Congestive heart failure in the ER Cheryl Trempala DVM, 3 rd Year Resident Speaker Notes On the

Transcription

1 Congestive heart failure in the ER Cheryl Trempala DVM, 3 rd Year Resident Speaker Notes On the This talk will be a discussion of the pathophysiology, approach to, and management of heart failure in the emergency setting. Pathophysiology of heart failure Heart disease and heart failure are two distinct problems. Heart disease is any structural abnormality of the heart that may or may not result in heart failure, whereas heart failure is a pathophysiologic state that occurs when the heart can t function at a level capable of meeting tissue needs or can only do so at elevated filling pressures. Our understanding of heart failure as a progression from asymptomatic heart disease to symptomatic heart failure has grown from a focus on biomechanical dysfunction to an emphasis on neuroendocrine dysfunction secondary to chronic biomechanical dysfunction. Systolic and diastolic dysfunction is the inevitable result of many heart diseases and activates many of the compensatory mechanisms. Chronic activation of compensatory mechanisms leads to congestive heart failure. Systolic dysfunction implies the hearts ability to pump blood in a forward direction is impaired, whereas diastolic dysfunction refers to an impaired ability to relax. Components of systolic function that can become impaired or dysfunctional include myocardial contractility, valvular competence, preload, afterload, and heart rate. Diastolic dysfunction is anything that limits relaxation or ventricular filling. Abnormal systolic and diastolic function can result in elevated venous and capillary pressures that lead to pulmonary edema and ascites We can talk about heart failure in a number of different ways, including myocardial, congestive, low-output, right and left heart failure. Myocardial failure refers to failure resulting from a defect in myocardial contractility, as might occur with dilated cardiomyopathy (DCM). Not all patients with heart failure, however, have decreased myocardial contractility. Congestive heart failure is a clinical syndrome, as opposed to a disease, where abnormal cardiac function results in the accumulation and retention of sodium and water with the resulting signs of congestion and edema. Most patients in heart failure develop systemic or pulmonary congestion because increased cardiac diastolic filling pressures result in elevated venous and capillary hydrostatic pressures with subsequent edema formation. Low-output failure occurs when cardiac function doesn t produce adequate cardiac output to maintain blood pressure and tissue perfusion. Right heart failure occurs when the right atrium or ventricle develops elevated filling 2011 DoveLewis Annual Conference presented by Butler Schein Animal Health Page 1

2 pressures associated with valvular insufficiency, pericardial disease, outflow tract obstruction or pulmonary hypertension. Right heart failure develops slowly because the systemic venous reservoir is large, and blood volume has to increase a lot to raise pressure. Left heart failure occurs when the left side of heart develops elevated filling pressures associated with valvular insufficiency, impaired contractility, or diastolic dysfunction. Elevated left ventricular filling pressures are transmitted to the left atrium and pulmonary venous and capillary beds, causing pulmonary edema. Pulmonary venous capacitance is relatively small, so small changes in blood volume or its distribution can cause a rapid rise in pulmonary venous pressure that leads to pulmonary edema The compensatory mechanisms that arise in response to heart disease are very important because these create the problems we see clinically and have important implications for our treatment strategies. Ideally, understanding the pathophysiology of the disease in question and of heart failure in general dictates treatment to manage the condition. The body responds to reduced cardiac output and tissue perfusion by retaining sodium and water to increase blood volume, heart rate and contractility, with a goal of increasing cardiac output. Generalized vasoconstriction also occurs in order to maintain blood pressure and perfusion of vital organs. Eventually compensatory mechanisms lead to excessive sodium and water retention and excessive vascular resistance. Compensatory mechanisms activated during congestive heart failure (CHF) include the Frank-Starling mechanism, the renin-angiotensin-aldosterone system, the sympathetic nervous system (SNS), myocardial