We next proceed to physical examination, beginning with the pulse and arteries, and passing on to the heart and associated structures. The characters of the præcordial impulse--particularly the seat of the apex-beat and the strength of the impulse--are closely (I might almost say laboriously) investigated. We must never yield to the temptation to disregard weakness or absence of the impulse. Like many other negative signs it is apt to be overlooked. Then the præcordial dulness is mapped out by means of light percussion. Finally, auscultation reveals to us the presence or absence of murmurs and the characters of the sounds--in the standing and recumbent postures, and, if necessary, after a little exertion. The relative loudness of the first and second sounds over the different parts of the præcordia is particularly worthy of note. Now let us suppose that we have found a mitral systolic murmur. We ask ourselves whether it is structural or whether it is functional, that is, due to relaxation and dilatation of the ventricular walls. If structural, with which (if any) of the diseases elicited in the man's previous history would it correspond? Most probably with gout or glycosuria. Thus we attempt to connect the lesion with its cause, and the cause with its effects, and have reached the ultimate diagnosis. So with other valvular murmurs: for example, an aortic diastolic murmur proves to be related to syphilis. If there be no murmur audible, we naturally think of dilatation with failure, or of enlargement from strain, from Bright's disease, from arterial sclerosis, from emphysema, from an insufficient or impure blood-supply in the coronary arteries, from disordered innervation, or from some rarer cause, such as adherent pericardium; and then, with these associations in our minds, we review once more the patient's history, and generally succeed in our diagnosis.