Page 1020 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

Cardiovascular system 995

VetBooks.ir serum biochemical profile. cTnI should be tested. some protection in acute cases via free-radical scav-
Elevations in CK and AST may be present on a
enging. Corticosteroids (dexamethasone 0.05–0.2
Hypocalcaemia and hypokalaemia may also be pres-
ent. Elevations in urea, creatinine and bilirubin have mg/kg i/v, i/m or p/o q24 h) may decrease the inci-
dence and severity of arrhythmias. Antiarrhythmic
been reported. therapy is indicated only if the arrhythmia is life-
Multiple arrhythmias may be noted on the ECG. threatening because it will have effects on cardiac
Electrocardiographic abnormalities are not consis- function. Digoxin is contraindicated if ionophore
tent, but signs of left ventricular volume overload toxicosis is suspected because of exacerbation of the
may be evident. Left ventricular functional indices effects of monensin.
are not consistently abnormal. Advanced cardiac
imaging may be of value in showing depressed func- Prognosis
tion of a portion of myocardium (tissue Doppler The immediate prognosis is dependent on the dose
imaging). ingested and the severity of clinical signs. Some
horses, especially those with high exposure, develop
Management severe clinical signs and have a grave prognosis for
No specific treatments are available. If contaminated survival. Multiple organ involvement also warrants
feed is suspected, an alternative source should be a poor prognosis. Myodegeneration and replacement
provided. Nasogastric administration of activated with fibrous tissue may lead to long-term abnormal
charcoal (0.75– 2 g/kg) or mineral oil (4 l/450 kg cardiac impulse conduction and the potential for
horse) may delay and decrease further absorption arrhythmias. Due to the potentially late onset of
if recent ingestion has occurred. Intravenous fluid clinical signs, the prognosis for exposed horses is
therapy is indicated in acute cases. Strict stall rest is guarded regardless of the initial clinical signs, espe-
of the highest importance. Vitamin E may provide cially for return to performance.

PERICARDIAL DISEASE

Congenital pericardial disease is very rare and loss syndrome. The pathophysiological mechanism
acquired pericardial disease is uncommon in the for pericarditis with this condition has not been
horse. Pericardial disease is usually caused by elucidated.
inflammation of the pericardial sac and pericarditis, As the volume of fluid within the pericardial sac
and is classified as effusive, fibrinous or constrictive. increases, so does the pressure within the pericar-
Benign pericardial effusion may be present during dial sac. When this pressure equals or exceeds that
disturbances of fluid homeostasis, such as congestive for the right heart, signs of right-sided heart failure
heart failure or hypoproteinaemia. ensue. Initially, compression of the right atrium
results in decreased venous return. Venous conges-
PERICARDITIS tion follows. As the pressure within the pericardial
sac increases, more pressure is required to fill the
Definition/overview right heart. Signs are more severe with sudden-onset
Pericarditis is inflammation of the pericardial sac. pericardial effusion because the pericardial sac does
not have time to stretch.
Aetiology/pathophysiology
The aetiology is usually unknown, and the condition Clinical presentation
is classified as idiopathic. Bacterial pericarditis may Tachycardia, a weak rapid pulse, muffled heart
occur. Neoplastic pericarditis is rare in the horse. sounds, venous hypertension, jugular vein distension
Fibrinous pericarditis was reported in mares dur- and ventral oedema are common. Peripheral perfu-
ing 2001 in association with the mare reproductive sion is decreased and, therefore, the extremities are