Exercise Intolerance Secondary to Congestive Heart Failure
History. An 8-year-old female Great Dane has been diagnosed previously with idiopathic dilative cardiomyopathy. Severe, generalized cardiac enlargement was evident on thoracic radiographs.
The dog has been losing weight and is unable to complete daily walks with her owners.Clinical Examination. Femoral pulses are weak but regular at 140 beats/min. The mucous membranes are pale, and the capillary refill time is prolonged. Heart sounds are muffled, and a murmur is heard on the left side over the atrioventricular valve. Respiratory rate is greater than normal (45 breaths/min). Auscultation reveals increased bronchovesicular (respiratory) sounds. The abdomen is distended, and the abdominal organs are difficult to palpate. The electrocardiogram shows sinus tachycardia with broad, high-voltage QRS complexes. Thoracic radiography reveals a greatly enlarged heart and moderate pulmonary edema. Echocardiography reveals dilation of all four cardiac chambers. Ejection fraction is below normal, and there is mitral regurgitation.
Additional diagnostic tests are conducted to help assess the degree Ofcomplications secondary to the heart failure. The percentage saturation of hemoglobin in arterial blood is 78% (normal, 95%-100%), the difference in oxygen content between arterial and venous blood is 8.5 mL of O2 per deciliter of blood (normal, 4-6 mL), the serum creatinine concentration is 3mg∕dL (normal, reserves the available cardiac output for the heart and brain. The vasoconstriction is evident in the pale color and slow refilling of the mucous membranes. Renal vasoconstriction reduces the rate of urine formation. Urinary loss of salt and water is further reduced by the actions of ADH and the renin-angiotensin- aldosterone system. The urine that does form has a high solute concentration (high specific gravity). Metabolic products (e.g., creatinine) that are normally eliminated by the kidneys accumulate in the blood.
Salt and water retention increases blood volume above normal.Most of the excess blood volume is in the veins, so venous and atrial pressures are above normal. The elevated atrial pressure (preload) increases ventricular end-diastolic volume above normal, which helps the failing heart to pump a larger stroke volume than it otherwise would. However, the excessive volume and pressure of blood in the veins also cause systemic edema (distended abdomen caused by ascites) and pulmonary edema (visible on the radiograph). Pulmonary edema impairs the ability of the lungs to oxygenate blood. Therefore the hemoglobin saturation and the oxygen content of arterial blood are both below normal in this dog. The tissues of the body respond to the low rate of oxygen delivery by unloading as much oxygen as they can from the blood as it flows through the tissue. This makes the arteriovenous difference in oxygen content greater than normal. The general inadequacy of cardiovascular transport leads to poor gastrointestinal function and metabolic stresses on the tissues of the dog, and weight loss occurs.
Despite many compensatory mechanisms, this dog is unable to deliver a normal amount of well-oxygenated blood to the body tissues, even at rest. When the dog tries to exercise, cardiac output increases very little. Therefore, when exercise-induced vasodilation occurs in the exercising muscles and total peripheral resistance decreases, blood pressure falls dramatically. There is a further decrease in blood flow in the tissues of the systemic circulation that were already Vasoconstricted (e.g., mucous membranes), and these tissues become hypoxic and cyanotic. Inadequate blood flow in the exercising skeletal muscles leads to hypoxia and acidosis, and the dog collapses.
Treatment. The ideal treatment strategy for this dog is to improve the contractile performance of the myocardium. Theoretically, β-adrenergic agonists or cardiac glycosides could be administered to increase cardiac contractility.
However, currently available drugs are either ineffective or only mildly effective in dogs with severe, chronic heart failure. Therefore, treatment should emphasize symptomatic therapy, with the goals of controlling pulmonary congestion and improving cardiac output. Diuretics or Venodilators reduce venous pressures and are usually effective in controlling signs of congestion. They must be used cautiously, however, because they create the risk of lowering preload and therefore exacerbating the low cardiac output. Arteriolar vasodilators can augment the output of a failing heart by reducing the afterload (arterial pressure) against which the heart must eject blood. An appropriate initial treatment for this dog includes a diuretic (furosemide) and a cardiac glycoside (digitalis). If digitalis fails to improve cardiac contractility in this advanced case of cardiomyopathy, an arteriolar vasodilator (hydralazine) or a mixed vasodilator-Venodilator (enalapril) can be added to the furosemide regimen.Despite therapy, the prognosis for a dog with such severe, chronic heart failure is poor.