Specific Heart Diseases

Degenerative Valve Diseases

Brief Review of Diagnostics

Degenerative valve disease affects mainly the mitral and tricuspid valves. It is also called myxomatous mitral valve disease due to the pathology and endocardiosis although this term has fallen out of favor as it does not help describe the disease.

As the mitral valve is most commonly affected, the disease has a reliable biomarker, the presence of a left apical systolic murmur. Typically initially, this is quiet, grade 1 or 2, with little evidence of cardiac remodeling, but as the disease progresses, the murmur becomes louder often radiating to the right. In a third of cases, the tricuspid valve is also affected and a right apical systolic murmur can be appreciated.

Blood samples: In asymptomatic dogs, these are usually normal but with the onset of heart failure mild elevation of renal param­eters is often seen due to the pre-renal renal failure caused by the poor cardiac output. Biomarkers such as atrial natriu­retic peptide (ANP) and brain natriuretic peptide (BNP) rise in the few months prior to heart failure and in the dyspneic dog, a high level of BNP is strongly suggestive of heart failure.

ECGfindings: These are usually non-specific. A tall or wide R wave can represent left ventricular enlargement and a wide P wave can suggest left atrial enlargement. Arrhythmias are not uncommon. Atrial or supraventricular premature complexes (SVPC) are seen and atrial fibrillation (AF) is occasionally found especially in larger dogs secondary to the left atrial dilation.

Radiographs are very helpful to document progression of the disease and confirm the presence of congestive heart failure. In asymptomatic dogs, the heart and lungs can be normal in class B1. The pulmonary vasculature should also be normal. Once cardiac remodeling develops, dogs enter class B2 and left atrial and ventricular enlargement can be seen on the radio­graphs due to the volume overload of the regurgitation. This is typically observed with tracheal elevation which suggests left ventricular enlargement and a triangular soft tissue density on the caudodorsal mar­gin of the cardiac silhouette on the lateral radiographs. On the DV radiograph, a bulge at the 2-3 o'clock position suggests enlargement of the left auricle. As left atrial pressures start to rise, the pulmonary vein dilates and this can be used as a sign that heart failure is imminent. Once heart fail­ure develops, an interstitial/alveolar pat­tern develops in the caudodorsal lung fields on the lateral and the right caudodorsal lung field first, obscuring the outline of the left atrium. This is particularly evident in the left lateral view where the right lung is uppermost and should be filled with air.

Echocardiography can be used to confirm the etiology of the murmur. The thickened mitral valve leaflets can be seen and volume overload of the left ventricle and left atrium can be assessed. The left atrium to aorta ratio is a reliable way to document left atrial enlargement as the disease progresses. The disease affects the chordae tendineae and if these rupture, valve prolapse or a flail leaf­let may be seen. Color flow with variance mapping will show the turbulent jet of mitral regurgitation and mitral regurgita­tion can been seen on echocardiography before a murmur is audible. The size of this jet can be used to roughly assess severity (Figure 5.4).

There are few differential diagnoses for a left apical systolic murmur and in an older small breed dog, degenerative valve disease is the likely cause. In younger animals, mitral valve dysplasia is seen particularly in the bull terrier breed. Co-morbidities are mainly those of an aging dog. Renal failure presents a significant problem as it may reduce the dosage of diuretic that can be used.

Therapeutics Acute, Chronic, and Expected Outcome

See section on treatment of acute and chronic left sided congestive heart failure

Trials involving angiotensin converting enzyme inhibitors (ACEi) and beta blocker have not demonstrated a delay in the onset of congestive heart failure in asymptomatic dogs. A recent trial showed that the calcium inodilator, pimobendan, delayed the onset of congestive heart failure by 15 months when used in dogs with stage B2 degenerative mitral valve disease. The entry criteria were strict including a large heart on x-ray and echocardiography as well as a loud murmur. Current recommendations for asymptomatic dogs include avoiding a high sodium diet and the use of omega 3 fatty acids. The recom­mended dose of DHE and EPA are 25 mg/kg and 40 mg/kg respectively.

Once heart failure is controlled and the patient returns home, heart failure can recur after a period for a number of reasons:

1) Rupture of a chordae tendinae - this is probably the most common cause and can result in acute death. It can be visualized with echocardiography.

Figure 5.4 Echocardiogram of a dog with advanced degenerative mitral valve disease. This right parasternal long axis 2D view (Figure 5.4a) shows the thickened mitral valve especially the anterior leaflet. The left atrium and left ventricle show eccentric hypertrophy due to the volume load. On color flow (Figure 5.4b), the green turbulent jet of mitral regurgitation can be seen filling the left atrium during systole.

2) Development of an arrhythmia usually AF. When AF develops, the dogs lose the atrial component of left ventricular filling and the heart rate increases, decreasing diastolic filling. Rate control is usually sufficient to bring the failure under control.

3) Left atrial tear - the mitral regurgitant jet produces fibrous scars on the left atrial wall, so called “jet lesions” and can even­tually puncture the left atrial wall causing a hemopericardium. These are difficult to treat as the pericardium should not be drained unless the cardiac tamponade is life threatening. Then a small volume is withdrawn. The pressure in the pericar­dium helps reduce the leak which, in some cases, can heal. Cage rest and drugs to reduce blood pressure to 90-100 mmHg are used to reduce the afterload and hence regurgitant fraction and left atrial pres­sures. Recurrence is not uncommon.

2) Increasing systolic dysfunction - the vol­ume-loaded left ventricle becomes unable to eject blood into the circulation without elevated filling pressures and pulmonary edema. This may be seen with a gradual increase in breathing rate necessitating changes in medications. For patients that have recurrence of heart failure with none of the previous three causes, treatment is continued as:

a) Optimize medications: Ensure the drugs are given correctly, for example, every 12 hours for twice daily medication, ensure spironolactone is given with food which enhances its absorption and pimobendan is given on an empty stom­ach.

b) Change medications: If furosemide is being given twice daily, increase fre­quency to 3 or 4 times as it has a rela­tively short duration of action. Alternatively, a parenteral route can be considered if the owner is able to inject the furosemide subcutaneously twice daily. This can be more effective for patients who have concomitant right heart failure and so may not be absorb­ing medications well. If this is ineffec­tive consider adding a thiazide diuretic to encourage sequential nephron blockade. Beware when adding in thi­azide diuretics as dehydration and electrolyte depletion can easily occur. Start at the lower end of the dose range and titrate up to effect. Alternatively, consider switching to a more potent loop diuretic such a torsemide. The starting dose of torsemide is typically 1/10 of the total daily dose of furosem­ide. That dose is halved and given twice daily. For example if a dog is receiving 10 mg furosemide three times daily, the starting dose of torsemide would be 1.5 mg twice daily. Again electrolyte depletion and dehy­dration are common side effects and may necessitate dose reduction.

Another complication of advanced degenera­tive mitral valve disease is the development of pulmonary hypertension. Dogs with pulmo­nary systolic pressures over 55 mmHg have a worse prognosis than those with lower pres­sures. While syncope can be a sign, lethargy and other non-specific signs are common. Treatment with a phosphodiesterase 5 inhibi­tor, for example, sildenafil 2-3 mg/kg BID - TID, often reduces clinical signs although a reduction in pulmonary artery pressure may be hard to document with increased flow.

Low sodium diets rich in omega 3 fatty acids have been advocated but there is little evidence in veterinary literature regarding their benefit.

Prognosis is variable with degenerative mitral valve disease, making prediction of survival time difficult. Some dogs with mild disease never develop congestive failure, while others have a more rapid progression of their disease. Patients with class B1 disease can be monitored with an annual echocardio­gram or radiograph to assess cardiac size. Patients in class B2 warrant closer monitoring with a review every 6 months. It is helpful to actively enroll the owner in monitoring their pet. Counting their resting respiratory rate has been shown to be one of the most effec­tive ways of detecting the onset of heart fail­ure. Rates less than 30 breath/minute are normal while rates over 40 require further investigation. When patients are in the com­pensated stage of congestive heart failure (class C) continuing to monitor breathing rate is a useful way of monitoring the effectiveness of diuretics and guide dose adjustments.

Once heart failure develops, the mean survival time is 9-12 months. However as chordal rupture, for example, may cause acute decompensation at any time, predict­ing the lifespan of an individual dog is impos­sible. There are certain parameters that are associated with poorer prognosis such as larger LA:Ao ratio, high E wave velocities of mitral inflow or larger LV but ultimately they suggest that the more advanced the disease, the poorer the prognosis.

Quality of Life with Euthanasia Decision

Initially once heart failure is controlled, quality of life is usually normal with few clinical signs and reasonable exercise tolerance. However with more advanced disease, quality of life deteriorates and increasing doses of diuretics are required to control the congestive heart failure. The high doses of diuretics produce electrolyte depletions which can predispose the patient to weakness and arrhythmias. In addition elevation of urea and creatinine sug­gest increasing renal compromise. This can cause the patients to have poor appetites which contributes to their cardiac cachexia and electrolyte depletion. Ultimately, for some patients, the heart failure cannot be controlled without producing unacceptable renal failure. Sudden death is uncommon but can occur. It may be due to a malignant ventricular arrhyth­mia or rupture of a major chordae and fulmi­nant pulmonary edema.

Cardiomyopathies

Cardiomyopathies refer to the primary heart muscle diseases suffered by dogs and cats. As a result, all secondary causes must be ruled out to make the diagnosis. Secondary causes include:

• Hyperthyroidism especially cats

• Tachycardiomyopathy where a sustained fast heart rate can lead to a dilated poorly contractile ventricle, for example, supraventricular tachycardia.