hypertrophy, and other neuroendocrine mechanisms. The Frank-Starling mechanism is an adaptive mechanism where an increase in preload enhances cardiac performance (results in more vigorous contraction) by allowing muscle sarcomeres to function near optimal length, generating maximal contractile force. During heart failure, increased preload and ventricular end diastolic pressures are required to maintain cardiac output. This is problematic because when chronically active, increasing volume and pressure reach a point of diminishing returns and congestion and pulmonary edema can result The renin-angiotensin-aldosterone system (RAAS) helps maintain blood pressure and tissue perfusion despite reduced cardiac output. Decreased renal perfusion and sodium delivery, and sympathetic nervous system stimulation of beta-1 receptors and the renal juxtaglomerular apparatus cause renin release. Renin leads to formation of angiotensin II, further activates the SNS, and increases synthesis and release of aldosterone and anti-diuretic hormone (ADH). Aldosterone causes sodium and fluid retention, and promotes myocardial and vascular smooth muscle fibrosis. Angiotensin II also stimulates release of growth factors that promote vascular and myocardial remodeling. Vascular remodeling decreases vascular compliance and increases afterload. Myocardial remodeling results in pathologic hypertrophy and cardiac dysfunction. Sympathetic nervous system activity increases due to baroreflex stimulation and RAAS activation. Early SNS activation helps maintain cardiac output, blood 2011 DoveLewis Annual Conference presented by Butler Schein Animal Health Page 2

3 pressure and tissue perfusion via increased venous return to the heart and positive inotropic and chronotropic effects. Chronic activation results in sympathetic desensitization, beta receptor downregulation, and abnormalities in baroreceptor function. Chronic SNS activation overloads the heart by increasing venous return to an already volume overloaded heart, increasing myocardial oxygen consumption and damaging the myocardium. Hypertrophy is another way the heart can respond to dysfunction. Eccentric (volume-overload) hypertrophy allows the ventricle to pump approximately the normal amount of blood despite abnormal systolic function and is characterized by chamber dilation. Concentric (pressure-overload) hypertrophy is characterized by thickening of the ventricular walls in response to increased systolic wall stress. Increases in the thickness of the ventricular wall helps compensate for increased systolic wall stress. With increased myocardial mass, oxygen has to diffuse farther from capillary to mitochondria, leading to myocyte hypoxia, death and fibrosis. Finally, other neuroendocrine mechanisms also play a compensatory role. Endothelins regulate vascular tone and blood pressure. They are a vasoconstrictive agent with inotropic and mitogenic actions, and a strong stimulus for RAAS and SNS activation. Natriuretic peptides regulate salt and water homeostasis, and blood pressure, and have potential diagnostic and prognostic value. Brain natriuretic peptide (BNP) is primarily produced in the atria in response to stretch and results in natriuresis, diuresis, and balanced vasodilation. BNP antagonizes the RAAS and SNS, inhibits ADH release, prevents myocardial fibrosis and modulate cell growth and myocardial hypertrophy. Left heart failure Left heart failure results from the progression of many cardiac diseases, with hypertrophic cardiomyopathy (HCM), chronic mitral valve disease (MVD), and DCM being some of the most common. HCM in cats results in concentric or asymmetric left ventricular hypertrophy. The pathophysiology of HCM includes increases in wall thickness that reduces enddiastolic volume and cardiac output, and hypertrophy and fibrosis that increase left ventricular stiffness. Abnormal mitral valve motion and ventricular muscle changes distort the mitral valve and cause mitral regurgitation and an increase in left atrial pressure. Increased myocardial oxygen consumption and decreased perfusion damage heart muscle. Decreased myocardial relaxation and compliance leads to CHF by affecting diastolic function and filling. Impaired relaxation and compliance result in high diastolic pressures that lead to atrial enlargement, venous congestion, reduced stroke volume and cardiac output. Acquired primary valvular disease in dogs is usually degenerative in nature. Myxomatous degeneration of the mitral valve is the most common canine heart disease. The exact cause is still unknown, though the breed predispositions seen with the disease suggest a genetic component. Mitral valve degeneration results in regurgitation and progressive cardiomegaly because some of the left ventricular 2011 DoveLewis Annual Conference presented by Butler Schein Animal Health Page 3

