The message does not vary, by using one's bedside skills alone we can very elegantly define our patient's diagnosis. Not only the diagnosis, but often the severity of the lesion and its etiology. And this was clearly a care in point.
We started out by observing our patient's general appearance, their blood pressure, and the carotid arterial pulse and we found nothing abnormal. Those were normal, but when we got to the jugular venous pulse, the wave form of that jugular venous pulse provided us a clue to this patient's diagnosis. We didn't see the normally dominant "a" wave and smaller "v" wave, rather, we saw a slightly more prominent than normal "v" wave, so that it was equivalent to the "a" wave, maybe even slightly greater, and that sent us a clue, a message. Could our patient have a minor degree of tricuspid regurgitation, wherein this could be seen? Could our patient have an atrial septal defect? Why an atrial septal defect? Why, because when there is an atrial septal defect you basically have a common chamber - physiologically. So the pressures equilibrate across tham chamber, the left and the right and that means that the normally dominant "v" that is normally seen in the left atrium, gets transmitted to the right side and hence the more prominent "v" wave. A clue to the diagnosis.
Then we went to the chest wall, no apical impulse. Right away that says to us this patient could have an enlarged right ventricle. Why? Because the left ventricle is basically a behind ventricle, is a posterior ventricle, and when the right side is enlarged, it can push back the left ventricle. And that is what happened in our case, because we then felt the left parasternal edge and we felt a dilated pulmonary artery in the second interspace and the dilated right ventricle at the mid-to-lower left sternal edge, and those impulses were not sutained, as one would see in a pressure loaded ventricle, but rather they were dynamic, early in systole, as one would see in a volume loaded ventricle. Getting clues all along the way.
And auscultation really did pretty much define our diagnosis. We listened at the upper left sternal edge and the lower left sternal edge. Upper left sternal edge: well, the door was open to some differential possibilities when we focused and tuned in on the murmur. The murmur was systolic, it was short, crescendo-decrescendo and that could even be an innocent murmur due to flow. Or, it could be due to very mild pulmonary stenosis, remember it wasn't a very long murmur. Or it could be due to an atrial septal defect, again, excess flow early in systole. And when we listen to the second heart sound, we pretty much pinned down our patient's diagnosis. Because we did not heart normal respiratory variation. We did not hear normal width of splitting, we heard wide splitting and fixed splitting. Instead of the usual [sounds], no. We heard [sounds]. It was unyielding that is was fixed and wide. That essentially tells us our patient has an atrial septal defect. And then, an index of severity came. We listened at the lower left sternal edge, we focused on diastole, we heard [sounds] and that [sounds] is a diastolic flow rumble. That low frequency flow rumble at the lower left sternal edge is a result of excess flow across the tricuspid valve. Not only is the right atrium in a patient with a significant atrial septal defect receiving blood from the systemic veins, but also from the left atrium. Blood goes poring across that tricuspid valve and the result is a rumbling flow murmur.
So we have defined our patient's diagnosis - atrial septal defect; we have defined that it is big, it is severe, by virtue of the flow rumble and, of course, we know it is congenital because atrial septal defects are congenital.
One last little pearl. Sometimes, when the patient is lying, the second heart sound may seem fairly widely and even fixed split. By sitting, or better, standing them up, and reducing venous return, one often then does find out that the patient has in fact not really true fixed splitting. Our patient could have been put in any posture, our patient had wide, fixed splitting. Our patient has an atrial septal defect.
Key to diagnosis
The key to defining the diagnosis of an atrial septal defect in our patient was the recognition of the systolic outflow murmur across the pulmonary valve and wide, fixed splitting of the second heart sound. We also defined the size and severity of the defect by the company it keeps, including the mid diastolic murmur at the lower left sternal edge. Associated findings consistent with a large atrial septal defect included equally prominent jugular venous "a" and "v" waves and hyperdynamic parasternal impulses.