EXAMINATION OF THE PATIENT (WITH ATTENTION TO THE CARDIOVASCULAR SYSTEM)

Transcription

1 THE NORMAL HEART In land mammals, the heart is divided into top (receiving) chambers and bottom (pumping) chambers. The receiving chambers are called atria and the pumping chambers are called ventricles. The heart has right and left sides, each with one atrium and one ventricle. o The right heart receives deoxygenated blood from the body through veins called the venae cavae and delivers it to the lungs via the pulmonary artery. The right side of the circulation (leaving the right ventricle and returning to the left atrium) is referred to as the pulmonary circulation. o The left heart receives oxygenated blood from the lungs via the pulmonary veins and delivers it to the body via the aorta. The left side of the circulation (leaving the left ventricle and returning to the right atrium) is referred to as the systemic circulation. Between the atria and ventricles, and the ventricles and the great vessels (aorta and pulmonary artery) are valves. o The valve between the right atrium and right ventricle is the tricuspid valve. o The valve between the right ventricle and the pulmonary artery is the pulmonic valve. o The valve between the left atrium and the left ventricle is the mitral valve. o The valve between the left ventricle and the aorta is the aortic valve. The heart and the origins of the great vessels are surrounded by a fibrous sac called the pericardium. There is a scant volume of fluid between the pericardium and the surface of the heart (the epicardium). The heart rate is set through automatic discharge of the SA (or sinus) node in the right atrium. Electrical signals pass through specialized heart muscle cells, which comprise the conduction system. The signal passes from the conduction system into the muscle of the atria and ventricles, which causes contraction. o The signal from the SA node spreads through the atrial chambers, and then pauses at the AV node near the center of the heart, where the atria and ventricles meet. o From the AV node, the signal passes through the bundle of His and into the Purkinje fibers, which conduct the signal into the ventricles.

2 EXAMINATION OF THE PATIENT (WITH ATTENTION TO THE CARDIOVASCULAR SYSTEM) Patient History o General When/where was pet acquired; Indoor vs. Outdoor; Vaccine status, Travel history, Flea/tick and heartworm prevention being used (Year round vs. seasonal) Major medical/surgical history Diet: specific diet being fed? Treats/table food? Appetite (normal, decreased, increased) Medications: Names, Doses, Indications. For cardiopulmonary medications, effectiveness and perceived adverse effects o Cardiac-specific history Attitude and Activity: what is pet s normal? Any decline? If yes, for how long? Acute onset or chronic progressive? Cyanosis? Lethargic or depressed Winded Short of breath Panting more with activity Turning blue/purple Coughing: if present, for how long? How frequently? Worse morning, evening, or throughout day? Any consistent triggers for cough (on rising, with excitement/activity, when drinking, when pulling on leash, etc.)? Is the patient able to get comfortable lying down and sleep through the night? If not, why? Coughing, getting up to drink/urinate, orthopneic, etc. Any episodes of fainting or weakness? How frequently? What do the episodes look like? How long do they last? Does the pet recover to normal within seconds/couple of minutes? Any associated triggers (excitement/activity, coughing, defecating/vomiting, etc.)? For cats appetite, hiding (if usually social) is important Observation of the Patient o Attitude alert, responsive? Bright, quiet, dull, or obtunded? Anxious or distressed/uncomfortable? o Body condition; abdominal distension or peripheral edema? o Ambulatory? Lame (especially for cats)? Apparent weakness? o Respiratory pattern Rate and apparent effort. Extraneous noise (stridor, stertor, wheezing, congestion)? Coughing? Orthopneic? Veterinarian s Physical Examination o A cardiologist does a full physical examination as in general practice. Of particular interest in the patient with cardiovascular disease are: Pulses: arterial pulse quality and synchronicity with auscultated heart rhythm? Weak/thready, normal, strong, bounding? Variation from beat-to-beat or with respiratory cycle? Generally use femoral ± dorsal pedal arteries. Jugular veins: persistently distended after occlusion? Pulsations? Hepatojugular reflex present? Abdominal palpation: Ascites? Fundic examination: retinal hemorrhage or detachment? Cardiac auscultation Normally only S1 and S2 auscultated representing closure of the mitral/tricuspid valves and aortic/pulmonic valves, respectively

