflet is seen in B; the leaflet appears wide and “fuzzy” compared with the thin, discrete posterior leaflet.

The diameter of the aortic root and sometimes its motion are measured with M-mode. The parallel walls of the aortic root shift rightward in systole. During diastole one or two aortic valve cusps may be seen as a straight line parallel to and centered between the aortic wall echoes. At the onset of ejection, the cusps separate toward the walls of the aortic root and then come together again at the end of ejection. The shape of these echoes (two cusps) has been described as a train of boxcars or little rectangular boxes attached together by a string. Aortic diameter is measured at end diastole. The amplitude of posterior-to-anterior motion of the aortic root is often decreased in animals with poor cardiac output. The LA dimension (behind the aortic root) is measured at maximal systolic excursion. In normal cats and dogs, the (M-mode) ratio of LA to aortic root diameters is about 1 to 1. However, LA size is underestimated with this M-mode view because (especially in dogs) the M-mode cursor usually transects the LA close to the left auricle, not at its maximal dimension. In cats the M-mode beam is more likely to cross the body of the LA, but its orientation can be inconsistent. Echo beam placement may be difficult in some animals, and the pulmonary artery can be inadvertently imaged instead. Therefore LA size assessment is best done from 2-D images.

Systolic time intervals (STIs) have been used sporadically to estimate cardiac function, but they are influenced by cardiac filling and afterload. These intervals can be calculated if the opening and closing of the aortic valve are clearly seen on M-mode and a simultaneous ECG is recorded for timing. The STIs are left ventricular ejection time (duration of time the aortic valve is open), preejection period (time from the onset of the QRS to aortic valve opening), and total electromechanical systole (left ventricular ejection time plus preejection period). STIs can also be derived with Doppler echocardiography.

Pulsed Wave Doppler

Pulsed wave (PW) Doppler uses short bursts of ultrasound to analyze echoes returned from a specified area (designated the sample volume) along the Doppler cursor line. The advantage of PW Doppler is that blood flow velocity, direction, and spectral characteristics can be calculated from a specific location in the heart or blood vessel. The main disadvantage is that the maximum measurable velocity is limited. The pulse repetition frequency (time required to send, receive, and process returning echoes), as well as the transmitted frequency and the distance of the sample volume from the transducer determine the maximum measurable velocity (called the Nyquist limit). The Nyquist limit is defined by two times the pulse repetition frequency. Lower frequency transducers and closer sample volume placement increase the Nyquist limit. When blood flow velocity is higher than the Nyquist limit, “aliasing” or velocity ambiguity occurs. This is displayed as a band of velocity signals extending above and below (“wrapped around”) the baseline, so neither velocity nor direction is measurable (Fig. 2-30). The velocity spectrum displayed with PW Doppler when blood cells in the sample volume are moving in the same direction and at the same velocity is relatively thin (tight). Variation in velocity causes spectral broadening (widening).

FIG 2-30 Mitral diastolic inflow and systolic regurgitant flow in a dog with degenerative mitral valve disease recorded with PW Doppler from left caudal parasternal position. The direction of mitral regurgitant flow is away from the transducer (below baseline); however, this direction cannot be discerned with PW because the flow velocity is too high. The signal is instead “wrapped around” the baseline (aliased).

Characteristic blood flow patterns are obtained from the different valve areas. Flow across both AV valves has a similar pattern; likewise, flow patterns across the semilunar valve areas are similar. Normal diastolic flow across the mitral valve (Fig. 2-31) and tricuspid valve consists of an initial higher velocity signal during the rapid ventricular filling phase (E wave), which is followed by a smaller velocity signal associated with atrial contraction (A wave). Breed, age, and body weight appear to have little influence on normal Doppler measurements. Peak velocities are normally higher across the mitral (peak E usually ≤0.9 to 1.0 m/sec; peak A usually ≤0.6 to 0.7 m/sec) compared with the tricuspid valve (peak E usually ≤0.8 to 0.9 m/sec; peak A usually ≤0.5 to 0.6 m/sec). The four-chamber left apical view usually provides optimal alignment for assessing mitral inflow velocities; the left cranial short axis view is usually best for tricuspid inflow, although several other imaging planes may provide adequate alignment. Doppler-derived diastolic function indices include the isovolumic relaxation time, mitral valve E/A ratio, and others.

