Incidental murmurs are common in small animals, particularly in young dogs or dogs that may be subjected to high-stress environments,1,2 and determining whether a grade I/VI to grade III/VI systolic murmur is pathologic (ie, structural cardiovascular lesion is present) or nonpathologic (ie, functional or innocent murmur) based on auscultation alone can be difficult. Guidelines are available to help determine the best approach for treating these murmurs.3,4 Criteria such as a murmur that can be heard at all times (at rest or with activity), that is loud through the majority of systole, that is diastolic or continuous in nature, that is grade III/VI or higher intensity, or that is accompanied by abnormal heart sounds (eg, gallop rhythms, split heart sounds, clicks, arrhythmias) is more likely to be pathologic in nature as compared with a murmur that is characterized as soft, focal, or short or with a systolic murmur that is softer or absent at rest, which is more likely to represent a nonpathologic murmur. Localization of the point of maximal intensity, timing, and grade of the murmur in conjunction with patient signalment can help either heighten or decrease the concern for any potential underlying cardiovascular disease. A grade II/VI murmur in a young healthy golden retriever, as in this patient, could represent a functional murmur or indicate a lesion such as mild SAS. Even if mild SAS is present, it is unlikely to substantially impact the lifespan and health of this patient.5,6 More important clinical implications arise in patients being considered for breeding.
SAS is a common obstructive congenital heart defect in large-breed dogs, with a strong prevalence in golden retrievers.7 Hereditary transmission is suspected via an autosomal recessive trait.8 Dogs with moderate-to-severe SAS are at an increased risk for arrhythmias, sudden death, infective endocarditis,9,10 and other complications (eg, congestive heart failure [CHF]).5
Anesthetic considerations for cardiac disease are best determined via echocardiography to evaluate the severity of the cardiovascular lesion and secondary chamber enlargement, cardiac function, and fluid tolerance. General recommendations and anesthetic goals for patients with underlying structural cardiac disease include maintaining heart rate and limiting vasodilation. Extreme fluctuations in heart rate and blood pressure should be avoided. Tachycardia and hypertension should be avoided in patients with aortic stenosis, as there are fewer cardiovascular reserves and these extremes may worsen myocardial work against a fixed obstruction.
It is important to maintain adequate preload and optimize ventricular filling in patients with SAS or other underlying disease processes that can impair ventricular compliance (eg, hypertrophic cardiomyopathy). Inappropriate preload or volume contraction can contribute to myocardial oxygen deficit, which may precipitate arrhythmias. Cardiac output for these patients can be highly dependent on heart rate; thus, bradycardia can result in a significant decrease in cardiac output. Cardiac output is a product of heart rate and stroke volume. Alternatively, tachycardia can result in decreased coronary artery perfusion.
The use of certain drugs that can alter hemodynamics and/or precipitate arrhythmias should be avoided, including α2 agonists (eg, dexmedetomidine), ketamine (due to increased myocardial oxygen demand), acepromazine, and anticholinergics (unless indicated for bradycardia).11 Because patients with SAS have an increased risk for endocarditis due to blood flow turbulence and endothelial damage, prophylactic antibiotics (eg, cefazolin) are recommended intraoperatively. Although there is no evidence-based medicine to support that postoperative antibiotics are necessary, their use is common among some cardiologists, in part due to the difficulty of treating endocarditis if it develops and the serious sequelae that may result (eg, acute CHF, immune-mediated disease [eg, glomerulonephritis, polyarthritis], thromboembolic disease, arrhythmias). Endocarditis can result in permanent damage to the cardiac valves, causing significant regurgitation, and is difficult to treat due to the relatively avascular composition of the heart valves. Therefore, antibiotics are sometimes administered intra- and postoperatively if there is a concern about an increased risk for endocarditis; it may be easier (and less costly) to prevent endocarditis and/or prophylactically treat it with antibiotics as compared with treating the endocarditis itself. Antibiotics should not be administered to every patient; the cardiologist should discuss with the pet owner the degree of risk for the development of endocarditis and determine appropriate antibiotic use based on the severity of the lesion.