3 A gallop sound is an audible S3 (representing rapid filling) or S4 (atrial contraction/late filling), only present in heart disease in dogs and cats. This sound occurs in diastole, while the heart is relaxing. A systolic click is a sound similar in frequency/duration to S1 and S2 that occurs during systole. Noted in dogs with mitral valve prolapse (usually when mild) and cats with hyperdynamic (more vigorous than usual) systolic (pumping) function A murmur is a wooshing (sometimes whistling) noise that occurs in between the normal heart sounds. Murmurs are described by when they occur (systolic, diastolic, continuous), where they are loudest (left or right? Apex or base?), how loud they are (1-6), and how they sound (harsh, musical, crescendo, decrescendo, crescendo-decrescendo, plateau). o Murmurs are caused by turbulent blood flow, which can happen with increased flow velocity (physiologic v. valve stenosis), valve regurgitations, obstructed or stenotic outflow from the heart, rapid flow through a defect. Rhythm described by rate and regularity (regular, regularly irregular, irregularly irregular, extrasystoles [early beats]). o Specific arrhythmias cannot be diagnosed on auscultation alone.

4 DIAGNOSTIC MODALITIES IN VETERINARY CARDIOLOGY Thoracic Radiographs o Thoracic radiographs allow evaluation of the size of the cardiac silhouette, and particular patterns are associated with specific chamber enlargement. Heart size can be quantified by a vertebral heart score (VHS). VHS is obtained by converting the long axis length (carina to heart apex) and short axis length (widest dimension of the heart 90º to the long axis) to the number of vertebral bodies (from T4 caudal) and summing the numbers. A normal VHS is in dogs, and < 8.0 in cats. Normal dogs occasionally have a VHS near 11, with some breeds (Boxers) significantly larger than that. A VHS of 9.0 or greater is almost never normal in a cat. o Thoracic radiographs allow evaluation of the lungs and pulmonary vessels that exceeds the capabilities of the echocardiogram. o Definitive diagnosis of left heart failure is made on a thoracic radiograph (showing pulmonary edema). o Thoracic radiographs are especially useful in dogs with respiratory and cardiac disease in distinguishing a cardiac cough from a cough due to airway or lung disease. o Proper/straight positioning and proper collimation of radiographs is critical for best evaluation of the cardiac silhouette, pulmonary vessels, and lung fields. Echocardiogram (Echo) o The echo is an ultrasound (sonogram) of the heart. The echo allows for visualization of individual heart chambers, walls, and valves, as well as the proximal parts of the aorta and pulmonary arteries. Pleural and pericardial effusion and blood clots or tumors within the heart chambers are easily visualized on echo. o 2D measurements and M-mode allow evaluation of heart size and systolic function. o Color Doppler shows a visual representation of blood flow and is helpful in identifying regurgitations, intracardiac shunts, PDAs, and turbulent blood flow. Blue color represents flow away from the probe (down the screen). Red color represents flow toward the probe (up the screen). o Continuous and pulsed wave Doppler allow measurements of blood flow velocity in specific areas of the heart. Specific measurements on Doppler wave forms give information regarding diastolic and systolic function, allow for estimation of systemic and pulmonary blood pressures, and provide variables for quantification of pressure differences (important in cases with stenotic/narrowed heart valves, and septal defects) and severity of shunts. o The echocardiogram is the gold standard for the diagnosis of the most common heart diseases of dogs and cats. Electrocardiogram (ECG, EKG) o The electrocardiogram is a representation of the vector of the wave of electrical activity (depolarization and repolarization) graphed over time. o The different leads of the electrocardiogram show the electrical activity in different planes between the electrodes. Most often, 6-leads are examined when a cardiologist records an ECG. In dogs and cats, the electrodes are placed on the elbows and knees.