4 stroke volume is ejected through the faulty valve and back into the left atrium. This increases the volume load on and the end-diastolic pressures of the left ventricle and atrium, leading to ventricular dilation and eccentric hypertrophy. High filling pressures cause pulmonary venous congestion, pulmonary edema, and heart failure. DCM is the most common form of canine cardiomyopathy and is characterized by progressive ventricular dilation and loss of myocardial contractility. DCM has an asymptomatic or occult phase during which it is difficult to identify the disease and a clinical phase with a high rate of CHF and sudden death in dogs with severe disease. History Cats with HCM often have no previous symptoms, and sudden decompensation without warning is possible. Cats may have history of weight loss, an unkempt appearance, tachypnea, dyspnea, sudden death, aortic thromboembolism (paralysis, pain, pulselessness, pallor, and firm gastrocnemius muscles). Age range of those affected varies between 6mo-19yrs. Sudden death may be due to arrhythmic, thromboembolic, or hemodynamic (eg. acute worsening of outflow tract obstruction) causes. Any cat can develop HCM, though certain breeds, like the Ragdoll and Maine Coon, are predisposed. Dogs more commonly have some historical evidence of heart disease. Certain breeds are more readily identifiable as associated with certain types of heart disease. For example, small breed dogs like Shih Tzu s and Cavaliers are most commonly affected by MVD, whereas larger breed dogs, like Dobermans and Great Danes, typically get DCM. Coughing, tachypnea, dyspnea, exercise intolerance, lethargy and weakness are common. Dogs may also have a history of inappetence, weight loss and syncope. Exercise intolerance can be an early sign of heart failure, but may only be noted in those animals that are active on a regular basis. Respiratory symptoms usually result from pulmonary compromise and include tachypnea, dyspnea, lethargy, exercise intolerance. LCHF in dogs tends to cause pulmonary edema, whereas in cats it can be associated with pulmonary edema and pleural effusion. Pulmonary edema stimulates receptors in the interstitium that reflexively increase the respiratory rate, thus making it an effective way to monitor the development and resolution of CHF. With regard to coughing, cats do not usually cough due to heart failure because they lack the receptors in their lower airways to detect and respond to edema with a cough. Dogs will frequently cough in association with heart disease, especially dogs with MVD. In dogs with MVD, a cough can arise from atrial compression of the mainstem bronchi or from pulmonary edema. It is also important to keep in mind that other diseases can make a dog cough, such as tracheal collapse, chronic bronchial disease, and pneumonia DoveLewis Annual Conference presented by Butler Schein Animal Health Page 4

5 Exam Common abnormalities on exam may include respiratory and cardiac abnormalities, mucus membrane changes, jugular distension, or signs of low cardiac output. The initial exam may need to be staged and prioritized due to patient distress, especially in cats. By the same token, not every animal needs to be sedated on presentation. Those animals whose distress and agitation is working against their efforts to breathe are prime candidates for sedation, but sedation is not necessary in a calm animal and may even be harmful due to reduction of respiratory drive. The patient can be observed carefully while waiting for initial interventions to have an effect. Animals with CHF will usually be tachypneic and may have expiratory or mixed respiratory effort patterns indicative of pulmonary edema, or rapid shallow breathing suggestive of pleural space disease. Cats with pleural effusion may have labored inspiration with inward abdominal movement during inspiration. Once the animal is more stable, blood pressure is best obtained using the Doppler method. This is more accurate than oscillometric methods, especially in small patients. Despite this, it may still be difficult or impossible to obtain a blood pressure in lowoutput states. Just as cats may have no historical signs of heart disease, they may also have normal physical exam findings and still have heart disease. Once they are in