Memorias del XXXVI Congreso Nacional AMMVEPE 2018

AMMVEPE 1968 - 2018

MEMORIAS DE LAS PONENCIAS EN EL XXXVI CONGRESO NACIONAL 2018 ACAPULCO, GUERRERO “DR JESÚS PAREDES PÉREZ”

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

ÍNDICE TEMÁTICO DE LAS PONENCIAS

ACQUIRED HEART DISEASE IN THE DOG – CAUSES, DIAGNOSIS & MANAGEMENT John D. Bonagura, DVM, DACVIM (Cardiology, Internal Medicine) Ohio State University College of Veterinary Medicine, Columbus, Oh.

CARDIAC ARRHYTHMIAS IN VETERINARY MEDICINE – REFERENCE NOTES John D. Bonagura, DVM, DACVIM (Cardiology, Internal Medicine) Ohio State University College of Veterinary Medicine, Columbus, Oh.

RADIOGRAPHIC DIFFERENTIAL DIAGNOSIS John D. Bonagura, DVM, DACVIM (Cardiology, Internal Medicine) Ohio State University College of Veterinary Medicine, Columbus, Oh.

BRACHYCEPHALIC AIRWAY SYNDROME Eric Monnet, DVM, PhD, FAHA Diplomate ACVS and ECVS Colorado State University, Fort Collins, Colorado

DIAPHRAGMATIC HERNIA Eric Monnet, DVM, PhD, FAHA Diplomate ACVS and ECVS Colorado State University, Fort Collins, Colorado

FELINE HEART DISEASE CARDIOMYOPATHIES & ARTERIAL THROMBOEMBOLISM John D. Bonagura, DVM, DACVIM (Cardiology, Internal Medicine) Ohio State University College of Veterinary Medicine, Columbus, Oh

LAPAROSCOPY IN SMALL ANIMAL PRACTICE IS IT POSSIBLE? Eric Monnet, DVM, PhD, FAHA Diplomate ACVS and ECVS Colorado State University, Fort Collins, Colorado

LARYNGEAL PARALYSIS Eric Monnet, DVM, PhD, FAHA Diplomate ACVS and ECVS Colorado State University, Fort Collins, Colorado

OA EN EL GATO MC Gerardo Garza Malacara

PERICARDIAL DISEASES IN DOGS: DIAGNOSIS & MANAGEMENT John D. Bonagura, DVM, DACVIM (Cardiology, Internal Medicine) Ohio State University College of Veterinary Medicine, Columbus, Oh

SURGERY OF THE LUNG Eric Monnet, DVM, PhD, FAHA Diplomate ACVS and ECVS Colorado State University, Fort Collins, Colorado

SURGERY OF THE LIVER AND GALL BLADDER Eric Monnet, DVM, PhD, FAHA Diplomate ACVS and ECVS Colorado State University, Fort Collins, Colorado

SURGERY OF THE TRACHEA Eric Monnet, DVM, PhD, FAHA Diplomate ACVS and ECVS Colorado State University, Fort Collins, Colorado

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

ACQUIRED HEART DISEASE IN THE DOG – CAUSES, DIAGNOSIS & MANAGEMENT John D. Bonagura, DVM, DACVIM (Cardiology, Internal Medicine) Ohio State University College of Veterinary Medicine, Columbus, OH Introduction The most important heart disease of the dog is chronic mitral regurgitation due to degenerative valvular disease. The condition is variously termed “degenerative valvular disease (DVD)”, “myxomatous mitral valve disease (MMVD)”, “valvular endocardiosis”, or simply “mitral regurgitation” (MR) although the latter term is not very specific considering MR also occurs with malformations, endocarditis, or cardiomyopathy. Chronic MMVD often leads to congestive heart failure (CHF) in the dog. The latter is a clinical syndrome triggered by impaired cardiac systolic or diastolic function and characterized by stereotypical changes in neurohormonal activation, renal sodium retention, and cardiac and vascular remodeling.

Functional characteristics of heart failure include impaired exercise capacity, secondary pulmonary dysfunction, and metabolic disturbances related to impaired organ perfusion.

Both quality and duration of life are limited by cardiac failure and there is keen interest not only in treating well‐defined CHF, but also preventing heart failure if possible. From the author’s perspective five things matter in terms of therapy: 1) Is the onset of CHF significantly delayed by a treatment; 2) Do the patients live longer; 3) Is quality of life better with treatment; 4) Are unplanned hospitalizations reduced; and 5) Are adverse effects related to quality of life and mortality acceptable? From a client’s perspective (and therefore of our interest) are the practicalities of cost‐effectiveness and convenience of medication, since both of these can influence client compliance with medications. Cost of drugs is often influenced by the locale of the client and local regulations regarding generic drug availability and usage in animals. Cost‐ effectiveness is especially important when drugs are used for prevention of CHF because a long duration of therapy and a potentially high cost of treatment might be involved (sometimes with marginal evidence for its use). When there is a potential for benefit based on favorable effects on markers of disease or ambiguous results of clinical trials, some clinicians will empirically recommend therapy; however, clients should understand the lack evidence and appreciate the costs of such treatment as well as potential unintended adverse effects.

These points become very relevant when we consider the various clinical trials involving cardiac drugs, especially the angiotensin converting enzyme (ACE) inhibitors and pimobendan (Vetmedin®). For example, the initial QUEST study showed the efficacy of pimobendan therapy in CHF caused by chronic MR in small breed dog. This study involved a well‐constructed comparison of pimobendan versus benazepril in dogs with CHF due to DVD treated with a background of furosemide and spironolactone. The “survival” (endpoints) benefit of pimobendan was evident when compared to the selected dosage of benazepril and this has previously been reported in the initial paper from this trial. The more recent report compared a number of quality of life indicators between the two groups. (In this study there was not a “combined” group receiving both pimobendan and an ACEI; such combined treatment would represent the typical standard of care for canine CHF). In this recent report, there was (somewhat confusingly) no demonstrable benefit in the quality of life indicators between groups, although the time to Acquired Canine Heart Disease (Dr. Bonagura) – Page 1

intensification of therapy was delayed in the pimobendan group and there was probably less free‐water retention with inodilator therapy. Recently the EPIC trial was presented which showed a statistically‐significant and clinically meaningful delay in the onset of CHF in dogs with asymptomatic MMVD. These results will clearly change our practices and will be one of the main discussion points of these presentations on chronic valvular disease in the dog.

Differential Diagnosis of Canine Heart Disease The most common heart diseases leading to CHF in dogs are valvular endocardiosis (MMVD), dilated cardiomyopathy, pulmonary hypertension, and pericardial effusion. Various congenital malformations (including patent ductus arteriosus, pulmonic stenosis, subaortic stenosis, atrioventricular valve dysplasia) are important causes of heart disease and heart failure young animals.

Valvular endocardiosis is characterized by progressive mitral/tricuspid valvular degeneration and apical systolic murmurs typical of mitral regurgitation (MR) and tricuspid regurgitation (TR).

Atrial arrhythmias, left mainstem bronchus compression, PH, and rarely atrial tearing may complicate the clinical picture. Systemic hypertension from renal or Cushing’s disease increases the regurgitant fraction and represents a comorbid condition. In contrast to endocardiosis, infective endocarditis is a multisystemic inflammatory disorder originating from a cardiac infection and is a relatively rare cause of CHF in dogs. The conditions should not be confused.

Dilated cardiomyopathy (DCM) is a primary myocardial disorder caused by an inexplicable loss of myocardial contractility. This idiopathic/genetic disease is often associated with cardiac arrhythmias, such as atrial fibrillation (AF) and ventricular tachycardia (VT). Occult or preclinical DCM refers to the echocardiographic finding of reduced left ventricular (LV) ejection fraction in the absence of CHF. Left‐ and right‐sided CHF as well as sudden cardiac death are common outcomes of DCM. In some breeds such as Doberman pinschers, development of ventricular or atrial arrhythmias can predate the development of DCM. Right ventricular arrhythmogenic cardiomyopathy (ARVC), is especially common in boxers and English bulldogs. Cases of DCM are infrequently related to dietary issues and have been observed when there is taurine or protein deficiency with certain vegan diets, some lamb & rice diets, and some grain‐free diets (there is more to understand here).

Pulmonary hypertension (PH) stems most often from three disorders: chronic left sided heart failure; dirofilariasis; and severe interstitial lung disease. This disorder also can be idiopathic (primary) in dogs. PH is very common in dogs with chronic mitral regurgitation (MR) and typically leads to a progressively louder murmur of tricuspid regurgitation, signs of low cardiac output, right sided failure (including ascites and exertional syncope). With the exception of heartworm disease, PH due to primary lung disease infrequently leads to heart failure.

Pericardial effusion is a frequent cause of heart failure in dogs but often is misdiagnosed. Acute effusions can provoke collapse related to hypotension. Right‐sided CHF, including pleural effusions, can develop in chronic cardiac tamponade. In younger dogs (and some older ones) idiopathic pericardial hemorrhage is the underlying cause and carries a very good prognosis with proper management. In dogs >7 years of age there is often a cardiac‐related neoplasia involved with the effusion (hemangiosarcoma, chemodectoma, mesothelioma, ectopic thyroid neoplasia).

Treatment of pericardial disorders does not involve drugs, but instead, pericardiocentesis often followed by form of surgical or endoscopic procedure.

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Cardiac arrhythmias often complicate the atrial and ventricular remodeling observed in structural heart diseases. Heart rhythm disturbances can precede the development of heart failure in some disorders, especially in forms of cardiomyopathy. Tachyarrhythmias, if relentless (as with atrial flutter, atrial fibrillation, reentrant supraventricular tachycardia, or sustained ventricular tachycardia) induce a potentially reversible decrease in ventricular function called tachycardia‐induced cardiomyopathy. This impairment of cardiac output is additive to any preexisting structural heart disease. Bradyarrhythmias such as sinus arrest and atrioventricular blocks are more often related to primary disease (degeneration) of the conduction system in dogs and can lead to collapse, syncope, or CHF. Management approaches for arrhythmias may involve directed follow‐ups (with no therapy), antiarrhythmic drugs, cardiac pacing, or catheter based interventions.

Diagnosis of Valvular and non‐Valvular Heart Diseases & Heart Failure The diagnosis of heart disease and the recognition of CHF require a careful history and clinical examination. There is clearly epidemiologic risk for cardiac disease related to species, age, breed, and sometimes sex. These predispositions are learned with experience or can be identified by consulting reference textbooks. The historical findings of cardiac disease are not specific. Exercise intolerance often can be identified and respiratory signs are common in patients with heart failure.

Physical diagnosis might identify objective signs of CV disease. Auscultation may indicate a heart murmur, arrhythmia, or gallop sound. Realistically, the diagnosis of MMVD as a cause of respiratory signs (cough/dyspnea) or apparent cardiomegaly is untenable without an obvious systolic murmur over the apex or mitral valve area. The lungs can be abnormal to auscultation if there is pulmonary edema or cor pulmonale. Blood pressure in heart failure may be normal (from cardiac, autonomic, endocrine, and renal compensations); low in profound CHF (cardiogenic shock); or surprisingly high, indicating the co‐morbid condition of systemic hypertension.

Diagnostic imaging is an important aspect of cardiac diagnosis. Echocardiography is the noninvasive gold standard for diagnosis of heart disease and is helpful in confirming the cause in cases of suspected CHF. While not necessary in all cases, Echo studies are pivotal for confirmation of DCM, pericardial diseases, endocarditis, and pulmonary hypertension (as well as for the diagnosis of congenital heart defects). Thoracic radiography is useful for evaluating heart size and following the progression of cardiomegaly. Radiographs are also essential in the differential diagnosis of respiratory signs. Many dogs with compensated heart disease are symptomatic because of a primary respiratory, pleural, or thoracic disorder, not CHF. When CHF is suspected, chest radiographs obtained before and after diuretic treatment can support the clinical diagnosis because radiographic findings of acute or severe CHF are significantly “improved” following successful therapy.

The electrocardiogram (EKG, ECG) in advanced heart disease may delineate cardiac‐ enlargement patterns (wide or tall P‐waves or QRS complexes), conduction disturbances, or arrhythmias. Unfortunately, the 6‐ or 9‐lead ECG is too often within normal limits or equivocal and therefore cannot be relied on for establishing a diagnosis of heart disease. Simply stated, the EKG has low diagnostic sensitivity for heart disease in many dogs. Of course, the EKG is the test of choice for delineating heart rhythm disturbances.

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Confirmation of the diagnosis of left‐sided CHF requires integration of history, physical examination, and radiography; echocardiography can also be instructive when performed by an experienced examiner. Most CHF patients have some cardiac abnormality on auscultation, but it may be subtle, such as soft heart sounds (pericardial disease, DCM) or a gallop sound. Resting tachycardia is common but not always evident. Key radiographic findings of left sided heart failure include left atrial and ventricular enlargement; pulmonary venous congestion or distension (this is variable); and pulmonary infiltrates compatible with cardiogenic edema. These are typically bilateral, caudo‐dorsal interstitial and alveolar infiltrates when heart failure is severe. There may be a slight, right‐sided preponderance to the infiltrates. Radiographic signs of cardiogenic pulmonary edema should improve within 24 to 48 hours of diuretic therapy, and this improvement is often accompanied by reduction in overall heart size, indicating reduced venous pressures and cardiac filling. Pleural effusions also may be evident in biventricular CHF and especially with pericardial disease or end‐stage CHF complicated by atrial fibrillation.

The diagnosis of right‐sided CHF is usually suspected from physical examination (resting tachycardia, jugular venous distention, abnormal jugular pulses, abdominal distension from hepatomegaly and ascites, and abnormal cardiac auscultation). Confirmation requires identification of cardiomegaly or pericardial effusion by radiography and often with echocardiography (to establish the exact type of heart disease).

Clinical laboratory tests can be contributory in canine patients with heart disease. Elevated blood troponin (cTnI) indicates heart muscle injury and is likely to be high in cases of myocarditis or acute ischemic injury. High circulating BNP (brain natriuretic peptide) or part of the prohormone (NT pro‐BNP) suggests structural heart disease and volume overload, with or without overt CHF. There are emerging data regarding the use of this biomarker for both diagnosis and prognosis in canine heart disease, but the test should not be assessed in isolation (as it might also be high in some dogs with primary respiratory disease, compensated disease, and noncardiac conditions). Serum biochemistries, especially renal function tests and electrolytes, should be evaluated in CHF patients. These can be abnormal owing to pre‐existing disease or drug therapy. Anemia and hyperthyroidism (from excess or inappropriate supplementation) increase demands for cardiac output and should be ruled out in cardiac patients. Thyroid function tests (including free T4 and TSH) are indicated in dogs with inappropriate sinus bradycardia or when serum cholesterol is significantly elevated. A heartworm antigen test should be obtained from dogs living in or arriving from geographic regions endemic for dirofilariasis.

Staging of Canine (Valvular) Disease The ACC/AHA classification of human heart disease (Stages A‐B‐C‐D) has been applied to dogs with chronic valvular heart disease. Treatment approaches can be based on these modified ACC/AHA stages, especially when considering chronic home management of heart disease. Stage A includes dogs at high risk for development of heart disease/failure, but currently without signs of structural disease. Examples include the Doberman pinscher (risk for DCM) and the Cavalier King Charles spaniel (risk for chronic MR). No therapy is indicated, but monitoring by auscultation or other methods (e.g. echocardiography or perhaps biomarkers line NT proBNP) may be appropriate in some cases. Stage B includes dogs with a structural heart abnormality (e.g. murmur of MR or echo findings compatible with “occult” DCM) but never showing signs of heart Acquired Canine Heart Disease (Dr. Bonagura) – Page 4

failure. Subclass B1 includes dogs with a normal‐sized heart and subclass B2 includes dogs with remodeling (cardiomegaly). There is some tendency to consider treatment in dogs in subclass B2 (see below). Stage C includes those dogs with current or previously treated heart failure. Once in stage C, the patient can never return to stage B. Dogs in this stage are prescribed life‐long cardiac therapy. Some Stage D includes dogs with clinical signs of CHF that are refractory to “standard therapy” (defined by a consensus panel as “standard dosages of furosemide, spironolactone, ACE‐inhibitor, and pimobendan”). These dogs require treatment that is more aggressive and may benefit from referral to a cardiologist. Dogs with acute CHF requiring hospital stabilization are somewhat difficult to classify in this system. Following hospital therapy, some dogs that have never received any treatment will stabilize and reside in stage C. Other dogs with long‐standing CHF will clearly fall into Stage D. In staging pre‐clinical (asymptomatic) valvular heart disease, some of the key features relevant to the EPIC clinical trial are: intensity of the systolic murmur of MR; the size of the heart based on vertebral heart scale (score); the size of the left ventricle based on a projected size that is normalized to bodyweight (LVEDDN); clear evidence of MMVD and MR by echocardiography with Doppler; and size of the left atrium relative to the aorta using a short‐axis (Swedish) approach.

Specific entry criteria for EPIC included: Grade 3/6 murmur or louder; VHS >10.5 (note this normal for some dogs!); LVEDDN ≥1.7; and LA/Ao (Swedish) ≥1.6. These criteria and how to evaluate these in canine patients is a focus of this presentation.

After staging, the basic management of heart disease involves the usual drugs previously mentioned, and related to the stage of disease. These drugs are summarized below.

Drugs Used in the Management of Congestive Heart Failure A large number of drugs can alter heart and vascular functions. Some treatments for congestive heart failure (CHF) affect ventricular pumping (inotropes), while others reduce venous pressures and ventricular preload (diuretics and venodilators), improving or preventing CHF. Drugs with arterial vasodilator effects will most likely decrease blood pressure, ventricular afterload, and mitral regurgitant volume, with a consequence of increasing stroke volume from the ventricle.

Some drugs, demonstrate very rapid hemodynamic effects (IV diuretics and inotropes), while others modulate chronically activated neurohormonal or inflammatory mediators of CHF (offering “cardiac protection”). The clinician should be mindful of the clinical pharmacology of these agents and appreciate that many drugs used in veterinary practice are prescribed in an extra‐label manner. For example, all of the antiarrhythmic drugs are human drugs used empirically in an unapproved manner based on current “standards of care”. The following is a summary of “bullet points” related to commonly‐used cardiovascular drugs in dogs.

Diuretics – Furosemide and other diuretics are administered to cardiac patients in hospital for the mobilization of edema fluid, and given chronically to counteract fluid retention. Low doses also may be useful (combined with an angiotensin converting enzyme (ACE) inhibitor for management of cough related to left bronchial compression is stage B2 chronic valvular heart disease. Diuretics should be used with progressive degrees of sodium restriction. Dietary therapy is discussed elsewhere in these proceedings.

Furosemide (2–4 mg/kg IV, IM, SQ, and PO) is a potent loop diuretic that blocks the 2‐chloride transporter and increases urinary losses of chloride, sodium, potassium and water. A relatively Acquired Canine Heart Disease (Dr. Bonagura) – Page 5

high initial furosemide dose (2–4 mg/kg, IV) is administered in cases of severe canine CHF as renal blood flow and drug delivery may be reduced. Once diuresis begins, the dose can be reduced to 2 mg/kg q6–12h, IV, IM, or SQ depending on severity and response. In life‐threatening pulmonary edema, a constant rate infusion of furosemide should be considered (after one or two IV boluses, a constant rate infusion 2 mg/kg/hour can be administered over the next 6 hours until diuresis begins). Oral maintenance dosages of furosemide typically range from 2 to 4 mg/kg two to three times daily but can be increased to 12 mg/kg daily in refractory cases of heart failure; alternatively, intermittent subcutaneous dosing (2 mg/kg) can be helpful (replacing three weekly oral doses with a subcutaneous injection of 2 mg/kg). Torsemide is another alternative substituted at about 1/8 to 1/10 of the furosemide dose. This loop diuretic may have better bioavailability and longer duration of effect.

Spironolactone (2 mg/kg PO daily in one or two divided doses) is a weak, cardioprotective, potassium‐sparring diuretic. It also may normalize baroreceptor function. There is some evidence‐though it is not definitive‐for a survival benefit in canine heart failure. Spironolactone is prescribed as chronic co‐therapy with furosemide for management of CHF. Some also use this drug empirically in preclinical DCM for potential cardioprotection.

When fluid retention becomes refractory (Class D heart failure) other options should be considered. The use of torsemide, another loop diuretic, may be considered at approximately one‐tenth to one‐twelfth of the daily furosemide mg dose (divided into two treatments) for dogs with refractory ascites or edema. It can be combined with or substituted for furosemide. This drug is better absorbed in humans; canine studies are still needed but preliminary reports are encouraging and the drug is approved for canine usage in the UK. Hydrochlorothiazide (HCT) is occasionally used in combination with furosemide for management of refractory fluid retention. This drug blocks the sodium transporter and inhibits sodium, chloride and water reabsorption in the distal tubule and the connecting segment. When used in combination with furosemide, HCT prevents some of the distal sodium reabsorption that escapes the effects of the loop diuretics (sequential nephron blockade). HCT is often formulated with spironolactone (25 mg of each in the 50‐mg tablet). Usual dose is 2‐4 mg/kg of the combined product once daily (or 1‐2 mg/kg of HCT). To prevent rapid volume depletion and electrolyte disturbances, when HCT is added to furosemide, the author recommends administering the drug every other day, starting at the lower end of the dosage range. Profound hypokalemia and hypochloremia can develop with HCT, regardless of treatment with spironolactone or an ACE inhibitor. If renal function and electrolytes remain stable, increase the frequency of dosing to daily if beneficial. The author’s personal preference is for torsemide but other clinicians seem to prefer adding HCT. Adverse effects of diuretics include polydipsia, polyuria, reduction in blood pressure, azotemia, electrolyte depletion, and elevated blood potassium (with spironolactone). Monotherapy will activate the renin‐angiotensin‐aldosterone system so chronic diuretic use should include an ACE‐ inhibitor as part of the treatment plan. Clients should be instructed not to administer the drug at bedtime and should not restrict water except in rare circumstances. Mild azotemia is not a reason to discontinue diuretic therapy, but moderate to severe azotemia should prompt a dosage reduction. Potassium supplements are rarely needed in dogs receiving combined therapy of furosemide, spironolactone, and enalapril as the latter two drugs “spare” potassium, reducing urinary losses.

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Diet & Nutraceuticals – Diuretics therapy is usually discussed in conjunction with control of sodium intake. There is also interest by many clients and veterinarians in holistic treatments with demonstrated cardiovascular effects. There is some evidence supporting the use of sodium‐ restricted diets for reduction of plasma volume and heart size in heart failure. Conceivably this diet would also reduce daily diuretic dosages. Restriction of salt must be balanced with issues of palatability and protein/caloric intake, which can be insufficient in dogs with CHF and cardiac cachexia. Rigid sodium restriction is generally considered about 12 mg sodium/kg bodyweight/day, but this is rarely achieved. Freeman has recommended moderate restriction of 50 to 80 mg sodium/100 kcal of dietary energy as a starting point for dogs. Both prescription diets (Cardiac Support diet, h/d – Heart Diet, and CV Diet) and over the counter senior diets restrict sodium to varying degrees. Perhaps as important as a special diet is simple avoidance of high‐ sodium treats (processed meats, hot dogs, sausages, some cheeses, etc.) that clients may use to entice pill taking. Lower sodium treats can be identified including carrots, apple slices, and a number of dog biscuits (read the labels).

A number of potential nutraceuticals have been discussed for the cardiac patient, but in terms of evidence, only the use of fish oils (omega‐3 fatty acids like EPA at 40 mg/kg/day and DHA at 25 mg/kg/day) have been shown to help prevent cardiac cachexia in dogs. L‐arginine supplementation (starting at 250 to 500 mg PO three times daily) is used by the author when severe PH is documented and a PDE‐5 inhibitor like sildenafil has been prescribed (this amino acid is the precursor of nitric oxide, the endothelial vasodilator maintained in an active state by phosphodiesterase‐V inhibitors).

Other supplements have minimal to no evidence for their use, except in very specific situations.

These nutraceuticals also can be very costly! Among this group are the supplements L‐carnitine (50 to 100 mg/kg every 8 hours) and taurine (500 to 1000 mg daily). L‐carnitine is considered for some boxers with DCM, as a familial deficiency may be present. Taurine is considered for treating dogs eating exclusive lamb‐rice diets, restricted‐protein (vegan) diets, some grain‐free diets, or “off‐brand” diets; it is also considered in spaniel breeds, golden retrievers, and Newfoundland dogs with DCM. While there is hypothetical value to coenzyme Q10 supplementation, there is no evidence this costly compound should be used.

Angiotensin Converting‐Enzyme Inhibitors & Other Vasodilators – The ACE‐inhibitors and vasodilators are mainstays of CHF therapy although their efficacy has been challenged in MMVD and there are insufficient data regarding the direct vasodilator drugs. Venodilation pools blood in systemic veins and reduces venous pressures, while arterial dilation reduces arterial blood pressure (BP) and ventricular afterload. Mitral regurgitation is usually reduced by lowering diastolic blood pressure, a potential benefit of ACE‐inhibitors and especially more potent arterial vasodilators such as amlodipine or hydralazine. The ACE‐inhibitors are widely used in treatment of mild systemic hypertension, somewhat controversially for advanced (stage B2) preclinical mitral valve disease, and as a standard of care for management of CHF. The ACE‐Inhibitors, including benazepril, enalapril, and ramipril, inhibit the renin‐angiotensin‐ aldosterone system by blocking the converting enzyme (a kininase) leading to decreased plasma angiotensin‐II and delayed degradation of vasodilating kinins. Reducing serum aldosterone concentration limits sodium retention and potassium loss in the urine. Additionally, ACE‐ inhibitors protect cardiac muscle, renal tissues, and blood vessels from RAAS induced injury while Acquired Canine Heart Disease (Dr. Bonagura) – Page 7

down regulating the sympathetic nervous system. Vasodilation is not as abrupt as with direct‐ acting drugs and overall is very modest when compared to agents such as the calcium channel blockers, especially when treating high BP. The usual dosage of enalapril and benazepril in North America is 0.25 mg/kg twice daily; the dose is often increased to 0.5 mg/kg twice daily at the time of first reevaluation if BP and renal function are acceptable.