5 White on the right; Smoke over fire. Reminder that the white electrode goes on the right elbow, the black electrode (smoke) goes on the left elbow, and the red electrode (fire) goes on the left knee. When a green electrode is present, it is placed on the right knee. o An ECG is required for diagnosis and characterization of arrhythmias. Changes to the shape of complexes on the ECG can be seen with heart chamber enlargement, abnormalities of the conduction system, and heart disease. o A normal ECG tracing has a p-wave (representing activation [depolarization] of the atrial chambers, a pr interval (representing slowing of the signal at the AV node), a QRS complex (presenting depolarization of the ventricles), and a T-wave (representing reset [repolarization] of the ventricles). o ECGs should be recorded at a faster paper speed (50mm/sec) to allow for analysis and measurement of complexes/waves and intervals, and a slower paper speed (25mm/sec) for evaluation of heart rhythm over a longer period of time. The amplitude or sensitivity (expressed in mm/mv, higher number = higher sensitivity) should be optimized so the complexes are readily visible but not overlapping other leads on a multilead ECG or running off the top or bottom of the paper on a single lead ECG. Holter Monitor o A 24-hour ECG used to determine the need for treatment in dogs with arrhythmias and the efficacy of antiarrhythmic therapy in dogs on antiarrhythmic medications. o Ideally baseline, post-treatment, and regular recheck ECGs are monitored in dogs with arrhythmias. o The test requires a dog to wear a small ECG recorder for 24 hours while the owner notes activity and clinical signs (if any) in a diary. o A Holter report includes reporting of maximum/mean/minimum heart rates, a tabulation of abnormal complexes and periods of abnormally fast or slow heart rate, and representative segments of ECG showing abnormalities or recorded during activities or clinical signs reported by the owner. Blood Pressure Measurement o Measurement Doppler measurement of blood pressure is preferred to and more accurate than oscillometric (Surgivet, Cardell, Bionet) measurement in conscious animals. Ideally, a Doppler blood pressure is recorded in a relaxed, still patient in lateral recumbency. The sphygmomanometer cuff width should be approximately 40% (just under half) the circumference of the limb. The cuff is placed on the antebrachium, above or below the hock (compress the Achilles tendon to relieve tension if above the hock), or at the tail base. Ultrasound gel is applied to the Doppler crystal, which is placed over the artery distal to the cuff. The cuff is inflated until no pulse is heard, and then deflated until the pulse is again heard. The pressure when the pulse returns is the systolic blood pressure. At least 3-5 readings within a narrow range of pressures should be taken and averaged. A systolic blood pressure between mmHg is normal for most patients in the clinic.

6 o Systemic Hypertension White Coat or stress-related hypertension and spurious high readings in tense or moving patients are common veterinary patients. Chronic systemic hypertension in dogs and cats is most often secondary to an underlying condition (kidney disease, Cushing s disease (in dogs), hyperthyroidism (in cats), diabetes mellitus, pheochromocytoma) that requires chronic management through a primary veterinarian or internist. Elevated BP readings in the clinic are corroborated by other physical exam findings (tortuous retinal vessels, retinal detachment, retinal hemorrhage on fundic exam; PE findings suggestive of Cushing s disease or hyperthyroidism), lab work results (suggestive of underlying cause [azotemia, increased T4, hyperglycemia, Cushing s changes] or end-organ damage [proteinuria], and echo findings (thickened heart walls, dilated aorta, aortic ± mitral valve regurgitation) suggestive of hypertension. Systemic hypertension is treated with one or several drugs including ACEinhibitors (enalapril or benazepril), calcium channel blockers (amlodipine), betablockers (atenolol), and rarely other therapies (hydralazine, phenoxybenzamine, nitroprusside CRI). BPs are rechecked within weeks of starting or adjusting medications and then every 3-4 months while controlled. o Systemic hypotension Seen often under anesthesia due to the effects of anesthetic drugs and in the ER due to dehydration, shock, and trauma. Occasionally seen in cardiac patients with severe heart disease and systolic dysfunction, secondary to brady- or tachyarrhythmias that reduce cardiac output, or as a side effect of medications (ACE-inhibitors, vasodilators, betablockers, diuretics). Depending on severity and clinical signs, treated with adjustment of cardiac medications, control of arrhythmia (when present), and/or hospitalization for pressor therapy (dobutamine, dopamine) ± fluids. Blood Work and Biomarkers o Serum chemistry (including electrolytes) monitoring is important in dogs receiving medications that might affect organ function, especially diuretics and ACE-inhibitors. o Monitoring of the PCV is necessary in pets with defects that shunt blood away from the lungs (right to left), as severe elevation in the PCV can develop and cause organ damage and neurologic signs. o Pets on digoxin should have serum digoxin levels checked after starting therapy, with dose adjustments, and every 6 months. Digoxin levels should be checked 6-8 hours after dosing. o NT-proBNP (CardioPet from Idexx) may be helpful in: Screening cats for heart disease and monitoring cats with heart murmurs and no signs of heart disease on echocardiogram. Discerning dogs and cats with respiratory distress due to heart failure from those with respiratory distress due to respiratory disease, however the turnaround time for the reference lab test (12-24 hours) and the low positive point for the SNAP test (around 130) make this application impractical. Adding prognostic information in cases of dogs with advanced valve disease prior to the onset of heart failure.