• Drug toxicity such as doxorubicin

• Infections, for example, trypanosomiasis

• Hypertension or increased growth hor­mone as a cause of LV hypertrophy

• Nutritional deficiencies. Both taurine and carnitine deficiencies have been report in dogs as a cause of heart disease with a DCM phenotype and taurine deficiency in cats. American cocker spaniels and Newfoundlands may be predisposed but taurine levels should be assayed in any unusual breeds with a DCM phenotype as supplementation can be curative. Blood carnitine levels reflect poorly myocardial levels so supplementation can be attempted with an improvement in systolic function expected in 2-3 months.

In dogs, the most common disease seen is dilated cardiomyopathy (DCM). The ventricle (mainly left) becomes dilated and poorly contractile and on histology the myofibers have a wavy appearance. Certain breeds such as the Doberman and Irish wolfhound are predisposed. Boxers have a variant with mainly right ventricular origin VPCs called arrhythmo- genic right ventricular cardiomyopathy (ARVC) or perhaps better, arrhythmogenic cardiomyo­pathy. On histology both the left and right ventricles have a Iibrofatty infiltration similar to the human disease.

Cats are more likely to develop hyper­trophic cardiomyopathy (HCM) with a spon­taneous increase in the thickness of the ventricular walls, usually the left ventricle so that the thickness exceeds 5.5 mm in diastole. This may start with papillary muscles abnor­malities which in some cats develop into symmetrical hypertrophy of the left ventri­cle. In other cats, the hypertrophy is more asymmetrical with discrete bulges. If these occur in the left ventricular outflow tract, a dynamic murmur can be appreciated. A murmur may also be caused by mitral regur­gitation which can also develop due to sys­tolic anterior motion (SAM) of the anterior mitral leaflet.

Cats can also suffer from DCM although this is rare since feline diets are now supple­mented with taurine. Restrictive cardiomyo­pathy (RCM) is also seen. In this disease, the ventricle becomes fibrotic unable to relax and fill with blood. The muscle walls may have a normal thickness but the atria are usually very dilated. ARVC in cats is similar to the boxer form of the disease and if the heart muscle disease does not fit into any of these categories, it is called unclassified car­diomyopathy. Most of the discussion will be restricted to HCM as it is the most common feline cardiomyopathy.

Dilated Cardiomyopathy

Brief Review of Diagnostics

Dogs have a long asymptomatic period where echocardiographic changes are evident although in some breeds such as the boxer and Doberman, a Holter analysis of the heart rhythm over 24 hours can be more helpful. Over 500 VPCs in 24 hours or the presence of ventricular couplets is suggestive of the disease although other causes such as abdominal disease may have to be ruled out.

Blood Samples: As for degenerative valve dis­ease, serum biochemistry is usually in the reference range in asymptomatic patients although renal parameters rise with heart failure. The pattern with ANP and BNP is also similar to degenerative valve disease with values rising at or just prior to heart failure. Troponin may be elevated espe­cially in patients with frequent ventricular arrhythmias and may have prognostic util­ity as patients with higher troponin have a poorer prognosis.

ECG findings: These can be variable with some dogs having a normal rhythm but may show the wide P wave and tall R wave suggestive of left atrial and ventricular enlargement respectively. In others atrial and ventricular premature complexes can be seen and the later can vary from iso­lated complexes to bigeminy to runs of ventricular tachycardia. Atrial fibrillation (Figure 5.5) is not uncommon and often precipitates the onset of heart failure with the reduced diastolic filling and loss of the atrial component of LV filling. Irish wolf­hounds may develop slow atrial fibrillation without concurrent myocardial disease, so called lone atrial fibrillation although many go on to develop DCM later in life. Holter monitoring may be the most sensi­tive and specific way to diagnose this dis­ease is some breeds.

Radiographs: In the asymptomatic stage, the cardiac silhouette maybe enlarged although this can be difficult to document especially in breeds such as the Doberman. Once heart failure develops, an interstitial/ alveolar pattern is seen in the caudodorsal lung lobes, especially the right due to the presence of pulmonary edema (see Figure 5.1). The pulmonary veins are usually dis­tended. In some dogs, a pleural effusion is also seen. If right-sided heart failure is also present, a ground glass appearance to the abdomen suggests ascites and this will obscure the hepatomegaly. A distended caudal vena cava would support this.

Echocardiography: The presence of a dilated thin walled poorly contractile left ventricle and dilated left atrium are seen in advanced cases and in those with heart failure. In dogs with asymptomatic disease, the changes are more subtle and reference to breed stand­ards or an allometric scaling system such as Cornell may be needed. The right ventricle and right atrium may also be affected espe­cially in ARVC in boxers. In clinical cases the various measures of systolic function would be expected to be depressed. These include fractional shortening, ejection frac­tion, systolic time intervals, and E point sep­tal separation as well as tissue Doppler parameters. On color flow Doppler, a small jet of mitral regurgitation is often seen which explains the soft left apical systolic murmur. This is caused by dilation of the mitral annulus which drags the leaflet tips apart, leading to incompetence (Figure 5.6).

Therapeutics Acute, Chronic, and

Expected Outcome

Both pimobendan and ACE inhibitors have been shown to be beneficial in the asympto­matic case delaying the onset of heart failure. Asymptomatic dogs with frequent arrhythmias may be given anti-arrhythmic medication

Figure 5.5 ECG from an 8-year-old Labrador with atrial fibrillation. This ECG shows the hallmarks of this rhythm abnormality: tachycardia, irregularly irregular, no P waves and a narrow supraventricular QRS. Note the irregular baseline which represents the atrial fibrillation. This movement, called F waves, can be fine or coarse. 50 mm/s and 1 cm/mV.

especially if the coupling interval is very short (R on T phenomenon) which may suggest ventricular fibrillation is likely. Although, there is no evidence that drug therapy makes sudden death less likely, it may reduce synco­pal episodes. Once a dog is started on anti- arrhythmic medication, the Holter monitor should be repeated after one month to assess response, as all anti-arrhythmic drugs have the potential to be pro-arrhythmic. Once sta­ble, the Holter monitor is usually repeated every 6 months and again one month after any drug change.

Treatment for acute heart failure is as pre­viously described. Some patients with poor myocardial function may have low blood pressure and require positive inotropic sup­port with dobutamine. Patients with atrial fibrillation require careful reduction of their heart rate as they may be relying on this ele­vated heart rate to maintain output. Often resolving their heart failure will reduce heart rate as it reduces the sympathetic drive. At discharge, dogs receive the same 3 or 4 medications as described previously as well as medication to control heart rate if necessary.

Atrial fibrillation requires drugs to slow the heart rate as the underlying mechanism for its development is atrial enlargement which cannot be addressed. As a result, the beneficial effects of cardioversion to sinus

Figure 5.6 Echocardiogram of dog with dilated cardiomyopathy. The left atrium and left ventricle are dilated and the ventricle appears thin walled (Figure 5.6a). On M mode (Figure 5.6b), the reduced fractional shortening can be appreciated and this is consistent with reduced contractility.

rhythm are likely to be short lived. Digoxin, calcium channel blockers (diltiazem) and beta blockers (usually atenolol) can all be used to slow heart rate. Beta blockers tend to have more negative inotropic effects which are usu­ally dose related so are less frequently used. Diltiazem also has some negative inotropic effects but this is less severe. Digoxin acts cen­trally via vagal centers to slow heart rates. A combination of digoxin and diltiazem has been shown to provide better rate control than either drug alone and presumably this will translate into longer survival. The optimum heart rate for patients with atrial fibrillation has yet to be determined but rates of 140­160 bpm in the clinic and 120-140 bpm on Holter monitor have been reported.

Quality of Life with Euthanasia Decision

As for degenerative valve disease, dose esca­lation of diuretics and ACE inhibitors is seen with progressing disease. The owner should be advised that many dogs with DCM are at risk of sudden death especially if they have frequent VPCS or runs of ventricular tachy­cardia. Options for patients who are diuretic resistant include:

• More frequent administration of furosemide

• Parenteral administration of furosemide

• Addition of a thiazide diuretic

• Switching to the more potent loop diuretic, torsemide, as described previously

Right heart failure can contribute to the development of cardiac cachexia. Severe weight loss is not uncommon in dogs with chronic disease. This can be caused by increased catabolism (heart failure is an inflammatory disease), poor nutritional intake with poor appetite, poor absorption and poor metabolism from the under-per­fused liver. Poor appetite can be due to:

• Advancing renal failure

• Altered taste sensations with medications

• Digoxin toxicity

Use of a calorie dense food can help to miti­gate weight loss. Supplementation with omega 3 fatty acids has been shown to be beneficial in human patients with cardiac cachexia and the same is likely to be true in dogs. The dose of omega 3 fatty acids is as described previously.

Balancing diuretic requirements between controlling heart failure and not exacerbat­ing renal failure is an act that will ultimately be lost with advancing renal failure in the face of increased diuretic requirements. Sudden cardiac death is always a possibility.

Hypertrophic Cardiomyopathy

Brief Review of Diagnostics

Cats can have a long asymptomatic period and although 30% of cats may have a mur­mur with 50% of those having structural heart disease, many cats never go on to develop heart failure. For cats with mild left ventricular hypertrophy and no left atrial enlargement, annual evaluations are suffi­cient as the disease is slowly progressive. The only way to assess disease stage is with echocardiography. However, once left atrial enlargement is documented, heart failure is likely to occur and more frequent re-evalua­tion is prudent.

There is no firm evidence that treatment prior to the onset of heart failure is benefi­cial. However, if the hypertrophy is severe or there is significant left atrial dilation, treat­ment is often started.

Blood samples: In the asymptomatic patients, routine blood work will be normal. Biomarkers may be helpful especially in cats with other signs of heart disease such as murmur or gallop. Elevated BNP would increase the suspicion of cardiac disease and prompt further evaluation with an echocardiogram. Once heart failure devel­ops, pre-renal renal failure causes eleva­tions of urea and creatinine.