Different direct acting vasodilators used for acute, life‐threatening pulmonary edema. These include hydralazine (an arterial dilator) and the nitrovasodilators. Topical 2% nitroglycerine ointment (15 mg/inch; dosed between ¼ to one inch topically, q12h for 24 to 48h), and sodium nitroprusside (infused at 0.5 to 5.0 micrograms/kg/minute IV to achieve the systolic BP to approximately 85–90 mm Hg) are hospital treatments used in acute CHF. Nitroprusside is also a potential treatment for severe systemic hypertension in dogs. Evidence for benefit of nitrates in managing acute CHF is lacking, but nitroglycerine ointment is commonly used in part due to simple application and theoretical benefits. Many cardiologists view sodium nitroprusside as a life‐saving drug for dogs, especially when there is fulminating pulmonary edema from ruptured chordae tendineae; however, recent cost increases have made the drug challenging to use.

Hydralazine is not often used but can be an effective arterial vasodilator in acute situations, reducing LV afterload and the volume of mitral regurgitation. Chronic use activates the RAAS. The phosphodiesterase‐5 inhibitors such as sildenafil (Viagra®, usual dose: 1–3 mg/kg PO q12h but as often as q8h) and related compounds like tadalafil are reserved for treatment of severe, symptomatic pulmonary hypertension. These drugs demonstrate relatively selective pulmonary arterial vasodilation and thereby lower pulmonary vascular resistance to blood flow. Some dogs respond significantly to this therapy with a reduction in collapsing or syncopal attacks and improved exercise capacity.

The dihydropyridine calcium channel blockers such as amlodipine are used mainly for control of systemic hypertension (where amlodipine is the drug of choice). Another use is as a load reducer in end‐stage Class D, left‐sided CHF. The initial dose of amlodipine for CHF patients is 0.05–0.1 mg/kg PO q12h; however, much higher doses (usually 0.2 to 0.4 mg/kg PO q12 to 24h) are needed to treat most dogs with systemic hypertension. The drug has a long elimination half‐ life (about a day), so it may take a number of days before dosage changes are manifest.

The main adverse effects of vasodilator drugs are systemic hypotension (causing weakness or lethargy) and impairment of renal function. Some drugs, including amlodipine and hydralazine (1–3 mg/kg PO q12h), cause reflex neurohormonal activation and potentially sinus tachycardia.

Hyperkalemia is a risk with the ACE‐inhibitors, especially when combined with spironolactone (mild Hyperkalemia is ignored). Amlodipine can cause severe generalized edema in dogs; this rare but reversible side effect should be appreciated.

Inotropic Drugs – The positive inotropic drugs include catecholamines (dobutamine, dopamine), the glycoside digoxin, and the inodilator pimobendan (Vetmedin®).

Catecholamines are used only in the hospital setting. Dobutamine (2.5–20 micrograms/kg/minute constant rate infusion) is reserved for dogs with cardiogenic shock (defined clinically as CHF accompanied by systolic BP <80 mm Hg + hypothermia + impaired peripheral perfusion + elevated blood lactate). Dobutamine is infused for 24 to 48 hours and is often an effective bridge to oral medications. The dose is titrated to effect with adjustments made every 15 to 30 minutes until the cardiovascular status is more stable. Tachycardia and Acquired Canine Heart Disease (Dr. Bonagura) – Page 8

ectopic complexes are signs of overdose. Weaning can usually be accomplished by cutting the dose in ½ every 2 to 4 hours and measuring BP to insure it can be maintained.

Digoxin (0.005–0.0075 mg/kg PO q12h in dogs with normal renal function) is a modest positive inotropic drug that also slows heart rate by sensitizing baroreceptor function and altering autonomic neural tone to the CV system. The main indications for digoxin today are refractory CHF or CHF with AF. In the latter situation, the drug’s vagal‐stimulating effect helps to slow AV nodal conduction and heart rate. Contraindications to use include complex ventricular arrhythmias, bradyarrhythmia, and moderate to severe renal dysfunction. The adverse effects of digoxin – anorexia, vomiting, diarrhea, depression, and cardiac arrhythmias (sinus node and AV nodal depression; PVCs) – are best avoided by monitoring therapy with a serum digoxin level.

Pimobendan or Vetmedin® (0.2–0.3 mg/kg PO q12h) is a potent, orally administered inotropic drug with vasodilator properties. It is classified as a calcium sensitizer with phosphodiesterase‐3 (and possibly PDE‐5) inhibitory properties. Pimobendan is useful in both acute and chronic heart failure of dogs as shown in a number of studies and reports, including the QUEST trial. When used chronically it is combined with furosemide, an ACE‐inhibitor (at least in the USA), and spironolactone; this represents the current standard of care for management of chronic CHF due to chronic valvular disease or cardiomyopathy based on an ACVIM consensus panel. Another indication based on recent study is for delaying heart failure in dogs (in particular, the Doberman pinscher) with well‐defined, preclinical dilated cardiomyopathy (PROTECT trial). The value of this drug in advanced but preclinical mitral disease has recently been reported in the EPIC trial and (when compared to placebo) it delayed on the onset of CHF in small breed dogs with asymptomatic mitral valve disease by approximately 15 months. Adverse effects are uncommon.

Extralabel usage three times daily may be considered for end‐stage heart failure (Stage D).

Beta‐adrenergic Blockers – The beta‐blockers, particularly carvedilol (0.1 to 0.6 mg/kg q12h PO), metoprolol (long acting), bisoprolol, and atenolol (0.25 to 1 mg/kg q12h PO) are sometimes prescribed to protect the heart muscle. The hope is that with chronic use, myocardium at risk will be protected from neurohormonal assault and demand ischemia; heart rate will be controlled; and LV ejection fraction will improve (as observed in human patients). In canine model studies, beta‐blockers are cardioprotective, but this effect has not been proven in preliminary clinical studies of dogs with DCM or chronic mitral regurgitation. Dogs with advanced heart disease but not yet in CHF (e.g. “occult” or preclinical DCM) tolerate beta‐blockade reasonably well.

Importantly, while beta‐blockers are prescribed empirically by many cardiologists for treatment of preclinical dilated cardiomyopathy, for cardioprotection in canine aortic and canine pulmonic stenosis, and as anti‐arrhythmic drugs for a variety of rhythm disturbances, unlike the case in humans, these agents are not considered a standard of care for chronic CHF in dogs.

The dog with normal ventricular function and a healthy conduction system can generally tolerate high dosages of beta‐blockers with little apparent difficulties. However, beta‐blockers should never be used in uncontrolled CHF (i.e., never to a “wet patient”), and gradual dose up‐ titration is most appropriate when prescribed to dogs with systolic ventricular dysfunction or following stabilization of CHF. Concurrent use of pimobendan seems to offset some of the negative inotropic effects of beta‐blockers in dogs with heart failure. Anticipated adverse effects of these drugs include weakness, hypotension, bradycardia, and worsening of edema or effusions.

Acquired Canine Heart Disease (Dr. Bonagura) – Page 9

Antiarrhythmic Drugs – In atrial fibrillation (AF) heart rate control is usually gained by the combination of digoxin plus the calcium channel blocker diltiazem (starting dose of 0.5 mg/kg PO q8h uptitrated every 8 hours to as high as 2.5 mg/kg PO q8h for standard diltiazem; an alternative is long‐acting diltiazem at a dosage range of ~1.0 to 4 mg/kg q12h). Hypotension and bradycardia are adverse effects of over‐dosage. Target in‐hospital heart rate response for dogs with AF is about 120–160/minute, and an ambulatory ECG (Holter) monitoring can be done to assess rate control. A hospital rate of <150/minute is a good target.

Treatment of severe ventricular arrhythmias in the setting of CHF is difficult because most drugs depress ventricular function and represent yet another “pill” for clients to administer. IV lidocaine (2–4 mg/kg IV boluses to 8 mg/kg; 50 microgram/kg/minute constant rate infusion) can be used in the hospital in dogs with rapid or dangerous‐morphology ventricular. While useful for short‐term treatment only, it does not significantly depress heart function or heart rate. A related compound, mexiletine (5–8 mg/kg PO q8h) may be effective chronically if adverse effects are not an issue and the client can tolerate t.i.d. dosing. Side effects of both drugs include anorexia, vomiting, tremors, and seizures.

The class 3 (potassium‐channel blocking) antiarrhythmic drug sotalol (1–2 mg/kg PO q12h) is generally effective well tolerated, but since this drug exhibits beta‐blocking properties as well it can depress heart rate and myocardial contractility and is therefore best avoided in CHF until heart failure has been stabilized. It can then be used cautiously.

The sodium channel blocker flecainide has not been studied sufficiently in dogs and is more likely to be proarrhythmic, worsening ventricular ectopy, in the setting of a failing heart.

Ventricular dysfunction is considered a relative to absolute contraindication for this Class IC drug.

Amiodarone is a complex drug that is sometimes used for rhythm control after electrical or drug‐induced cardioversion of AF. It also can be used for suppression of malignant ventricular arrhythmias and may be highly effective (dose: 8 to 10 mg/kg PO once daily for one to two weeks; thereafter 4–6 mg/kg PO once daily). However, owing to liver toxicity, liver enzymes/function tests (as well as thyroid function and a CBC) must be followed. Dogs who become ill from amiodarone may take days to recover owing to the very long elimination half‐life.

Therapy of Canine Heart Disease & Heart Failure Early introduction of CV drug therapy in “preclinical” or “asymptomatic” dogs with heart disease has always been controversial. There is a greater tendency to treat dogs with echo‐evidence of dilated cardiomyopathy or dogs with chronic valvular heart disease with severe remodeling, but these therapies should be guided by clinical trials, not simply theoretical benefits.

Cardioprotective drugs might be useful, but require more detailed study; currently their use is considered reasonable but empirical. However, as shown in two recent trials (PROTECT in Doberman pinschers and EPIC in small breed dogs with chronic mitral valve disease) the early use of pimobendan (Vetmedin®) has shown clear benefit in delaying CHF and prolonging life in dogs meeting the specific entry criteria for the study.

There is some evidence that early “cardioprotective” therapy is of value to dogs with well defined, preclinical (“occult”) DCM (note: Large breed dogs with chronic mitral regurgitation and demonstrable cardiomegaly or LV dysfunction are treated as if they have occult DCM.). In these cases, an ACE‐inhibitor such as enalapril or benazepril is initiated at 0.25 mg/kg b.i.d. and then increased to 0.5 mg/kg b.i.d. after two weeks. When cost‐effective (e.g., generic) the addition of Acquired Canine Heart Disease (Dr. Bonagura) – Page 10

spironolactone (2 mg/kg/daily in one or two divided doses) is also appropriate for cardiac muscle protection. Consideration also should be given to the use of a beta‐blocker considering these are likely to be well tolerated at this time. The use of digoxin is not recommended in this setting unless there is atrial fibrillation. In the USA, pimobendan labeled for CHF and is therefore tends to be withheld until radiographs indicate that pulmonary edema is imminent or careful observations suggest there is demonstrable exercise intolerance due to “preclinical” DCM. However, most cardiologists initiate pimobendan if LV systolic dysfunction is moderate to severely reduced based on multiple variable measurements. Additionally, introduction of pimobendan in stage B2 DCM (an echocardiographic diagnosis) is a definite consideration in light of the PROTECT clinical trial that showed benefit in delaying CHF in the Doberman pinscher with occult DCM. This study compared pimobendan to placebo treatment of preclinical DCM and demonstrated a substantial improvement in both cardiac and all‐cause mortality with pimobendan. The median time to the primary endpoint (CHF or sudden cardiac death) was 718 days (interquartile range of 441‐1152 days) for dogs treated with pimobendan versus 441 days (IQR of 151‐641 days) for dogs treated with the placebo (so about a 9‐month delay with pimobendan compared to placebo). Although the study was small, it was well designed and controlled. Importantly, as a group, ventricular ectopy did not seem to increase in the pimobendan treated dogs (based on 24h ECG) although some individual dogs did worsen in the raw data plots. This certainly recommends the use of pimobendan in this breed with clear evidence of pre‐clinical DCM is evident based on echocardiographic findings. The major question is whether the study results can be generalized to other breeds with occult DCM. This is attempting to be addressed using a (retrospective) case‐control study (SHIELD) and it will be interesting to see those results. The critical issue will be if the “case‐controls” are sufficient to provide pivotal evidence for using pimobendan in preclinical DCM of other breeds.

Unfortunately, in PROTECT any benefits of potentially cardioprotective treatments (ACEI, beta‐ blockers, or spironolactone) along with pimobendan were not investigated.

In contrast to DCM, studies of chronic degenerative valvular heart disease in dogs have failed to show clear benefit of ACE‐inhibition for this group and certainly no therapy can be justified for dogs in subclass B1 (MR without any remodeling). In dogs in subclass B2 (i.e. significant remodeling) an ACE‐inhibitor can be considered for empirical use to delay development of CHF based on the “trend” for benefit –albeit a modest effect size – in the VETPROOF trial (this is the author’s personal approach). Others are not compelled by the evidence for introducing ACE‐ inhibition and offer no therapy until there are clinical signs of heart failure (issues to be presented in the lecture). Certainly in this group of patients, there might be other indications for considering an ACE‐inhibitor prior to CHF, including dogs with cough from left bronchial compression or dogs with other medical disorders (systemic hypertension, chronic kidney disease). In the author’s practice, an ACE‐inhibitor is also initiated once a dog reaches the “EPIC‐criteria” discussed below.

The EPIC trial of CHF prevention in dogs with degenerative valvular disease was recently ended prematurely due to efficacy. The entry criteria were presented earlier in notes, and when dogs with chronic MR achieve these criteria (in terms of cardiac remodeling), pimobendan (Vetmedin) is initiated as a therapy to prevent the development of CHF. The results of the EPIC study showed the “median time to primary endpoint was 1228 days (95% CI: 856‐NA) in the pimobendan group and 766 days (95% CI: 667‐875) in the placebo group (P = .0038). Hazard ratio for the pimobendan group was 0.64 (95% CI: 0.47‐0.87) compared with the placebo group. The Acquired Canine Heart Disease (Dr. Bonagura) – Page 11

benefit persisted after adjustment for other variables. Adverse events were not different between treatment groups. Dogs in the pimobendan group lived longer (median survival time was 1059 days (95% CI: 952‐NA) in the pimobendan group and 902 days (95% CI: 747‐1061) in the placebo group) (P = .012).” In bottom line terms, the initiation of pimobendan therapy in dogs fulfilling the EPIC criteria delayed the onset of CHF by nearly 15 months, on average”. There was a trend towards more sudden cardiac deaths in the pimobendan group, but the overall number in both groups was small, and this risk is probably overshadowed by the benefits on delaying CHF and all‐cause mortality. In our practice, we also initiate enalapril (or benazepril) therapy with pimobendan. When an echocardiogram cannot be performed, six‐monthly interval evaluations are recommended for radiography. In these cases, an absolute VHS of 11.5 or a “VHS velocity” of 0.5 VBs per 6 months (or 1 VB per year) represents (to the author and to some other cardiologists) sufficient evidence to initiate pimobendan and an ACE‐inhibitor.

Managing Initial Clinical Signs In Mitral Valve Disease The transition between stage B2 and C can be difficult to discern even with a full workup. The onset of clinical signs in dogs with advanced valvular endocardiosis is often very gradual and usually heralded by intermittent coughing. While this can indicate pulmonary edema and CHF (Stage C), the lungs may be very clear radiographically and the coughing caused by compression of the left mainstem bronchus (between the descending aorta and dorsal left atrium). This feature of chronic MR in dogs is not synonymous with left‐sided CHF, but can be difficult to distinguish from signs of pulmonary edema. The author’s approach to management of these dogs is initial treatment with enalapril or benazepril (0.25 mg/kg q12h for two weeks then 0.5 mg/kg q12h thereafter) along with low‐dose furosemide (1‐2 mg/kg PO once daily). In most cases, the cough improves if it’s due to bronchial compression (or early CHF – it CAN be hard to tell!). If the cough returns weeks to months later or if respiratory rate increases at home (>40/min), radiographs are repeated and often full CHF therapy is initiated (see below). Pimobendan is also added if the patient fulfills EPIC criteria (see above).

It should be emphasized that failure of the cough to respond to a low dose of a diuretic and full dose of an ACE‐inhibitor (+/‐ pimobendan) should prompt reconsideration of the diagnosis; in particular, the clinician should rule out chronic bronchitis, bronchomalacia, other airway diseases (laryngeal disease, tracheal collapse), and pulmonary parenchymal disorders (pneumonia, neoplasia, heartworm disease, etc.). These patients are ideally evaluated by radiography and fluoroscopy (consider obtaining a second opinion on the chest films) and by appropriate respiratory diagnostics (such as bronchoscopy with airway cytology/culture). When diagnostic testing is limited, a trial course of doxycycline or prednisone may be instructive (and relieve signs related to infection or bronchitis). Cough suppressants can be prescribed as a last resort for symptom relief.

Acute Pulmonary Edema from Left‐Sided CHF The combination of furosemide, oxygen, nitroglycerine (or sodium nitroprusside) & sedation with butorphanol (0.25 mg/kg IM, repeated in 30 to 60 minutes if needed) closely followed by oral administration of pimobendan (0.25 to 0.3 mg/kg q12h) represents the initial treatment plan applicable to most cases of CHF regardless of cause. This can be remembered by the mnemonic “SO FINE”, for Sedation, Oxygen, Furosemide, Inotropic support (pimobendan), Nitroglycerine, Acquired Canine Heart Disease (Dr. Bonagura) – Page 12

and Extra treatments. With this protocol, diuresis is initiated; oxygen saturation is increased; ventricular loading is reduced; the tendency towards pulmonary edema is decreased; anxiety is relieved; myocardial contractility is supported, and ventricular load is reduced. If patients are heavily sedated, the torso is positioned in sternal recumbency, the chin supported with a towel or soft pad, and nasal oxygen prongs are inserted for better oxygenation. After an initial IV or IM bolus of 2 to 4 mg/kg, the dosage, route, and frequency of furosemide can be adjusted to the clinical response (respiratory rate, anxiety, auscultation). In life‐threatening pulmonary edema due to mitral disease, a constant rate infusion of furosemide along with aggressive afterload reduction with sodium nitroprusside should also be considered. Less‐potent and less controllable alternatives to sodium nitroprusside include oral hydralazine or an ACE‐inhibitor. The inodilator pimobendan is generally considered a drug for chronic CHF in dogs, but it also exhibits effects acutely and is therefore helpful in the acute treatment of heart failure. This drug functions as a preload and afterload reducer as well as a potent inotrope and can be started as soon as the dog is capable of swallowing, typically within an hour of starting other treatments.

Cardiogenic Shock The findings of cardiogenic pulmonary edema or pleural effusion with severe hypotension (BP <80 mm Hg), along with other indicators of low cardiac output (pallor, hypothermia, depression, elevated blood lactate) are highly suggestive of cardiogenic shock. Dogs with dilated cardiomyopathy (often Doberman pinschers) represent the typical case of cardiogenic shock.

Other potential causes of cardiogenic shock include myocardial infarction and massive pulmonary embolus as might occur following treatment for adult heartworms or after a spontaneous pulmonary embolism. Initial treatment is the same as discussed above with Furosemide‐Oxygen‐Nitrate‐Pimobendan. As these patients are hypotensive and often very depressed, sedation is rarely needed and diuretics alone can further lower BP; therefore, more aggressive hospital therapy is needed. The clinician should determine if centesis is necessary, as dogs with cardiogenic shock can have both pulmonary edema and large cavity effusions.

Generally, volume infusion (i.e. fluid therapy) is not appropriate to raise BP in this setting, as it will only worsen edema. In most cases, there is a need to stimulate myocardial contractility to improve pump function and facilitate diuresis. Dobutamine (or dopamine) is administered as a constant rate intravenous infusion, starting at 2.5 micrograms/kg per minute and increasing the infusion by 1‐2 micrograms/kg/minute every 15 to 30 minutes until systolic BP is 90 mm Hg. This end‐point is generally reached at an infusion of 5–10 micrograms/kg/minute, though higher infusion rates may be needed. Once the BP is stable (systolic BP in the 90 to 100 mm Hg range).

Otherwise, the approach to the patient with cardiogenic shock, aside from the addition of a catecholamine, is similar to that discussed in the previous section. The main difference is the requirement to address BP and tissue perfusion aggressively and to avoid drugs that depress BP until it is supported by a catecholamine. After 24 to 48 hours of dobutamine therapy, the dobutamine rate is reduced by 50% every 2–4 hours, and once the dose has been lowered to ~1.25 micrograms/kg for 2‐4 hours, the infusion is discontinued. By that time, the dog should be taking oral drugs for CHF.

Acquired Canine Heart Disease (Dr. Bonagura) – Page 13

Arrhythmias in Acute CHF Drugs used for management of heart rhythm disturbances were summarized previously. Atrial fibrillation can precipitate CHF in previously stable canine patients. This problem is usually managed with heart rate control as opposed to cardioversion (to normal rhythm). Rate control involves initiation of oral digoxin followed within 24 hours by up‐titration of oral diltiazem.

Diltiazem is titrated to a hospital heart rate of 120 to 160/min and is optimally evaluated later by a 24‐hour (Holter) ECG. Effective treatment of CHF is also useful as it allows for some withdrawal of sympathetic tone with reduction of ventricular rate response. Electrical cardioversion from AF to sinus rhythm has been used by some in managing this arrhythmia, but our experience is that dogs in CHF usually revert to AF in short time, so we mainly recommend rate control in our practice. Isolated premature ventricular complexes (PVCs) are not treated in CHF cases. However, sustained runs of rapid ventricular tachycardia require treatment to maintain BP; these are managed with boluses of lidocaine followed by a constant rate infusion of lidocaine. As previously discussed, mexiletine, low‐dose sotalol, flecainide, and amiodarone are all potentially useful for suppression of life‐threatening ventricular tachycardia but each drug carries serious adverse effects.

Chronic Home Management of CHF (Stages C & D) The transition from hospital to home therapy of CHF usually begins within 48 hours of admission.

During that interval, the initial diagnostic workup should have been completed. The typical transition to “Home Therapy” includes the following steps: 1) parenteral furosemide is replaced with oral furosemide; 2) oxygen is discontinued; 3) nitrates (if used) are replaced by an ACE‐ inhibitor; 4) pimobendan is continued (digoxin is used only for rate control in AF); 5) spironolactone is initiated mainly for cardioprotection at release or at the time of first follow‐up; and 6) the client is counseled regarding a sodium‐restricted diet and pros/cons of nutraceuticals.

These specific uses of these drugs (as well as dosages) have been summarized above in Part 2 of “Acquired Valvular Heart Disease in the Dog.”

Long‐term Home Therapy The basic home treatment of chronic CHF in the dog with Stage C heart disease involves “Dogs Are For Special People” therapy: Dietary sodium restriction, an ACE‐inhibitor, Furosemide, Spironolactone, and Pimobendan. As previously stated, it can be very difficult to initiate therapy with beta‐blockers due to their negative effect on contractility and there is a lack of clinical evidence to support this treatment. Additional therapy may be added for special problems as a dog progresses from stage C to stage D. In cases of severe PH with symptoms such as exertional collapse or ascites, sildenafil is considered as a relatively selective pulmonary vascular vasodilator to unload the right ventricle. Arrhythmias have been discussed previously; again, if AF complicates CHF, both digoxin and diltiazem are added to gain better heart rate control. Isolated premature ventricular complexes (PVCs, VPCs) and nonsustained runs of VT are not treated, unless the QRS morphology or timing appear “dangerous” (such as R on T; very rapid; multiform VT; or torsade de pointes): In reality, most clients are willing to assume a risk of sudden death for their dog (and most hope that will occur instead of intractable CHF or euthanasia). Sustained ventricular arrhythmias – especially when causing signs – are managed with mexiletine, amiodarone, flecainide, or sotalol.

Acquired Canine Heart Disease (Dr. Bonagura) – Page 14

Stage D Heart Failure Strategies for managing refractory edema or ascites (Stage D) include first reviewing client compliance and optimizing the dosages of currently prescribed drugs. Pimobendan (Vetmedin®) dosage is generally increased to 0.25 ‐0.3 mg/kg PO q8h (extra‐label). Client administration of subcutaneous furosemide is suggested (begin by substituting one oral dose of furosemide for a subcutaneous injection, three times weekly then go to every other day if necessary).

Alternatively, torsemide can be substituted for furosemide or a low dose of hydrochlorothiazide can be started (1‐2 mg/kg daily or every other day) with monitoring of serum biochemistries within a week (or earlier). The author prefers torsemide and doses this drug at approximately 1/8 to 1/10 of the furosemide daily dose. For example, if the dog received 50 mg of furosemide daily, the torsemide dose would be ½ of a 5 mg tablet, PO, twice daily. Abdominal paracentesis should be considered to reduce tense ascites. Sildenafil (Viagra®) plus L‐arginine supplementation is offered when severe PH is documented by echocardiography.

Follow up evaluations Rechecks for dogs with chronic CHF are scheduled initially at 7‐14 days after release, then one month later, then every 3 to 4 months if possible. Drug dosing and adverse effects of treatments are discussed with the client at all stages of therapy. Emphasis for effective treatment is on quality of life (eating well, sleeping comfortably, capacity for walking/mobility, family interaction, resting respiratory rate, and clinical signs of disease or drug toxicity). Additional examinations of importance include physical examination findings of controlled CHF; bodyweight/cachexia; BP; renal function; heart rhythm; and thoracic radiography if respiratory symptoms are still present.

Prognosis The prognosis is a key client question and it is very difficult to predict the outcome for a single canine patient. The general prognosis for canine heart disease and CHF in particular depends on the cause, severity, and care received. Many dogs survive > 1 year following the first signs of CHF provided they receive optimal veterinary and home care. It may take weeks to obtain complete stabilization of the seriously‐ill dog with CHF. Clients should understand that not every dog will be well overnight, and regrettably, some clients run out of patience or financial resources and request euthanasia. As patients become well managed, other problems might become evident.

Some dogs with chronic left‐sided CHF appear to develop pulmonary fibrosis at an accelerated rate. This comorbidity should not be misdiagnosed as uncontrolled CHF; the usual findings are tachypnea + crackles + “clear lung fields” radiographically. Dogs with chronic airway disease (tracheal or primary bronchus collapse, chronic bronchitis) may become symptomatic due to these diseases requiring other treatments for control (doxycycline, prednisone, cough suppressants). Development of chronic renal failure with moderate azotemia is a poor prognosis, especially if diuretic dosages cannot be reduced due to fluid accumulation. A number of small studies have evaluated biomarkers (especially NT‐pBNP) in dogs with CHF in terms of prognostic considerations. Clearly, there is a statistical trend to higher levels to indicate a worse prognosis and that failure of natriuretic peptides to decrease with therapy is a poor prognostic sign. Specific guidelines for modifying therapy based on natriuretic peptides still need to be developed.