heart failure however, it is more common to hear a murmur and/or arrhythmia, crackles, muffled heart and/or lung sounds, and to see cyanosis, open mouth breathing, jugular distension, increased respiratory rate and/or effort, hypothermia, or hepatomegaly. Heart murmurs are frequently 2-4/6 left sternal systolic murmur originating from mitral valve regurgitation, aortic outflow tract obstruction, or systolic anterior motion of the mitral valve. It is important to keep in mind that a murmur may result from non-cardiac disease (stress, anemia, etc); there is a high prevalence of murmurs in healthy cats. Gallop arrhythmias are common due to stiff ventricles and atrial contraction signifying diminished ventricular compliance and high atrial pressures. A gallop more specifically identifies cats with heart disease than does a murmur. HCM should be a differential for any cat with a murmur or a gallop, but also should not, on its own, be an indication for empiric treatment. Dogs will frequently have heart murmurs when in heart failure, though this is not a specific finding for failure. Arrhythmias are also relatively common in dogs with CHF. Atrial fibrillation and ventricular arrhythmias are perhaps the most common arrhythmias in dogs with DCM and chronic MR. An S3 gallop is common in dogs with CHF from volume overload, especially dogs with DCM. Poor cardiac output causes weakness, exercise intolerance, fatigue, cold extremities, slow CRT, poor mucus membrane color, and hypothermia. Blood pressure may be low. Diagnostics, whether obtaining blood pressure or radiographs, or drawing blood, can greatly increase stress and result in acute decompensation of patients, especially cats. Consequently, patients should always be stabilized prior to performing diagnostics DoveLewis Annual Conference presented by Butler Schein Animal Health Page 5

6 Cardiac biomarkers NT-proBNP may be able to help discriminate between cardiac and non-cardiac causes of respiratory distress. Several studies have found that very elevated levels are consistent with heart failure as opposed to other causes of respiratory distress or systemic disease. There is, however, a fair amount of overlap between values for animals with and without cardiac disease and with some systemic diseases. Cardiac troponin I can be used to search for significant cardiac damage, especially in animals with severe cardiac arrhythmias where troponin concentrations may provide prognostic information. ECG ECG is a specific, but not a very sensitive diagnostic. Findings are variable, and may be normal, show patterns of heart enlargement, or demonstrate arrhythmias. Continuous ECG monitoring helps better assess animals with syncope, collapse, severe systemic disease, arterial embolism, and CHF. Continuous ECG allows for monitoring arrhythmias over time, tracking responses to treatment, and identifying problems such as reperfusion injury. Heart rate changes can indicate change in disease condition or trends that might result in arrest. Thoracic radiographs Thoracic radiographs in cats may reveal cardiomegaly, but the concentric nature of the hypertrophy can result in a normal appearing heart, despite the presence of significant disease. Many cats with left atrial enlargement also have pulmonary arterial and venous distension on the DV. Tortuous pulmonary veins returning to the left atrium from the caudal lung lobes may also be evident. Edema may manifest as an increased interstitial pattern that coalesces into an alveolar pattern as CHF worsens. This often develops ventrally or is distributed into multifocal, patchy areas of edema rather than the more classic dorsal distribution seen in dogs. Pleural effusion may be seen in association with hepatomegaly and caudal vena cava enlargement. Thoracic radiographs in dog may reveal left-sided or generalized cardiomegaly and pulmonary venous congestion. Interstitial edema may manifest as a diffusely increased radiopacity of the lung fields due to increased interstitial opacity. The margins of the pulmonary vessels may be indistinct as a result of perivascular edema. When fluid enters the alveoli, a coalescent alveolar infiltrate results along with air bronchograms. Pulmonary vascular margins are frequently obscured. The alveolar pattern associated with pulmonary edema in the dog can be asymmetrical, with the right lungs affected more than the left. Echocardiography Echocardiography is a valuable diagnostic tool in both cats and dogs. It is helpful for evaluation of anatomic information, congenital abnormalities, myocardial abnormalities, functional information, indirect chamber size and wall thickness, direct fractional shortening and Doppler information. Multiple M-mode and 2- dimensional views are used so regional changes are not missed DoveLewis Annual Conference presented by Butler Schein Animal Health Page 6