ECG: This may be normal or consistent with left ventricular hypertrophy - tall or wide R wave. Atrial or ventricular premature complexes may be present but malignant arrhythmias are uncommon. A particular branch block is recognized in cats and its detection again increases the suspicion of cardiomyopathy. A left anterior fasicular block is seen in cats where the R wave is negative in leads 2 and 3 but positive in lead 1. When cats develop heart failure, their rate does not increase as dramatically as dogs.

Radiographs: The hypertrophy is concen­tric so the cardiac silhouette can be nor­mal even in significantly affected cats. However if atrial dilation is present a dis­crete enlargement can be caudodorsally. If biatrial enlargement is present, the car­diac silhouette can have a Valentines's shape on the DV. When cats develop heart failure the interstitial alveolar pat­tern can occur anywhere in the lung fields (Figure 5.7). Cats in heart failure can also develop significant pleural effu­sions that may warrant treatment. Thick pulmonary veins support the diagnosis of heart failure. Ascites is rare in cats with heart failure

Echocardiography: This is the definitive test that allows the diagnosis and disease

Figure 5.7 Lateral (Figure 5.7a) and DV (Figure 5.37b) chest radiograph from a 13-year-old DSH cat with congestive heart failure. A moderate pleural effusion is present and patches of pulmonary edema. In cats, these can occur anywhere in the lungs unlike the perihilar distribution seen in dogs.

severity to be identified. The hypertrophy of the left ventricle can be visualized and the size of the left atrium assessed. The left ventricular walls should be less than 5.5 mm in diastole and the left atrial diam­eter under 16 mm in long axis. In addition, the LA:Ao ratio should be under 1.6. In some cats, mitral regurgitation due to SAM or dynamic left ventricular outflow tract obstruction (DLVOTO) is present. The left auricle can be examined for the presence of a thrombus (Figure 5.8). Also, the presence of spontaneous echo contrast in the left atrium which looks like swirling smoke suggests an increased likelihood of thrombosis and would warrant the intro­duction of antithrombotic medication.

Therapeutics Acute, Chronic, and

Expected Outcome

There is no good evidence currently that medication of asymptomatic cats is benefi­cial. Previously it was believed that cats with DLVOTO benefited from beta blockage. However, recent evidence suggests this is not the case. If the left ventricle thickness exceeds 9mm in places, the addition of an ACE inhibitor can be tried due to the effects on myocardial remodeling. If the left atrium is very large, over 19 mm, the cat is at increased risk of a thromboembolic event. The sluggish blood flow in the left atrium predisposes cats to this. The recent FAT CAT (feline aortic thromboembolism clopidogrel v. aspirin trial) study indicated that clopi- dogrel is superior to aspirin in prevention of re-thrombosis. Clopidogrel is administered as 75 mg ¼ tablet once daily. It is bitter and can be administered in a gel capsule to improve palatability. The dose of aspirin is more variable with doses as high as 10-25 mg/ kg every 48 hours but for platelet inhibition, 0.5 mg/kg is probably sufficient.

Cats with cardiomyopathy can develop heart failure with pulmonary edema and/or pleural effusion. However they can also have a thromboembolic event. Pulmonary edema is treated as for canine left heart failure with oxygen, cage rest, and furosemide. Pimobendan can be given if inotropic sup­port is needed. Cats are particularly sensitive to the stress of further investigations so these may be delayed until the disease is under control. It is also easy to create electrolyte

Figure 5.8 Echocardiogram from a cat with hypertrophic cardiomyopathy. The right parasternal long axis view (Figure 5.8a) shows the thickened left ventricular walls and dilated left atrium. During systole (Figure 5.8b) color flow shows the green turbulence shows high velocity flow in the left ventricular outflow tract caused by dynamic obstruction with end systolic cavity obliteration. There is also a jet of mitral regurgitation secondary to systolic anterior motion (SAM) of the anterior mitral valve leaflet.

and renal abnormalities with high diuretic dose and this should be carefully monitored. Once the respiratory rate and effort start to decrease, the cat can be switched to oral medications.

If a cat has a pleural effusion, thoracocen­tesis is indicated to obtain a sample and to therapeutically remove the fluid. No amount of diuresis will reduce the pleural effusion in the short term but treatment including diu­retics is aimed at slowing the recurrence of the fluid. Thoracic ultrasound can be used to confirm the clinical suspicion of a pleural effusion and to guide location for drainage. A butterfly or over the needle catheter is advanced into the pleural cavity and suction applied with a three way tap. As much fluid as possible should be drained from each side. In cats with severe life threatening dyspnea, this can be life-saving although it may have to be performed in two stages. The first proce­dure removes a small amount of fluid with minimum restraint and stress. The cat can then recover in oxygen for 30 minutes before a second procedure to remove the rest of the fluid. Even the removal of a little as 20 ml in the first procedure can make a significant difference to the respiratory effort of the cat.

Thromboembolic events are life threaten­ing for cats as recovery is often poor with up to 50% of cats not surviving to discharge despite appropriate intensive care. The ter­minal aortic trifurcation is the most common site with the classic signs of paresis, pallor, lack of pulse, and pain. The stress can also precipitate the onset of heart failure which can complicate treatment. Other arteries can be affected including the renal, cerebral, and forelimb, usually the right. For these arteries, the prognosis is better with cats with fore­limb thromboses recovering within a week. Aortic thromboembolism requires prompt treatment. The heart failure should be man­aged as previously. Pain is often the most severe problem and can be difficult to con­trol even with appropriate opiate analgesia. Use of thrombolytic medication such as tis­sue plasminogen activator is associated with high fatality rate probably because the cat is not presented early in the course of its disease. Beyond 6 hours, high levels of p otassium and toxic metabolites such as myocardial depressant factors build up in the ischemic tissues and sudden release of these into the circulation can cause sudden death. Instead, heparin or low molecular weight fragments such as dalteparin may be used to help clot dissolution. The dose of heparin is 250-300 IU∕kg TID while the dose of daltepa- rin is less well established with 100IU∕kg every 8 to 12 hours often used. Symptomatic treatment is provided which may include management of the heart failure and pain and encouraging feeding. Hospitalization for at least 7 days is required in severe cases and at the end of that period, cats that are likely to survive, will show some improvement in hind limb function although this is often uni­lateral initially. Weak pulses may be felt, the limb is slightly warmer and some return of function is seen although knuckling is com­mon. Some cats develop a dry gangrene of the limb and the lower portion becomes hard and dry resembling mummification. For these cats, amputation is required.

Quality of Life with Euthanasia Decision

If a cat is presented with a severe aortic thromboembolism, the owner needs to be involved in the decision making process as treatment is not inexpensive and the outcome is often poor. If pain cannot be adequately managed, euthanasia should be considered. A brief echocardiogram is helpful as if fur­ther thrombi are identified in the left auricle, recurrence in a short period is likely. Large thrombi can result in sudden death. Anorexic cats in heart failure rapidly develop electro­lyte abnormalities and increasing renal parameters further depress appetite creating a downwards spiral which is difficult to treat. Cats that survive to discharge are at risk of recurrence although clopidogrel will help to reduce that risk. Most owners are unwilling to allow their cat to be treated for a recurrence.

Cats with compensated congestive heart failure have an average survival of 9-12 months depending on the severity of their heart disease. Recurrence of heart failure with escalating doses of diuretics is com­mon as the disease progresses and as with dogs, the balance between renal and heart failure often determines ultimate outcome. Cats seem to be more sensitive to the addi­tion of a thiazide diuretic or switching to torsemide.

Congenenital Cardiac Diseases

Dogs and cats with congenital heart disease can vary in the severity of their signs from those that are minimally affected with normal life expectancies although they should not be used for breeding to those with severe disease who will die prematurely from heart failure or sudden cardiac death. While the most com­mon congenital heart disease seen in cats is probably a ventricular septal defect, this section will discuss the three most common congenital cardiac diseases seen in dogs:

• Subaortic stenosis

• Pulmonic stenosis

• Patent ductus arteriosus (PDA)

Brief Review of Diagnostics

The presence of a heart murmur in a young puppy is the clinical sign that should raise suspicion of congenital heart disease. Subaortic and pulmonic stenoses both have a left basilar murmur. However while subaor­tic stenosis is associated with a murmur that radiates up the carotid arteries and weak femoral pulses, the murmur of pulmonic ste­nosis tends to radiate dorsally on the chest wall. The murmur of a PDA is also left basilar but characteristic as it is continuous, waxing and waning during the entire cardiac cycle but reaching a peak in systole. Pulses tend to be bounding due to the increased difference between systolic and diastolic pressures. As PDA and pulmonic stenosis are potentially treatable diseases, it is important to have a definitive diagnosis so that treatment can be recommended as appropriate.

Blood samples: Routine hematology and bio­chemistry would be expected to be normal in dogs with congenital heart disease that is not cyanotic unless heart failure devel­ops. However, in right to left shunting PDAs, polycythemia can develop due to the caudal cyanosis. Biomarkers are usu­ally unremarkable until heart failure develops.

ECG: In PDAs, the ECG is usually normal. In subaortic stenosis, the pattern can suggest left ventricular hypertrophy with a tall, wide R wave. The ECG appearance of pul­monic stenosis is more helpful. In severe cases right axis deviation is seen with a negative lead 1 and positive leads 2 and 3. This, together with deep negative S waves in leads 1, 2, and 3, is the characteristic of right ventricular hypertrophy. This finding in a puppy with a left basilar systolic murmur increases the suspicion of pulmo­nic stenosis and should prompt referral.

