Our patient has hypertension and that hypertension is significant, not just significant by the numbers - although surely the level of pressure we determined was impressive - but significant because the thorough physical examination we carried out together determined that this patient's hypertension is having an effect on his circulation.

We first determined the blood pressure, but immediately looking for possible complications or secondary causes, palpated the peripheral vessels and we found no support for those complications or secondary causes of hypertension. Then we evaluated the carotid arterial pulse and the jugular venous pulse and they were normal. But then, when we palpated the chest wall, we found something compelling. We found unequivocal evidence that this patient has left ventricular hypertrophy, non-displaced but enlarged apical left ventricular impulse. And when we analyzed the contour of this apical impulse we found even more compelling evidence for left ventricular hypertrophy because, we not only found that that impulse was sustained throughout systole, but we palpated a presystolic movement, and that presystolic movement, the palpable equivalent of an audible fourth heart sound, is telling us that the left ventricular hypertrophy, or thickening, from hypertension is significant enough that when the left atrium goes to push blood in presystole into that thickened, hypertrophied, less compliant ventricle, vibrations are set off because of that lack of compliance and this can be appreciated at the bedside as a palpable fourth sound.

And then we listened to the patient. Upper right sternal edge: an expected finding - not just [sounds] - an enhanced second sound due to aortic closure, because of the higher closing pressure in the aortic root. And then, normal splitting of the second sound at the upper left sternal edge. And finally, at the apex, confirmation of what we palpated, an expected finding [sounds] light pressure on the bell bringing out that low frequency fourth heart sound.

So, the physical examination in our patient went so far beyond just defining our patient has hypertension. We defined that it has had an effect on the patient's circulation and we did not define any specific serious complications or secondary causes. The bedside examination has been of enormous help to us in our patient.