Chapter 5 Pathophysiology of heart failure
The term heart disease refers to any abnormality of the heart; whereas the term heart failure refers to a clinical syndrome characterized by congestion and oedema and/or poor peripheral perfusion, either at rest or with exercise. If heart failure is severe enough to produce a marked reduction in cardiac output, systemic hypotension may be present also (cardiogenic shock). However, cardiogenic shock is rare in veterinary patients. Congestive heart failure (CHF) is a more specific term that refers to heart failure with congestion of one or more vascular beds. Although heart failure is the result of severe heart disease, heart disease may be present that does not lead to heart failure.
MECHANISMS OF HEART FAILURE
Heart failure is a clinical syndrome that can be caused by a variety of etiologies and mechanisms. The most common haemodynamic mechanism responsible for heart failure in horses is volume overload caused by valvular regurgitation or by a left to right shunt. However, myocardial systolic failure (reduced contractility) is also recognized in horses and may lead to heart failure. Less commonly heart failure is the result of impaired diastolic function as a result of inadequate cardiac filling in horses with pericardial disease.
Regardless of the etiology or mechanism of heart failure, CHF is associated with two primary haemodynamic abnormalities: (1) increased ventricular filling pressures and (2) reduced cardiac output. Increased ventricular filling pressures are responsible for signs of congestion and oedema; whereas reduced cardiac output causes clinical signs of inadequate tissue perfusion. The haemodynamic abnormalities and resulting clinical signs that characterize heart failure are illustrated using ventricular function curves in Figure 5.1.
Figure 5.1 A ventricular function curve (Starling curve) from a normal animal (top curve) and from an animal with myocardial systolic failure (bottom curve). The dashed vertical line in the centre represents the upper limit of normal preload (normal ventricular filling pressure). The dashed horizontal line represents the lower limit of normal cardiac output. A horse with valvular regurgitation (volume overload) and normal myocardial contractility is likely to have an operating point on the upper curve and will, therefore, have either no clinical signs or signs of circulatory congestion (oedema). However, a horse with valvular regurgitation and reduced contractility is likely to have an operating point in the lower right quadrant of the graph. Thus, a horse in this situation is quite likely to have clinically apparent oedema in addition to signs of hypoperfusion.
Horses with left-sided failure have increased left ventricular filling pressures and subsequently increased left atrial and pulmonary venous pressures leading to pulmonary oedema. Thus, clinical signs may include tachypnea, dyspnea, coughing, haemoptysis and the appearance of frothy white or blood-tinged fluid at the nostrils. Horses with right-sided CHF have increased right ventricular filling pressures and subsequently increased right atrial and systemic venous pressures leading to peripheral oedema. Subcutaneous oedema in the dependent areas such as the ventral abdomen, the prepuce and the distal extremities is the most common manifestation of increased right-sided filling pressures. Jugular venous distension and pulsation may also be present. In horses, an increase in left-sided filling pressure frequently stimulates pulmonary vasoconstriction and pulmonary vascular remodelling, changes that result in secondary right-sided heart failure. Thus, in some horses, systemic oedema and jugular distention may be the first clinical signs of chronic left-sided heart disease. Reduced cardiac output causes clinical signs referable to poor tissue perfusion, namely fatigue, weakness, exercise intolerance, cold extremities, prolonged capillary refill and hypothermia. With the exception of exercise intolerance and fatigue, these signs are not likely to become apparent until heart failure has become severe. Laboratory evidence of reduced cardiac output includes reduced venous oxygen tension in patients that are not hypoxaemic or anaemic as well as azotaemia and lactic acidosis if cardiac output is markedly decreased. ( AF, PC, VMD)