Radiographs: Radiographic changes can vary depending on the severity of the lesion. Dogs with mild disease may have normal thoracic radiographs. In dogs with moder­ate to severe stenosis, the radiographic changes are often disappointing as there is concentric hypertrophy so the evidence of left or right ventricular hypertrophy may be hard to identify. However, the DV view is helpful as the post stenotic dilation of the main arteries can be identified. The post stenotic bulge of the aorta can be vis­ualized at the 12-1 o'clock position in cases of aortic stenosis whereas that of the pulmonary artery is seen at 1-2 o'clock in pulmonic stenosis. The typical left to right shunting PDA causes volume overload of the left atrium and ventricle. As a result, a left-sided enlargement pattern would be expected. However, while cardiomegaly is usually documented the typical appear­ance of left atrial enlargement with a trian­gular soft tissue density extending from the caudodorsal border of the heart is not seen. Instead on the DV a classic appear­ance of three bulges may be seen, the aorta and pulmonary artery at the 12-1 and 1-2 o'clock positions respectively. The third bulge is the left auricle which is at 2-3 o'clock. However the three knuckles are seen in about 25% of cases. Perhaps more useful is documenting the overcirculation of the lungs. Both the pulmonary artery and vein should be dilated and this is per­haps best seen by the ability to follow these vessels far into the periphery beyond where they would normally fade.

Echocardiography

• Aortic stenosis: In mild to moderate cases, the changes can be minimal with little to no left ventricular hypertrophy. However, in these cases, a small ridge under the aortic valve is usually visible. With increasing severity a fibrous ring may be seen causing various degrees of stenosis and there may be a change in the aortoseptal angle which may have a role in the etiology (Figure 5.9). The left ventri­cle becomes increasingly hypertrophied

Figure 5.9 Echocardiogram from a 1 year old Chow Chow with subaortic stenosis. In this right parasternal 5 chamber view optimized for the left ventricular outflow tract, the discrete sub valvular ridge can be seen. The left ventricle shows concentric hypertrophy due to the pressure load.

and hyperechoic areas may been seen especially in the papillary muscles sug­gesting fibrosis which is probably the result of hypoxia. On Doppler examina­tion, a high speed turbulent jet can be seen in the left ventricular outflow tract. Aortic regurgitation may also be seen but is not usually significant. The assess­ment of aortic regurgitation can be dif­ficult and can vary from assessment of the size of the jet to measuring the pres­sure half-life. The severity of subaortic stenosis is determined by the pressure gradient (Table 5.1), which is related to the velocity by the modified Bernoulli equation:

Pressure gradient (mmHg)

= 4? velocity² (m/s)

To assess the velocity accurately, it is critically important that the ultrasound beam is correctly aligned with flow. Hence although the left apical long axis view can be used, higher velocities are often obtained from the subcostal angle so this should always be interrogated to accurately assess severity.

• Pulmonic stenosis: Again, in mild to moderate cases, the changes can be min-

Table 5.1 Severity of aortic regurgitation.

imal. With increasing severity, the right ventricle becomes hypertrophied. As pressures in the right ventricle exceed those in the left ventricle the septum becomes flattened and the right ventri­cle may become dominant with the sep­tum moving towards the right side in systole - paradoxical septal motion. Pulmonic stenosis is usually valvular and is more common in small breed dogs especially the bulldog (Figure 5.10; Figure 5.11). Two types are recognized although there is significant overlap. In type A, the valve leaflets are normal but appear fused together along the commisures. In type B, the valve leaflets are more thickened and dysplastic. The pulmonary artery may also be

Figure 5.10 Echocardiogram from a 2 year old cavalier King Charles spaniel with severe pulmonic stenosis. In the right parasternal short axis view (Figure 5.10a), the right ventricular free wall is hypertrophied due to the increased pressure with flattening of the interventricular septum as the pressures in the the right ventricle near or exceed those in the left ventricle. On color flow (Figure 5.10b), the green jet of turbulent flow can be seen starting at the valve and the pulmonary artery is dilated post stenotically.

hyperplastic. In bulldogs, an abnormal arrangement of the coronary arteries may complicate the stenosis. In these dogs, the left coronary artery arises as a branch of the single right coronary artery. This left coronary artery then circles round the pulmonary artery to reach the left ventricle. This R2A anomaly may con­tribute to the stenosis. Again, alignment with flow is critical for accurate assess­ment of severity. Maximal velocities should be obtained from both the right and left short axis views and the higher value used. In severe cases hypertrophy in the outflow tract can cause a dynamic stenosis where the thickened muscle crushes the outflow tract. This can complicate the Bernoulli equation caus­ing underestimation of pressure gradients. Pulmonic regurgitation is not uncom­mon but is rarely significant. The tricus­pid valve may become incompetent and

Figure 5.11 Lateral chest fluoroscopic image from a small breed dog with pulmonic stenosis showing contrast being injected into the right ventricle. The right ventricle is hypertrophied with prominent papillary muscles and the outflow tract can be visualized. The discrete valvular stenosis and the post stenotic dilation can be seen.

assessing the speed of the regurgitant jet can help confirm severity. Fortunately in most dogs the degree of tricuspid regur­gitation remains small as this valve pro­tects the right atrium and systemic veins from the high pressures present in the right ventricle.

• PDA: The volume overload of the left side of the heart can be documented in moderate and severe disease. The dilated left atrium and left ventricle can be seen and the left ventricle can appear to have depressed systolic function with a reduced fractional shortening although this is not signifi­cant in the long term. The dilated left side can lead to secondary mitral regurgitation due to dilation of the annulus. On the short axis, the pulmo­nary artery is dilated and color flow confirms the turbulent flow arising from the ductus heading towards the transducer as it enters the pulmonary artery. In most cases, the ductus can be visualized and measured and importantly the size of the narrow ending as the ductus enters the pulmo­nary artery, assessed (Figure 5.12).

Therapeutics Acute, Chronic, and

Expected Outcome

Aortic and pulmonic stenosis: Dogs with mild to moderate aortic and pulmonic stenosis do not usually require treatment and may not require further evaluation. As disease severity moves into the moderate/severe category, there is a potential for the disease to progress and those dogs may benefit from annual re-evaluations with an echocardiogram.

Aortic stenosis: In dogs with severe disease, beta blockers are initially used to reduce the risk of arrhythmias and sudden death. For subaortic stenosis, this is continued long term although more recent evidence has questioned the benefit of beta blocking agents. Valve replacement and infundibu­lar myectomy has not been shown to pr olong survival and is no longer performed. Cutting and high pressure bal­loon dilation of the subvalvular region has been described and although the pressure gradient may decrease in the immediate post-operative period, there are no long­term data to indicate this is translated into increased survival and many dogs experi­ence an increase in their gradients over time. Clinical experience suggests that beta blockers reduce the risks of sudden death and syncopal episodes which usually occur at exercise.

Pulmonic stenosis: For dogs with severe pulmonic stenosis, balloon dilation of the obstruction has been shown to reduce gra­dients and prolong survival. Beta blockers are usually administered for 2 weeks prior to the procedure to reduce dynamic obstruction and reduce the risk of serious arrhythmias during the procedure. This is performed under general anesthesia with fluoroscopic guidance. The diameter of the pulmonary artery can be measured on fluoroscopy and the obstruction visualized. Balloons measuring 1.2 to 1.5 times the

Figure 5.12 Echocardiogram from a dog with a patent ductus arteriosus. This left parasternal cranial view (Figure 5.12a) shows the pulmonary artery with blood flowing away from the transducer coded blue. The ductus enters the pulmonary artery distally and the red flow of blood in the ductus flowing toward the transducer changes to a green turbulent jet when it enters the pulmonary artery. The pulmonary artery is dilated. The transesophageal view (Figure 5.12b) shows the blood from the ductus on top entering the main pulmonary artery. In this color compare view the shape of the ductus can be appreciated as it narrows at the pulmonary artery entrance.

diameter of the pulmonary artery are selected and a reduction of the pressure gradient of 50% would be a successful result. Higher pressure balloons and the use of a double balloon technique in larger dogs may improve outcomes. In dogs with type A pulmonic stenosis, 95% would be expected to respond well. In dogs with type B, the results are poorer due to the thickened leaflets and hypoplastic pulmo­nary artery with about 2/3 expected to improve. Dogs are followed with a repeat echocardiogram to assess gradients in 2-3 months and then as necessary depending

on the pressure gradient. Dogs that return to mild disease, can be weaned off their beta blockers once right ventricular hyper­trophy has resolved but if dogs remain in the moderate to severe category, beta blockage may be needed for life. Some dogs especially type B initially respond well but restenosis can recur presumably because the stenotic lesion is stretched rather than torn. For dogs that have a restenosis or respond poorly, beta block­age should be maintained. Further treat­ment involves the patch graft technique where a patch is sewn over the stenosis and the entire area opened up during brief inflow occlusion. Severe incompetence of the pulmonic valve is created but dogs seem to cope well with this despite the risk of chronic right-sided volume overload. At the University of Florida, we have been placing a bare metal stent across the steno­sis with a similar effect.

PDA: Dogs with small PDAs may not require treatment if the volume of blood is so small it is hemodynamically insignificant. However, these dogs may be at increased risk of developing infective endocarditis and prophylactic antibiotics should be given as needed. Dogs with larger ductuses will die prematurely if their ductus is not closed with 75% not surviving to one year of age. Closure can be achieved two ways. Either a thoractomy and surgical ligation can be performed or a minimally invasive technique used to close the ductus. Both have similar success rates with 95% of dogs expected to survive. Recovery is faster from the minimally invasive technique but it is usually more expensive due to the implants used. These include coils, vascu­lar plugs and more recently the Amplatz canine duct occluder (Figure 5.13; Figure 5.14). Such techniques require the use of fluoroscopy although more recently, transesophageal echocardiography has reduced this requirement and allows visu­alization of ductus in detail. After closure, an echocardiogram is repeated in 1 month to assess closure and remodeling. A small

Figure 5.13 This lateral chest fluoroscopic image shows a catheter in the aorta injecting contrast. The PDA can be visualized as a finger like projection extending ventrally towards the pulmonary artery. It narrows at the pulmonary artery entrance and the pulmonary artery is dilated. This is the most common type of PDA and is amenable to closure with an Amplatz canine duct occluder (ACDO).