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References Atkins C, Bonagura J, Ettinger S, Fox F, Gordon S, Haggstrom J, et al: ACVIM Consensus Statement: Guidelines for the Diagnosis and Treatment of Canine Chronic Valvular Heart Disease. J Vet Internal Med 2009; 23:1142‐1150.

Bonagura JD, Keene BW: Drugs for Canine Heart Failure. In In Bonagura & Twedt (eds): Current Veterinary Therapy XV, Philadelphia, WB Saunders/Elsevier, 2013 Borgarelli M, Haggstrom J. Canine Degenerative Myxomatous Mitral Valve Disease: Natural History, Clinical Presentation and Therapy. Vet Clin North Am (Small Anim Pract), 2010 40(4):651‐663.

Boswood A, Häggström J, Gordon SG, Wess G, Stepien RL, Oyama MA, Keene BW, Bonagura J, MacDonald KA, Patteson M, Smith S, Fox PR, Sanderson K, Woolley R, Szatmári V, Menaut P, Church WM, O'Sullivan ML, Jaudon JP, Kresken JG, Rush J, Barrett KA, Rosenthal SL, Saunders AB, Ljungvall I, Deinert M, Bomassi E, Estrada AH, Fernandez Del Palacio MJ, Moise NS, Abbott JA, Fujii Y, Spier A, Luethy MW, Santilli RA, Uechi M, Tidholm A, Watson P: Effect of Pimobendan in Dogs with Preclinical Myxomatous Mitral Valve Disease and Cardiomegaly: The EPIC Study‐A Randomized Clinical Trial. J Vet Intern Med. 2016 Nov;30(6):1765‐1779. doi: 10.1111/jvim.14586 Häggström J, Boswood A, O'Grady M, et al.: Longitudinal Analysis of Quality of Life, Clinical, Radiographic, Echocardiographic, and Laboratory Variables in Dogs with Myxomatous Mitral Valve Disease Receiving Pimobendan or Benazepril: The QUEST Study. J Vet Intern Med. 2013 Sep 6. doi: 10.1111/jvim.12181.

Keene BW, Bonagura JD: Management of Heart Failure in Dogs. In Bonagura & Twedt (eds): Current Veterinary Therapy XV, Philadelphia, WB Saunders/Elsevier, 2013

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

Cardiac Arrhythmias in Veterinary Medicine Reference Notes

John D Bonagura DVM, MS, DACVIM (Cardiology, Internal Medicine) Professor, Veterinary Clinical Sciences, The Ohio State University

Heart rhythm disturbances (arrhythmias, dysrhythmias) can be classified based on the ventricular heart rate (normal, bradyarrhythmia, tachyarrhythmia); anatomic origin of the rhythm disturbance (sinoatrial node, atria, atrioventricular, or ventricular); or electrophysiologic mechanism, if evident. An overview of electrophysiologic mechanisms of arrhythmias is presented in class. These include abnormalities of impulse formation (enhanced automaticity, triggered activity) and various abnormalities of impulse conduction (including major conduction blocks such as atrioventricular (AV) block and right and left bundle branch blocks; “macro‐retry” as with atrial flutter; disordered re‐entry as with myocardial fibrillation; and other forms of re‐ entry around a focal zone of myocardial disease.) Detailed models of arrhythmogenesis represent a major focus of research, but are beyond the scope of this course.

DIAGNOSIS Keys to recognizing and diagnosing cardiac arrhythmias include an analysis of the atrial and the ventricular rates, regularity of the rhythm, identification of any patterns in irregular rhythms, P to QRS relationship, atrial waveform morphology (e.g. different than sinus node; flutter or fibrillation waves); morphology of the QRS complex (supraventricular or ventricular origin); and conduction intervals (especially duration of PR interval and duration of QRS complex). In terms of a methodological approach to rhythm diagnosis, it is recommended that one consider analysis of the ECG (EKG) as follows: 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; 3) Identify regularity or lack thereof and search for repetitive patterns in irregular rhythms; 4) Identify P and QRS complexes and the relationship between these waveforms (P‐R intervals and the distance between the QRS and following P‐waves (R‐P) 5) Scrutinize morphology and consistency of the P‐waves, QRS complexes, and T‐waves; 6) Consider the conduction intervals across the atria (P‐wave duration), atrioventricular

conduction system (P‐R interval), ventricles (QRS duration), and repolarization (Q‐T) 7) Estimate the frontal axis and analyze the amplitude and terminal orientation of the QRS; 8) Evaluate the QRS morphology for conduction disturbances, obvious bundle branch or fascicular block patterns, and for changes typical of cardiomegaly; 9) Assess the ST segment and T‐wave (ST‐T) for repolarization abnormalities; and 10) Interpret the ECG with consideration of the entire clinical and laboratory picture.

These are simply guidelines, but can assist with a methodical ECG analysis.

The main clinical concerns about cardiac arrhythmias are hemodynamic effects such as reduced blood pressure (BP) and tissue perfusion and the promotion of further electrical instability leading to myocardial fibrillation. Bradyarrhythmias, as third‐degree atrioventricular (AV) block, can reduce cardiac output by decreasing heart rate. Supraventricular tachyarrhythmias encroach on the diastolic filling periods, reducing preload and stroke volume.

In the case of atrial fibrillation (AF), atrial contribution to ventricular filling is also lost, further impairing filling. Many ventricular arrhythmias are well‐tolerated, but in other patients cause John D Bonagura, DVM, DACVIM – Introduction to Cardiac Arrhythmias – Page 1

hypotension from reduced diastolic filling time, loss of normal atrioventricular coordination, and decreased mechanical synchrony between the two ventricles (due to abnormal current spread).

Additionally, a relentless tachycardia can lead to a tachycardia‐induced cardiomyopathy, a type of dilated cardiomyopathy that is reversible with cessation of the arrhythmia. Ventricular ectopy also predisposes to ventricular fibrillation (disorganized electrical activity with loss of mechanical function of the ventricles). This is a cause of sudden death in some animals.

SINUS RHYTHMS Sinus rhythms are those in which the electrical impulse originates in the cells of the SA node, the normal “pacemaker” of the heart. These rhythms are characterized by a P‐QRS‐T relationship.

The P‐waves are normal in morphology (positive in lead II; positive and notched in the base‐apex lead of horses and cattle); there is an appropriate P‐R interval indicating atrial and ventricular activities are related; and the QRS occurs once the impulse conducts from the internodal pathways through the AV node, the His‐Purkinje system, and finally enters the ventricular myocardium.

Physiologic sinus rhythms during routine exam include normal sinus rhythm (NSR) and sinus arrhythmia. Normal sinus rhythm is characterized by a normal heart rate, regular rhythm (varying by <10% between cycles), and consistent P‐QRS relationship. Sinus arrhythmia is due to variation in vagal input to the sinus node and is most often observed in dogs, horses and some camelids.

The sinus node discharge rate cyclically slows and speeds and the QRS‐T complexes follow suit; thus, the overall ventricular rate is normal but the instantaneous heart rate (i.e., between consecutive R‐waves) varies by >10%. In dogs, sinus arrhythmia is most often associated with ventilation and termed respiratory sinus arrhythmia. Spillover of inhibitory input as the lungs stretch at end‐inspiration somehow influences vagal output to the sinus node, leading to slowing of heart rate during expiration. As respiratory inhibition decreases during expiration, the vagal input to the sinus node also starts to decline and the heart rate speeds up again. This repeats in a cyclical pattern and can be thought of to lag slightly behind the respiratory cycle (i.e. at end‐ inspiration the sinus node starts to slow down; at end‐expiration the sinus node starts to speed up). Dogs with respiratory disease often show pronounced sinus arrhythmia as do some other conditions associated with high vagal tone (such as some gastrointestinal disorders). In horses, sinus arrhythmia – as with physiologic second‐degree AV block – is often associated with blood pressure regulation and likely reflects varying vagal influence associated with the baroreceptor reflex.

A common feature associated with sinus arrhythmia is wandering atrial pacemaker in which the P‐waves vary in morphology as the current originates from different portions of the SA node (“wanders”) and crosses the atria in a slightly different activation sequence. Wandering atrial pacemaker is normal and is recognized by higher‐amplitude P‐waves in lead II during inspiration and flattening of the P‐waves during expiration. The changes in P‐wave morphology are usually gradual, but this rhythm can be confused with premature atrial complexes.

Sinus arrhythmia is less common in animals that are likely to be stressed during examination (such as cats and cattle); these species will usually have a regular rhythm (NSR) or sinus tachycardia. However, occasionally sinus arrhythmia is detected in resting cats or when blood pressure increases inappropriately during times of (psychic) stress and vagal input increases in response to baroreceptor input in an attempt to lower blood pressure (BP).

Sinus rhythm disorders include sinus bradycardia and sinus tachycardia. These are simply sinus rhythms at slower or faster discharge rates than is normal for the species. These rhythms John D Bonagura, DVM, DACVIM – Introduction to Cardiac Arrhythmias – Page 2

are often physiologic, as occurs with sleep or exercise. In most cases sinus bradycardia or tachycardia are due to high vagal or sympathetic tone, respectively. Therefore, any patient with one of these rhythms should be evaluated with the likelihood of some autonomic nervous system influence in mind. Additionally, drugs, anesthetics, body temperature, and endocrine diseases (especially thyroid or adrenal) can affect sinus node rate. For example, elevated CSF pressure (which stimulates vasoconstriction to raise BP and better perfuse the brain) stimulates the baroreceptors leading to reflex sinus bradycardia (“Cushing’s reflex”). Other causes of sinus bradycardia include sedatives and tranquilizers, inhalation anesthetics, hypothermia, and hypothyroidism. Counterintuitively, this rhythm is also observed in some cats with profound shock (along with hypothermia and marked hypotension). Sinus tachycardia is associated with any cause of sympathetic nervous system activation (exercise, pain, anxiety, anemia, and hypotension), as well as anticholinergic drugs (atropine/glycopyrrolate), fever, and hyperthyroidism.

If the sinus node fails to discharge, the rhythm is termed sinus arrest. Strictly speaking, this is defined as an absence of sinus node discharge exceeding two normal P‐P intervals. What is “normal” is easy to determine when the underlying rhythm is a regular NSR, but when there is a marked sinus arrhythmia, it can be hard to decide if the pause is abnormal or just part of the sinus arrhythmia. Short periods of sinus arrest are well tolerated, but when prolonged (e.g. >5 seconds), and if there is no escape complex to rescue the heart, weakness or syncope are more likely to occur. When sinus arrest is associated with clinical signs, the term sick sinus syndrome is used. This is most common in dogs (see in‐class notes). Chronic, progressive, sinus node dysfunction is especially common in miniature Schnauzers, West Highland white terriers, and cocker spaniels. These patients often have abnormal conduction in other parts of the heart (e.g. atrioventricular block) and insufficient escape activity in the AV junction and ventricles indicative of diffuse conduction disease. Additionally, these dogs are prone to inappropriate sinus tachycardia and ectopic supraventricular (atrial) tachyarrhythmias.

Management of sinus rhythm disturbances is focused first on treating any underlying conditions. For example, if one encountered sinus tachycardia in a post‐operative patient the first considerations would be hypotension (Rx: Fluids/Colloids), pain (Rx: opiates), increased body temperature (Rx: underlying cause), or emergence delirium (Rx: tranquilizer). Occasionally inappropriate sinus tachycardia is treated with a beta‐blocker (e.g. in some cats with hyperthyroidism or in dogs with certain sympathomimetic intoxications). Sinus bradycardia can be treated in the hospital with atropine or glycopyrrolate, two drugs that block the muscarinic receptor and reduce vagal influence. In emergencies, catecholamines can be used to stimulate the beta‐receptors of the SA node and increase heart rate as well as myocardial contractility. Sick sinus syndrome is often treated in practice with an oral anticholinergic drug (hycosamine) or the sympathomimetic drug (terbutaline, a beta‐2 agonist or theophylline, a PDE inhibitor). However, these drugs are rarely effective in treating clinically important SSS, and the best long‐term therapy is permanent transvenous pacing. Pacemaker programming is critical for optimal system performance and long‐term outcomes are very good.

SUPRAVENTRICULAR ARRHYTHMIAS Supraventricular rhythm disturbances are among the most common and sometimes difficult of all cardiac rhythms to diagnose and manage. Supraventricular arrhythmias are considered “ectopic” as these originate outside of the sinus node. The arrhythmias include premature atrial complexes, atrial tachycardia, atrial flutter, atrial fibrillation (AF), and re‐entrant supraventricular John D Bonagura, DVM, DACVIM – Introduction to Cardiac Arrhythmias – Page 3

tachycardia (SVT), which uses the atria as part of the circuit loop. These rhythms can be transient, recurrent, or persistent to permanent. Atrial standstill is a unique atrial rhythm disturbance characterized by inexcitable atrial myocardium.

Supraventricular arrhythmias are most often caused by structural heart diseases associated with atrial enlargement, especially in dogs and cats. Atrial dilatation can stem from some congenital heart defect or an acquired valvular, myocardial, or pericardial disease. Atrial dilatation alters atrial electrical activity, and promotes abnormal heart rhythms through abnormal impulse formation or electrical conduction. Cardiac size influences the likelihood of sustaining an atrial arrhythmia such that atrial flutter and fibrillation occur more often in larger canine breeds and in horses. In contrast, the small size of the feline atria decreases the risk of atrial fibrillation in the absence of relatively severe atrial remodeling or disease.

Supraventricular arrhythmias can occur in the absence of overt structural disease and with a normal echocardiogram. One prominent example is atrial fibrillation (AF) in this setting of a structurally normal heart; the term “lone atrial fibrillation” is applied. Of course, it is likely that microscopic lesions, such as myocarditis or fibrosis, or genetic or acquired cell membrane channelopathies form the basis of some of these recurrent arrhythmias. This might explain why some animals develop recurrent atrial fibrillation (AF), even after successful conversion back to NSR. However, such lesions cannot be detected clinically (or without a biopsy sample). In some canine cases, atrial arrhythmias are forerunners to cardiomyopathies, but this is not always the case. Atrial arrhythmias are also detected in large animals, including horses, cattle and camelids, due to electrolyte (potassium) disturbances; these are often short‐lived and not caused by underlying heart disease.

Another special example of a supraventricular arrhythmia that can occur without over structural heart disease is the reentrant supraventricular tachycardia (SVT) using an accessory pathway. This tissue provides a second electrical bridge between the atria and ventricles, which are normally insulated by the AV valves and the fibrous cardiac skeleton. As shown in class, this can lead to a reentrant circuit that sequentially depolarizes the AV node  ventricles  accessory pathway (retrograde direction)  atria (retrograde)  AV node (antegrade direction)  ventricles. These accessory pathways are a special form of congenital heart disease (and beyond this overview, a topic beyond this introductory course).

A premature atrial complex (PAC or APC) arises outside of the SA node, timed early (prematurely) relative to the dominant sinus cycle. The arrhythmia is characterized by premature P wave (P’) with a morphology that differs from P waves of sinus origin. The premature P’ wave is followed by a normal duration to prolonged P‐R interval (if the AV node has not fully repolarized) and then by a related QRS complex. In most cases, the QRS complex is of normal‐ duration and morphology, indicating the impulse originated above the ventricles (“supraventricular”). Occasionally the conducted QRS complex will be slightly different than a sinus conducted QRS or even much wider: this indicates the ventricular conduction system had not yet repolarized fully; the phenomenon is called aberrant ventricular conduction. This situation is analogous to a conducted beat with bundle branch block (in fact right or left BBB can occur when premature atrial complexes are conducted into the ventricle). Sometimes the AV node is so refractory to premature stimulation from the atrium the impulse is blocked. Isolated nonconducted PACs are especially common in horses and can be an explanation for sudden pauses in the rhythm. In these situations, the P’ is so early it appears within the T‐wave of the previous supraventricular complex.

The rhythm atrial tachycardia is essentially a “run” of repetitive PACs. This usually arises from John D Bonagura, DVM, DACVIM – Introduction to Cardiac Arrhythmias – Page 4

a single atrial focus, and the term “focal atrial tachycardia” is sometimes used for such arrhythmias. The rhythm is characterized by an abrupt increase in the heart rate with abnormal P’ waves preceding each QRS complex. Finding the P’ waves can be difficult because they are usually buried in the T‐wave of the preceding QRS‐T complex. Although the QRS complexes should be relatively normal in appearance during a PAT, sometimes the first premature QRS complex of the atrial tachycardia exhibits aberrancy (abnormal ventricular conduction), leading to confusion with premature ventricular complexes. When the atrial tachycardia is nonsustained (<30 sec) with a sudden onset and termination, the term paroxysmal atrial tachycardia (“PAT”) is often used. Focal atrial tachycardias can also be sustained or persistent. Atrial tachycardia can be confused with atrial flutter if the atrial rate is very fast and large atrial repolarization waves (Ta waves) deviate the baseline.

Sustained atrial arrhythmias include focal atrial tachycardias, atrial flutter, and atrial fibrillation (AF). As indicated above, atrial tachycardia is a series of premature atrial complexes.

Atrial flutter is thought to represent a macro‐reentry circuit involving the right atrium and is characterized by saw‐toothed flutter waves in the baseline and the lack of an isoelectric shelf (i.e. the atrial activation does not return to the baseline but “saws” it back and forth). The atrial rate in atrial flutter is about ~300 to 400/minute in dogs; in horses an atrial flutter rate of 170 to 275/minute has been reported. QRS complexes are caused by conduction of flutter waves into the ventricles. Inasmuch as the normal AV node, His bundle and bundle branches are available for conduction, the resultant QRS complexes are usually normal in morphology.

Atrial fibrillation is a very important heart rhythm disturbance. The genesis of AF is likely an electrical scroll wave, micro‐reentry circuit, or focus of abnormal automaticity within the pulmonary venous entries or the left atrium itself. Varying conduction across the atrial mass leads to fragmented and chaotic myocardial activation (with measured atrial impulses of ~275 to 500 per minute in horses and even faster atrial activity in dogs and cats). Sometimes in horses the activation pattern seems to alternate with atrial flutter (“flutter‐fib”). The ECG diagnosis is straightforward and characterized by a lack of any consistent P‐waves, presence of fibrillation waves in the baseline, and an irregularly irregular (unpatterned) ventricular rhythm of supraventricular complex morphology. As with the other atrial tachyarrhythmias, the QRS complexes are due to conduction of atrial impulses across the AV node; consequently, the ventricular rate depends on AV nodal conduction. The amplitude of the fibrillation waves varies: these are obvious in horses but less clear as the species decreases in size. In cats the diagnosis is secured by recognizing a rapid rhythm, irregular R‐R intervals, narrow (supraventricular) QRS complexes, and absence of consistent P‐waves.

In dogs and cats, AF is usually characterized by a rapid, irregular supraventricular tachycardia.

The admonition: “if it’s rapid and irregular it is atrial fibrillation until proven otherwise”, is a useful guideline. However, the ventricular response rate depends on AV conduction. In lone AF, cardiac output is usually normal at rest so arterial BP is normal, sympathetic tone low and resting heart rate normal. In contrast, during exercise – when sympathetic activity is high and vagal traffic low – the AV nodal cells conduct supraventricular impulses rapidly so ventricular rate response is higher than would be normal for the degree of activity. This is why horses (and dogs) with lone AF are fine at rest, but at peak activity develop exercise intolerance. Recall: most ventricular filling occurs in early to middle diastole, but when the ventricular rate response is rapid and irregular, the diastolic filling periods are abbreviated and preload is often reduced.

Furthermore, the normal response to faster heart rates is a greater atrial contribution to filling in the form of a vigorous atrial contraction; however, this contribution is absent in AF. Carrying this explanation to a patient with heart failure, where sympathetic tone is generally high, it John D Bonagura, DVM, DACVIM – Introduction to Cardiac Arrhythmias – Page 5

should be clear that AF will lead to a sudden increase in resting heart rate, chaotic cardiac cycles, reduced ventricular filling, and decreased cardiac output. In fact, AF often precipitates CHF in previously compensated animals with heart disease.

Physiological AV block is often observed with atrial tachycardia and atrial flutter and is always present in AF. This block helps to prevent excessive ventricular rate response and can be understood by appreciating that AV nodal cells might not conduct current if there has been insufficient time for repolarization. Whereas the ventricular rate response to AF is “always” irregular, with atrial tachycardia or atrial flutter the rhythm can be regular or irregular as the atrial waves are better organized and regularly spaced. It can be challenging if there is a regular AV conduction sequence, for in these cases, ectopic P’ or F‐waves are buried in the QRS or ST‐T and it might require multiple lead traces or sudden depression of AV conduction for identification (as with a vagal surge or after administration of diltiazem).

Thus, the ventricular rate response in any supraventricular tachycardia is determined by the type of atrial arrhythmia and the 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). Even in the absence of heart failure, a SVT due to focal atrial tachycardia, atrial flutter or re‐entrant SVT can induce a ventricular response of nearly 400/minute (in small animals). Unlike AF, other supraventricular tachyarrhythmias form regular and organized impulses within the atria. With atrial tachycardia or atrial flutter, the ventricular rate can suddenly double or half as the atrioventricular conduction ratio suddenly changes. Supraventricular tachyarrhythmias also can be conducted with subtle electrical alternans (a diagnostic clue!) or even with a bundle branch block pattern so that the resultant QRS complexes are so wide as to be confused with ventricular tachycardia.

Conceptually it can be helpful to consider that the most common atrial arrhythmias (PACs, FAT, atrial flutter and AF) are inter‐related. Many dogs and horses exhibit more than one of these rhythm disturbances at one point or another. For example, during quinidine cardioversion of AF in horses it is common to observe a period of atrial flutter and later what appears to be a sustained focal atrial tachycardia (FAT). After successful conversion, many horses continue to manifest isolated or repetitive PACs. The basic management of supraventricular arrhythmias involves either heart rhythm control or heart rate control. Rhythm control means suppressing ectopic atrial activity. Heart rate control focuses on maintaining a more normal ventricular rate by depressing AV nodal conduction. For example, if a focal atrial tachycardia of 320/minute is conducted 1:1, then the ventricular rate is 320/minute. If every other impulse is blocked in the AV node, the ventricular response rate falls to 160/minute, a rate that is better tolerated hemodynamically.

When managing atrial tachyarrhythmias, the clinician should decide if the arrhythmia is more likely of recent onset or chronic in nature. Additionally, therapy will differ if the rhythm is “lone” (i.e., without structural heart disease) or associated with cardiac enlargement or heart failure. If the latter situations are evident, heart rate control is more commonly pursued.

Heart rhythm control (also called “conversion”) can be obtained in some patients with drugs that suppress ectopic rhythms. These drugs are typically in the Vaughan‐Williams Classes I and III, although this is a generalization. Lidocaine (Class 1B) can be effective in some peracute conditions, but typically does not suppress atrial arrhythmias. More often, the class IA drugs and class III drugs are used for rhythm control. The IA drug quinidine (by nasogastric tube) is reserved for horses with sustained atrial tachyarrhythmias, especially AF. Quinidine therapy of horses with lone AF is about 85% effective in attaining conversion to NSR. Procainamide (IV) also can be John D Bonagura, DVM, DACVIM – Introduction to Cardiac Arrhythmias – Page 6

used in dogs and horses for hospital therapy of atrial arrhythmias. The class III drugs (sotalol, amiodarone) are used for both hospital and chronic suppression of atrial arrhythmias in dogs and occasionally in horses. Sometimes class II drugs (beta‐blockers) and class IV drugs (calcium channel blockers) will suppress an ectopic atrial rhythm, but drugs in these two classes are more often used for heart rate control (see below).

Many atrial tachycardias are resistant to drug suppression and require heart rate control.

Sometimes rate control is needed prior to cardioversion. One important example is when quinidine – which exerts an atropine like effect on the AV node in addition to its sodium channel blocking on myocytes – speeds conduction of AF impulses across the AV node prior to cardioversion. In this case, the horse can experience an increased heart rate that can exceed 120/minute and be associated with signs of hypotension. Digoxin (due to its vagomimetic effect) can be administered to block conduction within the AV node, slowing the ventricular response rate, and allowing time for quinidine to convert AF to NSR. This is just one of various and sometimes nuanced treatment strategies applicable to these supraventricular arrhythmias. Not every contingency can be discussed in an introductory presentation; but these are the principles of rhythm control.

Synchronized DC cardioversion is another therapeutic approach to converting a sustained supraventricular tachyarrhythmia back to NSR. This approach is particularly relevant to dogs with lone AF or to horses with lone AF that are resistant to quinidine sulfate or develop side effects from the drug. Electrocardioversion requires general anesthesia and involves a timed, DC shock delivered on the R‐wave to depolarize all of the heart muscle cells simultaneously and disrupt reentry electrical circuits. This should not be confused with ventricular defibrillation, which is a stronger, untimed DC shocking of a heart (without any QRS complexes) in an attempt to depolarize all the cells and allow the sinus node or another pacemaker to assume control.

Amiodarone (dogs) or sotalol (dogs or horses) is often prescribed empirically after cardioversion to maintain sinus rhythm. These drugs are usually continued for some months to prevent reversion to atrial fibrillation; however, the efficacy and the benefit to risk of such therapy have not been published.

Frequently, heart rate control of supraventricular tachycardia is the more logical treatment goal. In the setting of significant cardiomegaly or heart failure, ventricular rate control – not rhythm control – is generally preferred. Rate control involves administering a drug that depresses AV nodal conduction, reducing the transmission of atrial impulses into the ventricle. The three drugs used for this purpose are digoxin, diltiazem, and beta blockers. Recall, stimulation of parasympathetic muscarinic receptors depresses AV conduction. Digoxin increases the vagal input to these receptors, albeit indirectly, by sensitizing the baroreceptor reflex to prevailing BP. Diltiazem works by blocking the L‐type calcium channel, and thereby the calcium current essential for phase 0 depolarization in AV nodal cells. Beta‐blockers (__lol) depress calcium entry indirectly, because the beta‐receptor exerts ligand‐operated control of calcium entry across the L‐type channel.

