References
Anaesthetic management of dogs with myxomatous mitral valve disease
Abstract
Myxomatous mitral valve disease is the most commonly acquired heart disease in the dog. Affected dogs have a reduced forward stroke volume as a result of the regurgitant flow back through the compromised mitral valve leaflets. Primary care practitioners will be all too familiar with the challenges of performing a general anaesthetic on these animals and unfortunately, there is no ideal protocol for every case. Having knowledge of the haemodynamic changes that occur with myxomatous mitral valve disease, compared to structurally normal hearts, as well as a good understanding of pharmacological effects of agents used in general anaesthesia, is essential in the safe management of these cases. This article will summarise disease pathophysiology, concurrent cardiac medications and commonly used pre-anaesthetic, induction and maintenance agents available in primary care practice for use in dogs with myxomatous mitral valve disease.
Myxomatous mitral valve disease (MMVD) manifests as degeneration of the atrioventricular valve of the left side of the heart. It is characterised by regurgitant blood flow travelling from the left ventricle back into the left atrium during ventricular contraction. This disease is the most commonly acquired heart disease in dogs, affecting approximately 1/30 dogs attending primary care practices in the UK (Mattin et al, 2015). As a degenerative disease, it is more prevalent in older dogs, with studies reporting that approximately 30% of dogs over 10 years of age are affected (Detweiler et al, 1961; Beardow and Buchanan, 1993).
This disease can be seen in any breed, but the highest prevalence is among small-to medium-sized dog breeds such as Cavalier King Charles Spaniels, Yorkshire Terriers, Dachshunds and miniature Poodles, with higher incidences observed in male dogs (Thrusfield et al, 1985; Beardow and Buchanan, 1993). The aetiology of the disease is not completely established, although a hereditary link is strongly suspected in some breeds (Swenson et al, 1996; Olsen et al, 1999). The disease has a long subclinical course, which may or may not progress to congestive heart failure (Borgarelli and Buchanan, 2012).
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