7 Contributing to screening of dogs predisposed to dilated cardiomyopathy. o Cardiac troponin I can be used to rule-out myocarditis in dogs with ventricular arrhythmias and to determine the likelihood of hemangiosarcoma in dogs with pericardial effusion.

8 HEART DISEASE AND HEART FAILURE Heart disease can be divided into those conditions that a patient is born with (congenital heart disease) and those conditions that develop with time (acquired heart disease). Acquired heart disease is more commonly seen in the clinic than congenital heart disease. Heart Disease vs. Heart Failure Any abnormality of cardiac structure or function is termed heart disease. Heart failure is a clinical syndrome that results from an inability of the heart to maintain an adequate cardiac output (forward or low cardiac output heart failure) and/or to load at a pressure that does not result in elevated capillary pressure and fluid accumulation (congestive heart failure or CHF). CHF manifests as fluid in the lungs (pulmonary edema left heart failure) and/or fluid in body cavities (pleural effusion, ascites, pericardial effusion right heart failure). Swelling of the dependent extremities (subcutaneous edema) is seen rarely in cases of right heart failure in dogs, but is quite common in people with CHF. CHF is treated with medications to reduce filling pressure by reduction in blood volume (diuretics, like Lasix and spironolactone) and dilation of veins (Pimobendan, nitroprusside, rarely nitroglycerin), to improve systolic function (Pimobendan, digoxin, dobutamine), and to decreased afterload/workload (vasodilators like enalapril/benazepril, Pimobendan, and occasionally amlodipine, nitroprusside). Congenital Heart Disease The three most common congenital heart defects seen in a veterinary cardiology practice are patent ductus arteriosus, pulmonic stenosis and subaortic stenosis. Abnormal development of the mitral and tricuspid valves (mitral valve dysplasia, tricuspid valve dysplasia) and communications between the right and left sides of the heart (atrial and ventricular septal defects) are seen less commonly. Other defects (Tetrology of Fallot, etc.) are seen rarely. Many more dogs than cats present with congenital heart defects. PDA, mitral valve dysplasia, and VSD are the most common congenital heart defects in cats. Patent Ductus Arteriosus (PDA) o The ductus arteriosus is a normal vessel between the aorta and pulmonary artery in the developing fetus that shunts blood away from the pulmonary circulation/lungs (not breathing, no need for gas exchange) and to the systemic circulation. When this vessel does not close shortly after birth, the ductus arterious is patent a PDA. o PDA causes a loud (usually grade 4-6), continuous murmur at the heart base and bounding femoral pulses. o The shunting of blood after birth switches to go from the aorta to the pulmonary artery. This shunted blood shows up back at the left heart after passing through the lungs, resulting in left heart dilation, reduction in left heart systolic function, and potentially congestive heart failure. o Surgery for PDA (occlusion of the vessel with a device by catheter or ligation by thoracotomy) is curative and can result in a normal to near normal life span, often without the need for medications. Patients with advanced secondary heart changes and heart failure may not have such a positive outcome.

9 o Medications (Lasix, ACE-inhibitor, Vetmedin, +/- spironolactone) are used when heart failure is present o A reversed or right-to-left shunting PDA occurs rarely when a PDA is present along with severe pulmonary hypertension (severe elevation in the blood pressure in the pulmonary circulation). This can result in symptoms of cyanosis and elevated red blood cell count (polycythemia). These patients often have a soft heart murmur or no heart murmur at all. Pulmonic Stenosis (PS) o Condition where the pulmonic valve (or, less commonly, an area just above or below the pulmonic valve) is narrowed, resulting in increased work for the right ventricle. o PS causes a systolic murmur at the heart base that is loud (grade 4-6) in moderate to severe cases. Some patients with PS have arrhythmias. o The increased pressure work results in thickening of the right ventricular walls and dilation of the right ventricle and right atrium. o Pets with PS may have syncope (especially with activity), arrhythmias, and/or rightsided congestive heart failure (ascites). Patients with severe PS may die suddenly due to arrhythmia. o In cases of moderate and severe PS, balloon valvuloplasty may help to reduce the work on the right heart by dilating/opening up the narrowed valve. Surgery can reduce symptoms and prolong survival time. Valvuloplasty is performed by catheter (through the jugular vein) under fluoroscopy. o Beta-blockers to slow heart rate, reduce incidence of arrhythmias, and reduce heart muscle oxygen consumption are used in patients with moderate to severe PS, and are sometimes required even after a successful surgery. o Pets with mild PS usually live a normal lifespan without therapy or surgery. Subaortic Stenosis (SAS) o Condition in which there is a narrowing just below the aortic valve (a nodule in the mildest forms, more commonly a ridge of fibrous and muscular tissue, in severe cases a circumferential tunnel of muscle), resulting in increased work for the left ventricle. o SAS causes a systolic murmur at the heart base that is usually loud (grade 4-6) when moderate to severe. o Causes thickening of the left ventricular walls that can progress to left heart dilation, decreased systolic function, and congestive heart failure. Dogs with severe SAS often have ventricular arrhythmias. o Clinical signs include exercise intolerance, syncope, and sudden death. Some dogs may live long enough with severe disease to develop congestive heart failure, though many die suddenly due to arrhythmia before this occurs. o There is currently no readily available, consistently effective surgical option for SAS. o Beta-blockers to slow heart rate, reduce incidence of arrhythmias, and reduce heart muscle oxygen consumption are used in patients with moderate to severe SAS. Exercise restriction may help in preventing syncope. o Dogs with mild SAS usually live a normal lifespan without therapy or surgery. o SAS increases the risk for heart valve infection (endocarditis).