When atrial tachyarrhythmias are associated with CHF and if there is no contraindication for digoxin (such as renal failure or ventricular ectopy), this cardiac glycoside is administered. Digoxin can be used in horses as well as dogs (it is rarely used in cats due to prolonged elimination half‐ life). However, the CCB diltiazem (Class IV) is usually more effective for depressing AV nodal conduction than digoxin, and this drug is often used in dogs and cats for this purpose.

(Infrequently diltiazem will actually convert the arrhythmia back to NSR.) There is some debate about which drug should be started first in the heart failure patient, but practically speaking, most clinicians use combined therapy with digoxin and diltiazem to control heart rate in atrial John D Bonagura, DVM, DACVIM – Introduction to Cardiac Arrhythmias – Page 7

tachyarrhythmias of dogs. Remember that while digoxin is a positive inotropic drug, diltiazem actually depresses myocardial contractility and reduces systemic vascular resistance. Thus diltiazem should not be given to CHF patients without concurrent therapy to manage edema and reduced cardiac output (such as diuretics and pimobendan in dogs). In most cases, the dose of diltiazem is gradually increased to gain ventricular rate control while minimizing the negative inotropic impact of the drug.

When atrial tachyarrhythmias in dogs or cats are not associated with heart failure, most clinicians select diltiazem or a beta‐blocker such as atenolol to control ventricular rate response.

The situation in horses is more complicated as these drugs are not often used chronically and cannot be administered in the setting of drug testing (some horse shows, racing). Diltiazem and a beta‐blocker also can be used together, but care must be taken to avoid excessive AV nodal conduction block that might lead to ventricular bradycardia.

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

Atrial standstill is another type of atrial arrhythmia, but does not result in tachycardia. This diagnosis indicates that the atrial muscle is inexcitable. It should not be confused with sinus arrest wherein the failure resides in the SA node discharge, not the atrial muscle depolarization. Atrial standstill is caused transiently by high serum potassium or persistently by atrial muscle disease (dogs, cats) or severe atrial dilation (in cats). The main ECG findings of atrial standstill are due to hyperkalemia include complete absence of P‐waves, widening of the QRS complex, and increased amplitude of the T‐waves (with abbreviated ST‐T relative to heart rate). The P‐wave and QRS changes are caused by partial depolarization of the cardiomyocytes, which inactivates fast sodium channels and slows or depresses depolarization. The ST‐T changes are due to opening of potassium channels allowing for more rapid repolarization (despite the higher extracellular K+, intracellular K+ is still >>> extracellular K+). SA impulses can still conduct to the AV node via functional (microscopic) internodal pathways, and the rhythm is sometimes termed “sinoventricular”, as no P waves are seen. The sinus discharge rate is usually depressed in hyperkalemia, but in cats, this is less common, so that wide QRS complexes and T waves associated with severe hyperkalemia can be confused with an ectopic ventricular tachycardia.

When atrial standstill is due to primary muscle disease (replacement of atrial muscle with fibrous tissue), either no P‐waves or tiny, non‐conducted P waves are evident. Generally, the AV conduction system is also involved in the fibrotic process so the patient depends on a junctional (AV nodal) or ventricular escape rhythm to initiate heartbeats. Persistent standstill caused by atrial myocardial disease and fibrosis is most common in English Springer spaniels, but can also occur in larger retriever breeds. In cats, apparent atrial standstill can be observed with severe John D Bonagura, DVM, DACVIM – Introduction to Cardiac Arrhythmias – Page 8

forms of cardiomyopathy.

VENTRICULAR ARRHYTHMIAS Arrhythmias arising ectopically in the ventricle parallel those of the atria in terms of nomenclature. However, there are some very important differences: 1) the AV node need not be activated to generate a QRS complex; therefore, rate control is not an effective strategy; and 2) there is greater potential for sudden death if the rhythm degenerates to ventricular fibrillation or asystole. Unfortunately, currently it is difficult to predict which patients will die suddenly or will benefit from therapy. The other obvious difference between rhythms of supraventricular and ventricular origin is the morphology of the QRS‐T. Most ventricular arrhythmias cannot enter the His‐Bundle Branch‐Purkinje system normally. Therefore, depolarization spreads along abnormal conduction pathways, and propagates in some regions using slower cell‐to‐cell conduction. This results in a wider than normal QRS complex, often in the opposite direction, and frequently a “bizarre” morphology when compared to the normal activation process typical of sinus‐rhythm impulses. The T‐wave is also very large and oriented in the opposite direction, representing a secondary repolarization change (due to abnormal depolarization).

Idioventricular “escape” complexes are rescue mechanisms for sinus arrest, atrial standstill, or AV blocks and should not be suppressed by drugs. These complexes or rhythms originate from subsidiary pacemakers, usually residing in the AV junction or Purkinje system of the ventricle.

The idioventricular (escape) rhythm is initiated when there is a failure of a normal impulse to depolarize the ventricles. If the escape originates near the bundle of His, the QRS is relatively normal, but will not be preceded by a related P wave. If the impulse starts deeper in the ventricle, the resultant QRS complex is wide with a more bizarre morphology when compared to normal sinus QRS complexes. These escape foci discharge at 20 to 40/minute in dogs and horses, but in the cat, the rate is much faster, approaching 130/minute in many cats with complete AV block.

In contrast to a ventricular escape, the premature ventricular complex (PVC, VPC) arises early compared to the dominant R‐R cycle to suddenly assumes pacemaker control of the ventricles.

These ectopic complexes can be uniform or multiform in morphology suggesting a single focus or multiple foci (or different conduction patterns). A fusion complex might also be seen in some cases. This complex is a “sandwich” of a PVC and a sinus impulse that occurs when both impulses arrive simultaneously and collide in the ventricles. These are usually recognized by a preceding P wave, but shorter than normal PR interval, along with intermediate QRS morphologies between sinus and PVC. The finding of three or more linked PVCs constitutes a “run” of ventricular tachycardia (VT). These ectopic ventricular rhythms can be “slow” (near the sinus node rate) or “fast”; paroxysmal or sustained; monomorphic or polymorphic; or rapidly varying in orientation (torsade de pointes = turning on point). The ventricles also can flutter (creating sine waves), or fibrillate (disorganized reentry currents without mechanical contraction = a lethal activation). In very sick animals or in those with CHF, death can occur from asystole, which is essentially ventricular standstill.

PVCs are among the most common rhythm disturbances. Causes include primary electrical or structural heart diseases, including arrhythmogenic cardiomyopathies and dilated cardiomyopathy. Other causes include electrolyte and metabolic disturbances, autonomic imbalance, drugs, toxins, and the “usual suspects”, such as splenic masses and gastric dilatation in dogs and ileitis‐jejunitis in horses. The electrophysiologic mechanism for the arrhythmia is rarely known.

It can be difficult to decide if PVCs are “clinically significant” or not, but the issue is important.

John D Bonagura, DVM, DACVIM – Introduction to Cardiac Arrhythmias – Page 9

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 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 very high. Arrhythmogenic right ventricular cardiomyopathy is common in Boxers and English bulldogs. These predispositions can prompt antiarrhythmic therapy in a Doberman or Boxer dog, recognizing there is no proof treatment will prolong life. Conversely, some asymptomatic boxers have PVCs for years without signs and these patients are best assessed by reviewing history and an ambulatory (Holter) ECG recording before starting any treatment.

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 medical workup includes drug and medical history, consideration of clinical signs (weakness, collapse or syncope), Echo findings, laboratory tests (CBC, chemistries, cardiac troponin‐I), and abdominal ultrasound in older dogs at risk for splenic disease. These are obtained to determine the most likely cause and overall clinical significance of the arrhythmia. A Holter (24h ambulatory) ECG can contribute to assessing the severity and complexity of the PVCs as well as response to therapy. Based on some Holter ECG studies, >10/day in cats and >50/day in dogs would be considered abnormal (others use lower limits). The absolute number of PVCs per day needing treatment is controversial. Spontaneous daily variation is common (up to ~85%); this should be taken into account. In general, clinical signs (collapse, syncope); clinical situation (anesthesia; hypotension); and modified “Lown criteria” are used to assess severity and need for therapy. The latter include (a) “uniform” vs. “multiform” PVCs; (b) “monomorphic” vs. “polymorphic” VT; (c) “late” versus “R on T” timing of premature complexes; and (d) “slow” vs. “fast” ventricular rhythms – with the second of each pair considered more hemodynamically or electrically destabilizing.

Management of ventricular ectopic rhythms involves determining the most likely cause, advancing an educated guess about the clinical significance, considering the need for therapy, and possibly choosing one or more drugs. All antiarrhythmic drugs carry the potential for side effects and worsening of the arrhythmia (proarrhythmia).

Lidocaine remains the drug of choice for acute management of serious PVCs or VT in animals.

Doses are important with cats and horses more sensitive to neurotoxicity of the drug. Any underlying electrolyte disturbances, especially involving potassium or magnesium, should be corrected. As sympathetic input can trigger or worsen VT, any pain should be controlled. Fluids or colloids might be needed to support blood pressure. Second‐line treatments include intravenous procainamide, amiodarone, esmolol, and magnesium salts (which stabilize membranes). These are often trial‐and‐error treatments, and experience has brought these drugs to the fore.

For chronic oral therapy, sotalol (class III drug with beta‐blocking properties) is generally the best tolerated, and it often reduces the frequency and complexity of ventricular ectopy (beware: negative inotropic effects in CHF). Sotalol can be administered to dogs, cats, and horses.

Alternatives are mexiletine (class IB, similar to lidocaine, but oral) or sotalol plus mexiletine.

Amiodarone (class III) can be effective in dogs, but deserves respect, especially in terms impairing liver function. Flecainide is a potentially useful drug but experience is low and the drug can lead to serious “pro‐arrhythmia”, especially in settings of a failing heart.

John D Bonagura, DVM, DACVIM – Introduction to Cardiac Arrhythmias – Page 10

CONDUCTION DISTURBANCES In addition to sick sinus syndrome, persistent atrial standstill, and ventricular pre‐excitation (each mentioned above), conduction disturbances include the AV blocks; bundle branch blocks, and intraventricular conduction disturbances. Bundle branch blocks and fascicular blocks do not cause clinical signs.

The AV blocks are classified as first, second (Mobitz I, Mobitz II), and complete (third‐degree block). First‐degree AVB is characterized by a P wave preceding each QRS complex but with a longer than normal PR interval for the species. Second‐degree AVB is “incomplete”, meaning some impulses conduct to the ventricles and others do not. Mobitz type I, second‐degree AVB (also called Wenckebach type) is typical of high vagal tone and drug effects and is characterized by a progressively longer PR interval until a P wave is blocked. Mobitz type II second‐degree AVB is often due to conduction disease, as occurs with senile degeneration in the bundle of His or bilateral bundle branches. In this rhythm, the PR interval is relatively fixed, and often prolonged, and one or more P‐waves are blocked at a time. “High‐grade” second‐degree AVB usually refers to blocking of three or more P waves before one is conducted. Third‐degree AVB is “complete”, meaning no atrial impulses conduct into the ventricles. The block occurs in the AV node, bundle of His, or both bundle branches. It is usually due to degeneration of the conducting pathways, although other causes (myocarditis, tumors, concentric hypertrophy in the area) are other potential causes. Since atrial impulses are blocked, the heart can only discharge from an escape pacemaker (idioventricular rhythm), typically from the His‐Purkinje system and below the level of the block (see previous discussion under Ventricular Arrhythmias).

Treatment of symptomatic AV blocks generally involves referral for permanent pacing. Single or dual chamber pacing systems can be used, depending on a variety of patient and technical factors. When AVB is due to vagal input or drugs, atropine can often abolish the block.

John D Bonagura, DVM, DACVIM – Introduction to Cardiac Arrhythmias – Page 11

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

Radiographic Differential Diagnosis

John D Bonagura DVM, MS, DACVIM (Cardiology, Internal Medicine) Veterinary Clinical Sciences, College of Veterinary Medicine 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. 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)

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 is 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).

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

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 breathe 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).

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 the Table. 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 are 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., Dr. Bonagura – Radiographic Interpretation (for case studies) Page 2

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 is helpful in determining the underlying reason for respiratory sign.

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 is 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 is 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) is 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) is done with sedation.

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

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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 “washes” 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 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 3‐ way stopcock as an adaptor in the end of the inflated endotracheal tube to obtain a “tracheobronchial” 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 is 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‐ Dr. Bonagura – Radiographic Interpretation (for case studies) Page 4

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.

Table: 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 denser 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 Dr. Bonagura – Radiographic Interpretation (for case studies) Page 5

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.

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 11 to 11.5 is likely to indicate cardiomegaly in most canine breeds; even more useful are serial evaluations in a dog. A VHS “velocity” of 0.1 vertebral bodies per month is taken as a significant progression. There are multiple 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.  Bulges: Are any distinctive bulges or rounded borders evident that might 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.

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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.

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 over‐ interpreted. 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.

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BRACHYCEPHALIC AIRWAY SYNDROME Eric Monnet, DVM, PhD, FAHA Diplomate ACVS and ECVS Colorado State University, Fort Collins, Colorado Eric.Monnet@ColoState.EDU Brachycephalic breeds (Shih Tzu, boxer English and French Bulldog, Pekingese, pug and Boston terrier) have a shortened skull compared to the other breeds. Compression of the nasal passage and distortion of the pharyngeal tissue result in an increase in airway resistance. Brachycephalic airway syndrome includes stenotic nares, elongated soft palate, everted laryngeal saccules and laryngeal collapse. There is a high incidence of hypoplastic trachea found in brachycephalic dogs that contributes to airway distress.

Stenotic nares and elongated soft palate are the primary anatomic components of the syndrome while everted laryngeal saccules with laryngeal collapse are thought to be secondary. Excessive negative pressure generated at inspiration because of stenotic nares creates inflammation and stretching of soft tissue and eventually eversion of the laryngeal saccules and laryngeal collapse. Stenotic or obstructed nares affect the mechanics of the lungs and provoke degenerative changes of the nasal mucous membrane. Severe upper airway obstruction can result in pulmonary edema because of a reduction of intrathoracic pressure. The greatest changes are observed in dogs with partial bilateral nasal obstruction and high nasal resistance. Inadequate pulmonary ventilation due to upper airway obstruction can lead to a reduction of arterial oxygen content. The hypoxia is a potent pulmonary vasoconstrictor to divert away blood from poorly ventilated alveoli. Pulmonary vasoconstriction and pulmonary hypertension result in cor pulmonale and right sided heart failure.

CLINICAL FINDINGS AND DIAGNOSIS Brachycephalic breeds are presented for excessive noisy breathing and inspiratory dyspnea. Inspiratory dyspnea is exacerbated by exercise and augmentation of the ambient temperature. Some English Bulldogs have been presented for vomiting not associated with meals. An increase frequency of hiatal hernia seems to be present in English Bulldogs with brachycephalic airway syndrome. The mean age for dogs presented is 3 to 4 years old.

Many of these animals have a high potential to decompensate and develop acute respiratory distress. Therefore, they must be handled carefully to prevent stress and acute decompensation. It is important to keep the animal calm and in a cool environment.

Supplemental oxygen might be required.

Physical examination of the nares for stenosis should be performed. Breathing pattern should be observed. Brachycephalic dogs are presented with an inspiratory dyspnea that is corrected by open mouth breathing if only the nares are involved in the syndrome. If the soft palate is elongated, the laryngeal saccules and/or the larynx collapse the dyspnea is inspiratory and expiratory. The severity of inspiratory dyspnea depends on the length and congestion of the soft palate and other restrictive or obstructive conditions present. An obstructive breathing pattern, characterized by a slow inspiratory phase followed by a rapid expiratory phase is seen frequently in brachycephalic breed even if the airway diameter is not comprised more than 50%. In nonbrachycephalic breed, a reduction of more than 50%

of the airway diameter is required to modify the breathing pattern. The greatest airway noise is usually noticed in the larynx. Auscultation of the lung field is difficult because of enhanced upper airway sounds.

A radiological examination of the larynx shows an elongated soft palate protruding in the rima glottidis. It is also important to evaluate the diameter of the trachea in dogs with brachycephalic syndrome. It is very common to diagnose an hypoplastic trachea, which worsens the prognosis. Comparison of the diameters of the thoracic inlet (TI) and the tracheal lumen (TD) makes the diagnosis of tracheal hypoplasia. In normal Bulldogs the ratio TD/TI is 0.106 English Bulldogs have the highest incidence of hypoplastic trachea within brachyocephalic breeds (55%). Thoracic radiographs allow evaluation of lung fields for signs of pulmonary edema, pneumonia and the heart for signs of right-sided dilation. If there is cardiac enlargement an echocardiography and an electrocardiogram are required to evaluate myocardial function and arrhythmias. Diagnosis of hiatal hernia can also be done with radiographs.

Blood work is usually within normal limits since the animals are young at the time of diagnosis. An augmentation of the pack cell volume might be indicative of a mild to moderate hypoxia.

A laryngeal examination is required under light general anesthesia to visualize the soft palate, the laryngeal saccules and the function of the larynx. The soft palate should not extend passed the tip of the epiglottis. Position of the soft palate is influenced by the position of the head, traction on the tongue and presence of an endotracheal tube.

Evaluation of the soft palate should be performed without an endotracheal tube in place and with the tongue in a normal position. Everted laryngeal saccules are white shiny dome shape structures located cranial to the vocal cords. Tonsils should also be evaluated as well as the presence of redundant mucosal folds in the pharynx/larynx. A medial tipping of both corniculate processes both and medial flattening of the cuneiform processes of the arytenoid cartilage characterize a laryngeal collapse. The vocal cords are usually not visualized if the larynx is collapse. Usually the corrective surgery is performed during the same anesthesia because recovery from anesthesia with compromise airways could be life threatening.

Stenotic nares are frequently diagnosed in younger, brachycephalic dogs (less than 2 years) with an overlong soft palate and have a favorable prognosis after surgical treatment.

In brachycephalic dogs older than 2 years, stenotic nares are associated with additional airway obstruction, and these patients have a guarded prognosis even with treatment.

Surgical treatment is therefore recommended as soon as possible to prevent further deterioration of the animal condition and prognosis. English Bulldogs are not responding as well as the other breeds to surgery probably because of the higher incidence of hypoplastic trachea in this breed.

SURGICAL TREATMENT Stenotic Nares In brachycephalic breed the cartilage plates are short, thick and displaced medially.

Stenotic nares are present in 48% of dogs presented for brachycephalic airway syndrome.

Stenotic nares are frequently found in brachycephalic dogs and interference with inspiration by the obstructed nares leads to secondary airway changes (i.e., everted saccules, laryngeal collapse, tracheal collapse). Stenotic nares have also been reported in cats.

The wing of the nostril is examined to determine the amount of tissue to be removed for optimal airflow. The technique of removing a vertical wedge from the wing of a nostril and extending the incision caudally to include part of the alar cartilage has been useful in eliminating stenosis. The incision is made with a # 11 BardParker blade. The tip of the blade is introduced at the apex of the wedge and directed caudally, with the cutting edge directed medially to the free edge of the wing of the nostril. The apex of the wedge is the pivot point of the flap created to allow the edges of the incision to come together evenly and without tension. The blade is again introduced at the apex of the wedge, and the cutting edge directed ventrolaterally as the tip is pushed in caudally to end at the same point as the first incision. The width of the base of the wedge (free edge) determines the opening of the nostril. The wedge is removed, and the edges are sutured with two or three interrupted sutures performed with 30 or 40 absorbable material using a small halfcircle cutting needle.

The surgical site is kept clean and protected from rubbing (selfmutilation) with an Elizabethan collar. Additional medical care is usually not needed.

Elongated Soft Palate In brachycephalic breed the soft palate extends beyond the epiglottis obstructing the airway passage. Vibration of the soft palate in the pharynx induces inflammation and swelling that will obstruct even more the airway. Approximately 80 per cent of cases of overlong soft palate are found in brachycephalic dogs, English and French bulldogs being the most frequently afflicted. Edematous pharyngeal mucosa and enlarged, protruding tonsils are common. The intention of palate resection is to shorten the soft palate so that its free border lies at the tip of the epiglottis or just covers it with the tongue in a normal position.

The mouth is held open with a mouth gag, and the tongue is extended to provide adequate exposure of the oral pharynx. A pair of malleable ribbon retractors is helpful in moving soft tissues while the resection level is being determined. The free border of the palate is grasped with forceps, and both sides of the palate as well as the oral cavity are swabbed with antiseptic.

The tongue is relaxed, and the point at which the tip of the epiglottis touches the soft palate is noted and marked with a scalpel cut or a sterile felttipped marking pen. The caudodorsal part of tonsils can also be used as a cranial landmark for the soft palate. A pair of Allis forceps or a traction suture is placed in the free edge of the palate and retracted rostrally. An absorbable suture (40 to 50) is placed in the mucosa at the lateral edge of the free soft palate. The visualization is not always good in the mouth of brachycephalic dogs.

It will open the surgical field and improve the visualization if the procedure is performed with long and curved instruments. The palate is incised from the lateral traction suture to the reference mark at its midline with a scalpel or scissors while low tension is applied on the forceps and lateral traction suture. The soft palate is completely excised. The incised edge is sutured with a simple continuous pattern, with sutures placed through both the nasal and oral mucosa, 1 mm from the cut edge and 2 mm apart. The layer of muscle is avoided so that the mucosa is pulled over the exposed muscle when the sutures are tightened. The closely placed sutures provide a smooth hemostatic closure and do not shorten the width of the soft palate. Postoperative hemorrhage or edema is minimal.

Everted Laryngeal Saccules Everted laryngeal saccules are most frequently encountered in brachycephalic breeds, with a prolonged history of upper airway obstruction. Everted laryngeal saccules have been

present in 48% of the brachycephalic dogs in a study. The mucosa of the laryngeal saccules evertes in the larynx because of the high negative pressure during inspiration. The prolapse mucosa is edematous and creates a mass in the larynx that contributes to the obstruction of the ventral rima glottidis. Resection of everted saccules is not performed routinely.

Correction of other components of the syndrome might result in the reduction of the everted saccules.

A temporary tracheostomy is necessary to ensure an adequate airway during surgery and during postoperative recovery. Temporary tracheostomy allows removal of the endotracheal tube from the surgical site and helps manage the airway after the surgery.

A patient is placed in sternal recumbency with the mouth held open as described for partial laryngectomy. The saccule is grasped with long hemostats or Allis forceps, and rostral traction applied. The saccule is amputated at its base with scissors or a longhandled scalpel. Hemorrhage is minor and controlled by pressure. Avoiding the electroscalpel reduces inflammation Resection of everted saccules is associated with edema and swelling of the larynx.

Dexamethasone intravenously (1 mg/kg) is used to reduce the amount of edema after surgery. The temporary tracheostomy is maintained for 24 hours after surgery. The patient is challenged before removal of the temporary tracheostomy tube.

Laryngeal Collapse Laryngeal collapse occurs as a result of a loss of the supporting function of the cartilages.

It represents a very advance form of the brachycephalic airway syndrome. The cuneiform and corniculate cartilages are drawn medially by the excessive inspiratory negative pressure. Laryngeal collapse is a progressive disease in which the prognosis worsens with time. Collectively, stenotic nares, elongated soft palate and everted laryngeal saccules predispose dogs to abnormal stresses within the larynx that lead to progressive distortion and ultimate collapse of the arytenoid cartilages.

Three stages of laryngeal collapse have been described (stages 1 to 3) stage 3 being the most advance. The first stage in the pathogenesis of laryngeal collapse involves eversion of the laryngeal saccules into the cavity of the glottis. This is caused by an abnormal negative pressure created at the glottis during inspiration. The vacuum that develops in the glottis results from the increased inspiratory effort necessary to ventilate through the stenotic nares or elongated soft palate. Inflammation and edema of the mucosa usually accompany saccule eversion and contribute to the dyspnea. During stage 2, the cuneiform process of each arytenoid cartilage, which normally extends to the caudolateral region of the pharynx during inspiration, loses its rigidity and gradually collapses into the laryngeal lumen. In stage 3, the corniculate process of each arytenoid cartilage, which normally maintains the dorsal arch of the glottis, collapses toward the midline, resulting in complete collapse of the larynx. Loss of laryngeal cartilage rigidity is speculated to contribute to the collapse of the cuneiforme and corniculate process. Dogs with stenotic nares, an elongated soft palate, or everted laryngeal saccules are treated for these conditions first. A dog is allowed to recover, and the clinical response suggests whether further resection is necessary.

Dogs with persistent stage 2 disease, even after resection of the soft palate and nares, may require partial arytenochordectomy to enlarge the laryngeal opening. Dogs with stage 3 laryngeal collapse may not show significant improvement when treated with partial laryngectomy. An alternative treatment for dogs with severe laryngeal collapse that does

not improve after resection of the elongated soft palate, stenotic nares, or laryngeal saccules is a permanent tracheostomy.

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DIAPHRAGMATIC HERNIA Eric Monnet, DVM, Ph.D., FAHA Diplomate ACVS, ECVS College of Veterinary Medicine Colorado State University, Fort Collins, Colorado Eric.Monnet@ColoState.EDU A hernia is an abnormal protrusion of an organ or part of it through the containing wall of its cavity, beyond its normal confines. A diaphragmatic hernia is a protrusion of the abdominal viscera through the diaphragm. In the dog and cat, traumatic diaphragmatic hernias are common, whereas the congenital type is infrequently seen. The diaphragm is not essential for life as the entire diaphragm can be removed in a newborn cat or dog and the animal will survive.

APPLIED ANATOMY The diaphragm is a musculotendinous structure that separates the thoracic and the abdominal cavities. The diaphragm projects into the thoracic cavity like a dome. On the thoracic side it is separated from the pleura by the endothoracic fascia and on the abdominal side, is separated from the peritoneum by the transversalis fascia. The fascia and serosa are so thin in the dog that over the tendinous portion they can only be visualized microscopically. Diaphragm attaches to the lumbar vertebrae, the ribs, and the sternum. Contraction of the diaphragm is a major force contributing to ventilation. The diaphragm is composed of a U shaped central tendon and 4 muscle groups: the pars sternalis, the pars lumbalis and the paired pars costalis. The pars lumbalis of the diaphragmatic musculature is formed by the right and left diaphragmatic crura, the right crus being considerably larger than the left. Seen from the abdominal cavity each crus of the diaphragm is a triangular muscular plate whose borders produce the tendinous portions. The musculature of the crus medial is the thickest (5-6 mm). The pars costalis on each side consists of fibers radiating from the costal wall to the tendinous center. The pars sternalis is an unpaired medial part unseparated from the bilateral costal portions. The diaphragm is composed of only one layer of muscle and two layers of tendon and therefore is weaker than the multilayered abdominal wall.