7 Echocardiography is the most sensitive means of diagnosing heart disease in cat. It is the gold standard in diagnosis of heart disease because cats can have substantial cardiac wall thickness changes without marked radiographic changes. HCM is characterized by left ventricular concentric hypertrophy without chamber dilation. The left ventricular lumen is typically small. Left atrial enlargement is common and may be the site of spontaneous echo contrast ( smoke ) or a thrombus. Mitral regurgitation is common and SAM of the mitral valve occurs in approximately 1/3 of HCM cats. If outflow obstruction is present due to SAM, it is called hypertrophic obstructive cardiomyopathy (HOCM). Echocardiography is similarly valuable in the canine patient, but may not be required for definitive diagnosis. Echocardiography provides more specific and definitive information regarding the size of cardiac chambers and indicators of systolic and diastolic dysfunction. Cardiac ultrasound in the ER is also a great tool, does not require being a cardiologist to answer a few important questions, and can frequently be performed with little to no patient stress or restraint. Some of the key questions to answer include the presence of pleural effusion, pericardial effusion and, depending on user comfort and experience, size of the left atrium, size and subjective function of the left ventricle and the size of the right heart. Treatment Initial treatment should focus on patient stabilization. Oxygen support should start immediately and rapid initial patient observations and exam should be performed to localize the problem and establish whether CHF is suspected as the primary cause of respiratory distress. If the patient will allow, try to obtain vascular access as soon as possible. Minimize stress during any patient manipulations to minimize the risk of acute decompensation. Sedation may be helpful in patients who are so distressed they are working against their efforts to breathe and actually increasing their oxygen needs and the effort required to breathe. Opiods +/- benzodiazepines are effective sedation options that have minimal negative effects on the cardiovascular system. If intubation is necessary due to fulminant CHF and imminent decompensation and arrest, a rapid acting IV anesthetic should be used, like ketamine/valium, etomidate, or propofol. Propofol is a highly hypotensive agent and should be used sparingly, if at all if other appropriate options are available. Ketamine has the potential to exacerbate cardiac instability in HCM cats and should be avoided in these cases if possible. The primary goals of treatment are to improve quality of life (exercise capacity and comfort at rest) and increase survival time if quality of life is acceptable to the owner. Thus, treatment aims to prevent edema and effusion, and to increase cardiac output. These goals are generally accomplished by improving pump function, resolving congestion, and reducing the work of the heart though a combination of medications, supportive care and procedures DoveLewis Annual Conference presented by Butler Schein Animal Health Page 7

8 Thoracocentesis can be life-saving and diagnostic for moderate to large volume effusions. Thoracocentesis can usually be accomplished with use of low dose diazepam and butorphanol, +/- a local block. While it is helpful to remove as much effusion as possible, it is not necessary to remove all of the pleural fluid to see a clinical improvement. If patient compliance or stability limits handling, even modest fluid removal can help improve and stabilize respiratory status. The mediastium is fenestrated, so it is not very important how much fluid is obtained from one side relative to the other. After initial thoracocentesis, it is usually best to try to mobilize remaining fluid with cardiac medications rather than rely on repeated thoracocentesis. Furosemide is a loop diuretic that reversibly inhibits the sodium/potassium/chloride co-transporter in the thick ascending loop of Henle. Furosemide causes a significant contraction of intravascular volume, creating the conditions necessary for pulmonary edema to shift across the alveolar membrane and back into circulation. High doses (2-4mg/kg IV q 1-2hrs) may be required initially with acute severe