CHF Diagnostic Approach PDF 2000

The Diagnostic and Therapeutic Approach to the Patient in Acute Congestive Heart Failure Andrew W. Beardow, BVM6,r.S, MRCVS, Dipl ACVIM The patient presented in acute congesbve heart failure represents a diagnostic challenge. Life-threatening compromise of respiratory or cardtovascular function ren...

The Diagnostic and Therapeutic Approach to the Patient in Acute Congestive Heart Failure Andrew W. Beardow, BVM6,r.S, MRCVS, Dipl ACVIM The patient presented in acute congesbve heart failure represents a diagnostic challenge. Life-threatening compromise of respiratory or cardtovascular function renders the patient vulnerable to the stresses associated with many diagnostic tests. Before nsking any test tn thts situation, tt is ~mportant to understand the reformation that each test wtll give, and how that will impact the dtagnostm and therapeutic approach in this cructal early phase of pattent management. This arttcle describes the diagnostic tests commonly used m the evaluation of pattents in acute heart failure and the mformabon that each provides, and discusses how thts information can be used to guide therapy. Pericardiocentesis ts discussed in detail. Copynght © 2000 by W.B. Saunders Company Left-Sided Congestive Failure Elevation of left atrial pressure caused by underlying cardiac pathology and activation of compensatory mechanisms leads to elevations of pulmonary venous pressure, disruption of Starling's forces across the pulmonary capillary, and extravasadon of fluid, flooding the pulmonary intersntium and alveoli. Clinical signs are thus associated with disruption of gaseous exchange, ie, dyspnea, tachypnea, and orthopnea. A soft cough, which may produce serosanguinous frothy fluid, is seen. Characteristically tachycardia and arrhythmias associated with myocardial pathology and activation of the sympathetic nervous system are detected. Diagnosis of LCHF A patient in congestive heart failure is frequently presented to the veterinarian with a number of potentially hfethreatening changes that require rapid idennfication and appropriate intervention. Often the patient is hemodynamically unstable, rendering even relatively simple diagnostics dangerous. Appropriate selection of diagnostic tests is therefore critical, and clinicians must evaluate not only the diagnostic information that they are likely to glean from each test, but also the risk versus benefit to the patient. Although it is often necessary to take a symptomatic approach until the patient is stable enough to undergo tests required for a definitive diagnosis, it is important to understand which of the diagnostic data are most useful in assessing the cause of the patient's chnical signs The most appropriate therapeutic regimen will follow if the pathophysiological mechanisms that result in those clinical signs are understood. There are a limited number of syndromes that represent the final common pathways in the pathophysiology of heart failure. These syndromes differ according to the side of the heart affected and the nature of the inciting disease. Although each of these syndromes is discussed separately, it is important to note that they often occur concurrently in the cardiac patient. The syndromes are (1) left-sided congestive ("backward") failure (LCHF), (2) right-sided congestive failure (RCHF), (3) biventricular failure, and (4) low-output ("forward") failure. From Cardiopet Vetennary Associates, Little Falls, NJ. Address reprint requests to Andrew W Beardow, BVM&S, MRCVS, Dipl ACVIM (Cardiology), Cardtopet Inc, 48 Notch Rd, Little Falls, NJ 07424. E-mail abeardow @worldnet.att.net Copynght © 2000 by W.B Saunders Company 1096-2867/00/1502-0004510.00/0 doi:l 0 1053/svms.2000.6808 70 The cardinal clinical sign associated with left heart failure is pulmonary edema. The therapeutic goals in managing LCHF are discussed below, but one needs to establish this diagnosis first to ensure that appropriate therapeutics are selected. The following diagnostic tests are commonly available to most veterinarians. Their utility in establishing a symptomatic diagnosis is discussed here, but bear in mind that their utility in establishing a definitive diagnosis may be different, and where relevant, this is discussed. Cardiogenic pulmonary edema is often characterized by a history of a soft cough that may or may not be productive. A frothy serosanguinous fluid emanating from the nose or mouth is often seen when it is productive. Some animals may not cough at all. Cats with cardiogenic pulmonary edema are usually dyspneic but rarely cough. On auscultation lnmst crackles are heard, and may be more pronounced caudodorsally in early stages in dogs. Animals in severe LCHF may stand with their elbows adducted and with a serosanguinous nasal discharge. Radiography is the diagnostic test of choice for establishing a