The central tendon of the diaphragm of the dog is relatively small. In its tendinous portion, transverse fibers course from one side to the other as a reinforcing apparatus. The motor innervation of the diaphragm is supplied by the paired phrenic nerves. The phrenico abdominal arteries are the principal blood supply to the diaphragm. Several structures traverse the diaphragm through one of the three foramens. The caval foramen is located in the central tendon and allows passage of the caudal vena cava. The esophageal hiatus and aortic hiatus are located in the pars lumbalis of the diaphragm. The esophageal hiatus allows passage of the esophagus and vagal trunks. The aortic hiatus is bordered by the paired crural tendons and permits passage of the aorta, azygous vein, and thoracic duct.

The stomach and liver attach by ligaments to the concave peritoneal surface of the diaphragm.

TYPES OF DIAPHRAGMATIC HERNIAS -Congenital pleuroperitoneal hernia -Congenital peritoneopericardial hernia: most common congenital diaphragmatic defect, may remain asymptomatic, associated with other midline defects: ventricular septal defect, abdominal hernia.

-Traumatic diaphragmatic hernia: the most common form in dogs and cats: 80% of the cases. Nature of the trauma, multisystem injury, and shock are potential complications in traumatic diaphragmatic hernia -Hiatal hernia: usually congenital, common in Sharpei, sliding (Figure 1) or paraesophageal.

DIAGNOSIS Diaphragmatic hernia often is missed during the initial assessment after trauma, so a high index of suspicion for this condition should be maintained in animal that had experienced significant trauma. Clinical findings that Figure 1 suggest diaphragmatic hernia include dyspnea, tachypnea, cyanosis, paradoxical breathing, and muffled heart and lung sounds. The abdomen may appear empty on palpation. Auscultation may reveal muffled heart and lung sounds on one side of the chest. Radiographic findings that support a diagnosis of diaphragmatic hernia include loss of the diaphragmatic silhouette, pulmonary atelectasis, and presence of fluid dense structures in the chest or the pericardial sac. A gastric or bowel gas pattern within the thoracic cavity or the pericardial sac confirms the diagnosis. An upper gastrointestinal study might be required to confirm the diagnosis. Megaesophagus is commonly associated with a hiatal hernia.

Chronic diaphragmatic hernia occurs as a delayed presentation or failure of diagnosis after trauma. Presentation for chronic diaphragmatic hernia can occur years after the original trauma.

Usually presentation is due to entrapment of a liver lobe that produces significant pleural effusion.

PREOPERATIVE CONSIDERATIONS Immediate surgical intervention for the repair of a diaphragmatic hernia is rarely indicated.

Traumatic diaphragmatic hernia is a life threatening condition. It causes several concurrent pathophysiologic derangements. Ventilation is impaired by loss of diaphragm contraction and pleuropulmonary coupling. Gas exchange is impaired by pulmonary atelectasis as well as reduced resting lung volume. Ventilation perfusion mismatch and shunt are present. Oxygen delivery is impaired by decreased cardiac output resulting from impingement of venous return. Patients may also be compromise by trauma to other abdominal organs. Acute distension of a herniated stomach will further compromise the ventilation function and cause death in few minutes. Initial therapy of diaphragmatic hernia is primarily supportive, consisting of supplement oxygen, shock therapy, and treatment of concurrent injuries. Surgical correction should be undertaken early, usually within several hours after presentation. Delaying surgery beyond a few hours only increases the likelihood of cardiopulmonary decompensation and death.

Some animals present with severe

cardiopulmonary depression that will not stabilize with oxygen and other supportive therapies. In this case surgical correction should be undertaken without delay.

SURGICAL APPROACHES The dog or cat is positioned in dorsal recumbency The midline abdominal approach is the easiest and most versatile approach and is therefore the most commonly used. In some cases of congenital hernias or chronic diaphragmatic hernia where thoracic adhesions and/or complicating thoracic injuries are suspected the surgeon should be prepared to perform a median sternotomy.

By far the most common approach used is the abdominal midline.

SURGICAL PROCEDURE Diaphragmatic and peritoneopericardic hernias.

Using the abdominal approach, an incision is made from the xiphoid cartilage to the umbilicus. This incision can easily be extended if necessary. Once the peritoneal cavity is opened, the diaphragm is exposed and the situation evaluated. Some hernias, especially in the area of the dorsal attachments of the crura and the aortic hiatus are not easily visualized; therefore, this area should be carefully inspected even when another laceration is present. The herniated contents are replaced in their proper position and inspected for damage. Some of the complicating injuries that the surgeon must be prepared for a torsion of one or more liver lobes, ruptured viscus, intestinal intussusception, costal abdominal hernia, and others. If adhesions exist, they should be broken down using blunt dissection so as to avoid excess hemorrhage and inadvertent damage to a vital structure. Occasionally, in chronic cases, the hernial ring has to be excised because of adhesions between it and herniated structure. Those parts of the hernial ring that might be adhered to the liver should be dissected free from the diaphragm rather than stripping them from the liver and creating a raw bleeding surface.

Using large sponges or laparotomy pads moistened with warm saline, the liver and bowel are retracted laterally and posteriorly. The diaphragmatic tear is now more easily visualized so that a careful examination of the thorax can be done both visually and manually. All thoracic fluid should be aspirated. The lungs should be expanded to remove atelectasis and to inspect for pulmonary tears and persistent areas of collapse. The re-expansion of the lung parenchyma should be slow. Pulmonary edema could be a complication during re-expansion especially in cat after chronic diaphragmatic hernia. If the hernia is more than 48 hours old, the edges of the tear should be debrided. The hernia is closed using a single layer of absorbable material (dexon, vicryl, PDS, Maxon) or nonabsorbable material (nylon, prolene, novafil). The suture size should be 3-0 in cats and small dogs and 2-0 in medium and larger breed dogs. It might be necessary to preplace the most dorsal sutures for better visualization of the tear during suturing. It is also helpful to reconstruct the tear with several simple interrupted sutures to facilitate visualization of the rent.

When tears around the caudal caval foramen are sutured, larger stitches are to be avoided so as to prevent constriction of the vena cava. The same principle applies to the aortic and esophageal hiatus. When beginning the continuous suture line, this author finds it helpful to begin dorsally and work ventrally. Chronic diaphragmatic hernia may require a muscle flap (transverse abdominalis muscle) or an omentum flap to close the defect.

A thoracostomy tube should be placed for evacuation of the pleural space should be placed prior to complete closure of the diaphragm. The most convenient placement for the thoracostomy tube is the subcostal position just lateral to midline. Closure of the diaphragm is completed. With the use of a 3-way stop cock and 60 cc syringe, air is evacuated from the thorax until a gentle negative pressure is obtained. The celiotomy incision is closed in a routine fashion. When the

celiotomy closure is complete, the tube is again aspirated. The patient should then be placed through a series of positional changes (ventral recumbency, right lateral recumbency, left lateral recumbency, and dorsal recumbency) while attempting to aspirate air. The patient is monitored carefully for the next six to eight hours.

Hiatal hernia The purpose of the procedure is to bring back the lower esophageal sphincter in the abdominal cavity. Using the abdominal approach, an incision is made from the xiphoid cartilage to the umbilicus. This incision can easily be extended if necessary. Once the peritoneal cavity is opened, the diaphragm is exposed and the situation evaluated. The hernia is reduced by gentle traction on the stomach and the esophagus.

The omentum, small intestine, and liver lobes can also be herniated.

After reduction of the hernia the redundant phrenicoesophageal ligament is excised while preserving the vagal trunks.(Figure 2) The esophageal hiatus is reduced by Figure 2 mattress sutures placed in the medial diaphragmatic crura.(Figure 3) The hiatus is reduced to size of a finger. A simple esophagopexy is performed by placing interrupted sutures between the ventral esophagus and the diaphragmatic crura. A tube gastrostomy is then performed between the gastric fundus and the left abdominal wall. A Figure 3 thoracostomy tube should be placed for evacuation of the pleural space should be placed prior to complete closure of the hiatus.

POSTOPERATIVE CARE Post-surgical care includes systemic antibiotics and careful monitoring of the patient's breathing, temperature, and color. Small dogs and cats should be kept on a warming device for at least 24 hours. If complete bandaging of the chest is done, it should not be applied tightly because of the restriction of breathing. Analgesics may be used to relieve pain so that the animal can breathe more freely. The thoracostomy tube is checked every hours for the first 4 hours and then every 4 hours. The thoracostomy tube can usually be removed 24 hours after the surgery.

The gastrostomy tube after hiatal hernia is kept for at least 7 days. The stomach can be decompressed with the tube every 4 to 6 hours. Medications such as ranitidine, sucralfate and metoclopramide can be administered through the tube.

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Feline Heart Disease CARDIOMYOPATHIES & ARTERIAL THROMBOEMBOLISM John D. Bonagura, DVM, DACVIM (Cardiology, Internal Medicine) Ohio State University College of Veterinary Medicine, Columbus, OH

Overview of Feline Cardiovascular Diseases Genetic and idiopathic myocardial diseases are often termed ‘primary’ cardiomyopathies.

These include phenotypes of hypertrophic, dilated, restrictive, right ventricular, and unclassified cardiomyopathies, as well as myocarditis and a poorly defined disorder called “transient myocardial thickening”. Myocardial infarction is a poorly characterized disorder in cats that causes regional or global ventricular dysfunction. Of these conditions, hypertrophic cardiomyopathy (HCM) phenotype is most common.

These phenotypes can be genetically predetermined, adult‐onset disorders. However, these myocardial diseases can also stem from secondary defined disorders such as systemic hypertension, hyperthyroidism, taurine deficiency, diabetes mellitus, and growth hormone excess (acromegaly). Inasmuch as the echocardiographic findings overlap between primary and secondary myocardial disorders, these conditions should be distinguished whenever possible because as patient management and long‐term prognoses can differ.

Other causes of feline heart disease must be considered in the differential diagnosis of feline cardiomyopathies. Congenital malformations of the heart and great vessels are observed regularly in cats. Mitral valve malformation, ventricular septal defects, and atrial septal defects are encountered most often, but other lesions, including peritoneopericardial diaphragmatic hernia and patent ductus arteriosus must be considered. Although cardiac malformations usually are considered problems of kittens and young cats, these defects might go unrecognized until maturity.

Moderate to severe anemia is an under‐recognized reason for cardiac enlargement. As noted above, some cats with diabetes mellitus have myocardial heart disease, in some cases this is clearly related to a pituitary tumor, increased insulin like growth factor 1, and growth hormone excess. Additionally, severe respiratory diseases in cats can induce pulmonary hypertension and cor pulmonale, sometimes resulting in marked enlargement of the right heart. In contrast to other species, both degenerative valvular disease and infective endocarditis are very rare in cats. Pericardial effusions in cats are generally caused by congestive heart failure (CHF) and often resolve with effective treatment of the underlying condition.

Cardiac rhythm disturbances requiring treatment seem less common in cats when compared to dogs. However, atrial and ventricular ectopic rhythms do develop in association with cardiomyopathies, cardiomegaly, myocardial fibrosis, myocarditis, ischemia, infarction, increased sympathetic activity, electrolyte disturbances, hyperthyroidism, and cardiac or systemic neoplasia. Some persistent rhythm disturbances, including atrial fibrillation, can be idiopathic in cats. Atrioventricular blocks are observed most often in older cats from senile degeneration, although these can also occur with significant ventricular hypertrophy.

In terms of vascular disorders, idiopathic aortic dilatation, systemic hypertension, and arterial thromboembolism (ATE) are common diseases of mature cats. Idiopathic aortic dilatation

Feline Heart Disease (Cardiomyopathies & Arterial Thromboembolism) – Dr. Bonagura – Page 1

(aortoannular ectasia) is a seemingly benign disorder often observed in middle‐aged and older cats. Whether or not aortic stiffness is altered in this disease, or whether this vascular change contributes to systolic hypertension, has not been studied. This lesion is frequently associated with discrete upper septal thickening (DISH) or subaortic hypertrophy and a systolic murmur, clinical findings that can create confusion about the underlying cardiac diagnosis. Systemic hypertension is another common cause of LV hypertrophy in cats and also is associated with cardiac murmurs in cats; it rarely advances to CHF or aortic rupture. When blood pressure (BP) is severely elevated, retinal detachments and hemorrhages, renal injury, CNS depression, and hemorrhagic stroke are outcomes that are more common.

Types of Feline Cardiomyopathies The morphologic and functional characteristics, as well as the underlying etiology and severity of a cardiomyopathy, determine the classification, specific clinical findings, prognosis, and management of a particular myocardial disorder. The general clinical approach to feline cardiomyopathies is summarized later, as principles of management. This section reviews characteristic features of specific cardiomyopathies.

Hypertrophic Cardiomyopathy – Feline HCM is characterized by thickening of the left ventricular walls and papillary muscles unexplained by congenital disease, hypertension, or endocrinopathy.

(1, 2) Considering the prominence of HCM in the feline population and prevalence in certain breeds, it is not surprising that genetic mutations have been identified in some affected cats (including a mutation of myosin binding protein C). Some limited genetic testing is available currently; but this is mainly of value to breeders. Male cats are predisposed to HCM in some studies; however, there is no reported evidence of a sex‐linked mode of inheritance. Some specific breeds at risk for HCM include the Maine coon, Persian, Ragdoll, Bengal, Sphinx, American and British short‐hair cats, and Norwegian Forest cat.

The variable pattern of ventricular hypertrophy in this disease, ranging from concentric to focal (segmental) thickening, can be demonstrated at necropsy or by 2D echocardiography. The pattern of segmental or regional hypertrophy can influence the prognosis. For example, asymmetric free wall hypertrophy is often associated with significant LV dysfunction and progressive left atrial (LA) dilation. Conversely, focal subaortic, focal mid‐septal, or isolated papillary muscle hypertrophy are often well‐tolerated forms of HCM. However, these lesions progress in some cats and thus warrant follow‐up. As noted above, a specific variant of LV hypertrophy in older cats is a subaortic septal thickening associated with a dilated aorta. Whether this is actually a genetic HCM, or a degenerative aortic dilation (aortoannular ectasia) in which altered flow stimulates focal hypertrophy is undetermined. In most cases, this form is benign.

The key histologic findings of HCM are hypertrophy of cardiomyocytes with fiber disarray and interstitial fibrosis. Intramural coronary arteries are narrowed with foci of myocardial infarctions or replacement fibrosis observed. Some cats with HCM progress to a form of RCM or a type of DCM termed “burned out HCM”. In each of these conditions, extensive myocardial fibrosis is evident histologically.

Systolic ventricular function in most cats with HCM is hyperdynamic, but there can be regional or focal reductions that might require advanced (tissue) echo studies to identify and certainly systolic function can slowly degrade over time. When HCM evolves to an end‐stage or “burned Feline Heart Disease (Cardiomyopathies & Arterial Thromboembolism) – Dr. Bonagura – Page 2

out” form, the LV free wall or the entire left ventricle can be hypokinetic. RCM with severe biatrial dilatation also can evolve as a late phase of HCM although this is probably just a fibrotic end‐stage of HCM. Should atrial fibrillation develop, ventricular function is further impaired and this can precipitate severe CHF or ATE. Dynamic and labile pressure gradients between the LV and aorta are found frequently and confer the title of “obstructive” to HCM. These gradients stem from the combinations of septal and papillary muscle hypertrophy and systolic anterior motion (SAM) of the mitral valve. The latter is likely related to abnormalities of the papillary muscles or the valve itself. The major differential diagnosis is a primary mitral valve malformation.

The right ventricle is less often involved with HCM but can be affected in both structure (thickening) and function (occasionally impaired). The frequent finding of pleural effusions and jugular distension in cats with end‐stage HCM also suggests some role for RV involvement or secondary dysfunction. Septal thickening of HCM seems to facilitate dynamic RVOT obstruction, which is another common reason for a cardiac murmur in cats with HCM. The presumptive cause of CHF in feline HCM is diastolic LV dysfunction, which means that elevated left atrial and venous pressures are required to fill the ventricle. These abnormalities (discussed in the previous section) can be documented by advanced Doppler studies and generally evolve gradually, often over years, progressing from mild dysfunction due to impaired relaxation and shifting of filling to late diastole to severe diastolic failure with a restrictive form of ventricular filling. These filling disorders relate to the findings of atrial (S4) and ventricular (S3) gallops, respectively. Despite the long course of disease in most cats, sudden sympathetic stress or abrupt impairment of myocardial perfusion can lead to rapidly‐developing or “flash” pulmonary edema in cats with HCM with a need for emergent treatment. In some cases, diastolic function seems to improve with elimination of the stress, allowing a reduction in therapy over time. Some of these cats also reduce their wall thickness, suggesting a state of “transient myocardial thickening”.

Most cats with HCM are asymptomatic and recognized when a heart murmur or gallop sound is discovered during a routine examination, although it is emphasized that heart murmurs are quite variable in the HCM population and quite common as well in the normal/healthy cat population. As described previously, there are no unique clinical findings of HCM, and symptomatic cats can present with any combination signs. Similarly, other than the echocardiographic examination (or results of genetic testing), ECG, clinical laboratory, and ancillary studies do not sufficiently distinguish HCM from other forms of cardiomyopathy. Thus, a careful clinical workup including high quality cardiac ultrasound is required for definitive diagnosis. LV hypertrophy, including papillary muscle thickening, is the requirement for diagnosis.

The presence of significant SAM is invariably associated with an eccentric jet of mitral regurgitation (MR), and might represent an indication for beta‐adrenergic blockade.

Intraventricular or midcavitary obstructions often develop between the ventricular septum and papillary muscles and can be identified by Doppler studies.

Early diastolic dysfunction for the clinician is heralded by an atrial (S4) gallop. Progressive disease leads to decreased LV compliance, high venous pressures, a loud ventricular (S3) or summation gallop, and CHF. Progressive atrial dilatation and dysfunction go hand and hand with progressive loss of ventricular function. Thus, atrial size as observed by echocardiography or thoracic radiography stands as one of the best indicators of disease severity and short‐term prognosis.

Feline Heart Disease (Cardiomyopathies & Arterial Thromboembolism) – Dr. Bonagura – Page 3

The natural history of feline HCM can be benign or lethal; relatively brief or protracted; and some cats remain asymptomatic for many years before succumbing (if ever) to the disease. Even severely affected cats might be asymptomatic when first diagnosed. When present, severe LVOT obstruct has led to syncope or been associated with sudden cardiac death, but the frequencies of these complications is largely unknown. As in humans, there are seemingly different stages of HCM that range from 1) “occult” disease (with genetic mutations and subtle myocardial changes that are near or below thresholds of clinical detection); 2) established hypertrophic cardiomyopathy that is easy to diagnose by Echo but largely well‐tolerated, with no overt clinical signs and an overall low risk of sudden death, ATE, or CHF; and 3) progressive end‐stage HCM characterized by ventricular remodeling (including “burned out HCM”), progressive LA dilatation, impaired LV systolic function, and higher risks for CHF and ATE. These are generalities of course because some cats with seemingly mild LV hypertrophy will still experience bouts of thromboembolism or CHF. When clinical signs do develop with HCM, these are explained mainly by left‐sided CHF, complications of ATE, outflow tract obstruction, or arrhythmias. Left atrial size and left auricular function are probably the most important risk factors predicting ATE or CHF. Therapy of these complications is discussed below.

The REVEAL study in progress (Fox, et al, 2018) should provide more detailed prognostic information about the long term effects of having HCM. This study involves thousands of cats from around the world and will evaluate the risks for CHF, ATE, and cardiac death.

Restrictive Cardiomyopathy – Feline RCM represents a heterogeneous disorder, and some latitude is used in placing cats within this group as opposed to the “unclassified” category of feline cardiomyopathy (discussed below). The key pathologic feature of RCM is LV myocardial or endomyocardial fibrosis of uncertain pathogenesis. Antecedent myocarditis might be a cause, but in some cats RCM clearly represents a late stage of HCM as it does in human patients.

Burmese cats might have a predisposition to this disorder.

Post‐mortem lesions in cats with clinical features of RCM are dominated by fibrosis that is patchy, multifocal, or diffuse. The LV cavity is generally normal to decreased in size with variable but generally unimpressive hypertrophy, sometimes interspersed with regions of thinning or overt infarction. The latter changes are most evident in the LV free wall or apex. Prominent endocardial or papillary muscle fibrosis might be evident with extreme endocardial fibrotic scarring in some cases. Large moderator bands have been observed (and are classified by some as a congenital malformation or a separate form of cardiomyopathy). A consistent feature of RCM is striking left atrial or biatrial dilation. Histologic lesions include endocardial thickening, endomyocardial fibrosis, myocardial interstitial fibrosis, myocyte hypertrophy, focal myocytolysis and necrosis and arteriosclerosis. Systemic thromboemboli are common and LA and ventricular mural thrombi might be observed.

The clinical pathophysiology of RCM is compatible with a combined diastolic and systolic dysfunction syndrome. Increases of venous and atrial pressures, combined with ventricular dysfunction, atrial stiffness, and renal sodium retention, lead to CHF. Most cats with RCM are presented with overt clinical signs caused by CHF or ATE. Murmurs might not be evident, but loud gallop sounds are the rule, often punctuated by heart rhythm disturbances. The ECG is typically abnormal with wide P‐waves, ventricular conduction disturbances, and ectopic complexes common.

Feline Heart Disease (Cardiomyopathies & Arterial Thromboembolism) – Dr. Bonagura – Page 4

Echocardiography and Doppler studies generally demonstrate the following: mild systolic dysfunction; regional LV wall dysfunction; mild mitral or tricuspid valvular insufficiency; elevated LA pressures; and impaired LV distensibility with a “restrictive” filling pattern. Pulmonary edema, pleural effusion, jugular venous distention, and hepatic congestion are commonly identified through physical examination and diagnostic imaging. The ECG is often abnormal and atrial and ventricular rhythm disturbances are often evident, including atrial fibrillation or standstill. Stasis of blood in a dilated left atrium places affected cats at high risk for atrial thrombi and ATE. Management of RCM is based on control of CHF and prevention or treatment of ATE as discussed below. In cats with atrial fibrillation, diltiazem might provide the best control of ventricular heart rate. In the odd case that is diagnosed prior to onset of CHF, empirical use of an ACE‐inhibitor and anti‐platelet drugs such as clopidogrel seems warranted. Treatment of these disorders is considered at the end of these notes.

Dilated Cardiomyopathy – This disorder is uncommon today. Taurine deficiency can cause DCM in cats, and this is still observed in cats eating off‐brand or some “natural” diets, but most cases are idiopathic or related to diffuse myocarditis. The main postmortem lesions of DCM are left‐ sided or four‐chamber dilatation, generally with necropsy findings of CHF and with no demonstrable congenital, coronary, or valvular heart disease. Histological findings include myocyte loss, prominent interstitial fibrosis, and variable degrees of hypertrophy and myocytolysis or apoptosis. Some cases are characterized by diffuse myocarditis.

The clinical features of DCM in cats are indistinguishable from those of other cardiomyopathies.

Heart sounds can be soft owing to impaired contractility or pleural effusion. The principle functional disturbance as shown by echocardiography is marked reduction of LV ejection and shortening fractions, often with mitral and tricuspid regurgitation caused by ventricular dilation and dysfunction. While some cats are detected in the asymptomatic phase, cardiogenic shock, left‐sided CHF, or biventricular CHF are the most common presentations. These might be complicated by ATE. Prognosis is poor unless the condition is related to taurine deficiency. Oral taurine supplementation should be administered while awaiting results of a blood taurine test or at a minimum for 2 to 3 months following diagnosis. Management is discussed below.

Right ventricular cardiomyopathy – This condition, sometimes referred to as arrhythmogenic right ventricular cardiomyopathy, has been observed in cats, and the necropsy features have been described (Fox et al, 2000). The right ventricle is replaced by fat and fibrous tissue with the consequences of right‐sided myocardial failure and right‐sided dilatation with tricuspid regurgitation. Right Ventricular Cardiomyopathy is characterized in most cases by right sided CHF. Atrial standstill or atrial fibrillation might be apparent on the ECG. Ventricular ectopic rhythms are common as well. These cats generally present for clinical signs of pleural effusion, infrequently with concurrent ascites, owing to right‐sided CHF that can include development of chylothorax. Sudden death has been reported. Early cases might demonstrate only atrial or ventricular arrhythmias. Diagnosis hinges on echocardiography and exclusion of other predominately right‐sided diseases such as atrial septal defect and cor pulmonale. Treatment involves control of CHF and possibly antiarrhythmic therapy (see below).

Feline Heart Disease (Cardiomyopathies & Arterial Thromboembolism) – Dr. Bonagura – Page 5

Other Acquired Myocardial Diseases – A number of other cardiomyopathies are encountered in cats. Some of the key features of these are summarized below.

Reversible or transient ventricular thickening – This term is used to describe cats that typically present with pulmonary edema and other findings of acute left‐sided CHF. The LV walls appear thickened and the cats typically respond to diuresis and management with furosemide and an ACE‐inhibitor. Follow‐up examination indicates that the heart is no longer thick, atrial size normal, and some clients have actually stopped administering medication to their cats (without advise). Whether or not the so‐called corticosteroid induced cardiomyopathy (typically from Depo‐Medrol®) fits into this group is uncertain. The primary differential diagnosis is a misdiagnosis of CHF in a cat that is also dehydrated and has pseudohypertrophy of the LV walls due to volume depletion.

Unclassified cardiomyopathy – The term “Unclassified Cardiomyopathy” describes a myocardial disease of unknown etiology that does not readily fit into one of the above categorizations.

