5.5.3 Clinical diagnosis
VSDs in the semi-membranous part of the septum are usually associated with a characteristic loud plateau-type murmur. The point of maximal intensity (PMI) is on the right side of the chest, just above the sternum in the apex beat area (Figure 5.2). A palpable thrill is frequently present. The murmur may radiate to the left side of the chest. The murmur can be confused with that of tricuspid regurgitaalthough it is usually much louder and harsher and the PMI is slightly more ventral. If a significant left to right shunt is present, there may also be a functional ejection-type murmur heard over the pulmonary valve area at the left base related to the increased volume and velocity of blood flow into the PA. This is termed a murmur of 'relative' pulmonary stenosis.
Frequently, auscultation of the characteristic murmur will be the only sigclinical finding, but in some animals other abnormalities will be noted. The second heart sound may be markedly split due to the late closure of the pulmonary valve and early closure of the aortic valve which can result from the changes in effective stroke volume. A very loud second heart sound may be heard in animals with pulmonary hypertension, and a loud third heart sound may be related to volume overload of the LV. A brisk arterial pulse may be present in animals with moderate sized VSDs but without myocardial failure; a weak arterial pulse may be palpated in animals with more severe haemodynamic changes. CHF may develop in some cases. Sudden death has been reported in some animals with a VSD and is likely to be a result of rupture of the PA or malignant arrhythmias.
The murmur of a VSD may be less loud in animals in which there is pressure overload of the RV, thus the loudest murmurs are not necessarily the most sigSub-pulmonary VSDs have a PMI over the left base rather than the right apex. VSDs in the muscular septum have a variable PMI and radiation depending on their exact location. In some cases, a murmur of aortic regurgitation (AR) will also be associated with a VSD due to the effect of the defect on the aortic root. This results from prolapse of a cusp of the aortic valve, usually the non-coronary cusp, into the potential space created by the defect, resulting in regurgitant flow through the valve.