10 Acquired Heart Disease Acquired heart disease is not present at birth, but develops in adulthood (or less commonly in juvenile pets). In dogs, the most commonly diagnosed acquired heart diseases are (myxomatous) (chronic) degenerative (mitral) valve disease (MVD, DMVD), dilated cardiomyopathy (DCM), and (predominantly in Boxers) arrhythmogenic right ventricular cardiomyopathy (ARVC). Pericardial disease (most often pericardial effusion, often secondary to a tumor), also occurs, though less commonly that DMVD or DCM. Degenerative Mitral Valve Disease o Usual onset in middle aged to older in predominantly small breed dogs; occasionally seen to a significant degree in large breed dogs. o With age, irregular thickening of the mitral (and to a lesser extent tricuspid and semilunar valve leaflets) and laxity of the chordae tendinae result in prolapse of the valve leaflets, abnormal coaptation (closing) of the valve, and regurgitation. o Valve regurgitation at the atrioventricular (mitral or tricuspid) valves results in a systolic murmur of varying intensity between patients (from 1 in very mild cases to 6 with large, eccentric regurgitant jets) that is loudest over the most significantly affected valve (almost always the mitral valve, over the left apex). Dogs with advanced DMVD often have faster, regular rhythms, and may have arrhythmias (most often supraventricular premature beats, tachycardia, or atrial fibrillation). o Chronic mitral valve regurgitation results in enlargement of the left atrium and left ventricle. In late stages of degenerative valvular disease, there is often a decrease in systolic function. CHF generally develops in the later stages of DMVD, when there is severe heart enlargement. o There is no consensus on treatment of dogs with DMVD prior to CHF, though use of medications to blunt neurohormonal effects of progressive heart disease (like enalapril or benazepril and spironolactone) and control of blood pressure, when hypertension is present, are potentially beneficial in slowing progression. o Once in heart failure, Lasix (Salix, furosemide) and Vetmedin (pimobendan) are started in addition to enalapril/benazepril and, in many cases, spironolactone. The dose of Lasix is adjusted to adequately control clinical signs of heart failure (labored breathing, coughing, intolerance to activity). In dogs with chronic heart failure not responding to high doses of oral Lasix, Lasix as a subcutaneous injection or an additional diuretic (hydrochlorthiazide, HCTZ) may be added. An alternative loop diuretic (torsemide, Demadex) may be effective in place of Lasix in refractory patients. o Dogs with DMVD and arrhythmias also may require antiarrhythmic medications (often diltiazem, digoxin, and/or sotalol depending on the specific patient). o Monitoring of resting respiratory rates, coughing frequency, tolerance for activity, episodes of syncope, heart rate/rhythm, blood pressure, and body weight are important in cases of DMVD, especially when CHF is present/imminent. o Mean survival time following the onset of congestive heart failure is months. The time from the onset of a heart murmur from mitral regurgitation to heart failure is usually more than one year and often several years.