Findings of RCM and UCM are often very similar, and undoubtedly, what one cardiologist might call RCM is classified as UCM by another. Myocardial infarctions and primary atrial diseases might also lead to this diagnosis. Occasionally cats with left atrial dilation, impaired LV diastolic function, but no overt LV myocardial disease are identified (these might be a form of HCM without hypertrophy, a condition recognized in people). The assessment and management of the feline patient with unclassified cardiomyopathy can be “simplified” by describing completely the clinical, imaging, ECG, and biochemical findings evident in the patient and then directing treatments towards managing these abnormalities. Practically, most cases of unclassified cardiomyopathy present with CHF or ATE and are treated for these problems (see below).

Nonsuppurative and suppurative myocarditis occurs sporadically in cats. The cause is unknown and definitive diagnosis requires microscopic examination of the tissues. There is a tendency for cats with myocarditis to be young. Some are presented for ventricular arrhythmias, while others develop fulminant heart failure, ATE or RCM. Death during anesthesia is another common scenario. The clinical diagnosis is based on suspicion and exclusion of other diseases. Blood cTnI is generally elevated, but this is not a specific finding for myocarditis, and there is no “gold standard” short of myocardial histology to confirm the diagnosis. Myocarditis can also be associated with infectious diseases including toxoplasmosis, so this should be a consideration before anti‐inflammatory therapies are considered. It is likely that some cases of “transient myocardial thickening” are actually due to edema and myocardial inflammation associated with myocarditis that later reverses course. No therapies have been shown to be effective in treating myocarditis and patient management is generally supportive, related to identifiable clinical problems.

Hyperthyroid Heart Disease – Thyrotoxicosis causes cardiac hypertrophy related to a hypermetabolic state, peripheral vasodilation, and increased demands for cardiac output.

Increased sympathetic nervous system activity and elevated thyroid hormone levels might stimulate myocardial hypertrophy. In chronic cases of hyperthyroidism, the LV becomes thickened, and concurrent systemic hypertension probably contributes to this in many cases.

Echocardiography typically shows LV hypertrophy, often indistinguishable from idiopathic HCM. Feline Heart Disease (Cardiomyopathies & Arterial Thromboembolism) – Dr. Bonagura – Page 6

Typical findings in advanced cases associated with fluid retention are bi‐atrial dilatation with normal to reduced LV ejection fraction. These cats are at risk for CHF which is often precipitated by the administration of sodium containing fluids.

Circulatory Overload – This condition is usually observed in cats with comorbidities that predispose to sodium and volume retention (moderate anemia, hyperthyroidism, possibly some cats with primary kidney disease) and follows crystalloid therapy – typically 1.5 to 2x maintenance therapy with Plasmalyte® or lactated Ringer’s solution. These cats often have underlying diastolic dysfunction due to age, hypertension, or previously‐compensated hypertrophic cardiomyopathy. Echocardiography shows biatrial dilatation and the fluid accumulation is most often in the pleural space (as opposed to cats with moderate to severe HCM where fluid therapy often precipitates pulmonary edema). A helpful sign is to examine the cat for jugular venous distension, which is often present. In most cases a careful calculation of the sodium intake (in mg.) relative to the actual daily needs demonstrates that the cat is simply “over‐hydrated”. Reducing fluid intake, using lower‐sodium concentrations, and if necessary diuretic therapy will usually stabilize the situation. A large pleural effusion should be tapped.

Therapy of Acquired Feline Cardiovascular Diseases – Overview Risk stratification is important, especially when treatment evidence is lacking. This history should include past hospitalizations for congestive heart failure (CHF), arterial thromboembolism (ATE), or syncope as these place a cat into a high‐risk category. The size of the left atrium (LA) is probably the best overall predictor of current risk in asymptomatic cats. Other factors that may affect therapeutic decisions include the echocardiographic findings of systolic dysfunction of the left ventricle (LV); severe diastolic dysfunction of the LV (poor compliance/high filling pressures); severe morphologic changes of LV hypertrophy (e.g., “extreme hypertrophy” of 9 mm or more in diastole); myocardial scarring; regional wall motion abnormalities suggesting prior infarction; and mural thrombus, echogenic smoke, or impaired contractile function of the LA or atrial appendage. Finding a cardiac arrhythmia such as atrial fibrillation or complicated ventricular ectopy often prompts treatment. Of course a cat with cardiomyopathy secondary to systemic hypertension or hyperthyroidism will be treated and probably benefit most from control of the underlying disorder (e.g., amlodipine plus benazepril for systemic hypertension).

Optimally, therapies should affect major clinical endpoints. These include a) prolonging survival time, b) improving quality of life (enhancing activity and controlling “signs and symptoms” of clinical disease), and c) reducing the need for unanticipated, emergent veterinary visits.

Presumably, any effective treatment would somehow: a) delay disease progression, b) reverse‐ remodel the myocardium, c) prevent lethal arrhythmias, d) prevent thrombosis, e) improve ventricular function, or f) manage CHF. Up to this point, most treatments have evolved empirically and (at the time of this writing) there are no pivotal, prospective studies available.

Retrospective studies have suggested a role for various treatments, but none of these fulfill the evidence for a high‐grade treatment study (i.e., prospective, randomized, multicenter, double blinded, sufficiently powered). This session considers approaches to the cat with asymptomatic HCM, as well as management and prevention of CHF and ATE in cats with cardiomyopathy.

Feline Heart Disease (Cardiomyopathies & Arterial Thromboembolism) – Dr. Bonagura – Page 7

Asymptomatic Hypertrophic Cardiomyopathy The treatment of asymptomatic HCM is controversial with no clear benefit of any drug shown for asymptomatic cats with mild disease. Clients should be advised of this information prior to writing prescriptions for a difficult‐to‐treat species. A recent prospective study failed to demonstrate any 5‐year survival benefit of atenolol, although the study was limited by a small number of cats and low event rate. In a colony of cats with HCM, neither ramipril nor spironolactone significantly altered hypertrophy, diastolic function, or MRI‐estimated fibrosis.

However, these were healthy HCM cats and the effect of these drugs in advanced disease or in CHF might be different.

Dynamic LV outflow obstruction is a risk factor for syncope and sudden death in people with HCM, but some reports suggest the opposite situation for cats (an observation confounded by the frequency of cardiac murmurs found in obstructive HCM, when compared to cats with non‐ obstructive forms of disease that are likely under‐diagnosed). Despite the lack of evidence, many cardiologists treat dynamic LV obstruction associated with HCM. Atenolol is usually selected because it is well‐tolerated and better reduces heart rate, dynamic obstruction, and intensity of murmurs compared to diltiazem. Beta‐blockade also confers theoretical advantages of diminishing demand ischemia, prolonging ventricular and coronary filling periods, and protecting against sympathetically‐induced arrhythmias. However, none of these benefits have been proven or translated to major clinical endpoints. Some clients do report “greater activity” in cats after atenolol (as shown in a recent clinical report), but a placebo effect might be operative.

Overdosing of atenolol can lead to lethargy, bradycardia, and reduced left auricular function. The latter can develop on standard doses and is problematic if the risk of ATE is high. Atenolol doses (6.25–12.5 mg/cat PO bid) are usually adjusted based on exam room heart rate with a target of 120 to 160/minute.

Some clinicians prefer diltiazem, especially when there is no evidence of dynamic obstruction.

Theoretically, this calcium‐channel blocker can improve myocardial relaxation and induce coronary artery vasodilation (along with modest effects on heart rate and obstruction). However, there is no conclusive evidence of efficacy for this drug either and the higher adverse effect profile for the sustained release product (anorexia, weight loss, and skin lesions) limits its use. The author reserves its use to control of heart rate in cats with atrial fibrillation.

In the absence of clear evidence, the author discusses with clients the pros/cons of empirical therapy of HCM with moderate to severe LV outflow tract obstruction. In most cases, atenolol is initiated as discussed above, especially in younger cats, and for at least 6 months with reevaluation of any morphologic or obvious clinical benefits of treatment. In asymptomatic HCM cats with moderate LA dilation (two‐dimensional, long‐axis LA diameter of 20 mm), the atenolol dose should be reduced or not used (as it can depress LA function). In those cats, the author aso prescribes an ACE‐inhibitor along with antiplatelet therapy (clopidogrel ± aspirin–see below).

Either enalapril or benazepril is prescribed (both dosed between 0.25–0.5 mg/kg PO bid) and the client is dispensed a “rescue” prescription of furosemide and two preloaded syringes with buprenorphine (0.2–0.4 ml of the 0.3 mg/ml concentration). Furosemide is given should the cat develop resting tachypnea and buprenorphine (on the oral mucosa) if signs of ATE supervene.

(Clients are also instructed to seek prompt care for dyspneic or paretic cats).

Feline Heart Disease (Cardiomyopathies & Arterial Thromboembolism) – Dr. Bonagura – Page 8

Congestive Heart Failure Management of the cat with acute or severe CHF begins with gentle handling. Cats with pulmonary edema are managed with the “SO‐FINE” approach: Sedation (butorphanol 0.2–0.3 mg/kg IM), Oxygen (40–50%), Furosemide (2–4 mg/kg, IV/IM), ± Inotrope (see below), Nitroglycerine (1/8 to 1/4 inch of 2% NTG ointment), and “Extra” therapy as needed. Once diuresis occurs and symptoms improve, furosemide dose is reduced (1–2 mg/kg q12h).

Nitroglycerin is administered once for potential venodilation hoping to reduce ventricular preload. Inotropic drugs are not part of initial treatment of most cats with CHF due to HCM, but for the cat with impaired systolic function pimobendan (1.25 mg bid for an average sized cat) is administered. For cats with cardiogenic shock (hypothermia, bradycardia, systolic BP<70 mm Hg) dobutamine can be life‐saving (regardless of the type of cardiomyopathy). Dosing starts at 2.5 micrograms/kg/minute and is up‐titrated to 5 to 10 micrograms/kg/min with therapeutic targets of rectal temperature of >100oF (37.8 Co); heart rate >180/minute, and systolic BP >90 mm Hg. As indicated above, when a “FAST” thoracic scan shows systolic dysfunction and no outflow obstruction, pimobendan (1.25 mg/ cat, PO), is also considered appropriate therapy.

Thoracocentesis is the most important “Extra” therapy and indicated to treat moderate‐to‐large pleural effusions. With the cat sedated, positioned in sternal recumbency, and receiving supplemental oxygen by face mask, a small butterfly catheter is inserted in the intercostal space following a local infiltration of lidocaine (if needed). When pleural effusions are bilateral, tapping the right thorax might avoid puncturing a dilated left auricle.

The home therapy of chronic CHF centers on administration of furosemide (1–2 mg/kg, PO qd– bid), combined with an ACE‐inhibitor (enalapril/benazepril: 0.25–0.5 mg/kg, PO qd–bid).

Spironolactone (6.25–12.5 mg/cat, once daily) can be added. Antiplatelet therapy is initiated.

Neither atenolol nor diltiazem is recommended (both were ineffective in an unpublished multicenter study). Extralabel use of pimobendan (~0.25 mg/kg or 1.25 mg/cat PO q12h) provides an additional treatment option for chronic CHF. I prescribe pimobendan immediately for cats with CHF due to dilated, unclassified, or right ventricular cardiomyopathy, and hold it in reserve for refractory failure when CHF is caused by HCM, especially with HOCM. Pimobendan should be used with caution if at all in cats with HCM with dynamic LVOT obstruction. Although a retrospective study showed potential (marked) benefit of pimobendan in cats with HCM, a prospective study was less impressive and did not achieve the statistically‐significant endpoint.

However, clearly some cats with HCM do benefit and holding it in reserve (as discussed above) is probably a prudent approach. Rutin (250 mg/cat PO q12h) is considered when chylothorax complicates CHF. Famotidine (~5 mg/cat PO qd–bid) is an empirical treatment for anorexia.

Should the patient fail these treatments, consultation with a cardiologist is encouraged. Overall, therapy can be remembered as “Cats Are For Special People” – relating to Clopidogrel, ACE‐ inhibitor, Furosemide, Spironolactone, Pimobendan, with the caveat that pimobendan will not be used in all cases.

Clients are counseled regarding signs of decompensation (can’t breathe!/can’t walk!); treating cats (try: pill pockets, gelatin capsules, pill guns); and monitoring of activity level and interactions, ventilation effort, sleeping respiratory rate (<35/min is OK), and appetite. Follow‐up veterinary examination begins with a medical history and a conversation focused on treatment compliance.

A careful physical examination is critical. Diagnostic testing may involve BP, serum biochemistries, thoracic radiography, and cardiac/thoracic ultrasound.

Feline Heart Disease (Cardiomyopathies & Arterial Thromboembolism) – Dr. Bonagura – Page 9

Arterial Thromboembolism Arterial thromboembolism (ATE) is a sudden interruption of blood flow caused by a thrombus that forms proximal to the affected site and is carried by the bloodstream to the location of vascular obstruction. In most cases, the site of origin is the auricle of an enlarged left atrium (LA) from a primary or secondary cardiomyopathy (cardiogenic embolus). Uncommon causes of ATE are infective endocarditis, and mitral dysplasia. Pulmonary neoplasia is a noncardiac cause of ATE. Obstruction to flow leads to ischemia and tissue injury. In the absence of collateral flow, cell death or infarction occurs in the territory supplied by the obstructed vascular bed.

Risk Factors – Three pathophysiologic features of Virchow’s triad promote thrombosis in the LA; these are blood stasis; hypercoagulability; and endothelial (endocardial) injury. Blood stasis is predisposed by left atrial dilatation and loss of atrial contractility. In vitro studies have suggested a hypercoagulable state in cardiomyopathy. Dilatation and high‐pressure in a diseased LA could conceivably alter endocardial (intimal) function. Thrombi are platelet‐rich but also involve progressive incorporation of fibrin; thus, both anti‐platelet drugs and agents that inhibit fibrin formation can potentially prevent intracardiac thrombosis. From a practical perspective, the echocardiographic assessment of the size and function of the LA and its appendage are key when assessing risk of ATE. A previous ATE, presence of LA thrombus, and echogenic contrast (“smoke”) pose a high risk for a future event. A solid, round thrombus seen by Echo is a lesser concern than the soft thrombus with a “floating” or “waving” tail.

According to Hogan, the cardiogenic embolism has been reported in 6% to 17% of cats with heart disease. Males are overrepresented, and breeds that appear to have an increased risk are Ragdoll, Birman, Tonkinese, and Abyssinian. The typical history is of a sudden loss of limb function associated with acute onset of severe pain, especially if the thrombus goes to the typical location of the aortic trifurcation (at the origin of the iliac arteries). At necropsy, these “saddle thrombi” are relatively large and fill the distal aorta, external iliac arteries, and origin of the internal iliac arteries affecting blood flow to the rear limbs and the tail. Rarely three or even four‐limb paresis is observed. When the thrombus is massive and extends cranially to involve the mesenteric blood supply, the cat usually exhibits excruciating pain. Clients usually recognize loud vocalization.

Some cats are moribund with shock and metabolic acidosis at presentation. Obstructed blood flow in the axillary or brachial artery can lead to sudden forelimb paralysis.

The physical diagnosis of terminal aortic embolism is straightforward and characterized by vascular, musculoskeletal, and neurological deficits, and associated laboratory abnormalities.

The affected limbs are cool, pulseless, and pale. Generally, a Doppler crystal over the affected artery demonstrates the loss of blood flow. Occasionally the thrombus is located distal to the femoral triangle and pulses and Doppler flow can be detected proximally. The muscles become firm to rigid due to ischemia and are associated with elevations of serum creatine kinase, AST, and ALT. Lower motor neuron paresis/paralysis develops. If a large aortic thrombus is suspected, the abdominal aorta can be imaged with ultrasound. A very low temperature was associate with a poor outcome in the retrospective Smith study but distal rectal temperature also can be low due to poor regional perfusion. Radiographs of the thorax can document CHF (or lung cancer) if present. Heart failure is also a poor prognostic sign, reducing survival by about 1/3 in one study.

Echocardiography should delineate underlying cardiac disease.

Feline Heart Disease (Cardiomyopathies & Arterial Thromboembolism) – Dr. Bonagura – Page 10

Management of Feline Arterial Thromboembolism – The first and most important treatment is analgesia with a strong mu agonist for the first 24–48 hours following an event. Fentanyl is often used in our practice and provides excellent analgesia (beware: hyperthermia). Initiate therapy with 3 micrograms/kg and follow that with maintenance infusion of 1 to 3 micrograms per kg, IV per hour. Methadone, morphine or buprenorphine are other options. In the absence of hypothermia or hypotension, acepromazine (0.025 mg/kg subcutaneously) will sedate the cat further. Pain in most cats is diminished by 36 to 48 hours allowing transition to buprenorphine (10 to 20 micrograms/kg IM, SQ, or orally).

The current thrombotic issues can be managed actively with tissue plasminogen activator (tPA) plus heparin or conservatively by administering unfractionated or low‐molecular weight heparin. We dose tPA at 1 mg/kg (maximal total dosage of 6 mg/cat): 10% of the dose is given as a slow IV bolus and the rest is infused over ~one hour. Therapy with tPA therapy is only offered if the cat presents within 6h of a witnessed event. Heparin therapy is administered to prevent further thrombosis. Standard (unfractionated) heparin is dosed at approximately 250 to 300 units/kg IV. Thereafter either a constant rate IV infusion or subcutaneous dosing at approximately 150‐250 U/kg subcutaneously q6 to 8h for 48–72 hours. Alternatively, low‐molecular‐weight heparin (LMWH) can be administered. These have a smaller molecular weight than unfractionated heparin. Both dalteparin (100 IU/kg bodyweight subcutaneously q12h) and enoxaparin (1 to 1.5 mg/kg subcutaneously q12h) have been used. Some clinicians begin clopidogrel as well (18.5 mg PO daily), but the combination of tPA, heparin, and clopidogrel is not advised due to bleeding risk. When only heparin is given, clopidogrel can be started.

Most cats that do improve within 72 hours of admission. Home care includes: 1) protecting the limbs; 2) daily inspection for subcutaneous or muscle edema; 3) cleaning urine‐soaked hair and bedding; 4) providing a soft bed; 5) encouragement to eat; 6) stool softeners (Miralax®); and 6) a low stress area for convalescence. Oral buprenorphine is continued for 3‐5 days. Physical therapy of the limbs characterized by passive flexion of the limbs is encouraged.

Prevention of Thromboembolism – Possible approaches include: 1) aspirin monotherapy (dosed between 5 mg to 81 mg q72h); 2) warfarin (~0.5 mg per cat, PO daily); 3) low molecular weight heparins including enoxaparin (1 mg/kg) and dalteparin (100 IU/kg) subcutaneously once or twice daily; and 4) clopidogrel (Plavix®, 75 mg tablets, ¼ tablet – or 18.75 mg – PO once daily). The clinical trial evaluating clopidogrel versus aspirin (FATCAT) in secondary prevention of cats that have recovered from ATE indicates superiority of clopidogrel over aspirin for prevention of recurrent thrombosis. There was no group receiving both treatments (these drugs work by different mechanisms and might be complementary). In this study, median survival time significantly prolonged with clopidogrel and the median time to either death or the next ATE event was 443 days compared to 128 days in the aspirin group.

The author does not routinely prescribe antithrombotic therapy in asymptomatic cats with a near normal LA, provided auricular emptying velocities >25 cm/s. Clopidogrel (¼ of a 75 mg tablet) is prescribed for the cat with a moderate to severely dilated LA (≥20 mm), or when emptying velocities are <20 cm/s. Adult‐regimen 81 mg aspirin dosed at one tablet PO q72h is an alternative, but is less effective. For cats at the highest risk for ATE (LA dilation ≥25 mm, echogenic smoke in LA, auricular emptying velocities <20 cm/s, or a history of prior ATE) the author considers more aggressive therapy with both clopidogrel (¼ of a 75 mg tablet once daily) and a Feline Heart Disease (Cardiomyopathies & Arterial Thromboembolism) – Dr. Bonagura – Page 11

very low dose daily aspirin (compounded or “crumbled” to a dose of between 5 to 10 mg per cat daily, mixed in a gel cap (as both drugs are bitter). Another alternative for cats at high risk of ATE is once or twice‐daily administration of a low molecular weight heparin preparation, generally enoxaparin with clopidogrel. Warfarin is not prescribed. The use of inhibitors of factor Xa are also likely to be effective (e.g. apixaban or Eliquis®) but the author recommends waiting for published clinical trial data before replacing clopidogrel with this drug (it is likely both can be used).

Prognosis – Prognosis is guarded but better than most recognize. The main prognostic factor is probably the client’s willingness and ability to support treatment for 2‐4 days and to provide long‐ term care. The client should be advised about the 1) need for intensive therapy; 2) the high risk of ATE recurrence; 3) daily home medical care; 4) likelihood of underlying cardiomyopathy; 5) costs; and 6) potential for sudden death. These issues certainly can prompt euthanasia, although it is stressed that at least half of cats can be released from the hospital assuming the clients permit aggressive treatment. As indicated above, the positive results with clopidogrel prevention therapy has offered new hope for more favorable long‐term outcomes.

Reference Multiple Authors: The Feline Heart, Journal of Veterinary Cardiology (Special Suppl), Vol 17, Dec 2015k ppS1‐S359.

Feline Heart Disease (Cardiomyopathies & Arterial Thromboembolism) – Dr. Bonagura – Page 12

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LAPAROSCOPY IN SMALL ANIMAL PRACTICE IS IT POSSIBLE? Eric Monnet, DVM, PhD, FAHA Diplomate ACVS and ECVS Colorado State University, Fort Collins, Colorado Eric.Monnet@ColoState.EDU There is a number of minimally invasive surgical (MIS) procedures that are currently performed using laparoscopy. Many of these procedures require multiple trocar/cannula portals, specific minimally invasive surgical instruments, loop ligatures, clip applicators and monopolar electrosurgery. The techniques described below are the “tip of the iceberg” in as far as the potential for MIS in veterinary medicine. They can be performed in a small animal practice.

Intestinal Biopsy Small intestinal biopsies can be obtained using laparoscopy simply by exteriorizing a piece of intestine through the abdominal wall and then collecting the sample externally as would be done with a standard surgical biopsy. A 5-mm atraumatic grasping forceps with multiple teeth is used to grasp the intestine at the site to be biopsied. It may be necessary to “run” the bowel with two grasping forceps to select a location to biopsy. The antimesenteric boarder is firmly grasped with the forceps. The intestine is then pulled to the cannula. A 3-4 cm loop of intestine is exteriorized.

A small full thickness biopsy is then obtained in the same manner as one would use when performing an open abdominal surgical technique. The intestine is then returned to the abdominal cavity. If too much intestine is exteriorized it is difficult to return it to the abdominal cavity through a small incision.

Intestinal Feeding Tube Placement Duodenostomy or jejunostomy feeding tubes can be placed using the laparoscope simply by exteriorizing a respective piece of intestine through the abdominal wall and inserting the tube externally. Once the location of the bowel for tube placement is determined the antimesenteric boarder is firmly grasped with the forceps. The intestine is then pulled close to the cannula in which the intestine will be exteriorized. A 3-4 cm loop of intestine is exteriorized and four stay sutures (4-0 monofilament absorbable) are placed in the intestine to prevent the intestine from falling back into the abdominal cavity. A purse-string suture is placed on the antimesenteric border of the intestine. A number 11 blade is used to puncture the intestine in the middle of the pursestring suture and the jejunostomy feeding tube (5 French for cats and 8 French for dogs) is introduced in the loop of bowel in the aboral direction. The purse string suture is closed and the intestine is returned to the abdominal cavity except for the segment containing the feeding tube.

The stay sutures are then used to pexy the intestine to the abdominal wall using 4.0 monofilament absorbable sutures. The abdominal wall is then closed with simple continuous suture pattern.

Subcutaneous tissue and skin are closed in a routine fashion. The feeding tube exits through the incision.

Intestinal foreign body Single, non-linear foreign body in the jejunum or ileum can be removed under laparoscopy.

Dogs or cats with signs of peritonitis are not good candidates for this procedure. The surgical technique is the same as for a jejunostomy tube placement. The loop of intestine with the foreign body is exteriorized and an enterotomy or an enterectomy is performed outside of the abdominal cavity. The loop of intestine is then returned into the abdominal cavity at the end of the procedure.

Gastropexy A preventive gastropexy can be performed using the laparoscope simply by exteriorizing the pyloric antrum region of the stomach through the right abdominal wall. The animal is placed in dorsal recumbency and the telescope portal is placed on the midline at the level of the umbilicus.

A 5-mm atraumatic grasping forceps with multiple teeth is used to grasp the pyloric antrum middistance between the lesser and the greater curvature. The pyloric antrum is exteriorized after extension of the cannula site situated behind the last rib on the right side. An incisional gastropexy is then performed.

Ovariohysterectomy /Ovariectomy Ovariohysterectomy or ovariectomy can be performed using laparoscopy in any size dogs.

The space in the abdominal cavity of small dogs and cats make the procedure technically difficult.

The advantage of this technique is the perceived rapid patient recovery following the procedure and the improved visualization of the ureters and the pedicle for hemostasis.

The procedure is performed on dorsal recumbency and tilting the dog on the right and the left side to expose the ovaries.

Two cannulas are enough to perform an ovariectomy or an ovariohysterectomy. The ovariohysterectomy is laparoscopically assisted then. The cannula for the endoscope is placed caudal to the umbilicus.

For an ovariohysterectomy the second cannulas is placed caudal in the abdomen. The ovaries are suspended with a transcutaneous suture on the abdominal wall. Each ovarian pedicle is ligated with either suture, endoclips, electrocautery, or a vessel sealant device. After ligation of both ovarian pedicles, the uterus is exteriorized in the caudal abdomen through the caudal cannula.

The cervix is ligated outside the abdominal cavity like during a regular ovariohysterectomy. The cervix is then returned to the abdomen.

For an ovariectomy the second cannula is placed cranial to the umbilicus. The ovarian pedicles are ligated as described above. Another ligature will be placed on each uterine horn before transecting the ovaries from the uterus. Electrocautery or vessel sealant device can be used to transect the uterus at the level of the proper ligament. Both ovaries will be removed through one cannula site.

The enlarged cannula sites are sutured with a simple continuous suture pattern with 2-0 monofilament absorbable suture material. Subcutaneous tissue and skin are closed in a routine fashion. The other cannula site requires only subcutaneous and skin sutures.

Cryptorchid Surgery A testicle that is located in the abdominal cavity can be removed easily with laparoscopy.