FIG 2-31 Normal mitral valve inflow recorded with PW Doppler from left caudal parasternal position in a dog. The flow signal (above baseline) following the QRS-T of the ECG represents early diastolic flow into the ventricle (E); the second, smaller peak after the P wave represents inflow from atrial contraction (A). Velocity scale in meters/second is on the left.

Flow across the pulmonary and aortic valves (Fig. 2-32) accelerates rapidly during ejection, with more gradual decel eration. Peak systolic pulmonary velocity is ≤1.4 to 1.5 m/sec in most normal dogs. The left cranial views usually provide better flow alignment. Sample volume placement is at or just distal to the valve. Peak aortic velocity is usually ≤1.6 to 1.7 m/sec, although some normal dogs have peak aortic velocities above 2 m/sec related to increased stroke volume or high sympathetic tone, especially if unsedated. Ventricular outflow obstruction causes more rapid flow acceleration, increased peak velocity, and turbulence. In general, aortic velocities over 2.2 (-2.4) m/sec are suggestive of outflow obstruction. Between 1.7 and ∼2.2 m/sec lies a “grey zone” where mild LV outflow obstruction (e.g., some cases of subaortic stenosis) cannot be differentiated with certainty from normal but vigorous left ventricular ejection. Maximal aortic/LV outflow velocities are obtained in most dogs from the subcostal (subxiphoid) position; however, in some dogs the left apical view provides higher velocity recordings. The LV outflow region should be interrogated from both views and the greater maximal velocity value used.

FIG 2-32 Normal pulmonary flow recorded with PW Doppler from left cranial short-axis position in a dog. There is rapid blood acceleration (below baseline) into the pulmonary artery, with a peak velocity of about 1.0 m/sec. Velocity scale in meters per second is on the left.

Continuous Wave Doppler

Continuous wave (CW) Doppler employs continuous and simultaneous ultrasound transmission and reception along the line of interrogation. Theoretically, there is no maximum velocity limit with CW Doppler, so high-velocity flows can be measured (Fig. 2-33). The disadvantage of CW Doppler is that sampling of blood flow velocity and direction occurs all along the ultrasound beam, not in a specified area (so-called range ambiguity).

FIG 2-33 CW Doppler recording of high-velocity aortic outflow in a dog with severe subaortic stenosis, imaged from the subcostal position. Estimated systolic pressure gradient across the outflow region is 169 mm Hg based on a peak velocity of 6.5 m/sec. Velocity scale in meters/second is on the left.

Pressure Gradient Estimation

Doppler estimation of pressure gradients is used in combination with M-mode and 2-D imaging to assess the severity of congenital or acquired flow obstructions. In addition, regurgitant jet maximal velocity estimates the peak pressure gradient across the regurgitant valve. The instantaneous pressure gradient across a stenotic or regurgitant valve is estimated using the maximal measured velocity of the flow jet. CF Doppler is useful to depict jet orientation. Careful Doppler beam alignment is essential in order to measure maximum velocity. CW Doppler is employed if aliasing occurs with PW Doppler. A modification of the Bernoulli equation is used to estimate pressure gradient:

Other factors involved in this relationship are usually of minimal clinical importance and are generally ignored.

Pulmonary arterial systolic pressure can be estimated (if there is no pulmonic stenosis) by using the maximal tricuspid regurgitation jet velocity (TRmax). The calculated systolic pressure gradient plus about 8 to 10 mm Hg (or the measured central venous pressure) equals the peak right ventricular systolic pressure, which approximates pulmonary artery systolic pressure. Pulmonary hypertension (PH) is associated when TRmax exceeds 2.8 m/s. The severity of PH is often categorized as mild (∼35-50 mm Hg; TRmax 2.9-3.5 m/s), moderate (∼51-75 mm Hg; TRmax 3.6-4.3 m/s), or severe (>75 mm Hg; TRmax >4.3 m/s). Likewise, pulmonary diastolic pressure can be estimated from pulmonary regurgitant (PR) jet velocity at end-diastole. The calculated end-diastolic pressure gradient between the pulmonary artery and the right ventricle, plus the estimated right ventricular diastolic pressure, represents pulmonary arterial diastolic pressure. Pulmonary hypertension is also suggested by a peak PR velocity of >2.2 m/s.