pulmonary edema. A furosemide CRI between 0.1-1mg/kg/hr can also be used and may have a superior diuretic effect and fewer electrolyte derangements. Pimobendan is a calcium sensitizing drug useful as a positive inotrope, as well as having phosphodiesterase inhibitory properties that result in vasodilation. Pimobendan is rapidly absorbed from the GI tract, usually within 1-2hr, making its rapid onset of action useful in the ER setting. Common doses in chronic CHF range from mg/kg divided BID. Pimobendan improves quality of life in dogs and cats with CHF and may prolong survival in those with DCM. Nitroglycerin acts as a nitric oxide donor to create vasodilation. Venous, arterial and coronary vasodilation contributes to both the clinical benefits and side effects. A typical dose is 1/8-2 transdermally. The efficacy of transdermal administration in setting of CHF is controversial due to questionable absorption in action in patients that are often hypothermic and hypoperfused. Common side effects include hypotension, weakness, and lethargy. Diltiazem is a calcium channel blocker with primarily negative chronotropic effects and very weak vasodilatory actions. It is used primarily for rapid SVT or for slower or non-sustained SVT when seen in association with CHF. Ideally, treatment should aim to control CHF while antiarrhythmic and rate control drugs are started. Diltiazem can be given IV as a 0.25mg/kg IV slow bolus over 5-10min. Subsequent 0.25mg/kg boluses can be repeated at 15 min intervals until heart rate improves or a maximum dose of 0.75mg/kg is reached. Side effects include bradycardia, hypotension, and cardiovascular collapse. Side effects are more likely when diltiazem is given rapidly IV or used in combination with sotalol or other beta blockers. Lidocaine is Class Ib sodium channel blocker that slows ventricular conduction velocity, rate and force of contraction. It is used in the treatment of ventricular arrhythmias. Initial doses are usually given as boluses of 2-4mg/kg IV. If 2011 DoveLewis Annual Conference presented by Butler Schein Animal Health Page 8

9 arrhythmia improves, a CRI is required to maintain therapeutic concentrations. CRI rates vary from mg/kg/min. Signs of toxicity may be neurologic, gastrointestinal or cardiac. Amlodipine is a long acting calcium channel blocker with primarily vasodilatory actions used to reduce total peripheral resistance. It is most useful in reducing preload and afterload, and in treating hypertension. It tends to have fewer GI side effects than ACEI s due to its slower onset of action. Amlodipine can be used carefully in the setting of heart failure to reduce preload and afterload by titrating the dose and continuing other treatments until clinical improvement is noted. Blood pressure must be normal to high in order to safely use this drug and reduce the risk of hypotension. Hydralazine is a direct-acting arterial vasodilator used to reduce afterload in the setting of heart failure or added to treatment with an ACEI and amlodipine for refractory hypotension. Hydralazine is very rapidly acting, and can result in clinical hypotension if not used carefully. Doses range from mg/kg IV. Blood pressure should be normal to high and patients should be very closely monitored while small doses are titrated to effect. Nitroprusside is a nitric oxide donator that results in primarily arterial, but also venous, vasodilation. It is extremely potent and usually reserved for treatment of severe, decompensated, refractory CHF associated with MR or DCM under very close monitoring. Mean arterial blood pressure should be maintained higher than 65mmHg, and direct arterial pressure monitoring is ideal. Dosage range is 2-10ug/kg/min in a fluid volume equal to 1/16-1/8 maintenance needs for 12-48hrs. Combination therapy with dobutamine, digoxin, and/or pimobendan, and diuretics has the best effect. Hypotension, tachycardia, nausea and vomiting are the most common side effects. Dobutamine is a sympathomimetic agent used in the setting of CHF and lowoutput failure to help improve cardiac output and forward blood flow. Dobutamine CRI s can be adjusted up from 2.5ug/kg/min at 2.5ug/kg/min increments until signs of improved cardiac function appear, such as increased blood pressure, warm limbs, improved mm color and CRT, decreased respiratory distress. Typical effective dose is 5-15ug/kg/min in dogs. Heart rate increases > 20% above baseline and rates > 190 or arrhythmia formation dictates dose reduction. Dogs on beta blockers are not good candidates for dobutamine use. Side effects