diagnosis of LCHE Radiographic characteristics of left heart failure include left atrial enlargement, pulmonary venous distension, and an alveolar pattern with air bronchograms. It is important to ensure that all three of these characteristics are present. Coughing is common in those breeds in which concurrent airway and valvular disease occur. Ra&ographically these dogs may have an enlarged left atrium. If they do not have distended pulmonary veins or an alveolar pattern, however, then it is much less likely that they are coughing because of left heart failure. Similarly, looking for all three of these characteristics can help differentiate pulmonary edema from pneumonia, both of which will result in an alveolar pattern radiographlcally, It should be noted, however, that there may be a delay between the apearance of clinical signs and radiographic evidence of pulmonary edema. 2 In this situation, Clinical Techmques in SmallAmmal Practice, Vol 15, No 2 (May), 2000. pp 70-75 TABLE 1. Formulary of Drugs Used in the Emergency Management of Heart Failure* Furosemlde (Lasix) Nitroglycerine (Nitrobld 2%) injectable Nitroprusside Enalapril (Enacard) Benazapnl (Fortekor) Hydralazlne Digoxin Dobutamme (Dobutrex) Milnnone Amrinone Morphine Dogs 1-4 mg/kg every 2-8 h Cats 0.5-1.0 mg/kg every 6-8 h, watch hydration 0.125-1.0 inch percutaneously every 6 h for 24-48 h 1-5 IJg/kg/mln CRI 1-10 IJg/kg/mln CRI (monitor blood pressure, may cause severe hypotension) Dogs 0.5 mg/kg SID-BID Cats 0.25 mg/kg SID 0.25 mg/kg SID 0.5 mg/kg PO tltratlng up to 2 mg/kg 0.005 mg/kg BID PO Rapid IV dlgltalization: divide 0.01 mg/kg into four doses and give every 1 h to effect or toxicity. Cats 0 007 mg/kg EOD Dogs 1-101Jg/kg/min CRI Cats 1-5 IJg/kg/mln (watch for seizures) 1-10 IJg/kg/min CRI 1-3 mg/kg IV bolus (slow) then 10-100 pg/kg/mln CRI Dogs 0.1 mg/kg IM, IV Cats 0.05 mg/kg SQ, IM with caution NOTE. Laslx: Hoechst, Summerville, NJ Nitrobld" Hoechst, Kansas City, MO; Enacard: MerckAgVet, Rahway, NJ Fortekor: Novartls, Ontario, Canada (not currently licensed for veterinary use in the USA); Dobutrex: Lilly, Indianapolis, IN. Abbreviations: CRI, constant rate infusion, SID, once daily, BID, twice daily; PO, orally; IV, intravenously; EOD, every other day; IM, intramuscularly; SQ, subcutaneously. *All doses are for dogs unless otherwise indicated. the clinician will need to rely on history and physical findmgs, with close attention paid to monitoring the progression of the patient. Even if pulmonary edema is not present, clues such as the presence of a large left atrium and pulmonary venous distension will still be seen on chest radiographs. Echocar&ography is the diagnostic test of choice to provide a definitive diagnosis of the underlying cardiac disease, but may not help evaluate the underlying cause of a patient's clinical stgns when these results are used in isolation. In the coughing small breed dog with a murmur, echocardiography will help confirm the diagnosis of valve disease as the cause of the murmur, and will allow assessment of the consequences of that disease in terms of chamber size and function. Pulmonary venous distention can be recognized echocardlographically, but these findings in isolation, however, do not confirm that the patient is in LCHE The radiographic characteristics confirm that. The radiographs do not, however, in many cases give us a definitive diagnosis of the underlying cardiac problem, nor do they give information about cardiac function. A complete cardiac database should include both tests. If circumstance forces one to select tests in critical situations, then the radiographs give the information that helps differentiate heart failure from other causes of respiratory signs. The echocardiogram is invaluable in defining cause, severity, and consequently prognosis once the patient is more stable and able to undergo further testing. A tall R wave and P mitrale (a wide, notched P wave) provide electrocardiographic clues for a symptomatic diagnosis of LCHE although the absence of these changes does not rule it out, because many factors can influence complex amphtudes. ACUTE CHF An ECG is the only way to establish a definitive rhythm diagnosis if an arrhythmla is suspected as a complicating factor in a patient presenting with LCHE Therapeutic Goals and Pharmacological Interventions in LCHF Drug doses are listed in Table 1. Decreasing Left Atrial and Hence Pulmonary Venous Pressures Reduce preload using Lasix (Hoechst, Summerville, NJ), venodilator (ie, nitroglycerine) Reduce afterload using an arteriodilator (ie, hydralazine) Reduce both using balanced vasodilator (enalapril, benazopril, sodium nitroprusside) Increase output using positive inotropes (ie, digoxin, dobutamine, milrinone [also a vasodilator]) Clearing Pulmonary Edema Volume contraction using lasix Respiratory Support Oxygen at