Color Flow Mapping

Color flow (CF) mapping is a form of PW Doppler that combines the M-mode or 2-D modality with blood flow imaging. However, instead of one sample volume along one scan line, many sample volumes are analyzed along multiple scan lines. The mean frequency shifts obtained from multiple sample volumes are color-coded for direction (in relation to the transducer) and velocity. Most systems code blood flow toward the transducer as red and blood flow away from the transducer as blue. Zero velocity is indicated by black, meaning either no flow or flow that is perpendicular to the angle of incidence. Differences in relative velocity of flow can be accentuated, and the presence of multiple velocities and directions of flow (turbulence) can be indicated by different display maps that use variations in brightness and color. Aliasing occurs often, even with normal blood flows, because of low Nyquist limits. Signal aliasing is displayed as a reversal of color (e.g., red shifting to blue; Fig. 2-34). Turbulence produces multiple velocities and directions of flow in an area, resulting in a mixing of color; this display can be enhanced using a variance map, which adds shades of yellow or green to the red/blue display (Fig. 2-35).

FIG 2-34 Example of color flow aliasing in a dog with mitral valve stenosis and atrial fibrillation. Diastolic flow toward the narrowed mitral orifice (arrow) accelerates beyond the Nyquist limit, causing red-coded flow (blood moving toward transducer) to alias to blue, then again to red, and once more to blue. Turbulent flow is seen within the left ventricle at the top of the 2-D image.

FIG 2-35 Systolic frame showing turbulent regurgitant flow into the enlarged LA of a dog with chronic mitral valve disease. The regurgitant jet curves around the dorsal aspect of the LA. Imaged from the right parasternal long axis, four chamber view. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

The severity of valve regurgitation is sometimes estim-ated by the size and shape of the regurgitant jet during CF imaging. Although technical and hemodynamic factors confound the accuracy of such assessment, wide and long regurgitant jets are generally associated with more severe regurgitation than narrow jets. Other methods for quantifying valve regurgitation have been described as well. Maximum regurgitant jet velocity is not a good indicator of severity, especially with mitral regurgitation. Changes in chamber size provide a better indication of severity with chronic regurgitation.

Doppler Tissue Imaging

Doppler tissue imaging (DTI) is a modality used to assess the motion of tissue, rather than blood cells, by altering the signal processing and filtering of returning echoes. Myocardial velocity patterns can be assessed with color flow and pulsed wave spectral DTI techniques. Spectral DTI provides greater temporal resolution and quantifies velocity of myocardial motion at specific locations, such as the lateral or septal aspects of the mitral annulus (Fig. 2-36). Color DTI methods display mean myocardial velocities from different regions. Other techniques used to assess regional myocardial function and synchrony are derived from DTI methods; these include myocardial velocity gradients, myocardial strain, strain rate, and velocity vector imaging.

FIG 2-36 PW Doppler tissue image from a cat. The mitral annulus moves toward the left apex (and transducer) in systole (S). Early diastolic filling (Ea) shifts the annulus away from the apex as the LV expands. Additional motion occurs with late diastolic filling from atrial contraction (Aa).

Nuclear Cardiology

Radionuclide, or nuclear, methods of evaluating cardiac function are available at some veterinary referral centers. These techniques can provide noninvasive assessment of cardiac output, ejection fraction, and other measures of cardiac performance as well as myocardial blood flow and metabolism.

Cardiac Computed Tomography and Magnetic Resonance Imaging

Cardiac computed tomography and magnetic resonance imaging are available in some centers. These techniques depict greater contrast between cardiovascular structures and the blood pool as well as differentiate certain types of tissue. Because cardiac movement during the imaging sequence reduces image quality, some type of physiologic (ECG) gating, as well as rapid image acquisition, are needed. Identification of pathologic morphology is a major application, although myocardial function, perfusion, and blood flow studies may be done depending on the technical capability of the equipment. Novel MR techniques also allow noninvasive evaluation of blood vessels, including calculation of peripheral resistance.