11 Dilated Cardiomyopathy o Usual onset is in adult and geriatric dogs of larger and giant breeds. Doberman Pinschers appear to be especially predisposed to DCM. o DCM is a primary heart muscle disease characterized by a decrease in contractile function and dilation of the ventricles (usually left > right) and later the atria, leading to CHF. Dogs with DCM often develop mild to moderate valve regurgitations due to their primary heart enlargement. Arrhythmias, especially ventricular arrhythmia and atrial fibrillation, are common in dogs with DCM. o Dogs with DCM may or may not have a heart murmur. The heart murmur, when present, is often soft (less than grade 3). A gallop sound is occasionally noted. Dogs with moderate to severe DCM usually have weaker than normal peripheral pulses. Arrhythmias and pulse deficits are quite common. o Prior to the development of symptoms, benazepril and Vetmedin have been shown to increase time to heart failure and survival time in dogs with DCM. The studies demonstrating these potential benefits were performed in Dobermans. o Some dogs, generally of specific breeds (Cocker Spaniels) or being fed specific diets (vegan diet, lamb and rice diet in some dogs), may have significant improvement in heart function with supplementation of taurine and carnitine. Supplements do not make a significant difference in heart function in most dogs with DCM. o Following heart failure, treatment and monitoring is similar to that described for DMVD. o Antiarrhythmics are indicated in patients with significant ventricular arrhythmias. Mexiletine and/or sotalol are most often used with ventricular arrhythmias. Diltiazem, digoxin, and/or sotalol are often used to control atrial fibrillation rates. o Mean survival times in dogs with CHF due to DCM is 6-12 months. Sudden death from malignant ventricular arrhythmias occurs commonly. Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC) o Usual onset is adulthood or geriatric. Seen more commonly in Boxers than other breeds. Occasionally seen in English Bulldogs. Less commonly in other breeds. o ARVC is caused by infiltration of the heart muscle with fibrous and fatty tissue. This causes arrhythmias in almost all cases, and dilation of the right ventricle and atrium in some cases. Many dogs have a typical ventricular arrhythmia of ARVC without significant changes to the heart on echocardiogram. In dogs that do have enlarged right hearts, right-sided CHF (ascites, pleural effusion, subcutaneous edema) can be seen. Dogs with ARVC often have syncopal episodes. o Dog with ARVC are treated with medications to control their arrhythmias usually sotalol +/- mexiletine, and less commonly other antiarrhythmic medications. Fish oils have been shown to be an effective adjunct to medical therapy in reducing arrhythmia frequency. Response to treatment is evaluated best by Holter monitor. o Dogs with ARVC often die suddenly due to their arrhythmias. Pericardial Effusion (PCE) and Tamponade o PCE occurs when fluid accumulates in the pericardial sac surrounding the heart and great vessels. PCE is most often secondary to tumors of the heart (hemangiosarcoma and heart base tumor/chemodectoma are the most common of these) or idiopathic inflammation of the pericardium. Other cancers (like mesothelioma) and infection occasionally cause PCE.

12 o When the accumulated effusion causes compression of the right heart and impairs right heart filling, fluid accumulaton (ascites, pleural effusion, occasionally subcutaneous edema) result. This condition is called cardiac tamponade. o PCE is treated acutely with pericardiocentesis to remove the accumulated fluid and resolve cardiac tamponade. Fluid samples may be submitted for cytology and analysis, especially in atypical cases. o Long term treatment, especially in cases of idiopathic pericarditis and heart base tumors, may involve surgery to remove or perforate the pericardium to prevent recurrent tamponade. o Surgery and chemotherapy may prolong survival times in dogs with hemangiosarcoma, though they often survive less than 1 year even with aggressive therapy. o Dogs with idiopathic pericarditis (PCE without neoplasia or infection) can survive for years, though many experience at least one recurrent episode of effusion. o Yunnan Baiyao may be helpful in delaying recurrent hemorrhage in dogs with tumors. o No medications have been shown to consistently prevent recurrence of PCE due to idiopathic pericarditis. Less Common Acquired Heart Diseases o Tachycardia-induced cardiomyopathy o Adriamycin/doxorubicin-induced cardiomyopathy The above resemble DCM o Infective endocarditis (heart valve infection) o Atrial cardiomyopathy o Myocarditis (viral, Chaga s, rickettsial) o Infiltrative heart disease (neoplasia) Cats most often develop hypertrophic cardiomyopathy (HCM by far the most common type of heart disease), restrictive cardiomyopathy (RCM), or cardiomyopathy with components of each (unclassified cardiomyopathy - UCM). Rarely, DCM, ARVC or significant DMVD is seen in cats. Hypertrophic Cardiomyopathy (HCM) o Can be seen in young adults or in older/geriatric cats. Maine Coon, Ragdoll, American Shorthair, and Sphynx breeds may be predisposed. Changes to the heart resembling HCM can be seen in hyperthyroidism and systemic hypertension. o Cats with HCM will have varying degrees of thickening (hypertrophy) of the LV walls and reduction in LV chamber size. Some cats with HCM have abnormal motion of the mitral valve that causes outflow obstruction and mitral regurgitation (hypertrophic obstructive cardiomyopathy [HOCM]). As the disease progresses, the left atrium will enlarge due to impaired filling of the heart (diastolic dysfunction). In late stage disease, scarring (fibrosis) and thinning of the heart walls, ventricular dilation, and decreased systolic function can be seen. Some cats with HCM progress to CHF. Thromboembolism (blood clot, stroke, ATE) occurs commonly in cats with advanced heart disease, generally causing paralysis of one or both pelvic limbs or the right front limbs. Less commonly, blood clots embolize to the brain, kidneys, or elsewhere. o There are no consistent physical examination findings associated with HCM. Some cats may have heart murmurs due to outflow obstruction or valve regurgitations, which may be soft even with severe disease. Cats with HOCM often have louder (grade 3-4) heart