a FIo2 40% (up to 100% for 18 to 24 hours) by mask, nasal catheter, or oxygen cage Minimizing Stress Minimal handling and restraint. Monitor respiratory rate and effort. Abort procedure if a detrimental effect on respiratory rate, rhythm, or mucous membrane color is appreciated. Right-Sided Congestive Failure Elevation of right areal pressure leads to extravasation of fluid into body cavities and the interstitium because of increased systemic venous pressures. Ascites, pleural effusion, and subcutaneous edema are the cardinal pathophysiological consequences of RCHE Clinical signs are related to these changes and depend on the location of the fluid. Dyspnea, caused by pleural effusion or severe abdominal distension, is the most common complaint on emergency presentation of a patient with RCHE TABLE 2. Equipment Typically Included in a Pericardiocentesis Kit Anglocath 14-gauge 5.25-inch (shorter for small dogs and cats) Sterile surgical gloves (appropriate size) No. 11 scalpel blade 20-mL syringe 60-mL syringe (2) 3-mL syringe 25-gauge needle Surgical drape Extension set Th ree-way stopcock ACT tubes (to check for clotting) Red-top tubes Lavender-top tubes (for cytology, if required) Abbreviation" ACT, activated clotting time. 71 A - ~--~ ,'.', • ..'~ - ~ ;' C ' ' " ' " " ' "' • ", ', : "-. ". ", ,::~-'. .. • .:. "":'r:'~'~ ~,.Jv.\\.:~.~..\¢... r-.. : ! . • '"i ', ". , , "~;~ ~,~ L "/.: 5~ T.':t :'..'~ ~v**L , ;.'4", 72 : : :J ,~. i ,.'~ fl BEARDOW Diagnosis of RCHF Right heart failure is characterized by ascites in canine patients. Isolated right heart failure is rarely recognized in cats. Abdominal palpation may reveal hepatosplenomegaly if these organs can still be felt despite the ascites. Ballotment will confirm the presence of ascites. Transmission of a fluid wave across the abdomen will only occur when fluid is present and will not be felt when abdominal distension is caused by obesity, agerelated abdominal muscle weakness, or metabohc perturbances such as canine Cushing's syndrome. Close attention should be paid to both arterial and jugular pulses when examining a patient with suspected RCHE Jugular venous distension is supportive of a diagnosis of RCHE A positive hepatojugular reflex is also supportive when jugular venous distension IS less obvious. A positive hepatojugular reflex is seen when a sustained increase in intraabdominal pressure caused by sustained compression of the abdomen increases venous return, exacerbating jugular venous distension. It has been suggested that both right and left atrial pressures may be increased by this technique. Assessments of changes in left atrial pressure, however, are difficult unless invasive techniques that assess pulmonary capillary wedge pressure (PCWP) are used. Careful attenuon should be paid to palpation of the femoral pulses because the presence of pulses paradoxus in any patient presenting with right heart failure should bring pericardial effusion to mind. A paradoxical pulse is one that appears to increase in intensity during expiration and decrease or disappear during inspiration. Normally, pulse amphtude may decrease by up to 7% during inspiration because of an increase in venous return to the right side of the heart, which displaces the interventricular septum, causing a slight decrease in left ventricular size and hence stroke volume. When pericardial effusion and cardiac tamponade are present, increased intrapericardial pressure restricts right ventricular free wall distension, exacerbating this septal displacement and compromise of left ventricular filling. When marked, the femoral pulse may disappear altogether, even though, paradoxically, the heart is still beating. Right ventricular enlargement is a challenging radiographic diagnosis unless moderate to severe changes are present. The classic description of a reverse D is only moderately helpful at best and confusing at worst. On the lateral view, right ventricular enlargement should be suspected if the distance from an imaginary line drawn from the carina to the apex to the cranial border of the cardiac silhouette is greater than 2.5 times the distance from the same imaginary line to the caudal border. Other supporting evidence of right ventricular enlargement includes dorsal displacement of the apex from the sternum, the contact point between the heart silhouette and the sternum having been shifted cranially. On the dorsovental wew, right ventricular enlargement may cause a notching toward the apex or the appearance of a double apex. Displacement of the trachea as it courses over the cranial (right) portion of the cardiac silhouette may also be seen on the lateral chest radiograph, and this may be more marked when right atrial enlargement is present. Right atrial enlargement may also fill the cranial cardiac waist on the lateral view and cause a bulge in the 8 to 12 o'clock