The clinical signs of congestive heart failure (CHF) are a direct consequence of volume overload. A large regurgitant fraction is required before signs of congestive heart failure become apparent. With mitral incompetence, the rate at which progression occurs depends on the size of the regurgitant traction and also the compliance (distensihility) of the left atrium. In many cases signs of congestive heart failure will be accompanied by signs of low output failure, for example, cases of dilated cardiomyopathy where the signs of congestive heart failure are secondary to primary myocardial failure.
Left-sided congestive heart failure
The principal causes of left-sided congestive heart failure in the dog are acquired mitral valve incompetence (for example valvular endocardiosis or endocarditis), dilated cardiomyopathy (less frequently the hypertrophic form), congenital mitral valve dysplasia, aortic stenosis, ventricular septal defect and patent ductus arteriosus.
Interstitial or alveolar pulmonary oedema compounded by the presence of an enlarged left atrium impinging on the mainstem bronchi causes coughing, one of the early signs of left-sided failure. The cough may be more noticeable at night or first thing in the morning. Frequently the cough is paroxysmal with each bout terminating with the animal retching up phlegm or, in severe cases, flecks of blood. The animal may show exercise intolerance or may be overtly dyspnoeic. Severe pulmonary oedema may interfere with gaseous exchange and result in cyanosis of the mucous membranes especially with exertion. Some animals may become restless and have difficulty in breathing when lying down (orthopnoea).
Right-sided congestive heart failure
Disorders which may be associated with signs of right-sided congestive heart failure include pericardial effusion (cardiac tamponade), dilated cardiomyopathy, endocardiosis or endocarditis involving the tricuspid valve, dirofilariasis, cor pulmonale, congenital tricuspid valve dysplasia, pulmonic stenosis and cetralogy of Fallot. Increased right ventricular end-diastolic pressure and Increased central venous pressure may produce jugular distension. Hepatomegaly and less frequently splenomegaly may be evident; the former may be associated with portal hypertension, aseites and moderate increases in plasma alkaline phosphatase (ALP) and alanine aminotransferase (ALT) concentrations. The ascites always precedes subcutaneous oedema which may develop later during the course of the disease. Fluid, usually a modified transudate, may accumulate in the thoracic cavity (hydrothorax) and / or pericardial sac (hydropericardium).
Right-sided failure may occur secondary to left-sided failure. Pulmonary venous hypertension leads to an increase in pulmonary arterial and right ventricular end-diastolic pressures. The right ventricle hypertrophies in response to right ventricular pressure overload. Central venous and capillary hydrostatic pressures increase as the right ventricle becomes overloaded and signs of right-sided failure become apparent.
Not infrequently dogs with dilated cardiomyopathy (especially [hose in atrial fibrillation), pericardial effusion or ruptured chordae tendineae undergo acute decompensation and may present with signs of both left and right-sided congestive heart failure as well as signs of acute low output failure.
Causes and clinical signs of low output failure
Causes of low output failure include primary myocardial failure (for example dilated cardiomyopathy), decreased myocardial compliance (for example hypertrophic cardiomyopathy, myocardial fibrosis, pericardial effusion), hypovolaemia (for example acute haemorrhage), congenital cardiovascular shunts, severe valvular incompetence and tachy- or bradydysrhythmias. A marked reduction in preload, for example, obstruction to venous return by a large abdominal mass, ascitic fluid or the overzealous administration of diuretics to an animal with impaired myocardial Junction (particularly if the animal is already receiving a vasodilating drug) may significantly reduce cardiac output.
Low output failure may be classified as acute or chronic depending on the severity and rate of onset of clinical signs. Acute low output Lure is characterised by signs of tissue hypoperfusion and cardiogenic shock with collapse or syncope, weakness, recumbency or possibly even coma, pale mucous membranes (venous PO2<30 mm Hg in dogs) and a weak femoral pulse. Plasma urea and creatinine concentrations may be increased (prerenal azotaemia). The clinical signs of chronic low output failure may only become apparent with excitement or exercise. Typically the animal may experience episodes of exercise intolerance, weakness or collapse, the differential diagnoses for which include numerous metabolic, neuromuseular and central nervous system disorders.