13 murmurs. Occasionally, cats with HCM have arrhythmias. Cats with severe HCM often have a gallop sound. o There is no consensus regarding treatment of cats with HCM prior to heart failure. Atenolol (a beta-blocker) is often used to decrease heart rate and systolic function and can improve or resolve obstruction in cats with HOCM. Cats with enlarged atria are often started on medications to blunt neurohormonal activation (enalapril/benazepril) and decrease the risk for blood clots (Plavix or aspirin). Diltiazem is occasionally used, as it may improve diastolic function and improve blood flow to the heart muscle. o Following heart failure, Lasix is added to therapy with enalapril/benazepril if not already receiving. Pimobendan is occasionally used in cases not responding to standard treatment or in patients with poor systolic function. o There is wide variation in survival times in cats with HCM and CHF 6-12 months is typical. Restrictive Cardiomyopathy o RCM is a disease characterized by fibrotic (scarred), thin heart muscle with dilated heart chambers, diastolic dysfunction, and some degree of systolic dysfunction. Cats with late stage HCM often have echocardiographic findings similar to RCM. At the time of diagnosis, many cats have significant enlargement of both atrial chambers. o Like HCM, there are no consistent physical exam findings. Heart murmurs are occasionally present due to valve regurgitation. A gallop sound is often noted in severe cases. o Cats with RCM may be at higher risk for ATE than cats with HCM, and often have larger atria. o Treatment principles are similar to cats with HCM, though beta-blockers are not commonly used in this condition. o Survival times in cats with RCM and CHF is often shorter than that noted for cats with HCM. Less Common Acquired Heart Diseases o DCM more common historically due to taurine-deficient diets o Infective endocarditis (heart valve infection) often associated with Bartonella infection in cats o ARVC o Significant degenerative valvular diease o Tachycardia-induced cardiomyopathy o Infiltrative heart disease (neoplasia)

14 ARRHYTHMIAS Arrhythmias are the result of abnormal cardiac impulse formation, abnormal propagation of the cardiac impulse, or spontaneous impulse formation in tissues that normally are not spontaneously active. Bradycardias Abnormally slow heart rates are called bradycardias. In the clinic, heart rates below 70bpm in dogs and 120bpm in cats are bradycardic. Sinus Bradycardia o May be normal in athletically trained pet. o Can be seen secondary to gastrointestinal, central nervous system, or respiratory disease. o Can be seen with sedatives/opioids. o The heart rate should increase with atropine, though in most cases, this rhythm does not require specific therapy. Heart Block o First degree = slow conduction of impulse through AV node = prolongation of pr interval (> 130msec in dogs, > 90msec in cats); seen with normal heart rate, respiratory sinus arrhythmia or sinus bracycardia in most cases. o Second degree = intermittent failure of propagation of impulses through the AV node = occasional p waves without QRS complexes Can be low grade (i.e. most p waves are conducted) or high grade (half or fewer of p waves are conducted) May become more normal with atropine and managed at least partially with medications (theophylline, terbutaline, or hyoscyamine [Levsin]) Often, with severe bradycardia (< 60 bpm) and clinical signs of syncope or weakness/lethargy, a permanent pacemaker is required o Third degree/complete = complete failure of propagation of impulses through the AV node = p waves not associated with QRS complexes at regular intervals (p waves marching through QRSs). Cardiac output maintained by a slow escape rate generated by the AV node or ventricular conduction system/myocardium Seldom improves with atropine Almost always requires implantation of permanent pacemaker in dogs Cat escape rhythms are usually sufficiently fast to maintain adequate cardiac output for most activities, so pacemakers are not often required in this species Atrial Standstill (Silent Atrium) o Failure of the SA node to generate an impulse or the atrial myocardium to propagate a sinus impulse o Can be seen with hyperkalemia (e.g. in a blocked cat), atrial cardiomyopathy, or conduction system disease/fibrosis. o Absent p-waves on the ECG with a slow escape rate. o Requires a pacemaker to normalize heart rate and cardiac output in the absence of a reversible causes.

