Congestive heart failure (CHF)
The heart is unable to maintain circulatory equilibrium at rest and congestion of venous circuit takes place followed by dilatation of vessels, edema of lungs and enlargement of the heart. Congestive heart failure may be of either left side or right side depending on which ventricle is most affected.
Etiology: Diseases of pericardium, endocardium or myocardium in which there is interference with the blood flow cause CHF. Congenital valvular defects, valvular insufficiency or stenosis, obstruction to aortic or pulmonary valves also result in the congestive heart failure. Myocardial asthenia due to anoxia, toxemia and foot-and- mouth disease also causes this disease.
Pathogenesis: When increased load is placed for the ejection of blood from the heart or contractibility of myocardium is reduced, heart rate is increased as a compensatory mechanism. Dilatation of heart takes place to maintain the cardiac equilibrium. Cardiac reserve is reduced and the patient is not able to cope up with this load. The animal may be normal at rest but there is poor exercise tolerance. Edema develops due to increased hydrostatic pressure in the venous system. Due to anoxia there is tissue damage followed by leakage of plasma protein into the tissues. Right side failure causes involvement of kidneys and liver. Urine output is reduced due to reduced blood flow to the kidneys and plasma protein escapes in the urine. Pulmonary edema is seen in left side heart failure. However, congestive heart failure of one side leads to failure of the other side.
Clinical signs: (i) Left side congestive heart failure - There is increase in respiration and depth of respiration. Moist rales, cough, dyspnoea and cyanosis are also seen. There is murmur on auscultation of heart and heart rate is increased. (ii) Right side congestive heart failure is associated with signs of edema, anasarca, ascites or hydrothorax. There is enlargement of liver. Superficial veins are dilated while urine flow is reduced.
Diagnosis: Blood pressure is increased and the blood flows with high pressure when jugular vein is punctured. Changes in electrocardiogram are also noticed. Protein may be present in the urine. Estimation of lactose dehydrogenase (LDH), triglycerides and lipid profile are also valuable in its diagnosis.
Treatment: The cause of the disease may be ascertained before any treatment is given to the animal. The demand on cardiac output can be reduced by minimizing activity of the patient. If there is edema, salt should be restricted. Diuretics may be administered to reduce fluid accumulation. Venepuncture and withdrawal of 4 to 5 ml of blood/ kg body weight have been suggested as an emergency treatment in pulmonary edema. Drugs like digitalis or quabain can be administered to increase contractibility of myocardium. Dosage should be regulated according to the principle of digitalization. Paracentesis is tried for draining the fluids from the peritoneal cavity with caution that large volume of fluid should not be evacuated as it may lead to shock.