position on the ventrodorsal film. Whenever an older canine patient is presented in right heart failure, especially in the mid-sized to larger breeds, one should always consider pericardial effusion as a possible cause. Pericardial effusion typically appears as a pumpkin-shaped heart with loss of individual chamber detail and a clearly defined pericardial border caused by decreased pericardial motion. Acute tamponade, however, can occur with a relatively small volume effusion if insufficient time has elapsed to facilitate pericardial stretching. Subtle signs may be a rounding of the cardiac silhouette and a wide caudal vena cava. As a guide, the caudal vena cava should be no wider than the length of the fifth thoracic vertebral body on a right lateral chest film. Right ventricular enlargement may cause a right axis deviation on the ECG. Most sensitive in detecting right ventricular enlargement are a right axis deviation in the frontal plane and deep S waves in the chest leads. However, the absence of a right axis deviation does not rule out right heart failure. Electrical alternans may be seen if pericardtal effusion is present. This is identified as a beat-to-beat variation in the complex amplitude of the R wave but can be seen in the Q, S, or T wave. A swinging of the heart in the fluid-filled sac causes electrical alternans. This moves the source of the electrical activity relative to the electrodes, which are in a fixed position on the limbs. A similar variation in ECG configuration can also be seen with respiration, but this alternans pattern will match the respiratory pattern and is less often a beat-to-beat variation unless the patient is severely tachypneic. Patients in right heart failure tend not to be hemodynamically compromised unless the right heart failure is a consequence of pericardial effusion and cardiac tamponade, or unless venous return is compromised because of the presence of ascltes. A complete cardiac ultrasound may be performed at an earlier stage in the &agnostic work-up when compared with the hemodynamically compromised patient in left heart failure. A definitive diagnosis may therefore be available earlier in the management of right heart failure. Pericardial effusion is best assessed with an echocardiogram before pericardiocentesis. The presence of the fluid within the pericardial space acts as an excellent contrast medium for defining cardiac structures, and in particular, cardiac tumors. In this circumstance, the ultrasonographer should make every effort to visualize the entire right atrium, mcluding the right atrial appendage, and the base of the great vessels, especially the aorta. These are the most common sites for cardiac neoplasms, although they can form m any region of the heart. It should be stressed, however, that a patient in cardiac tamponade is a fragile patient, even if at first glance they appear hemodynamically stable. Increased demand for cardiac output can quickly lead to hemodynamic compromise necessitating immediate intervention. This should Fig 1. Technique for Pericardiocentesis. (A) The patient is placed in left lateral recumbency. (B) A 3-inch square is shaved and prepared for surgical intervention. A 14-gauge over-the-needle catheter is introduced as shown after it has been prepared with the addition of fenestrations at the catheter tip (see text). The catheter is introduced medially and dorsally, pointing toward the point of the opposite shoulder when the point of insertion is at or slightly below the costo-chondral junction. (C) An extension set and 3-way stopcock are attached to the hub of the catheter to facilitate drainage of the pericardial sac. The hub of the catheter should be stabilized in this position while the pericardium is completely drained. ACUTE CHF 73 always be borne in mind when deciding to postpone pericardiocentesls while awaiting an echocardiographic evaluation. Therapeutic Goals and Pharmacological Interventions in RCHF Remove the Fluid Pharmacologically, using Lasix (moderate doses), ACE inhibitors Mechanically, using thoracocentesis or abdominocentesis Improve Output Use positive inotropes, such as digoxin Use vasodilators, such as ACE inhibitors Pericardiocentesis Rapid drainage of the pericardia1 effusion is often the only intervention necessary in the management of this situation. The approach to the pericardium is controversial. If the pericardium is approached from the left side of the chest, there is a slightly greater risk for coronary artery damage, but less chance of confusion about needle placement if the left ventricle is inadvertently punctured. If the pericardium is approached from the right side, there is less risk of coronary damage but more risk of confusion if the right ventricle is inadvertently punctured. The right ventricle is a thin-walled, low-pressure chamber. It is more easily punctured, and