Figure 5.14 Lateral chest fluoroscopic image showing an ACDO deployed in the ductus. The first disc is in the pulmonary artery and the second in the ductus itself. Contrast is injected to check placement and lack of flow through the ductus.

percentage suffer from residual flow especially if the ductus is large. If this is small-volume, low-velocity flow, it may

close eventually but if it remains open, there should be no long-term conse­quence, although there may be an increased risk of infective endocarditis. If there is significant residual flow, the procedure may have to be repeated.

For dogs with a large PDA in which the ductus is not closed there are two possible outcomes:

• If the ductus remains left to right shunting, left heart failure can develop with pulmonary edema and breathlessness. Treatment is as for other causes of congestive heart failure with diuretics, usually furosemide, an ACE inhibitor, pimobendan possibly with spirono­lactone. The ductus can still be closed at this stage but the long-term outlook is poorer compared to dogs that have their ductus closed prior to the onset of heart failure.

• In some dogs, a reactive change occurs in the pulmonary arteries and pulmonary hypertension develops. As the pressure in the pulmonary artery rises, the velocity of blood flow across the PDA decreases until eventually the murmur disappears. Ultimately, they can become right to left shunting with de-oxygenated blood enter­ing the descending aorta causing caudal mucous membrane (differential) cyanosis. These dogs present with signs of exercise intolerance or due to signs associated with their polycythemia. The kidney responds to the de-oxygenated blood by producing more erythropoietin. The development of polycythemia is very variable and unpre­dictable. Unfortunately, once the PDA becomes right to left shunting, it cannot be closed as this will lead to the death of the patient - the PDA is acting as a pressure release valve for the pulmonary circula­tion. Drugs like the phosphodiesterase V inhibitor, sildenafil can be used to try to reduce pulmonary artery pressure but gen­erally have limited effect because the changes to the pulmonary arteries are structural. As the clinical signs are mainly due to polycythemia, repeated phleboto­mies may be needed to control clinical signs. The amount of blood removed depends on the PCV and size of the dog. For dogs where the intervals between phle­botomies is short or who are resistant to the treatment, hydroxyurea can be used to reduce red cell production. The rate at which the PCV can change is variable so it is difficult to give precise guidelines for each dog. Generally the PCV is checked one month then 3 monthly after phlebot­omy. This interval can be lengthened depending on the rate of rise of the PVC

Quality of Life with Euthanasia Decision

For dogs with small PDAs and mild aortic and pulmonic stenosis, these dogs should have a normal life expectancy. For dogs with large PDAs that are occluded at a young age and certainly before heart failure develops, again life expectancy should be normal. For dogs with significant cardiomegaly and poor systolic function, the prognosis is more guarded but these patient will have signifi­cant prolongation of life expectancy if the PDA is closed, surviving to middle to old age. Untreated dogs with a large PDA have a poor life expectancy and should be treated for heart failure as described when it occurs.

Dogs with severe pulmonic stenosis that is not treated or do not respond to balloon dila­tion and severe aortic stenosis should remain on beta blockers to try to prevent sudden death and decrease the dynamic obstruction. Dogs with severe disease have hypertrophied ventricles which may be poorly oxygenated especially during exercise. This can cause ventricular arrhythmias and result in col­lapse or, if ventricular fibrillation develops, sudden death. If dogs do not experience sud­den cardiac death, they can survive to middle to old age even with severe disease. Ultimately the dogs develop systolic dysfunction due to the severe chronic pressure overload and this can be seen with a dilating left ventricular chamber on echocardiogram. When left heart failure develops, treatment is similar to other causes of congestive heart failure. There is a concern that positive inotropes

such as pimobendan should be avoided as they may exacerbate the dynamic obstruction but in practice these seems to be more than balanced by the positive effects on contractil­ity. Sub-aortic stenosis tends to be poorly responsive to the usual treatments for con­gestive heart failure because of the underly­ing etiology. Hence progression is more rapid and the time before the heart failure becomes unresponsive to therapy short. For canine subaortic stenosis there seems to be a super- severe category with dogs that have gradients of 80-130 mmHg surviving to 8.3 years but those with gradients over 130 mmHg having a median survival of 2.8 years.

Arrhythmias

Both bradycardias and tachycardias can result in clinical signs. Signs often include exercise intolerance or lethargy and collapse. While the syncopal episodes can have the classic anamnesis of occurring at exercise with flaccid paralyisis and short duration with rapid recovery, this is not always the case. Cerebral hypoxia due to the cardiac event can cause seizure like activity. The nor­mal heart rate for dogs is extremely variable with average rates of 65-95 bpm over 24 hours. However, within that, the heart rate can vary from 40-50 bpm at rest to 250 bpm when exercising. In addition, pauses of up to 4 seconds at rest are not uncommon.

The important bradycardias include:

• Advanced (high grade) second degree AV block

• Third degree AV block

• Sick sinus syndrome (SSS)

• Persistent atrial standstill (PAS)

Significant tachycardias include:

• Atrial and supraventricular tachycardia (SVT)

• Atrial flutter

• Atrial fibrillation (AF)

• Ventricular tachycardia (VT)

Dogs with VT tend to be more symptomatic than dogs with SVT as the ventricular complex does not use the normal conduction pathways to the ventricle so the contraction is less efficient at ejecting blood.

Brief Review of Diagnostics

If an arrhythmia is detected, an ECG is essen­tial to determine the exact rhythm abnormal­ity. An echocardiogram can be helpful to confirm any structural changes and routine hematology and biochemistry can also be useful especially in collapsing dogs to rule out medical causes of collapse.

Second degree AV block has two forms. In type 1 (Wenckbach) the P-R length varies with subsequent complexes until there is an unconducted P wave. This usually represents high vagal tone and is atropine responsive. In type 2, the P-R interval is constant with occa­sional unconducted P waves. This suggests disease of the conduction system - fibrosis or degeneration - and is more likely to progress to third degree heart block in which there is no communication between the atria and the ventricles (Figure 5.15). The atria have their rate which is faster than the slow ventricular escape rhythm that keeps the dog alive.

Sick sinus syndrome (SSS) is a disease where impulse formation fails in the SA node as well as in other cardiac tissue so long pauses are seen (Figure 5.16). The disease is rarely fatal but dogs can be very symptomatic with it. Breeds typically affected include the West Highland white terrier and Miniature Schnauzer. The Miniature Schnauzer can get a particular form of SSS with periods of brad­ycardia and tachycardia. Often the bradycar­dia needs to addressed before medication given to control the tachycardia.

Atrial standstill can be caused by primary atrial myocardial disease but more com­monly by hyperkalemia. As a result patients with atrial standstill should be screened for hyperkalemia. Common causes include urethral obstruction usually in cats and Addison's disease. PAS is caused by atrial myocardial disease. The ECG is character­ized by a lack of P waves (Figure 5.17).

Supraventricular arrhythmias usually have a normal narrow complex appearance to the QRS as they use the conduction pathways of

Figure 5.15 ECG from a dog with 3 degree AV block. The P waves continue through the ECG with no relation to the QRS - every P-R interval is different. The QRS are wide and bizarre as they are ventricular escape complexes. The atrial rate is 180 bpm and the ventricular rate is 30 bpm. The atrial rate is fast as the intrinsic mechanisms are trying to increase the heart (ventricular) rate. 25 mm/s and 1 cm/mV.

Figure 5.16 ECG from a dog with sick sinus syndrome. There are long pauses and ventricular escape complexes. 50 mm/s and 1 cm/mV.

Figure 5.17 ECG from a dog with persistent atrial standstill due to atrial myocardial disease. There are no P waves on any leads. The QRS is narrow suggesting a supraventricular origin and this is because the SA node is still active with the impulse transmitted to the AV node via intermodal tracts. 50 mm/s and 5 mm/mV" as the rate is not slow.

the ventricles while ventricular arrhythmias tend to be wide and bizarrely shaped. The latter can be positive if the origin is in the right ventricle and negative if they originate in the left ventricle. SVT is caused by either a focal atrial tachycardia, an area of the atrial myocardium that spontaneously depolarizes or an accessory pathway which is an embryo­logical remnant of muscle that bridges the valvular fibrous ring allowing connection between the atria and ventricles outside the AV node. The P wave can be abnormal or hidden in the preceding QRS complex. However the complexes appear narrow like the sinus complexes (Figure 5.18).

Atrial flutter (Figure 5.19) and AF are par­ticular atrial tachycardias. In atrial flutter, a macro re-entry circuit revolves round the tri­cuspid valve. Hence the ECG has a saw-tooth like appearance to the baseline. Atrial fibril­lation is a micro re-entry circuit with at least fine or six small wavelets causing circuit rhythms in the atria (Figure 5.5). For these to be sustained, the atria must be a certain size, hence it is more common in larger breed dogs and with atrial enlargement.

While ventricular arrhythmias (Figure 5.20; Figure 5.21) can suggest primary heart mus­cle disease, the underlying cause is more likely to be extracardiac. Extra cardiac causes include:

• Abdominal neoplasia especially splenic

• Gastric dilation/volvulus

• Septicemia

• Pyometra

Basically, anything that irritates the heart muscle may cause VPCs.

Therapeutics Acute, Chronic, and

Expected Outcome

If possible identify the underlying cause and correct if possible. If a bradycardia is caused by high vagal tone, ocular, CNS, gastrointesti­nal, or respiratory disease should be suspected. In patients with hyperkalemia, the likely

Figure 5.18 ECG from a young Labrador with supraventricular tachycardia. The complexes are narrow

suggesting their supraventricular origin and the rhythm is regular. Vagal maneuvers help confirm the mechanism when the rhythm breaks to sinus. 50 mm/s and 1 cm/mV.

Figure 5.19 ECG from a miniature schnauzer with atrial flutter and one ventricular complex. The QRS complexes are narrow suggesting a supraventricular origin and the rhythm is irregular. A regular saw tooth like pattern can be seen on the baseline which represents the flutter wave going round the, usually tricuspid, annulus. 50 mm/s and 1 cm/mV.