include tachycardia, arrhythmias, and GI distress. Positive inotropes are typically not indicated in the HCM patient due to concern for worsening LVOT obstruction or drug related increases in heart rate that negatively impact diastolic function. ACEI s, like enalapril and benazepril, are frequently used in chronic heart failure, but benefits are not usually seen in the ER setting. Once patients are eating and can tolerate oral medication, however, an ACEI can be started. ACEI have been shown to prolong time until refractory heart failure or death occurs in dogs with MVD and DCM. These drugs have also been shown to reduce pulmonary edema 2011 DoveLewis Annual Conference presented by Butler Schein Animal Health Page 9

10 and improve quality of life and exercise capacity. While not yet demonstrated in dogs, ACEI s can prevent pathological remodeling and slow progression of heart disease in humans. There are fewer studies investigating the effects of ACEI prior to the onset of CHF, but they do seem to show a trend towards overall benefit. Spironolactone is an aldosterone antagonist and potassium-sparing diuretic used in combination with ACEI s and furosemide. Aldosterone antagonism may have a cardioprotective effect by reversing and inhibiting myocardial and vascular fibrosis. Studies in humans have shown that when spironolactone is added to convention therapy, mortality decreases. In dogs, initial studies suggest that the addition of spironolactone to conventional cardiac therapy with ACEI and furosemide +/- digoxin reduced the risk of severe worsening of MR and cardiac-related death and euthanasia. Dosages rage from 1-2mg/kg BID. Digoxin inhibits sodium-potassium-atpase in the sarcolemma, increasing intracellular calcium, and resulting in positive inotropic effects. It also has vagolytic effects that slow conduction through the AV node. Digoxin is used for rate control with SVT s, myocardial failure and chronic heart failure, and can be administered IV or po. Intravenous and rapid oral loading pose an increased risk of toxicity and is usually not necessary. It is usually sufficient to start treatment at the low end of a chronic oral dose of mg/kg po BID. Studies in dogs with atrial fibrillation and high ventricular rates indicate that superior rate control is achieved when digoxin is combined with diltiazem, versus when either agent is used alone. Sotalol is a potassium channel blocking drug with Class II (beta blockade) and Class III effects, though the Class III effects (delayed action potential phase 3 repolarization that results in prolongation of the action potential and refractory period) tend to predominate. It is used to treat ventricular and supraventricular arrhythmias. While its beta blocking activity is quite weak, a slight decrease in contractility and sympathetic compensation for CHF can occur, and dosages should be titrated carefully and used only with very careful monitoring. Dosage is 1-2mg/kg po BID. Clopidogrel is an antiplatelet drug used to try to prevent thromboembolic disease. Cats with cardiac disease and left atrial enlargement are candidates for use. Clopidogrel reduces platelet activation, degranulation, and inhibits modification of GP IIb/IIIa receptor, which leads to reduced aggregation. Clopidogrel is typically well tolerated, though reportedly approximately 20% of cats foam at the mouth. Daily dose 18.75mg/cat. Most animals start to look better clinically in hours. If a patient is not improving, or worsening during this time, both the diagnosis and treatment strategy should be reassessed. In general, dyspnea signals an ongoing need for heart failure treatment and indicates hypervolemia is present (though there can be a lag between diuretic administration and improvement in dyspnea). Once dyspnea is improving, the furosemide dose should be quickly and dramatically reduced DoveLewis Annual Conference presented by Butler Schein Animal Health Page 10

