Today's Veterinary Practice

MAY-JUN 2018

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PEER REVIEWED 26 CE: CONGESTIVE HEART FAILURE IN CANINES Aldosterone can increase myocardial fibrosis and cell death. It also potentiates the sympathetic nervous system, increasing the heart rate, and decreases potassium, predisposing the heart to arrhythmias. Treatment of CHF in dogs can be divided into two phases: acute and chronic. ■ The acute phase is aimed at treating the congestion and supporting cardiac output. This is potentially more critical for left-sided heart failure, as pulmonary edema will result in dyspnea, and urgent treatment is needed to avert death. ■ The chronic phase of treatment involves the long-term management of stable, compensated CHF. The goals are to prevent recurrence of decompensation, control clinical signs, and slow progression of the disease. TABLE 1 provides an overview of treatment options for CHF. ACUTE TREATMENT OF CONGESTIVE HEART FAILURE It is important to appreciate that patients in acute CHF may have little reserve cardiorespiratory function. Treatment should be prompt, and further investigations may need to be minimized, pending improvement in the clinical condition. Diagnosis of Congestive Heart Failure While a cage-side echocardiogram (eg, assessment of left atrial size) can provide support for a diagnosis of CHF if needed, the stress of a full echocardiogram could further decompensate the patient without providing additional information. Thoracic radiographs often confirm the diagnosis of left-sided CHF but should be postponed if the patient is unstable ( FIGURE 1 ). Radiographic cardiomegaly can be documented, and the presence of an interstitial/ alveolar pattern centered on the perihilar region, consistent with pulmonary edema, confirms the diagnosis of CHF. While dilated pulmonary veins can be suggestive of left heart failure, in acute cases, it is not uncommon for these to be normal in size. The clinical signs and history can also help in increasing the clinical suspicion of CHF. Sympathetic stimulation associated with heart failure should cause tachycardia, while cough and crackles are nonspecific signs. For example, an 8-year-old Cavalier King Charles spaniel presenting with tachycardia, pulmonary crackles on auscultation, and a several-year history of a left apical systolic murmur with progressively increasing intensity could be considered likely to have developed CHF secondary to degenerative mitral valve disease (DMVD). However, an 8-year- old Cavalier King Charles spaniel with a recently documented quiet murmur that presents with crackles on auscultation, a heart rate of 90 beats/ min, and a cough is unlikely to be in CHF. First-Line Therapy Any dyspneic patient should initially be provided oxygen supplementation to increase tissue oxygenation. This can be achieved several ways. The most effective TABLE 1 Summary of Treatment Options for Congestive Heart Failure ACUTE TREATMENT FIRST LINE SECOND LINE LONG TERM Oxygen supplementation Furosemide Pimobendan Arterio dilators (eg, hydralazine) Dobutamine or dopamine Furosemide Potassium supplementation (if needed) CHRONIC TREATMENT STANDARD ADDITIONAL Furosemide Pimobendan ACE inhibitor (eg, enalapril, benazepril) Spironolactone Antiarrhythmic drugs (eg, mexiletine, sotalol, digoxin, diltiazem) Dietary modification Omega-3 fatty acid supplementation Carnitine and taurine supplementation

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