Figure 5.20 ECG from a boxer with arrhythmogenic right ventricular cardiomyopathy showing sinus rhythm and an isolated VPC. The VPC is upright in lead 2 suggesting a right ventricular origin. 50 cm/s and 1 cm/mV.

Figure 5.21 ECG from a dog with dilated cardiomyopathy showing ventricular tachycardia. The rhythm is fast and regular and the complexes are wide and bizarre suggesting a ventricular origin. This responded to lidocaine. 50 mm/s and 1 cm/mV.

causes usually include Addison's disease and urinary tract obstruction. If no underlying cause can be identified, therapies to increase heart rate may be indicated. These include:

• Drugs to decrease vagal tone: atropine or oral propantheline

• Drugs to increase sympathetic tone: iso­proterenol or terbutaline

• Drugs that increase heart rate through other mechanisms: theophylline

• Pacemaker implantation

Patients with sick sinus syndrome occasion­ally respond to atropine and that can translate into response to oral anticholinergic agents. Unfortunately, the response can be variable and some patients continue to be sympto­matic either because of poor rate response or an increase in heart block. Patients with SSS can remain symptomatic for months to years so it seems to be relatively benign, rarely resulting in sudden death. However, it is progressive and those patients that respond initially may relapse in the future.

Dogs with high grade second degree AV and third degree AV block generally do not respond to anticholinergic drugs as there is no vagal innervation of the ventricles. They may improve temporarily with sympathomi­metic agents but this increase in heart rate declines with changes in the beta receptor population. These patients ultimately require pacemaker implantation as otherwise they are at risk of sudden death. In dogs, the pace­maker is implanted dorsally over the right neck with the endocardial lead introduced into the right ventricle via the jugular vein. In cats and small dogs, an epicardial lead is used with the pacemaker implanted in the abdo­men. Endocardial leads tend to cause chylous thoracic effusions in cats perhaps because of the small jugular diameter relative to the lead diameter. Potential problems include lead infection, dislodgement, and seroma forma­tion. In dogs, if the heart block is cause by fibrosis of the conduction pathway, the life expectancy should be normal with good quality of life. However, if neoplasia or myo­cardial disease is documented, the prognosis is poorer. In cats, pacemaker implantation seems to have little effect on longevity. However, the cats become less symptomatic.

Tachycardias are treated with one of the four classes of anti-arrhythmia agents:

1) Class 1 - sodium channel blockers

a) Quinidine and procainamide

b) Lidocaine and mexiletine

c) Flecainide and propafenone

2) Class 2 - beta blockers, for example, aten­olol, propranolol, and esmolol

3) Class 3 - potassium channels blockers, for example, sotalol and amiodarone

4) Class 4 - calcium channel blockers, for example, diltiazem

Generally, class 1 and 3 are effective against ventricular arrhythmias and class 2 and 4 act on the SA and the AV node. Drugs can be combined as they have different actions so it is common to use both a class 1 and class 3 agent together to control ventricular arrhyth­mias. However, calcium channel blockers should not be combined with beta blockers as both agents have negative inotropic effects and the results on myocardial contractility can be significant.

SVT can be controlled with sotalol alone or in combination with a class 1 agent such as mexiletine although digoxin may be used. In patients where it is difficult to obtain control, continued lethargy may be seen but syncope is uncommon. For these patients, a tachycardio- myomathy can develop where the sustained tachycardia ultimately causes the heart muscle to become dilated and poorly contractile and they usually present in right heart failure. If the tachycardia can be controlled, these changes can reverse. If the tachycardia cannot be controlled, referral for ablation of the focus or accessory pathway using intracardiac map­ping is indicated.

Atrial flutter can be a difficult arrhythmia to manage and frequently develops into atrial fibrillation. Rate response can be achieved as for atrial fibrillation but if this proves difficult, the patient can be shocked under general anes­thesia back into sinus rhythm. The decision whether to go for rate or rhythm control may depend on the presence of structural heart dis­ease, that is, large atria, and the degree to which cardiac output is dependent on atrial filling.

Atrial fibrillation is one of the most com­mon arrhythmias encountered in clinical practice. The classic signs include a tachycar­dia with an irregularly irregular rhythm, narrow complex and lack of P waves. There can be exceptions, for example, the Irish Wolfhound with slow AF that can mimic sinus arrhythmia or a dog with a concomitant bun­dle branch block that has a wide complex tach­ycardia which can be mistaken for ventricular tachycardia but is irregular. As the disease is usually associated with atrial enlargement and DC cardioversion usually reverts to AF after a short period, most dogs are treated with nega­tive chronotropes. These include:

• Beta blockers: Effective and the dose can be titrated upwards to give adequate rate control. Unfortunately the negative inotropic action limits their use

• Calcium channel blockers: Diltiazem is fre­quently used. While it has some negative inotropic action, this is not as marked as beta blockers. It may potentiate digoxin and dose reduction may be required when it is introduced. It should be given three times daily but the sustained release ver­sion may be administered twice daily.

• Digoxin: Because of the long half-life, this drug can take up to 5-7 days to become effective and reach steady state. As its action is vagally mediated, it is used in combination with diltiazem and the com­bination reduces heart rate more effec­tively than either drug alone. Hopefully this translates into increased long-term survival but this has yet to be demon­strated. The drug has a narrow therapeutic window so owners need to be aware of the toxic side effects which if they occur will be towards the end of the first week or beyond. These include:

î GI signs: Vomiting, diarrhea, anorexia. î Arrhythmias: Almost any arrhythmia may be cause by digoxin

î Neurological signs: Dogs often appear very “depressed” according to their owners.

• Blood samples should be collected after 7 days for serum levels and most laboratories suggest a trough level at 8 hours post pill.

This raises that question of what is adequate rate control. This is poorly defined in the veterinary world and no studies exist to con­firm actual numbers. It is evident that dogs presented in the clinic with controlled AF will have higher heart rates than those moni­tored with a Holter device. In the clinic, rates of 140-160 bpm are probably adequate, while using Holter monitors, an average rate of 120-140 bpm should be the target. If the rate is not adequately controlled and the digoxin level is low, the dose could be increased. However, if the dose is adequate, the dose of diltiazem should be increased.

Treatment of ventricular arrhythmias is a subject of ongoing debate among cardiolo­gists especially since the CAST study that showed an increased in sudden cardiac death associated with the use of the class 1 agents, encainide and flecainide. As a result in humans, there has been a move towards the use of intracardiac defibrillators which detect VT and deliver a shock to convert the rhythm to sinus. To date these require further refinement in dogs as the current algorhythms cannot differentiate an excited dog from one in VT.

Treatment of acute symptomatic VT involves the use of lidocaine. Typically boluses of 2 mg/kg are given intravenously with a pause between each administration to see if the rhythm converts. When the total dose reaches 6 mg/kg (third bolus), the patient is observed for signs of nausea (lick­ing lips, etc.) or tremoring, If either of these is seen, the final bolus should not be given as convulsions are likely to occur. If they do occur, they are usually short lived because of the short half-life of lidocaine in the blood stream. If lidocaine is unsuccessful, a review of whether this is truly VT should be consid­ered. The most common rhythm abnormal­ity that causes confusion is wide complex AF but this is usually irregular while VT is usually regular. Other agents that could be considered would include:

• Other class 1 agents: Procainamide. The failure of one class 1 agent does not neces­sarily mean that all class 1 agents will be unsuccessful

• Beta blockers: Esmolol is used as it is very short acting so if it is unsuccessful, other agents can be considered

• Class 3 agents: Sotalol or amiodarone. Intravenous amiodarone can cause hista­mine release due to the agent polysorbate 80 which increases solubility of amiodar­one. Pretreatment with anti-histamine is recommended.

• Magnesium: While hypomagnesemia is recognized as a cause of ventricular arrhythmias, the serum levels may not rep­resent actual tissue levels. Often this is tried when common anti-arrhythmic agents have failed and it should be given by slow intravenous injection.

Once VT has been controlled with lidocaine, the patient is continued on a CRI while oral medication is commenced. When the arrhythmia is adequately controlled on oral medication, the patient can be discharged.

Doberman Pinschers and Boxers have fre­quent ventricular arrhythmias as part of their DCM/ARVC. It has been shown that the combination of a class 1 agent and a beta blocker give better control than either agent individually. Practically, this translates into starting the patient on sotalol and repeating a Holter monitor after one month as all anti- arrhythmic medications have the potential to be pro-arrhythmic. If adequate control is not achieved, the dose can be increased or mexi- letine can be added. Again, after every dose change or medication introduction, the Holter monitor should be repeated. As the daily variation in VPC count can be up to 85%, a greater than 85% reduction in VPCs is considered a success.

While the treatment of VT is necessary, there is further debate on the treatment of VPCs and short runs of VT detected on a Holter monitor. Overall, the owner should be aware that there is no evidence that anti- arrhythmic medication reduces the risk of sudden cardiac death, although it may reduce syncopal episodes. A normal dog may have occasional VPCs on a 24 hour Holter moni­tor and the number increases with age. If ventricular arrhythmias are detected on a Holter monitor, the decision to treat may depend on:

• The number of VPCs: If there are many thousands, treatment is more likely to be recommended

• Speed of ventricular couplets: A ventricu­lar couplet represents two VPCs together and is never found in a normal dog. The coupling interval is important and should be reported from a Holter monitor. Although there is no published evidence, many cardiologists use a rate over 250 bpm as a guide to starting treatment.

• R on T phenomenon: This also represents a coupling interval whether between a cou­plet or a normal complex and a VPC. It suggests depolarization occurs during the repolarization which a dangerous sub­strate for ventricular fibrillation and would warrant treatment.

