Page 1023 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

998 CHAPTER 8

VetBooks.ir adequately, resulting in circulatory failure. The Clinical presentation
With acute left-sided heart failure the clinical signs
presence of circulatory failure alone does not nec-
essarily indicate heart failure, because other fac-
oedema, often with large volumes of frothy fluid
tors can produce evidence of circulatory failure. For are of respiratory distress and severe pulmonary
example, poor venous return secondary to a thoracic emanating from both nostrils. Chronic left-sided
mass may produce similar clinical signs. heart failure is often not obvious, as the lungs have
substantial lymphatic reserve and the oedema is
Aetiology/pathophysiology absorbed. Mild respiratory signs might initially be
A number of primary cardiac pathological processes attributed to respiratory diseases such as heaves.
may result in the development of heart failure. Weight loss is common. Tachycardia is almost always
Bacterial endocarditis, chordae tendinae rupture, present. The peripheral pulse may become weak.
cardiomyopathy, myocarditis, developmental defects Unsteadiness and syncopal episodes may develop.
and pericarditis are among the potential initiating Pulmonary venous pressures become increased and,
events. Right-sided heart failure may occur second- with time, the right side of the heart may become
ary to chronic respiratory disease, such as severe overloaded and clinical signs of heart failure become
small-airway disease. Pulmonary hypertension evident.
develops over time in response to alveolar hypoxia. Right-sided heart failure causes elevation of sys-
This eventually results in pressure overload of the temic venous pressure. Decreased cardiac output
right heart, which leads to failure. This condition is results in decreased renal blood flow and salt and
known as cor pulmonale. water retention. This increases body water content
Heart failure should be considered as a dynamic and, when combined with increased systemic venous
condition that is not necessarily present in the ani- pressures, peripheral oedema (Fig. 8.27) and venous
mal at all times. An animal with cardiac disease may engorgement result. Ascites, a common occurrence
have sufficient cardiac reserve such that no clinical during heart failure in small animals, is an uncom-
signs of heart failure are evident at rest. The same mon finding in horses.
animal may, at elevated heart rates, exceed its cardiac Decreased peripheral perfusion may result from
reserve and show signs of heart failure. left- or right-sided failure, therefore weight loss,
Concentric hypertrophy (muscular hypertrophy lethargy, renal or hepatic signs and diarrhoea may
without dilatation) is the typical response to pres- result. Dilatation of the atria often occurs in heart
sure overload, while eccentric hypertrophy (muscu- failure and AF is common.
lar hypertrophy combined with chamber dilatation)
is the typical response to volume overload and is Differential diagnosis
more commonly observed in the horse. • Acute left-sided heart failure: acute pneumonia,
Heart failure may be either acute or chronic. In anaphylaxis, pulmonary abscess rupture.
acute heart failure, the initiating event is sudden in • Chronic failure: other causes of emaciation
occurrence. Examples are acute severe blood loss (neoplasia, malabsorption), other causes of
leading to hypoxia, chordae tendinae rupture and car- peripheral oedema.
diac tamponade. Signs of acute left-sided heart fail- • Acute right-sided heart failure: overly aggressive
ure are primarily respiratory, due to acute pulmonary fluid therapy, particularly in neonates and in
oedema. Acute right-sided heart failure is vague and animals with compromised renal function.
peripheral oedema tends to develop over 3–4 days.
In chronic heart failure the underlying lesion will Diagnosis
have been present for weeks or even longer. Gradual Clinical signs are suggestive of heart failure but
decompensation occurs. Clinical signs are therefore are not diagnostic. Enlargement of the heart may
slower in onset. When compensatory mechanisms not be easily identified on thoracic radiographs. An
are overloaded, however, decompensation develops increased pulmonary interstitial pattern may be
rapidly. present but is non-specific.