Laparoscopic vasectomy can also be performed through this technique. The dog is placed in dorsal recumbency. The monitor is placed at the end of the table as described for ovariohysterectomy surgery. The procedure is performed with two cannulas. One is placed cranial to the umbilicus while the other is caudal to the umbilicus.

The ectopic testicle is usually readily visible upon entering the abdominal cavity. The ectopic testicle of one side rarely ever crosses the midline but stays lateral to the bladder on the effected side. The testicle is grabbed with a fine tooth grasper and a transcutaneous suture is placed through the abdominal wall to stabilize the ectopic testicle. The vascular pedicle and the vas deference are ligated with a pre-tied suture, clips, or electrocautery. The ectopic testicle is removed through one the cannula holes that generally must be enlarged. The enlarged cannula site is sutured with a simple continuous suture pattern with 2-0 monofilament absorbable suture material.

Subcutaneous tissue and skin are closed in a routine fashion. The other cannula sites require only subcutaneous and skin sutures.

Laparoscopic Cystoscopy Laparoscopic cystoscopy is an alternate method that allows placement of a laparoscopic telescope into the urinary bladder that has been exteriorized through the abdominal wall for examination, biopsy and calculi removal. The technique involves a standard laparoscopic entry with the telescope placement on the abdominal midline cranial to the umbilicus. Once the urinary bladder is visualized a second trocar cannula is placed directly over the urinary bladder at the location of exteriorization. Using atraumatic forceps with multiple teeth the bladder is grasped and pulled into the trocar cannula as described in intestinal biopsy section. Once the apex of the bladder is exteriorized stay sutures are placed from the bladder wall. The bladder is temporally pexied to the abdominal wall. A small incision is made in the bladder wall, the bladder is then flushed with sterile saline and the telescope is introduced into the bladder. Forceps can be placed in the lumen along the telescope to obtain a biopsy or remove calculi. At the conclusion of the procedure the bladder is closed in a standard manner and placed back into the abdomen. The cannula ports are then closed. The pexy is released and the abdominal wall closed in a routine fashion.

Laparoscopy is a minimally invasive technique for diagnostic and surgical procedures.

Once the basic technique of laparoscopy is mastered and the appropriate indications are applied to the procedures it becomes a simple and rewarding addition to small animal veterinary medicine and surgery. As our ability advances newer diagnostic and therapeutic procedures will no doubt be developed.

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LARYNGEAL PARALYSIS Eric Monnet, DVM, PhD, FAHA Diplomate ACVS and ECVS Colorado State University, Fort Collins, Colorado Eric.Monnet@ColoState.EDU The laryngeal functions are to regulate airflow, voice production, and prevent inhalation of food. If the intrinsic muscles and/or the nerve supply of the larynx are not normal laryngeal functions are compromised.

The dorsal cricoarytenoide muscle abducts the arytenoid cartilages at each inspiration.

The laryngeal recurrent nerve innervates this muscle. Central lesions or lesions to the laryngeal recurrent nerve or to the dorsal cricoarytenoide muscle result in laryngeal paralysis in dogs and cats. Laryngeal paralysis can be unilateral or bilateral ETIOLOGY Congenital and acquired forms of laryngeal paralysis have been recognized in dogs and cats.

Congenital Laryngeal Paralysis Congenital laryngeal paralysis has been reported in Bouvier des Flandres, bull terrier, Dalmatian, Rottweiller and Huskies. Bouvier des Flandres and bull terrier have mostly been reported from Europe while the Dalmatian and Huskies from United States. Laryngeal paralysis has a hereditary transmission in Bouvier des Flandres with an autosomal dominant trait. Dogs with congenital laryngeal paralysis are clinical at an early age (before one year old) than dogs with acquired laryngeal paralysis. Usually dogs with congenital laryngeal paralysis have several neurological deficits like ataxia.

Acquired Laryngeal Paralysis Acquired laryngeal paralysis is most commonly reported in Labrador retriever, Golden retriever, St Bernard and Irish Setter at an age of 9 years old. It has been reported in cats.

Acquired laryngeal paralysis is more frequently idiopathic; however, other causes should be ruled out. Several diseases and conditions may contribute to laryngeal paralysis. A cranial mediastinal or neck mass stretching or compressing the laryngeal recurrent nerves can induce a laryngeal paralysis. Trauma to the laryngeal recurrent nerve during dogfights or during surgery in the neck can cause of laryngeal paralysis. Laryngeal paralysis in the cat has been diagnosed after bilateral thyroidectomy. Finally, a ployneuropathy involving the laryngeal recurrent nerve is the most common cause of laryngeal paralysis. The polyneuropathy can be due to an endocrine insufficiency (hypthyroidism) . However most of the time a diagnosis of idiopathic polyneuropathy is made because no causes can be identified. A myopathy involving the intrinsic muscle of the larynx.

CLINICAL FINDINGS History The presenting signs are similar for the congenital and acquired forms. Progression of signs is often slow; months to years may pass before an animal develops severe respiratory

distress. Early signs include change in voice, followed by gagging and coughing, especially during eating or drinking. Endurance decreases and laryngeal stridor (especially inspiratory) increases as the airway occlusion worsens. Episodes of severe difficulty breathing, cyanosis, or syncope occur in severely affected patients. Male dogs are approximately three times more affected than female. Laryngeal paralysis can be accompanied with various degrees of dysphagia, which significantly enhances the probability of aspiration pneumonia after surgical correction of the laryngeal paralysis.

Physical Examination The physical examination of dogs with laryngeal paralysis is fairly unremarkable. Dogs have a difficulty breathing on inspiration that is not alleviated with open mouth breathing.

Mild lateral compression of the larynx significantly increases inspiratory effort. Referred upper airway sounds are present during auscultation of the thoracic cavity. Auscultation of the thoracic cavity and the lung field may reveal the presence of pneumonia in the cranial lung lobe due to aspiration. Palpation of the muscle mass may reveal skeletal muscle atrophy in cases of polyneuropathy. The tibial cranial muscle is very commonly atrophied in dogs with endocrine polyneuropathy. A complete neurological examination is required to evaluate the animal for a polyneuropathy.

Laboratory Findings Complete blood count and chemistry profile are usually within normal limits.

Hypercholesterolemia, hyperlipidemia, and augmentation of liver enzymes activity are present on the chemistry profile for dogs with hypothyroidism. A thyroid profile with endogenous TSH and free T4 is then required to further define the diagnosis. Laryngeal paralysis has inconsistent correlation with hypothyroidism.

Radiographic Examination It is necessary to perform a radiographic examination of the thoracic cavity for the evaluation of the lung parenchyma and the esophagus. Aspiration pneumonia is common finding pre-operatively in dogs with laryngeal paralysis. If aspiration pneumonia is present the surgical intervention should be delayed until the aspiration pneumonia resolved.

Pulmonary edema is not uncommon in dogs with an acute exacerbation of their clinical signs. Pulmonary edema needs to be treated aggressively and the surgery for the laryngeal paralysis does not need to be delayed. Megaesophagus might be present in dogs with laryngeal paralysis especially if the paralysis is due to polyneuropathy or polymyopathy.

Megaesophagus places the animal at more risk for aspiration pneumonia after surgery.

Radiographic examination of the larynx is unremarkable.

Laryngeal Examination A laryngeal examination under general anesthesia is required for the diagnosis of laryngeal paralysis. A light plane of anesthesia is required to be able to evaluate the laryngeal function during each inspiration. Thiopental or propofol is used intravenously as needed for the anesthesia. The animal should be anesthetized to the point at which the mouth can be opened easily and a laryngeal reflex is still present. If the animal is too deeply anesthetized the larynx looks paralyzed even in the normal animal. If the plane is too deep it is important to let the animal approach consciousness and examine the laryngeal function during this time. During the laryngeal examination, motion of the arytenoid cartilage is

observed during inspiration. Dopram intravenously can be used to stimulate the central respiratory center and have a better laryngeal examination. The animal should be placed in sternal recumbency and the head elevated to the level that it is normally carried. In the normal animal the vocal fold and the arytenoids should abduct during inspiration and passively relax during expiration. The arytenoid cartilages and the vocal cords are immobile and drawn toward midline during inspiration if the animal has laryngeal paralysis. If the paralysis is unilateral only one cartilage is not moving. Edema and erythema of the mucosa of the arytenoid cartilages is present on the dorsal part of the larynx and appear to be due to repeat trauma of the arytenoid touching each other at each inspiration. Paradoxical motion of the arytenoid can be present and makes the diagnosis more difficult. With paradoxical motion the arytenoid cartilages are sucked in the airway during inspiration and are moving back to a normal position during expiration. This gives the impression the patient does not have laryngeal paralysis.

TREATMENT Medical treatment is reserved for the emergency treatment while the surgical treatment is for the long term treatment of the condition. Surgery will improve the quality of life of the patient Medical Treatment: Emergency Treatment Animals are usually presented with acute cyanosis or collapse as a result of upper airway obstruction. Most animals in a cyanotic crisis precipitated by upper airway obstruction recover initially with medical therapy. Excitement or increase in the ambient temperature can trigger an acute onset of inspiratory dyspnea. Excitement or increase in the ambient temperature increases the respiratory rate, which results in trauma to the mucosa of the arytenoid cartilage. Inflammation and acute swelling of the mucosa of the arytenoid cartilages can exacerbate the chronic airway obstruction and induce an acute onset of inspiratory dyspnea. A vicious circle is then initiated.

Corticosteroids are given intravenously (dexamethasone, 0.2 to 1.0 mg/kg BID) to reduce laryngeal inflammation and edema. At the same time, oxygen is administered by mask or oxygen cage to alleviate hypoxia. Hyperventilating hyperthermic animals (temperature > 1050 F) must be cooled. Sedation with acepromazine intravenously is indicated (0.1 mg/kg with a maximum dose of 3 mg) if the animal is still stressed. Fluid therapy is administered with caution, because some animals with severe upper respiratory tract obstruction develop pulmonary edema. Diuretics are indicated in these patients. If the patient condition is deteriorating, an emergency tracheostomy is recommended to bypass the upper airway. Temporary tracheostotomy increases the risk of complication nine time in the post-operative period.

Surgical Treatment Laryngeal surgery is directed at removing or repositioning laryngeal cartilages that obstruct the rima glottidis. The surgical procedures commonly used to correct laryngeal paralysis are a unilateral arytenoid cartilage lateralization, aventricular cordectomy and partial arytenoidectomy via the oral or ventral laryngotomy approach, and a permanent tracheostomy. Arytenoid cartilage lateralization is getting the gold standard technique.

Arytenoid Cartilage Lateralization This procedure has been used successfully to treat laryngeal paralysis in cats and dogs.

Arytenoid lateralization has been performed bilaterally or unilaterally. Unilateral arytenoid lateralization is sufficient to reduce clinical signs of laryngeal paralysis. A unilateral lateralization can be performed through a ventral or a lateral incision. It is our preference to perform lateralization through a lateral incision.

The animal is positioned in lateral recumbency for a unilateral lateralization, and a skin incision is made over the larynx just ventral to the jugular groove. The sternohyoid muscle is retracted ventrally to expose the lateral aspect of the thyroid and cricoid cartilages. The larynx is rotated to expose the thyropharyngeal muscle, which is transected at the dorsocaudal edge of the thyroid cartilage. The wing of the thyroid cartilage is retracted laterally. The dorsal cricoarytenoide muscle or the fibrous tissue left is dissected and transected. The joint capsule of cricoarytenoid articulation is partially opened with Metzembaum scissors. The opening oft joint capsule should be minimal to prevent excessive abduction while tightening the suture. The sesamoid band connecting the arytenoid cartilages dorsally is left intact.

The arytenoid cartilage is sutured to the caudo-dorsal part of the cricoid cartilage. This provides an adequate laryngeal airway with only a unilateral tieback. Placement of the suture on the caudo-dorsal part of the cricoid provides a physiologic position of the suture.

One 2-0 non-absorbable suture is placed in a simple interrupted suture pattern from the muscular process of the arytenoid cartilage to the caudo-dorsal edge of the cricoid cartilage and tightened to maintain the arytenoid in position. The amount of tension on the suture should be limited to avoid to over abduct the arytenoids cartilage. The suture should be placed around the cricoid cartilage and at the level of the crico-arytenoid joint to limit the amount of abduction of the arytenoid cartilage.

In cats, it is recommended to use small suture material 3-0 or 4-0 mounted on a pledget to prevent tearing through the cartilage. The arytenoid cartilage does not need to be displaced caudally. It is the authorsâ&#x20AC;&#x2122; impression that the arytenoid cartilage needs only to be maintained in position and stabilized at inspiration. The wound is closed by suturing the thyropharyngeal muscle and routinely closing the subcutaneous tissue and skin.

At the time of extubation it is important to observe per os the size of the laryngeal opening achieved to ensure that adequate abduction of the laryngeal cartilages has been obtained. Excessive abduction may lead to aspiration of food or fluid.

Complications associated with laryngeal lateralization include aspiration pneumonia, persistent cough exacerbated after drinking, seroma, and breaking of the suture and fragmentation of the arytenoid cartilage. Breaking of the suture and fragmentation of the cartilage induce recurrence of the clinical signs of laryngeal paralysis. Laryngeal lateralization should then be performed on the other side. If the procedure has been performed bilaterally a

partial laryngectomy needs to be performed. Seroma formation is very common and is selflimited. Aspiration pneumonia is present in 10 to 20% of the cases. It affects the long term survival. Dogs are at risk for aspiration pneumonia during the rest of their life. The incidence of aspiration pneumonia is more common in bilateral laryngeal lateralization compared to unilateral. In a study, 42% of the dogs with bilateral lateralization experienced an episode of aspiration pneumonia.

Metoclopramide peri-operatively can be used to try to reduce the incidence of regurgitation and aspiration pneumonia in the peri-operative period.

Limited utilization of opiod is also recommended to allow sternal recumbency as soon as possible after surgery. A local skin block with bupivacaine might be valuable to control pain post-operatively and minimize the utilization of opioids. Water and food should be completely withdrawn after surgery until the patient is fully awake.

The animal should be closely watched for the next 2 weeks. The animal is at risk for aspiration pneumonia for its entire life after surgery. The quality of life of the dogs is significantly improved in the long term.

Permanent Tracheostomy Permanent tracheostomy is a surgical option for the treatment of dogs with laryngeal paralysis. The permanent tracheostomy bypasses the upper airway obstruction without inducing any modification in the size of the rima glottidis.

This surgical technique is therefore more valuable for dogs at high risk of aspiration pneumonia (myopathy, megaesophagus, hiatal hernia, gastrointestinal disorder).

Animals responded well to the treatment and owners were satisfied.

Permanent tracheostomy requires attention and maintenance from the owners.

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

OA en el Gato MC Gerardo Garza Malacara aracalam@prodigy.net.mx

La ausencia de conocimiento sobre la OA felina en el pasado se debió a varios factores, incluyendo el tamaño pequeño en comparación con otras especies, la capacidad del gato para compensar condiciones ortopédicas, mediante la redistribución del sostén del peso en las extremidades sanas, y el comportamiento felino normal que oculta los signos de claudicación, lo que en muchas ocasiones impide el análisis ambulatorio.

El reconocimiento de la OA en la actualidad se debe a la mayor atención y comprensión de la importancia de identificar y tratar el dolor y el papel que juega esta en el dolor crónico.

La osteoartritis (OA) o enfermedad articular degenerativa (EAD), es un disturbio de las articulaciones movibles, caracterizado por degeneración del cartílago articular y producción de hueso nuevo en los bordes articulares. El hecho de que los gatos en la actualidad sean más longevos hace que con mayor frecuencia se presenten y diagnostiquen patologías crónicas típicas de la edad avanzada.

En esta patología, se producen cambios degenerativos progresivos en el cartílago articular, el que va disminuyendo su capacidad de absorber impactos produciéndose rupturas y fricción, lo que ocasiona mucho dolor. Los gatos a diferencia de otros animales, por características propias y de supervivencia, ocultan los signos del dolor, lo que dificulta el diagnóstico e identificación de esta patología.

La EAD puede ser clasificada como primaria cuando se identifica como un fenómeno idiopático que se presenta en la ausencia de una causa aparente y se asocia al proceso de envejecimiento y secundaria cuando existe algún factor predisponente el cual por lo general es un trauma.

Los términos EAD y OA son empleados de manera indistinta, EAD puede ser definida clínica, radográfica y patológicamente y probablemente represente un estadio final de una variedad de problemas en la articulación más que una patología en sí. OA es empleado por médicos que quieren poner énfasis en la naturaleza inflamatoria de la enfermedad, en cambio, cuando la inflamación es mínima, se emplea el término osteoartrosis, lo que indica un proceso patológico que no presenta inflamación aguda.

Los signos de EAD pueden ser menos evidentes que en otras especies, de hecho siendo bastante sutiles. La cojera manifiesta puede ser observada en menos del 50% de los gatos afectados. En parte porque puede estar relacionado con el hecho de que los gatos no se ejercitan de la misma forma que los perros o los humanos, lo que dificulta el reconocimiento de la cojera, además puede ser en parte a que la enfermedad frecuentemente bilateral e insidiosa en el inicio y puede relacionarse también con el hecho de que pueden enmascarar los signos de enfermedad.

El trauma es una de las causas más importantes identificadas en la EAD u OA felina, sin olvidar la displasia de cadera, como OA coxofemoral con predisposición racial en los Maine Coon y en menor medida en los Persa y Siamés, a pesar de estas causas reconocidas los estudios sugieren en la mayoría de los casos son idiopáticos, no se han reportado cambios fisiopatológicos subyacentes, sin embargo se reconoce que en gatos con este padecimiento los cambios son bilaterales y afecta principalmente articulaciones del hombro y codos y en menor porcentaje cadera y rodillas.

El felino doméstico posee tres tipos de articulaciones, fibrosas, cartilaginosas y sinoviales, cada una con un nivel diferente de flexibilidad y con función diferente. Las articulaciones fibrosas no son flexibles y se encuentran en las líneas de unión de huesos fusionados; las articulaciones cartilaginosas se encuentran presentes entre las vértebras y tienen una capacidad de movimiento limitado, sin embargo, son mucho más flexibles en el gato que en otras especies, característica que los hace más flexibles en el torso; las articulaciones sinoviales las encontramos en donde se requiere de un alto grado de movilidad, poseen cartílago en su superficie de contacto y están rodeadas por una cápsula articular llena de líquido sinovial el cual actúa como lubricante.

La EAD puede afectar a cualquier articulación del esqueleto (axial o apendicular).

Las articulaciones sinoviales o diartrosis permiten un alto rango de movimiento y se encuentran al final de los huesos largos, particularmente en extremidades torácicas y pélvicas, se encuentran contenidas en una cápsula articular compuesta por una membrana fibrosa exterior y una membrana sinovial en el interior la cual recubre el espacio articular y secreta líquido sinovial que actúa como lubricante, reduciendo la fricción en la articulación, nutre y transporta los productos de desecho del cartílago hialino dentro de la articulación. Algunas articulaciones poseen estructuras adicionales que facilitan su función, como ligamentos intra articulares, meniscos y almohadillas de tejido graso.

Las articulaciones cartilaginosas o anfiartrosis son las que permiten un movimiento limitado de compresión o estiramiento, formadas por cartílago hialino, fibrocartílago o una combinación de ambos. Los cuerpos vertebrales están formados por fibrocartílago con una placa de cartílago en cada extremo (con la edad algunos se osifican), cuando la EAD afecta las articulaciones fibrocartilaginosas intervertebrales se conoce como espondilosis deformante(80% de gatos gerontes), en el caso de afectar las articulaciones sinoviales (diartrosis) se denomina OA, siendo esta la más común.

La OA, es un tipo de EAD definida como un desorden de las articulaciones diartrodiales, caracterizado por la degeneración del cartílago articular, remodelación ósea, cambios patológicos en los tejidos periarticulares (fibrilación del cartílago, erosión y agrietamiento, esclerosis del hueso subcondral, osteofitos y entesofitos, fibrosis de cápsula articular y sinovitis), inflamación y formación de nuevo hueso alrededor de la articulación. El dolor está dado por la sinovitis y cambios en el hueso subcondral ya que el cartílago hialino no posee terminaciones nerviosas.

La espondilosis vertebral es común en el gatos gerontes y muchos de estos presentan constipación.

Aunque no se ha documentado dolor en esta patología, la constipación puede ser sugestiva de la presencia de dolor, las vértebras lumbares se ven afectadas más que las cervicales pero menos que las torácicas, en el segmento torácico se ve más afectado la región craneal y de las lumbares de la región vertebral caudal.

Todas las patologías de las articulaciones que son producto de incongruencia o inestabilidad pueden causar OA secundaria. Los traumatismos articulares repetidos y la displasia articular son las causas iniciales de un cambio degenerativo, estos daños inducen a pérdida de proteoglicanos y agua por parte del cartílago articular, lo que se reduce su capacidad de recuperación y lo predispone a daño mecánico.

Las alteraciones del cartílago en la OA comprenden un aumento en la síntesis y degradación de proteoglicanos, aumento en la hidratación del cartílago, pérdida de la integridad del colágeno, disminución de la fuerza de tracción, fibrilación o desorden de la capa colágena superficial (por pérdida de proteoglicanos, haciendo que las fibras colágenas se presenten desnudas, el cartílago pierde su lisura) y aumento de la densidad cartilaginosa (eburnación). La pérdida de proteoglicanos se produce a pesar del aumento en su síntesis y es debido a la modificación de la naturaleza de los proteoglicanos sintetizados, menos condroitin sulfato de cadena larga y se presentan variaciones en el contenido de glicosaminoglicanos. Los proteoglicanos contienen menos cantidad de sulfato de queratina en relación a sulfato de condroitina. La disminución del contenido de proteoglicanos del cartílago artrósico también se cree que es debido a la acción de enzimas proteolíticas.

La degradación de proteoglicanos conduce a disminuciones considerables en el peso molecular de los agregados moleculares conformados por proteoglicanos y ácido hialurónico, esto conduce a una pérdida de agua en el cartílago articular que combinada a la pérdida de rigidez de la red de colágeno aumenta la probabilidad de una alteración mecánica del cartílago.

Las anormalidades de la membrana sinovial incluyen sinovitis con infiltración de células mononucleares y liberación de mediadores de la inflamación en el líquido sinovial. La liberación de enzimas que degradan el cartílago es fundamental en la patología de la OA (daños producidos son irreversibles).

Las lesiones de espondilosis se pueden observar en una radiografía de vista lateral: En etapas iniciales se presentan pequeñas proyecciones con forma de garfio en la región craneoventral y caudoventral vertebral adyacente a los espacios de los discos intervertebrales.

En pacientes más afectados se presenta más pronunciada la formación de nuevo hueso y las proyecciones aparecen más grandes, pudiendo desarrollarse ventrocaudalmente hacia el cuerpo de la vértebra siguiente o cranealmente hacia el cuerpo de la vértebra anterior.

En etapas finales se llegan a formar puentes óseos completos, fusionando a las vértebras.

El diagnóstico de la EAD se basa en tres aspectos; anamnesis, examen físico y hallazgos radiográficos.

Los signos clínicos relacionados con EAD comprenden cambios en el temperamento, agresividad, depresión, disminución del apetito o anorexia, pérdida ponderal, disminución de acicalamiento, sedentarismo, dificultad para saltar e inusualmente claudicación.

El diagnóstico físico de la EAD no es sencillo, ya que los gatos por lo general se resisten al manejo o a la manipulación durante el examen clínico, se encojen en la mesa y se quedan inmóviles, independientemente de que es difícil saber cuándo retira la extremidad por dolor o lo hace simplemente porque no quiere ser tocado, por lo que generalmente el diagnóstico se basa en observaciones hechas por el propietario.

Los hallazgos encontrados durante el examen físico son, dolor a la manipulación o palpación de articulaciones, inflamación de la articulación (articulaciones), efusión o derrame sinovial, disminución del rango de movimiento y atrofia muscular.

Los hallazgos radiológicos de EAD se deben usar para confirmar la sospecha de la enfermedad y no para guiar el tratamiento, además que en los gatos no se producen tantos cambios radiográficos como en otras especies, por lo que la ausencia de signos radiográficos evidentes no excluye la presencia de EAD, estos hallazgos pueden ser presencia de osteofitos y entesofitos, efusión sinovial, aumento del volumen de tejidos blandos, engrosamiento de la cápsula articular y esclerosis del hueso subcondral.

Un análisis del líquido articular con citología puede ser de utilidad para diferenciar esta enfermedad degenerativa de artropatías inflamatorias.

Debemos considerar que la EAD no es curable, por lo tanto el tratamiento debe dirigirse a proporcionar confort, buscando la calidad de vida, reduciendo el dolor articular y reducción de la destrucción del cartílago articular.

El tratamiento debe incluir modificación del ejercicio, control de peso, empleo de medicamentos, nutracéuticos solos o en dietas de prescripción y/o intervención quirúrgica.

El problema mayor en el tratamiento de esta patología en gatos es la escasez de conocimiento de esta patología en gatos, toxicidad a los medicamentos disponibles y dificultad de cambio de estilo de vida, por lo que se debe plantear de manera particular en cada caso.

Se recomienda la realización de estudios radiográficos de hombro, cadera y columna para que pueda iniciarse de manera temprana los manejos requeridos y evitar complicaciones de difícil manejo como la obstipación y constipación.

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

PERICARDIAL DISEASES IN DOGS: DIAGNOSIS & MANAGEMENT

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

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 may 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 may 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 may indicate inflammatory pericarditis; occasionally other signs of systemic disease such splenomegaly may 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 may be erroneously entertained. Arterial hypotension or pulsus paradoxicus, a marked inspiratory fall in BP may be 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 may be sharp, 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 may be

Pericardial Diseases – Dr. Bonagura 2

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 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 may 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 may 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 heartbase tumors exfoliate poorly so cytologic 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; BP cuff; ECG electrodes o ± Sedation (butorphanol 0.1 to 0.2 mg/kg). o Identify puncture site over right thorax; 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

Pericardial Diseases – Dr. Bonagura 3

FOLLOW‐UP CARE Other medical therapies are rarely administered. Judicious doses of furosemide (post‐ pericardiocentesis) 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‐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.