• History of syncope: This suggests that the ventricular arrhythmias are hemody- namically significant, that is, they are fast or sustained enough to reduce blood pressure. The actual cause of syncope can be difficult to document on a Holter monitor. The application of a Holter monitor may alter the dog's behavior so the episode does not occur. Indeed, many cardiologists believe that a Holter moni­tor is a good therapeutic tool to use in collapsing dogs!

• Runs of VT: Again these are not found in a normal dog and unless slow would suggest that treatment is indicated.

Quality of Life with Euthanasia Decision

If the ventricular arrhythmias can be well controlled, then the prognosis is reasonable given the underlying cause, for example, ARVC may be progressive. According to the Harpster classification of ARVC in Boxers, Boxers with VPCs and no evidence of systolic dysfunction have the best prognosis and have mean survival times of 2 years. However, the owner should always be counselled regarding the risk of sudden death.

Treatment of ventricular arrhythmias is never straightforward and the owner must understand that one drug will not work in all cases so they need to be engage as the clini­cian embarks on treatment, trying drugs to find one that is appropriate and not becom­ing frustrated when drugs are not successful. Clearly, the most commonly effective drugs with the least side effects are tried first but on occasions these will not control the arrhythmia and others must be tried. It is unlikely that medication will stop all the arrhythmias but if they can reduce the hemo- dynamically significant ones, signs should resolve.

In some dogs, it may prove impossible to stop syncopal episodes and the owner must understand that these are effectively aborted sudden death. If these episodes are frequent and distress the dog and/or owner, euthana­sia must be considered. In addition, most dis­ease causing ventricular arrhythmias are incurable and progressive, so if the signs are initially well controlled, ultimately they may escape that control.

Systemic Hypertension

Blood pressure is the result of cardiac output and systemic vascular resistance and cardiac output is the result of heart rate and stroke volume. Hence anything that raises heart rate, stroke volume or vascular resistance can cause hypertension. Chronically elevated blood pressure can result in a variety of end­organ damage and so should be identified and controlled. Primary hypertension is rare in dogs and cats and so diagnosis should prompt the search for an underlying cause.

Brief Review of Diagnostics

Diagnosis is by the detection of a persistently elevated blood pressure using a sphygmoma­nometer and Doppler technique or the oscil­lometric technique. Both have been validated in dogs and cats but many find the Doppler technique more reliable in small dogs and cats. The cuff should be about 40% of the diameter of the limb. The measurement is repeated until consistent results are achieved. This technique gives the systolic pressure while the oscillometric gives systolic, dias­tolic, and mean pressures. A blood pressure of less than 150/95 mmHg is normal while greater than 160∕100mmHg is now regarded as abnormal in dogs and cats and further diagnostics or treatment may be warranted. An ECG, echocardiogram, or chest radio­graph may show left ventricular hypertrophy.

Therapeutics Acute, Chronic, and

Expected Outcome

An ACVIM consensus statement has defined the risk categories for systemic hypertension:

• Mild risk (BP = 150-159/95-99): This is an equivocal level and is commonly seen in stressed cats (“white coat” hypertension). Underlying causes of hypertension may increase susceptibility to end-organ dam­age. No treatment is recommended but continue to monitor blood pressure

• Moderate risk (BP = 160-179/100-119): If confirmed by repeated measurements, begin search for underlying cause and begin anti-hypertensive treatment if end­organ damage or clinical signs

• Severe risk (BP > 180/120): Confirm and begin anti-hypertensive treatment even if no end-organ damage or clinical signs present.

Many diseases are found in association with systemic hypertension and the relationship can be causal:

• Renal disease: This is the most common underlying cause in dogs and cats and 20-30% of cats with renal disease have hypertension. The severity of renal injury is associated with a degree of hyperten­sion. Often it is unclear whether this is a cause or effect of the hypertension

• Adrenocortical disease: Hyperadreno- corticism is a common cause in dogs while primary hyperaldosteronism is rarely seen

• Diabetes mellitus: Hypertension is seen in diabetic dogs, but has not been reported in cats. However, they should be screened if proteinuria is present

• Hyperthyroidism: This is a common cause in cats with 10-30% of hyperthyroid cats having hypertension

• Pheochromocytoma: This catecholamine producing tumor can produce severe hypertension episodically

• Polycythemia: The increased blood vi scosity increases peripheral vascular resistance

• Acromegaly: This is recognized in cats.

Consequences

Many hypertensive patients are asymptomatic. Most vascular beds may autoregulate blood flow with vasomotor tone over a wide range of blood pressure. However, once the upper limit of blood pressure is exceeded, the elevated blood pressure is transmitted to the small arteries and capillaries leading to tissue damage:

• Cardiovascular: Concentric hypertrophy of the left ventricle rarely develops into congestive heart failure. Arteriosclerosis and hemorrhage, such as epistaxis, may be seen.

• Renal: Renal disease causes hypertension, but hypertension also worsens renal dis­ease. The glomerulus, nephron, and interstitium may all be damaged by expo­sure to increased blood pressure leading to progression of renal disease. Glomerular damage can lead to proteinu­ria and the degree of proteinuria is prog­nostic in cats.

• Ocular: Hypertensive retinopathy with tortuous retinal vessels and papilledema can be seen. Retinal edema, hemorrhage, and detachment may cause acute blindness especially in cats which may be permanent.

• Central nervous system: CNS signs may be evident especially if hypertension is over 180 mmHg. Signs include hypertensive encephalopathy due to cerebral edema, cerebrovascular accidents (stroke) from rupture of small arteries and local ischemia but these are rare in dogs and cats These manifest as behavior alterations such as depression, ataxia, focal neurologic defi­cits, stupor, coma, seizures, and death.

Treatment

The rationale for treatment is to eliminate clinical signs and prevent or potentially reverse end-organ damage. Therefore, the decision to treat should be based on the presence or relative risk of end-organ dam­age and clinical signs. Hypertension in dogs is often more difficult to control than in cats. Since hypertension is most often sec­ondary, underlying causes must be diag­nosed and managed. In most cases though, anti-hypertensive therapy is continued indefinitely.

Treatment is usually started with one ther­apy and titrated to effect. Two or more drugs may be combined if initial response is inadequate:

Salt restriction: The goal is to decrease total body sodium and extracellular fluid vol­ume but this alone does not reduce blood pressure, except in some cases of essential hypertension. Salt restriction may actually activate the renin-angiotensin-aldosterone system to increase peripheral vascular resistance and can worsen cardiovascular and renal consequences. As a result, salt restriction is not recommended, but high salt intake should be avoided.

ACE inhibitors: These act by blocking the conversion of angiotensin I to angiotensin II as well as decreasing breakdown of brad­ykinin and hence causing vasodilation. They also reduce secretion of aldosterone and antidiuretic hormone to cause sodium and water excretion. They are renoprotec- tive as they reduced glomerular pressure and proteinuria. However, they also decrease glomerular filtraction rate and may cause azotemia and hyperkalemia. As single agents, they are unlikely to provide sufficient blood pressure control alone but may help in cats with renal insufficiency and proteinuria. Decreases in blood pres­sure of 5-10 mmHg can be expected so they can be combined with other drugs (e.g., calcium channel blockers) in both dogs and cats. Enalapril and benazepril are the most commonly used but benazepril may be preferred as it is 50% cleared by the liver.

Calcium channel blockers: These decrease calcium influx into vascular smooth mus­cle cells to cause vasodilation but this may activate the renin-angiotensin-aldosterone system. Often used in combination with ACE inhibitors, the most commonly used drug is amlodipine which has almost exclusive vascular effects. Amlodipine is the first-line anti-hypertensive drug in cats and may be in dogs. It may cause preferen­tial vasodilation of afferent renal arterioles and increase intraglomerular pressure which can promote glomerular damage hence combining with an ACE inhibitor may be beneficial. As with any drug that lowers blood pressure, it can cause a reflex tachycardia in dogs.

Adrenergic blockers: Beta-blockers decrease heart rate and contractility to reduce cardiac output. They are the treatment of choice for hypertension due to hyper­thyroidism, combined with amlodipine. Some cats remain hypertensive and require therapy even when their hyper­thyroidism is controlled. They should not be used for pheochromocytomas before adequate alpha-blockage. The two commonly used beta blockers are propranolol which is a nonspecific beta­blocker and atenolol which is a cardio­selective β₁-blocker. α₁-blockers cause peripheral vasodilation and are the treat­ment of choice for pheochromocytomas, for example, phenoxybenzamine and prazosin which are non-specific alpha- and beta-blockers that decrease cardiac output and cause vasodilation.

Hydralazine: This causes direct vasodilation by an unknown mechanism and is a potent vasodilator with rapid onset of action. Reflex tachycardia is a significant and dose-limiting side effect.

Nitroprusside: This is a nitric oxide donor which is a potent vasodilator. It has a very rapid onset of action and very short half­life but must be administered by a constant rate infusion. High doses or prolonged treatment may lead to cyanide toxicity. While it may be needed in the emergency treatment of congestive heart failure, it has no role in chronic treatment.

Quality of Life with Euthanasia Decision

Control of blood pressure can usually be achieved although there may be exceptions. In many cases, it is the progression of the underlying disease that is the deciding factor in the decisions regarding quality of life. While some patients can cope well with acute onset blindness, others become very depressed and show marked behavior changes with poor quality of life.

Pulmonary Hypertension

Similar to systemic blood pressure, pulmo­nary pressures are the product of the blood flow, vascular resistance, and pulmonary venous pressure. An increase in any of these can result in pulmonary hypertension. The pulmonary vasculature is a low resistance, high capacitance circuit with a normal systolic pressure of 25 mmHg. Hypoxia leads to vasoconstriction regionally so that perfu­sion is matched to circulation. Vascular tone is maintained by a balance between vasodi­lating and vasoconstricting factors with the endothelium playing a key role locally.