blood is less apt to gush at high pressure from the penetrating trocar than if the left side is entered. Right ventricular blood is deoxygenated and dark and easily confused with the port wine effusate that is commonly seen. Whichever side is penetrated, you should always have a current packed cell volume (PCV) on the patient for comparison with the PCV of the tapped fluid. For additional confirmation, pericardial effusate is typically present in the pericardium for a sufficient time to become defibrmated and will fail to clot. When approaching the pericardium with any needle or catheter, it is best to have the animal connected to a continuous-lead II ECG because a ventricular premature beat or beats are typically seen as the needle approaches the epicardium. Several techniques for perlcardiocentesls are described. Below is a brief description of the technique favored by numerous clinicians. Table 2 lists the equipment typically included in a pericardiocentesis kit. The following is a technique for an approach from the left side of the thorax (Fig 1). 1. Site selection: if available, use the thoracic radiographs as a guide to the best position to enter the chest. This is typically in the region of the costochondal junction in the fourth, fifth, or sixth intercostal space. The dorsoventral radiograph will often show where the cardiac silhouette comes closest to the chest wall. 2. Catheter selection and preparation: a 14-gauge over-theneedle catheter is commonly used. Small fenestrations may be cut in the end of the catheter with a No. 11 scalpel blade while the needle is still in place, but care should be taken that this does not leave burs or compromise the integrity of the distal portion of the catheter. Remember that as the pericardium is drained, it will fall away from the chest wall, falling off the end of shorter catheters. An extension set is attached to the catheter. 74 3. Site preparation (Figs 1A and B): a 3-inch square is shaved at the selected site and prepared as a surgical site. The skin and deeper structures are anestheuzed with 2% lidocaine, and a small skin nick is made at the point of entry of the catheter with the point of a No. 11 scalpel blade. 4. Approach to the pericardium: the ECG is connected, and a continuous-lead II ECG is displayed. The needle is introduced medially and dorsally through the skin mck (Fig 1C). This wtll prevent burring of the catheter as it penetrates the tough subcuticular tissue. A faint scratching sensation is often appreciated just before the pericardium is punctured. Once the pericardium is penetrated, a port-wine-colored flash is usually seen in the needle and extension set, although if pericardial pressure is low, one might need to apply negative pressure with a 20-mL syringe. Once the flash is seen, the catheter is advanced over the needle until the hub of the catheter is pushed firmly against the body wall of the patient. A three-way stopcock is then placed at the end of the catheter/extension set. Once the catheter is placed, the operator should keep the hub stabilized at all times to prevent the catheter from migrating out of the pericardmm. An assistant with a 60-mL syringe should then empty the pericardium through the catheter/extension set/three-way stopcock. Slight rotations of the catheter may be necessary as the pericardium empties. Initial samples of the fluid should be evaluated for a PCV and lack of clotting. Once no further fluid can be obtained, the operator should slowly withdraw the catheter while the assistant keeps gentle suction applied. Pockets of pericardial fluid are thus emptied. Once the catheter is fully withdrawn, the patient is allowed to rest. If you are not sure whether you are withdrawing perlcardlal fluid or blood because of inadvertent ventricular puncture, the following should be considered: (1) The pericardial fluid will not clot; (2) The patient's heart rate on the ECG should decrease. If you are exsangulnating the patient, the heart rate will tend to increase; (3) The PCV of the effusate is typically substantially less than that of peripheral blood, unless acute bleeding has occurred, in which case it can be higher; (4) The supernatant when perlcardial effusate is spun is typically yellow (xanthochromic). If cardiac output is severely compromised in a patient with cardiac tamponade, shock doses of fluid (60 to 90 mL/kg/h IV m the dog, 40 to 60 mL/kg/h IV in the cat) should be administered. This may seem paradoxical in a patient showing signs of right heart failure, but makes sense when you consider that the low cardiac output is caused by a lack of cardiac filling. Increasing filling pressures will probably lead to an exacerbation of the ascites, but it will also help increase right ventricular filling and thus cardiac output. This will help provide time to perform a pericardiocentesis, after which all