15 Tachycardias Abnormally fast heart rhythms are called tachycardias. Heart rates above 160bpm in dogs (or 220bpm in puppies) and 240bpm in cats are considered tachycardic. Sinus Tachycardia o Can be seen in congestive heart failure and as a compensatory mechanism in shock, pericardial effusion/tamponade, and systemic hypotension. o Noted in normal animals that are actively exercising, hyperthermic/febrile, in pain, stressed/anxious, or very excited. o Generally reverses with resolution of precipitating cause. Does not usually require specific therapy, though some pets with persistent sinus tachycardia and heart disease may be placed on a beta-blocker or digoxin. Supraventricular/Atrial Tachycardia (SVT) o SVTs are the result of abnormally rapid formation of atrial impulses at a site in the atria other than the SA node or reentry of a cardiac impulse from the ventricles to the atrium causing excitation of the atria and rapid reexcitation of the ventricles. o On ECG, SVTs generally have normal-appearing QRS complexes ± with alternating QRS complex amplitude and p-waves that may appear different from normal sinus p-waves or may be obscured in the t-wave of preceding complexes. o Single or coupled early complexes originating from the atria are called atrial premature beats (APCs). o Sustained SVT or frequent runs of nonsustained SVT is treated with one or several of diltiazem, digoxin, sotalol, or atenolol in most cases. Other drugs are used less commonly. Atrial Fibrillation (A fib, AF) and Atrial Flutter o Arrhythmias characterized by rapid and, in the case of A fib, irregular excitation of the atria. o Generally occur in the presence of heart disease and atrial enlargement, but may occur in the absence of other heart disease in giant breed dogs. o Atrial flutter causes a rapid, regular heart rhythm. On ECG, a coarse, saw tooth pattern is noted on baseline (flutter wave). Generally only ¼ to ½ of the flutter impulses are conducted. QRS complexes usually appear normal. o Atrial fibrillation causes a rapid, irregular rhythm. On ECG, a low amplitude, irregular undulation (f-wave) might be visible, however the baseline is often flat. QRS complexes are usually narrow and normal, but may show changes due to ventricular enlargement or conduction abnormality. o The goals of therapy for both arrhythmias are to decrease the number of impulses passed through the AV node and slow the ventricular response rate. Digoxin, diltiazem and/or sotalol are most often used in rate control therapy for A fib and AF. Most dogs in A fib remain in A fib even with effective rate control therapy. o Electrical cardioversion using a defibrillator has been reported for A fib, and can provide (usually temporary) restoration of a sinus rhythm, however continued medication (sotalol or amiodarone) is required to prevent/delay recurrence of A fib.

16 Ventricular Tachycardia (VT) and Ventricular Fibrillation o Spontaneous activity of ventricular myocytes results in premature ventricular complexes (VPC, PVC) that may sustain in rapid heart rates VT. o VT appears as wide/bizarre QRS complexes unassociated with p-waves. o VT may devolve into chaotic, disorganized ventricular electrical activity ventricular fibrillation, which appears as irregular undulation of the baseline without obvious QRS complexes. A fibrillating ventricle does not generate a coordinated contraction, and cannot generate sufficient cardiac output. o Sustained VT is a life-threatening condition treated with injectable antiarrhythmic medications commonly lidocaine and procainamide, less commonly esmolol and amiodarone. Magnesium sulfate is occasionally given in the treatment of ventricular arrhythmias. In patients able to take oral medications, sotalol may be given while trying to break or convert the tachycardia to a normal sinus rhythm. When effective, lidocaine and procainamide are continue as CRIs in the hospital prior to transitioning to oral medications to be given at home. o Maintenance therapy for ventricular arrhythmias generally involves oral sotalol and/or mexiletine, less commonly beta-blockers (except in cats, where atenolol is used commonly) or amiodarone. o Ventricular fibrillation is a fatal arrhythmia unless converted with electrical defibrillation.