11 Right heart failure Right heart failure is a less frequently seen than left heart failure. Right heart failure results when the right atrium or ventricle develop elevated filling pressures secondary to valvular disease, pericardial disease, outflow tract obstruction or pulmonary hypertension. When the right ventricle is volume and pressure overloaded, hepatic congestion, ascites, pleural effusion and peripheral subcutaneous edema can result. Right heart failure can also lead to poor forward blood flow into the pulmonary circulation and, thus, the left heart, resulting in reduced stroke volume, cardiac output and, potentially, low-output failure. The most common cause of RCHF seen in the ER is pericardial effusion and cardiac tamponade. Other causes of RCHF include pulmonary hypertension, and tricuspid or pulmonic valve regurgitation or stenosis. History, clinical signs and exam findings arise from pericardial or pleural effusion, ascites, or peripheral edema. In general, patients with pleural effusion will be tachypneic and dyspneic, with dull lung sounds. Animals with ascites with have a distended abdomen and may also have respiratory difficulty. Jugular and abdominal subcutaneous veins may be distended when ascites is associated with right heart failure. In less severe fluid overload or right heart failure, the cranial abdomen (liver) can be gently compressed and the jugular vein observed. If there is a brief rise and then fall back to the original location, then the finding is normal. If there is a sustained rise in jugular pulsation, then either RCHF or fluid overload is imminent. Treatment usually involves management of CHF as discussed previously, thoracocentesis for pleural effusion, abdominocentesis if the volume is sufficient to place pressure on the diaphragm and impair ventilation. Patients with pericardial effusion may have abdominal distension from ascites, respiratory distress from pleural effusion, weakness, lethargy, or collapse. Exam usually reveals tachycardia, dull heart sounds, and, possibly, pulsus paradoxus (reduced pulse pressure during inspiration). Jugular distension and pulsation, abdominal distension with a fluid wave, and dull lung sounds due to pleural effusion may also be noted. ECG may show sinus tachycardia with decreased complex size +/- electrical alternans. Radiographs show an enlarged cardiac silhouette and distension of the caudal vena cava. Pleural effusion and metastatic pulmonary disease may also be present. A rapid thoracic ultrasound can confirm pericardial effusion. Cardiac tamponade is evident when there is collapse of the right atrium. Coagulopathy should be ruled out with PT/aPTT or similar diagnostics. Routine bloodwork may reveal hyponatremia and hypokalemia secondary to increased ADH secretion and reduced renal perfusion that occur in response to a low effective circulating volume. Pericardial effusion most commonly results from neoplasia, with hemangiosarcoma, lymphoma, mesothelioma and heart base tumors being the most common etiologies. Other causes include idiopathic, coagulopathic, inflammatory or infectious pericarditis, restrictive pericarditis, atrial rupture, and traumatic etiologies. Small volume pericardial effusion can occur with CHF, and is fairly common in cats. Treatment involves pericardiocentesis and volume expansion 2011 DoveLewis Annual Conference presented by Butler Schein Animal Health Page 11

12 with crystalloids. Diagnostic yield is usually very low, but pericardial fluid should be submitted for analysis in the event infectious organisms or exfoliated neoplastic cells are identified. Patients remain at risk of re-effusion at any time, depending on the underlying cause. Pericardiocentesis can be performed in lateral or sternal recumbency. Clip the right hemithorax (going on the right side helps avoid laceration of coronary vessels), block and aseptically prep between the 3 rd and 8 th ICS, from sternum to costochondral junction. Use the 4 th or 5 th ICS and long (5cm) large bore (18-16g) catheter to access the pericardial space. Use continuous ECG monitoring while advancing the catheter toward the heart, watching for fluid. Once pericardial fluid is obtained, advance the catheter over the needle into the pericardial sac and remove as much fluid as possible. Complications include coronary artery laceration, ventricular arrhythmias, and exsanguination into pleural space. Pulmonary hypertension is another cause of RCHF seen in the ER. Pulmonary pressure is usually low in relation to systemic circulation, with mean pulmonary pressures averaging <15mmHg and a systolic pressure of < 25mmHg at rest and <30mmHg during exercise. Elevated pulmonary pressures can result in syncope, weakness and fatigue, and ultimately RCHF. Echocardiography can be used to identify PHT and estimate severity based on tricuspid regurgitation and Doppler velocity of the tricuspid regurgitation. If moderate to severe PHT is present, then sildenafil and/or pimobendan may be helpful. Sildenafil is started at 1mg/kg TID and titrated up to 3mg/kg TID. TID administration is usually best. References available upon request 2011 DoveLewis Annual Conference presented by Butler Schein Animal Health Page 12