of the ascites will usually resolve spontaneously. Low-Output Cardiac Failure Diminished cardiac output may result from either systolic dysfunction, ie, failure to pump, or diastolic dysfunction, a failure to fill (Fig 2). Major causes of systolic dysfunction include dilated cardiomyopathy and end-stage chronic valve disease. Diastolic dysfunction occurs with hypertrophic cardiomyopathy, restrictive heart disease, pericardial effusion, and BEARDOW •DcMSYSTOLICDYSFUNCTION X Fig 2. Pathogenesis of low output failure. Activation of the body's compensatory mechanisms exacerbates falling cardiac output induced by both systolic and diastolic dysfunction. DCM, dilated cardiomyopathy; SNS, sympathetic nervous system; RAAS, renin-angiotensin-aldosterone system; HCM, hypertrophic cardiomyopathy. j,[Deoro i.g DIASTOLIC DYSFUNCTION i HCM I [ Pericardial Effusion / Ouut] IIncreasingAfterload I [Fall in Blood Pressure] / IVas°constricti°n [ Sensed by Baroreceptors] -,,. / Activation of compensatorymechanisms SNS & RAAS space-occupying lesions, ie, neoplasm. Clinical signs of lowoutput failure result from poor muscle perfuslon, pale mucous membranes, poor capillary refill time (CRT), and cold extremities. In most cases, these signs develop in addition to those of congestive failure. The diagnostic tests used are typically those for left heart failure because most animals presented for low output failure are typically also showing signs of left congestive failure. Clinicians should be cognizant, however, that clinical signs such as prolonged capillary refill, blanching of the mucous membranes, and a cool periphery may be indicative of concurrent low-output failure, and the appropriate therapeutic interventions should be considered. Therapeutic Goals and Pharmacological Interventions in Low-Output Failure Increase Cardiac Output The intervention will depend on whether the fall in cardiac output is caused by systolic or diastolic dysfunction. Systolic Dysfunction For positive inotropes, use digoxin, dobutamine, and milrinone. For afterload reduction, use arteriodilators and balanced vasodilators. Diastolic Dysfunction For extracardiac causes (ie, pericardial effusion), remove the cause/fluid (ie, pericardlocentesis). For cardiac causes, (ie, hypertrophic cardiomyopathy [HCM]), use negative inotropes, calcium channel blockers, or beta blockers. Cardiac Syndromes Associated With Common Cardiovascular Diseases In chronic valve disease, left CHF is seen initially. Low-output failure occurs in the end stages or after rupture of the cordae tendinaii. In dilated cardiomyopathy, left congestive and sys- ACUTE CHF tolic low-output failure occur concurrently. In hypertrophic cardiomyopathy, diastolic low-output failure and left or biventricular low-output failure occur. In pericardial effusion, lowoutput failure occurs because of extracardiac diastolic dysfunction. In heartworm disease, right congestive failure and possibly low-output failure with caval syndrome occur. Understanding the information that each diagnostic test yields and its implications in the pathogenesis of the clinical signs shown allows the clinician to make rational judgements about the diagnostic approach to the patient presented in heart failure. Classification of heart failure states also allows the clinician to make potentially life-saving therapeutic decisions when the fragility of the patient prevents us from establishing a complete diagnosis of the inciting disease process. It is impossible to overemphasize, however, that if a client is to be given an accurate assessment of long-term management and prognosis, then a complete cardiac database should be secured once the patient is stable enough to undergo further diagnostic testing. References 1. Hamlin RL. Pathophystology of the fading heart, in Fox PR, Sisson D, Morse NS (eds): Textbook of Canme and Feline Cardiology. PhiladeipNa, PA, Saunders, 1999, pp 210 2. Ware WA: Pulmonary edema, m Fox PR, Stsson D, Molse NS (eds): Textbook of Canine and Fehne Cardtology. Philadelphia, PA, Saunders, 1999, pp 257 3. Ttlley LP' Essenttals of Canine and Feline Electrocardtography. Philadelphia, PA, Lea & Febiger, 1992, pp 63 4. Ktttleson MD: Signalment, history and phystcal exammatJon, in Kittleson MD, Ktenle RD (eds): Small Antmal Cardiovascular Medicine. St Louis, MO, Mosby, 1998, pp 40 5. Lorell BH: Pencardtal effusion, in Braunwald E (ed): Heart Disease (ed 5). Philadelphia, PA, Saunders, 1997, pp 1488-1489 6. Lord PF, Suter PF: Radiology, in Fox PR, Stsson D, Morse NS (eds): Textbook of Canme and Felme Cardtology. PhiladelpNa, PA, Saunders, 1999 7. Buchanan JW, Bucheler J: Vertebral scale system to measure cantne heart size in radiographs. J Am Vet Med Assoc 206:194-199, 1995 8. Ware WA: Cardiac neoplasia, in Bonagua JD (ed). Current Vetermary Therapy XII. Phtladelphia, PA, Saunders, 1995, pp 873 75