Vasodilating factors derived from the endothelium include:

• Nitric oxide

• Prostacyclin (PGI₂)

While vasoconstricting factors include:

• Thromboxane and serotonin derived from platelets

• Endothelin 1 from the endothelium

• Angiotensin II both systemically and locally derived

Brief Review of Diagnostics

Clinical signs are usually non-specific includ­ing lethargy and anorexia although respira­tory signs including tachypnea and a cough can be seen. The patients may be cyanotic on exercise and may become syncopal. In chronic cases, right heart failure with ascites may be documented. On physical examina­tion, abnormal lungs sounds, cyanosis, and evidence of right heart failure may be found. A split S2 heart sound is suggestive and a right apical systolic murmur of tricuspid regurgitation may be auscultated.

Direct measurement of pulmonary artery pressures would require cardiac catheteriza­tion so this is not usually performed. Thoracic radiographs may show evidence of right heart enlargement and/or respiratory disease. The main pulmonary arteries are dilated in chronic disease with a bulge at the 1-2 o'clock position on the DV. The pulmo­nary arteries may be tortuous or rapidly tapering. An ECG may show evidence of right heart enlargement (tall P wave, deep negative S wave and right axis deviation). Echocardiography can demonstrate the right ventricular concentric hypertrophy with right atrial enlargement. The pulmonary artery is usually larger than the aorta. If tri­cuspid regurgitation is present, spectral Doppler can be used to estimate the pulmo­nary artery pressures by the modified Bernoulli equation (pressure gradient in mmHg = 4 ? V² in m/s). Pulmonic regurgita­tion may be used to estimate pulmonary diastolic pressure. Systolic pressures under 50 mmHg suggest mild disease, 50-80 mod­erate and over 80 severe (Figure 5.22).

Causes are usually divided into pre-capil- lary, capillary, and post-capillary. As for sys­temic hypertension, primary pulmonary hypertension is rare in dogs and cats. Pre­capillary causes include heartworm disease, pulmonary thromboembolism, congenital cardiac shunts (e.g., uncorrected PDA). Capillary hypertension is caused by lung dis­ease such as chronic bronchitis or interstitial pulmonary fibrosis. Post-capillary causes refer to disease associated with chronically elevated pulmonary venous pressure, for example, myxomatous mitral valve disease and DCM. Heartworm disease or myxoma­tous mitral valve disease are the most com­mon causes depending on which part of the world you live.

Therapeutics Acute, Chronic, and

Expected Outcome

Specific treatment for pulmonary hyperten­sion is usually unsuccessful as the pulmonary vasculature is already irreversibly damaged. However, clinical signs can be improved. Control of left heart failure can be beneficial and addressing heartworm infection will stop ongoing damage although the disease may show acute deterioration when the worms are killed. Treatment options include oxygen which is a potent vasodilator but not a long-term solution and nitric oxide which also must be inhaled.

For chronic disease, calcium channel block­ers, for example, diltiazem is used in humans but has not been studied in dogs and cats. ACE inhibitors have little effect on pulmonary artery pressure but may help delay pulmo­nary vascular remodeling. Phosphodiesterase 5 inhibitors are the most widely used agents, for example, sildenafil and tadalafil. Although the reduction in pulmonary artery pressure is modest and sometimes hard to document, clinical signs can improve significantly. However, they can increase left heart preload and precipitate congestive heart failure so in cases of advanced left-sided disease, they should be introduced at a low dose and titrated upwards. Pimobendan is a phospho­diesterase 3 inhibitor and may have some action on the pulmonary vascular tone. Endothelin antagonists, for example, bosen- tan, are effective but their costs prohibit their use in most cases.

Figure 5.22 Left parasternal long axis cranial systolic frame showing the right ventricle, right atrium, and tricuspid valve. There is a green turbulent jet of tricuspid regurgitation and the velocity can be measured. Using the modified Bernoulli principle, the pressure in the right ventricle and hence pulmonary artery can be estimated. This can be used to asses for pulmonary hypertension non-invasively.

Quality of Life with Euthanasia Decision

The prognosis depends on the underlying disease. In dogs with degenerative valve dis­ease, a pulmonary artery pressure over 55 mmHg suggests a poorer prognosis and may warrant treatment. Dogs with shunts such as a PDA cannot have the PDA closed as this leads to acute death but their poly­cythemia can be chronically managed. Heartworm disease should be treated as per the American Heartworm Association guidelines but the pulmonary hypertension does not usually resolve. If right heart fail­ure develops, it should be treated as described previously.

Pericardial Effusion

As fluid in the pericardium accumulates, the pressure rises. Initially there are no clinical signs until the pressure starts to exceed the pressure in the lowest pressure chamber, the right atrium. Cardiac tamponade describes the clinical syndrome of right heart failure sec­ondary to a pericardial effusion.

While heart failure is usually treated with diuretics, this is the exception as diuretics will decrease systemic venous pressure which is responsible for filling the right heart. In the short term, intravenous fluids may be used to augment cardiac output although unless the patient is critical, these are often not needed.

Causes include:

• Idiopathic: Seen in younger dogs especially St Bernards

• Neoplastic: Hemangiosarcomas are common in older dogs especially Golden Retrievers and German Shepherd Dogs, Heart base tumors (chemodectomas) are seen in brachycephalic breeds such as Boxers. Other tumors are occasionally recognized including mesothelioma, ectopic thyroid carcinomas, and lymphoma

• Left atrial tear secondary to chronic degen­erative mitral valve disease

• Infectious causes and secondary causes such as hypoalbuminemia are seen.

Brief Review of Diagnostics

Clinical examination: Muffled heart sounds with a weak rapid pulse may be detected. If right heart failure is present, a distended abdomen with a fluid thrill may be seen. Pulsus paradoxus is present in some cases. The pulse disappears during inspiration but returns during expiration. This is an example of ventricular interdependence.

ECG: Small complexes are seen due to the presence of fluid. In some cases, electrical alternans may be present with alternating heights of the R waves due to changing mean electrical axis as the heart swings in the fluid.

Radiographs: A round globoid “still” cardiac silhouette is seen. The caudal vena cava is enlarged especially if ascites is detected.

Echocardiography: This is the diagnostic test of choice (Figure 5.23). Not only can it con­firm the diagnosis showing the dark fluid around the heart and the cardiac tampon­ade with collapse of the right atrial wall but it can also guide treatment and help detect an underlying cause. Common places for neoplasia include the right auricle and right AV junction for hemangiosarcoma and the great vessels for chemodectomas. Masses are most easily visualized when some fluid is present. But it should be noted that echo­cardiography is not a good guide to identify tumor type. Echocardiography can also be used to guide treatment.

Therapeutics Acute, Chronic, and Expected Outcome

Acute drainage of the pericardium usually causes rapid resolution of clinical signs. In the short term, intravenous fluid should be

Figure 5.23 Right parasternal long axis echocardiogram from a dog with a pericardial effusion. The dark ring around the heart is the effusion. The collapse of the right atrial free wall can be visualized suggesting cardiac tamponade is present. Detection of a tumor is easier if fluid is still present but once this has been performed, drainage of the fluid is indicated.

given at a high rate to maintain systemic venous pressures and hence right atrial fill­ing. In critical patients, the effusion may need to be drained before a detailed echocar­diogram can be performed but in less severely affected dogs, an echocardiographic search for a neoplastic cause should be completed.

Pericardiocentesis is usually preformed from the right side with the patient in left lat­eral recumbency under mild sedation. Echocardiography is used to image a window such that the depth of fluid is maximized and the needle is likely to impinge on the pericar­dium at 90° hence there is less chance it will glance off into the surrounding lung tissue. (Figure 5.24) The needle is then advanced along the same line and angle as the echocar­diographic probe while negative pressure is applied to the syringe. A variety of pericar­diocentesis catheters are available but many use 14 G catheters with extra holes cut. An ECG should be attached to document any arrhythmias that may indicate the right ven­tricle has been touched with the needle. Once fluid starts to return, the catheter is advanced off the needle and a drainage system attached. The fluid should be retained as it does not usually clot unless the hemor­rhage is acute. In addition, the supernatent will differ from serum if spun down in a

Figure 5.24 Image of a dog undergoing drainage of a pericardial effusion. The dog has been sedated with an opiate and a local anesthetic was used in the chest wall. Having obtained an echocardiographic image maximizing the depth of pericardial effusion, a fenestrated catheter is advanced under suction along the probe line until fluid returns. The catheter is then fed off the needle and a three-way tap attached. Echocardiography can be repeated to assess the amount of fluid remaining.

centrifuge. Once the drainage starts to decrease, echocardiography should be per­formed. The right heart should re-expand and the pericardial effusion be reduced sig­nificantly. The volume of the effusion can vary up to 2 liters depending on the size of the patient and speed of development. The ascites usually resolves in 24-48 hours and diuretics are not needed although the ascites will resolve faster if they are used.

Although the pericardial effusion should be submitted for cytology, it is rarely helpful. It is rarely possible to differentiate reac­tive mesothelial cells from mesothelioma. However on occasions the fluid is not a mod­ified transudate or lymphoma cells are seen. The common neoplasia do not exfoliate.

Reevaluation depends on the underlying cause. For idiopathic effusion, they can re­effuse after very variable intervals so repeat echocardiography may not be helpful. Instead, the owner should be vigilant for the clinical signs and return if they recur. Owners should be warned that there is a 50% chance of recurrence. However, if the effusion recurs, the owner should be advised that per­icardectomy should be performed as repeated drainage increases the risk of con­strictive pericardial disease. Pericardectomy should be curative in these cases. Neoplastic causes are likely to have more rapid recur­rence of clinical signs but again, treatment would only be performed if the effusion was causing clinical signs. Pericardectomy may be offered for control although this depends on tumor type. For chemodectomas which are relatively benign and slow growing, peri­cardectomy can offer prolonged survival times of up to 3 years. Surgical resection of the tumor is not usually possible. Hemangiosarcomas have a poorer prognosis and surgical resection may not prolong life although survival times of 7-8 months with resection and chemotherapy have been