Pericardial Diseases – Dr. Bonagura 4

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SURGERY OF THE LUNG Eric Monnet, DVM, PhD, FAHA Diplomate ACVS and ECVS Colorado State University, Fort Collins, Colorado Eric.Monnet@ColoState.EDU The trachea divides into two principle bronchi which in turn subdivide into lobar bronchi that supply each lung lobe. Within each lung lobe, lobar bronchi divide into segmental bronchi that supply bronchopulmonary segments within each lobe. Dichotomous branching of the airway continues through subsegmental bronchi, terminal bronchioles, and respiratory bronchioles.

Respiratory bronchioles give rise to alveolar ducts, alveolar sacs, and pulmonary alveoli. The pulmonary arteries follow a lobar distribution in close proximity to the cranial dorsal aspect of each bronchi. Bronchial branches of the bronchoesophageal arteries provide oxygenated blood to the airways down to the level of the respiratory bronchioles where they terminate in capillary beds continuous with the pulmonary arteries. Pulmonary veins course on the caudal and ventral aspect of each bronchi collecting blood from both the pulmonary and bronchial arteries.

The left lung of dogs and cats is divided into cranial and caudal lobes. The left cranial lung lobe is divided into a cranial and caudal portion, but shares a common lobar bronchus. The right lung is divided into four distinct lobes: cranial, middle, caudal and accessory. The accessory lobe passes dorsal to the caudal vena cava and is located medial to the plica vena cava.

PNEUMOTHORAX Pneumothorax results from the accumulation of air in the pleural space. The air can come from the respiratory tract, the esophagus and through the skin. Spontaneous pneumothorax are classified as primary or secondary. Primary pneumothorax are usually resulting from the rupture of a bleb or a bullae. Primary spontaneous pneumothorax are more common in large breed dog with deep chest. Secondary spontaneous pneumothorax results from a lung pathology that eroded through a bronchioles (pneumonia, abscess0 or from chronic obstructive lung disease (emphysema). Primary spontaneous pneumothorax are treated with drainage of the pleural space by thoracocenthesis or thoracostomy tube. If a bullae is visible on thoracic radiographs, a lung lobectomy is then recommended. A pleurodesis can also be performed at the time of surgery to prevent recurrence.

NEOPLASIA Primary neoplasia of lung is the most common indication for pulmonary surgery in small animals. Presumptive diagnosis of primary lung neoplasia is based on characteristic radiographic appearance of a solitary lung mass. Fine needle aspiration can be undertaken prior to surgery.

Pulmonary lobectomy is indicated for suspected primary lung tumors without prior biopsy.

Excision biopsy of hilar lymph nodes is indicated for staging if they are visualized. Diagnosis is confirmed by histopathologic examination of the excised specimen. Adenocarcinoma is the most common primary lung neoplasia in dogs, representing approximately 75% of the cases. Alveolar carcinoma and squamous cell carcinoma also occur. Pulmonary carcinomas are classified as differentiated or undifferentiated. Prognostic indicators for primary lung neoplasia include involvement of hilar lymph nodes at surgery, histologic type, tumor size, and presence of pleural effusion. The prospect for cure or long term remission with surgery alone is good for small

differentiated adenocarcinomas. Undifferentiated carcinomas have over a 50% incidence of metastasis. The prognosis for squamous cell carcinoma is poor with a metastasis rate of over 90%.

Metastatic lung neoplasia is treatable by surgical excision under certain circumstances.

Guidelines for surgical treatment of metastatic pulmonary disease include: control of the primary site for at least several months, no evidence of metastasis to sites other than lung, favorable histology (i.e. sarcomas are better than carcinomas), slow growth of metastatic tumors (i.e. size doubling time > 30 days), and less than 5 metastatic nodules present. Metastatic lung tumors should be excised by partial lung resection whenever possible to preserve lung volume.

LUNG LOBE TORSION Lung lobe torsion is a rare condition that occurs most often in large deep-chested dogs. The condition may occur secondary to one of several predisposing factors including thoracic trauma, pleural effusion, diaphragmatic hernia, pneumothorax, or thoracic surgery. Lung lobe torsion occurs most often in the right middle lung lobe and less often in the left cranial lung lobe. Clinical findings associated lung lobe torsion include acute depression, weakness, dyspnea, tachypnea, cyanosis, nonproductive cough, hemoptysis, and tachyarrhythmias. Radiographically, lung lobe torsion appears as an isolated atelectasis of the right middle or left cranial lung lobes. Air bronchograms may be present early, but disappear over time. Pleural effusion is often apparent on radiographs. Evacuation of sanguinous effusion fails to expand the collapsed lobe.

Confirmation of the diagnosis can be made by contrast bronchography, bronchoscopy, or exploratory surgery. At surgery, the involved lung lobe appears as a solid liver-like mass due to engorgement of the lung with blood. Surgical treatment consists of complete lung lobectomy of the affected lung, preferably without derotation of the lung lobe.

PULMONARY ABSCESS Pulmonary abscesses occur secondary to severe pulmonary infections or pulmonary foreign bodies. Foreign bodies can enter by inhalation or impalement through the thoracic wall. Pyothorax can occur concurrently with pulmonary abscesses. Persistent pulmonary atelectasis and signs of pneumonia despite appropriate antibiotic therapy suggests the presence of a pulmonary abscess.

Pulmonary lobectomy of the affected lung lobe is indicated for suspected pulmonary abscesses.

Caution during surgical manipulation of an abscessed lung lobe is necessary to prevent expulsion of purulent material into adjacent lung lobes. Morbidity and mortality associated with this procedure is high in animals that have active diffuse pneumonia at the time of surgery.

PULMONARY RESECTION TECHNIQUES Possible indications for pulmonary resection include pulmonary neoplasia, pulmonary trauma, pulmonary abscess, lung lobe torsion, bronchoesophageal fistula, and spontaneous pneumothorax.

Normal animals can tolerate resection of as much as 50% of their lung capacity and still survive.

However, generalized pulmonary disease substantially decreases the amount of lung resection that can be tolerated. Chronic obstructive lung disease and pulmonary hypertension in particular limit the extent of pulmonary resection that can be undertaken.

Lung Lobectomy Lung lobectomy is indicated for severe traumatic injury, neoplasia, lobe torsion, or abscesses that are primarily confined to a single lung lobe. Lung lobes that can undergo separate lobectomy in small animals include the left cranial, left caudal, right cranial, right middle, and right caudal

lobes. The accessory lobe divides incompletely from the right caudal lobe and generally is resected with the caudal lobe. The standard surgical approach for lung lobectomy is a fifth intercostal thoracotomy in dogs and a sixth intercostal thoracotomy in cats. The procedure can be performed one intercostal space cranial or caudal to the ideal intercostal space, if necessary. Lung lobectomy also can be accomplished from a median sternotomy, if this approach is indicated for other reasons.

Lung lobectomy is performed by dividing the pulmonary vessels and oversewing the lobar bronchus. Lung lobes should be manipulated carefully during resection to avoid embolization of neoplastic cells or extrusion of purulent material into adjacent airways. The bronchus should be checked for leaks after closure by flooding the chest with saline and applying a positive pressure breath. Placement of a thoracostomy tube prior to closure of the thoracotomy is absolutely indicated.

Partial Lung Resection Partial lung resection is indicated for lung biopsy or excision of localized pulmonary lesions that do not require complete lung lobectomy. Partial lung resection can be performed by a standard suturing technique or with a surgical stapling device. Standard partial lung resection can be accomplished with readily available materials, but some leakage of air from the surgery site can be anticipated after surgery. Stapling devices, when available, are fast and less likely to leak after surgery. Partial lung resection can be performed using either the TA or GIA surgical stapling device. The 3.5 mm (blue) staples are most appropriate for stapling lung tissue. Any leakage of air after surgery is readily evacuated by a thoracostomy tube and usually will be self limiting after several hours.

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SURGERY OF THE LIVER AND GALL BLADDER Eric Monnet, DVM, PhD, FAHA Diplomate ACVS and ECVS Colorado State University, Fort Collins, Colorado Surgery of the liver and gall bladder is indicated for liver trauma, liver neoplasia, liver abscess, liver torsion, bile duct obstruction, and gallbladder mucocele. Liver and spleen are the two most common organs to induce a hemodabdomen after trauma. It rarely requires surgery unless the patient cannot be stabilized with appropriate fluid-therapy and blood transfusion. Liver trauma is treated surgically by compression, tamponnade with the omentum or liver lobectomy. Liver neoplasia is rare in dogs. Liver adenocarcinoma and lymphoma are the most common tumors found in dogs. Massive adenocarcinoma are well amenable to surgical treatment since they are slow growing and metastasize slowly. Liver abscess are rare in dogs and cats and usually their cause is not well known. Gram-negative aerobic bacteria are the most commonly found in the liver abscess. Liver lobe torsion usually involves the left liver lobes. Cholelithiasis has to be considered when obstructive icterus is present Stones could be solitary, numerous or sandlike. Most canine and feline stones are calcium salts of bilirubinate. Bile stasis and inflammation might be cause for the formation of bile stones. Cholecystitis has been reported in dogs. It could be acute or chronic and a necrotizing or emphysematous form has been described. Extrahepatic biliary obstruction occurs when disease processes interfere with normal flow of bile from the liver and the gallbladder into the intestine.

General considerations Regenerative capacity Removal of 70% of the liver is tolerated. The general condition of the patient conditions how much liver can be removed safely. If more is resected it will result in portal hypertension because there is not enough liver parenchyma left to access the entire blood flow from the portal vein. Regeneration of the liver starts with 24 hours of the surgery and peaks at 3 days. There is hyperplasia and compensatory hypertrophy of the remaining hepatocytes. The liver mass can be restored within six weeks after 70% hepatectomy.

Metabolic alterations Coagulation is evaluated in any patients with hepatobiliary disease. In one study, prothrombine time was elevated in 66% of the animal with liver disease. Plasma fibrinogen remain normal until almost liver function is lost Vitamin K deficiency resulting in coagulopathy may occur with prolonged complete bile duct obstruction. Vitamin K administration (1 to 2 mg/kg subcutaneously) is sufficient to increase their level in 3 to 12 hours. Fresh frozen plasma is administered if the coagulation times are still prolonged.

Hypoglycemia can occurs with 48 hours of partial liver lobectomy but does not always happened after major hepatectomy. Intravenous infusion f glucose (10%) would then be

required. Albumin concentration is reduced after massive liver lobectomy because of the low level of production. Bilirubin can increase but usually goes back to normal within one week. Increased liver enzymes will occur after major resection and will persist for 4 to 6 weeks.

Antibiotherapy Portal venous blood is an important source of bacteria for the liver. Infections of the liver and biliary tract commonly involve Gram-negative aerobic bacteria (E coli, Enterococcis faecalis, Proteus, Klebsiella). Anaerobic bacteria can also colonize the liver in dogs (Clostridium).

Antibiotics are routinely administered when hepatobiliary surgery is performed.

Cephalosporins provide broad spectrum coverage. When anaerobic bacteria are suspected metronidazole or enrofloxacine should be used.

Anatomy The liver has 6 lobes: left medial and lateral, right medial and lateral, quadrate lobe and the caudate lobe with two processes. The liver lobes are attached to the diaphragm by the triangular ligaments. There are also the hepato-gastric ligament, duodeno-hepatic ligament with the bile duct and hepato-renal ligament stabilizing the liver. The liver receives 70 % of its blood supply from the portal vein and 30 % from the hepatic artery. The blood from the hepatic artery and the portal vein mixes in the hepatic sinusoids and is released in the caudal vena cava through the hepatic vein. There is on hepatic vein per liver lobe.

Surgical techniques Liver Surgical biopsy Liver biopsies are commonly taken during abdominal exploration. The guillotine technique with a 3-0 braided suture is commonly used to remove a small fragment of the liver. Forceps can be used to make small indentation in the edges of the liver lobes. Several biopsy can be taken from different liver lobes. Biopsy can be submitted also for cultures.

If the edges of the biopsy are bleeding, cautery can be used to control the bleeding or gelfoam can be applied.

Partial liver lobectomy Partial liver lobectomy can be performed to remove the distal end of a liver lobe with a small lesion. Occlusion of the blood flow to the liver can be accomplish by compressing the hepatic artery and the portal vein with a vascular clamp or a Bulldog clamp.

After the line of resection has been decided, mattress sutures with 2-0 monofilament absorbable suture material are placed across the liver parenchyma and tighten to crush the tissue. This technique allows crushing of the parenchyma and ligation of the major vessels.

Several mattress sutures are placed across the section of the liver lobes. Mattress sutures should be 2 to 3 cm long. After all the sutures have been placed the blood vessels are cut

with a scissors. Stapling equipment can laso be used to performed a partial liver lobectomy.

Usually the section the liver lobs is bleeding significantly with this technique. Cautery can be used to cauterize the small vessels that are still bleeding. Alos Gelfoam can be applied to the liver or omentum can be patched to the liver to tamponnade the section of the liver.

Liver lobectomy Liver lobectomy requires ligation of the blood vessels and hepatic duct at the hilus of the liver. Each liver lobe can be removed separately. Right liver lobes and caudate lobes are the most difficult lobes to remove because of their close proximity to the vena cava. The dissection starts from caudally with exposure of the branch of the portal. IT is dissected and double ligated. Then hepatic artery and the hepatic duct draining the liver lobes are dissected and ligated next. Finally, the hepatic vein is identified after finger fragmentation of the liver parenchyma at the base of the liver lobe. Finger fragmentation reduces the amount of bleeding from the liver parenchyma and prevents laceration of major blood vessels. After the hepatic vein has been exposed it is double ligated and divided. The hepatic vein of the right caudal liver lobes is better clamped with a vascular clamp divided and then sawn as an open vessel. This technique avoid kinking of the vena cava or slippage of the suture of the stub of the hepatic vein. If the quadrate lobe has to be removed the gall bladder is dissected away from the liver parenchyma. At the end of the procedure either the gall bladder is removed or pexied to another liver lobes to prevent torsion and obstruction of the cystic duct.

Stapling equipment (TA 30 V3 or TA55) can be used to perform a liver lobectomy of the left liver lobes.

Gallbladder and bile duct Cholecystotomy Cholecystotomy is indicated to removed inspissated bile or biliary sludge, gelatinous bile or gallstones and bile duct stones. It is also performed to cannulate the bile duct to evaluate its patency.

Two stay suture of 3-0 monofilamet are placed on the gall bladder. A small incision is made between the two stay sutures and suction is used to aspirate the bile overflow before it contaminates the abdominal cavity. The incision is then enlarged with Metzembaum scissors. The incision should be long enough to perform the procedure. The bile duct needs to be catheterized before closure. It could be difficult to achieve a good catheterization because of the angle of the cystic duct with the common bile duct.

A biopsy of he wall of the gallbladder is taken for histology and culture before closure.

The gallbladder is then closed with a simple suture pattern with 4-0 monofilament absorbable suture. A one-layer closure is sufficient.

Cholecystectomy A cholecystectomy is required when the gallbladder is the primary cause of the pathological process or if the damages to the gall bladder are too severe and might contribute to the recurrence of the disease. Cholecystitis and gallbladder mucocele are best treated by cholecystectomy.

Cholecystectomy requires the dissection of the gallbladder form the quadrate lobe. The gallbladder is lodged in the hepatic fossa and it is covered by visceral peritoneum. The dissection starts at the fundus of the gall bladder by an incision through the visceral peritoneum. The dissection should not be in the liver parenchyma because severe bleeding will occur. The dissection is then carried with cautery toward the infudibulum of the gall bladder. The cystic duct and the cystic artery are isolated, clamped, and ligated. The cystic duct is ligated at a sufficient distance from the common bile duct to prevent kinking of the common bile duct. If the liver parenchyma is bleeding, cautery could be used to control the bleeding or gentle pressure could be applied for 5 minutes. Gelfoam could also be applied on the bleeding surface of the liver.

Cholecystectomy can also be performed with laparoscopy. Only cases without occlusion of the common bile duct can be operated with minimally invasive surgery. Usually the cystic duct is dissected first and ligated with clips. After successful ligation of the cystic duct the gall bladder is dissected from the hepatic fossa of the quadrate lobe. If the gall bladder is too large the dissection can be started at the level of the apex. IT is then important to establish a good plane of dissection between the gall bladder and the liver parenchyma. The cystic is then ligated last.

Cholecystoduodenostomy Cholecystoduodenostomy is the procedure of choice for bile diversion in dogs and cats when the gall bladder is not directly involved in the disease process that is causing the bile duct obstruction. It could be a palliative procedure for bile duct obstruction due to neoplasia.

The gall bladder is detached for the hepatic fossa as described for the cholecystectomy.

Then the gall bladder is brought in contact with the duodenum with two stay sutures.

Special attention should be placed on the cystic duct to avoid twisting and occlusion. The stoma between the gall bladder and the duodenum should be between 2 and 4 cm. A first layer of suture is applied between serosal layers on the back side of the duodenum. The gall bladder and the duodenum are then incised. A simple continuous suture is placed between the muscosa layers of the gall bladder and the duodenum. Finally, another layer of simple continuous suture is placed between the serosa of the duodenum and the serosa of the gall bladder. 4-0 monofilament absorbable suture material is used for the procedure.

After cholecystoduodenostomy, the patients are at risk for ascending cholangiohepatitis and needs to be maintained on enrofloxacin for long term.

Choledochoduodenostomy Choledochoduodenostomy can be performed if a benign obstruction occurs at the distal end of the bile duct. Significant dilation of he proximal art of the common bile has to be present to be able to perform this procedure.

The distal part of the common bile duct is separated form the pancreas and the duodenum.

It is then implanted more proximal into the wall of the duodenum with two simple interrupted sutures.

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SURGERY OF THE TRACHEA Eric Monnet, DVM, Ph.D, FAHA Diplomate ACVS, ECVS Colorado State University, Fort Collins, Colorado

The trachea originates caudal to the cricoid cartilage, passes through the thoracic inlet, and terminates at its bifurcation at the base of the heart. C-shaped hyaline cartilages give the trachea its rigid structure. The tracheal cartilages are united by the fibroelastic annular ligaments. The tracheal membrane forms the dorsal aspect of the trachea and is composed of the smooth muscle (trachealis muscle) and connective tissue. The trachea is lined by ciliated columnar epithelium rich in mucus producing goblet cells. Vascular supply to the trachea is carried by branches of the cranial thyroid, caudal thyroid, and bronchoesophageal vessels. These vessels form delicate lateral vascular pedicles on each side of the trachea.

Autonomic innervation to the trachea is supplied by branches from the vagus nerve (recurrent laryngeal nerve) and sympathetic chain. The recurrent laryngeal nerves must be preserved when performing tracheal surgery to avoid causing laryngeal paralysis.

SURGICAL TECHNIQUES Surgical techniques performed on the trachea include temporary tracheostomy, permanent tracheostomy, and tracheal anastomosis.

Temporary Tracheostomy Temporary tracheostomy is indicated for emergent or short-term relief of severe upper airway obstruction or for airway access to accomplish positive pressure ventilation or other forms of ventilatory therapy in conscious animals.

Temporary tracheostomy is accomplished by Outer cannula placement of a tracheostomy tube.

Commercially available tracheostomy tubes come in a variety of sizes, with or without an inflatable cuff, and with or without an inner Inner cannula cannula. It is preferable to have a temporary tracheostomy tube with an inner and an outer cannula (Schiley tube) An adequate tracheostomy tube can be fashioned by cutting Obturator an endotracheal tube. An inflatable cuff is only necessary if positive pressure ventilation will be administered, in which case a tube with a low-pressure high-volume cuff is preferred to minimize damage to the tracheal mucosa.

The majority of tracheostomy tube applications do not require a cuffed tube. In fact, if an inflatable cuff is available, it is better not to inflate the cuff because doing so disrupts

2 mucociliary clearance and increases the risk of tube obstruction by a mucus plug. Deflation of the cuff allows mucociliary clearance of mucus past the tube.

As long as a tracheostomy tube is in place, it must be periodically removed and cleaned with an antiseptic solution, such as chlorhexadine or povidone-iodine. This procedure is facilitated by an inner cannula that can be removed and cleaned without removing the entire tracheostomy tube. Airway maintenance should be performed every two to six hours depending on how quickly the tube is collecting debris and mucus. Airway maintenance must be performed with increasing frequency the longer a tracheostomy tube is in place.

Temporary tracheostomy is performed with the animal in dorsal recumbency if possible, but may have to be performed in a variety of positions and with a minimum of anesthesia.

If necessary, the procedure can be performed under local anesthesia only A longitudinal skin incision is performed caudal to the larynx over the trachea. After the dissection of the sternothyroideous muscle, the trachea is exposed. An incision in performed in the fibroelastic annular ligament between the 3rd and the 4th tracheal ring. The incision should be in the ventral portion of the trachea to avoid damaging the laryngeal recurrent nerves.

It is not necessary to cut tracheal rings to perform a tracheostomy and doing so only enhances the risk for tracheal collapse after surgery. Access to the tracheostomy is facilitated by externalizing a suture placed in the caudal margin of the incision. The temporary tracheostomy tube is then introduced in the trachea. The suture placed in the caudal margin of the incision allows for rapid replacement of the tube if it is dislodged or removed for cleaning. After placement, the tracheostomy tube is secured by cotton ribbons tied to the external flange of the tube and then tied over the neck.

The tracheostomy incision should be packed with povidone-iodine ointment and lightly bandaged. After the tracheostomy is no longer needed, the tube is removed and the tracheostomy wound is allowed to heal by second intention.

Permanent Tracheostomy Permanent tracheostomy is a salvage procedure for severe and refractory upper airway obstruction. Examples of such condition include severe laryngeal collapse, inoperable pharyngeal or laryngeal neoplasia, or complicated laryngeal paralysis. Complications associated with permanent tracheostomy include chronic respiratory infection, inhalation of foreign materials, aspiration of water during bathing or swimming, and chronic mucus

3 discharge from the tracheostomy. Stricture is a common complication after permanent tracheostomy in cats.

The patient is placed in dorsal recumbency. A longitudinal skin incision is performed caudal to the larynx over the trachea. After the dissection of the sternohydeus muscle, the trachea is exposed. The sternohydeus muscle can be pulled dorsal to the trachea to gain better exposure of the trachea.

Such a procedure may increase the risk of damaging the laryngeal nerves. The tracheostomy will be performed over 3 to 4 tracheal rings in length and a third of the tracheal diameter in width. The segment of the tracheal rings should be removed without damaging the tracheal mucosa. The tracheal mucosa is then incised and sutured to the skin with a 4-0 monofilament non-absorbable suture. A simple interrupted suture pattern is used.

Tracheal Anastomosis Indications for tracheal resection and anastomosis include severe traumatic injury to the trachea, congenital tracheal stenosis, tracheal stricture, tracheal granulomas, and tracheal neoplasia.

Several principles should be considered when performing surgery on the trachea.

Blood supply to the trachea is considered segmental and this limits the extent to which the trachea should be mobilized during surgery. The recurrent laryngeal nerves must be identified and preserved to avoid causing laryngeal paralysis. Avoiding excess tension on the anastomotic site is an important consideration both to prevent acute anastomotic dehiscence and to minimize luminal stricture as a late sequela. The extent of a tracheal resection is a major factor determining tension at the anastomotic site. Although as much as 40% of the trachea has been resected experimentally in animals, such extensive resections are not recommended. Resection of up to five tracheal rings is a reasonable upper limit for tracheal resection. Several techniques are available to relieve tension on the tracheal anastomosis including secondary tension sutures, division of tracheal annular ligaments, and cervical flexion bandages. Secondary tension sutures are routinely employed with tracheal anastomosis. Intraluminal granuloma is a potential late sequela after tracheal surgery. Monofilament suture with extraluminal placement of knots and careful apposition of tracheal mucosa are important for decreasing granuloma formation after surgery.

Approach to the cervical trachea for resection and anastomosis is by ventral midline cervical incision and separation of the paired sternohyoideus muscles. The thoracic trachea

4 may be approached either by median sternotomy or right intercostal thoracotomy. A combined ventral cervical and median sternotomy approach may be used when exposure to the cervical and thoracic trachea is needed. During exposure of the trachea it is important to preserve the laryngeal recurrent nerve and the blood supply of the trachea.

After exposure of the trachea, a stay suture is placed in the distal segment of the trachea.

The trachea is incised in the middle of cartilage ring. If a tumor is removed, the first incision is caudal to the tumor. The distal trachea is then intubated with a sterile endotracheal tube. The second is then performed cranial to the mass. Simple interrupted sutures are then preplaced starting from the dorsal part of the trachea. Tension will then be placed if required. The sutures are then tightened. Muscle, subcutaneous and skin are closed routinely. Temporary emphysema will develop in the neck. Usually it is selflimited and does not generate a pneumomediastinum.

COLLAPSING TRACHEA Collapsing trachea is a common condition of small dogs that occurs as a primary condition or as a secondary complicating condition to other cardiopulmonary disorders such as chronic bronchitis, reactive small airway disease, and mitral regurgitation. Primary collapsing trachea primarily affects the cervical trachea and may be a fixed or dynamic collapse, whereas secondary acquired collapsing trachea primarily affects the thoracic trachea and primary bronchi and is always dynamic.

Abnormal airway and transpulmonary pressures generated by chronic coughing and high airway resistance are the likely precipitating causes of secondary collapsing trachea. Primary collapsing trachea can occur in younger animals and may be heritable. Treatment of intrathoracic collapsing trachea should be directed at medical management of associated cardiopulmonary disease. Effective therapies include antibiotics, antitussives, bronchodilators, and anti-inflammatory drugs for chronic respiratory disease and arterial vasodilator drugs for mitral valve regurgitation.

Collapse of the cervical trachea can be managed in a similar manner with antibiotics, antitussives, and anti-inflammatory drugs. On occasion, collapsing trachea can become so severe that medical management strategies alone do not provide sufficient relief of airway obstruction or severe cough. In selected cases of cervical tracheal collapse, ring tracheoplasty can provide palliative relief as an adjunct to medical therapy. Spiral prosthetic repair of tracheal collapse also has been advocated. Access to the cervical trachea for ring tracheoplasty is gained by ventral midline cervical incision, which can be extended into a cranial median sternotomy if necessary to gain access to the cranial thoracic trachea.

5 NEOPLASIA Tracheal tumors in dogs and cats include chondrosarcoma, osteochondroma, leiomyoma, and adenocarcinoma. Adenocarcinomas appear as well defined ovoid masses within the tracheal lumen, are locally invasive, but slow to metastasize. Segmental resection of the trachea can be curative for adenocarcinoma and other localized tumors of the trachea.

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