Ideally, the BP should be measured after the patient has rested comfortably for at least 5 minutes (caffeine, exercise, and smoking should have been avoided for 30 minutes) sitting in a chair, with feet on the floor.12 The examiner’s chair should be arranged so that the patient’s right arm is always and inevitably presented for recording the BP. The arm should be abducted, slightly flexed, and supported by a smooth, firm surface. If the arm is unsupported, the BP may be elevated by as much as 10-12 mmHg due to added hydrostatic pressure induced by gravity. The brachial artery over which the BP is to be recorded should be at a level with the heart (Figure 4).12
A deflated cuff should be applied snugly around the right arm. The lower edge of the cuff should be 2-3 cm above the antecubital fossa. The radial pulse should be palpated and the rate noted. The compression cuff should then be inflated until the radial pulse disappears. The palpated radial pulse obliteration pressure should be used to estimate the SBP. In preparation for the auscultatory determinations the cuff is deflated, the brachial artery is palpated, and the bell of the stethoscope is applied lightly but snugly over it in the antecubital fossa to produce an airtight seal. The cuff is then rapidly inflated to about 20-30 mmHg above the estimated SBP, determined previously by the palpatory method, and then deflated at a rate 2-3 mmHg per second. SBP is the point at which the first Korotkoff sound is heard (onset of phase 1), and the disappearance of Korotkoff sound (onset of phase 5) is used to define DBP (Figure 5).12
Changing patterns of BP occur with increasing age. The rise in SBP continues throughout life. In contrast, the DBP rises until about age 50, then levels off over the next decade, and may remain the same or fall later in life. DBP is a more potent cardiovascular risk factor than SBP until age 50; thereafter, SBP is more important.12 The pulse pressure reflects the numerical difference between the SBP and the DBP. The “hammering” or “pounding” effect of elevated pulse pressure (noted when palpating the radial artery) damages arterial walls, contributes to arteriosclerosis, and leads to target-organ damage. The pulse pressure closely correlates with the SBP and is a reliable cofactor that provides further evidence of significant cardiovascular disease.