American Heart Journal
Volume 152, Issue 3 , Pages 417-419, September 2006

The blood pressure measurement—revisited

  • Michel E. Safar, MD

      Affiliations

    • Hopital Hotel Dieu, Paris, France
    • ,
  • Harold Smulyan, MD, FACC

      Affiliations

    • State University of New York, Upstate Medical University, Syracuse, NY
    • Corresponding Author InformationReprint requests: Harold Smulyan MD, Department of Medicine, State University of New York, Upstate Medical University, 750 E. Adams St, Syracuse, NY 13210.

Received 3 October 2005; accepted 20 March 2006. published online 30 June 2006.

Article Outline

 

The technique for the measurement of arterial pressure using the Riva-Rocci sphygmomanometer and the Korotokov sounds has been in use for >100 years, and its benefit to medicine and the care of patients has been inestimable. On the high side, the blood pressure (BP) makes the diagnosis of hypertension, assesses cardiovascular (CV) risk, and measures the effect of antihypertensive therapy. On the low side, it detects shock and severe circulatory disorders, whereas a wide pulse pressure (PP) predicts CV risk and contributes to such disparate diagnoses as anemia, thyrotoxicosis, and aortic insufficiency. The mean BP (MBP) can be calculated from the systolic BP (SBP) and the diastolic BP (DBP) by adding one third of the PP to the DBP. However, this is seldom used, probably because its lack of a clinical role and the annoying arithmetic involved.

Recently, a greater understanding of the physiologic underpinnings of the SBP, DBP, PP, and MBP have led to doubts about the accuracy and relevance of the brachial artery BP. These concerns are well known but grudgingly accepted in the absence of anything better. With regard to accuracy, the American National Standard for BP measurement, published by the Association for the Advancement of Medical Instrumentation,1 compared intra-arterial measurements with those obtained by the auscultatory method and found that for SBP, mean differences between the 2 methods ranged from 0.9 to 12.3 with standard deviations ranging from 1.3 to 13.0 mm Hg. For DBP, mean differences ranged from 8.3 to 18.0, with standard deviations from 1.1 to 9.3 mm Hg. Despite these weak comparisons, the auscultatory method is used by the American National Standard as the reference for the oscillometric automatic techniques because of the difficulty in obtaining intra-arterial values for validation. Validated or not, use of automatic methods has been spreading. They avoid the requirement for a stethoscope at home or for ambulatory BP recording and eliminate the mercury manometer that is gradually being phased out. It is also more convenient in hospitals, clinics, offices, and epidemiologic studies and avoids digit preferences, but has it own problems (see below).

Accuracy aside, another major issue is the relevance of the brachial artery BP for the assessment of CV risk. The major drawback of brachial arterial SBP or PP measurements is that they do not reliably represent central aortic pressure, and it is the central aortic pressure, against which the heart pumps, that is the important factor influencing the risk of heart disease and stroke. Large differences between brachial and central pressures are well described in youth, during exercise,2 and presumably also during stress testing. These differences can be explained by the details of arterial pulse propagation. After ventricular ejection, the pressure wave propagates through the arterial tree and is reflected from the peripheral resistance at reduced amplitude. The returning reflected wave then augments the oncoming primary pressure wave. The velocity of both forward and backward pulses depends largely on MBP and the distensibility of the conduit. Because distances from the heart vary, the summation of the forward and backward waves that produce the final SBP differs at each arterial site. Although MBP remains almost constant, and DBP decreases only slightly (<2 mm Hg) from central to peripheral vessels, the brachial artery SBP and PP may be 12 and 14 mm Hg greater than the aortic pressures. As the initially distensible central aorta stiffens with age, the aortic SBP and PP rise and the differences between aortic and brachial artery pressures become markedly reduced or even disappear. These inconstant relationships between central aortic and brachial artery pressure are of major importance for predicting CV risk and assessing antihypertensive therapy. Indeed the mechanical stress against which the heart pumps and the related CV mortality are determined by the local aortic, and not the distant brachial BP, where most measurements are made.

The inability to accurately estimate the central aortic pressure is a serious liability. It prevents an accurate prediction of left ventricular hypertrophy and its relief with antihypertensive therapy. Several therapeutic trials have compared different antihypertensive drug regimens producing the same reduction of brachial SBP and DBP, but significantly different effects on cardiac mass and/or CV mortality.3, 4 These differences suggest that similar drug-induced brachial BP reduction may be associated with different central BP reduction.5, 6, 7 Nitrates, angiotensin-converting enzyme inhibitors, and calcium entry blockers reduce central SBP and PP more than brachial SBP and PP.2, 5 Conversely, atenolol reduces MBP and DBP with little effect on central PP.6 This reduced effect of beta blockade on central pressures may have important therapeutic consequences.

A recent study8 showed that, at similar reductions in brachial artery MBP and DBP, an angiotensin-converting enzyme inhibitor/calcium channel blocker combination produced a greater reduction in LV mass than did a β-blocker. This result was best predicted from changes in the carotid artery PP (a surrogate for aortic PP), but not the brachial artery PP. The LIFE Trial3, 4 also showed similar reductions in brachial BPs with losartan and atenolol, but greater reduction in CV morbidity, mortality, and left ventricular mass with losartan. These results could be attributed to the salutary, but non–BP-lowering (pleiotropic) effects of angiotensin receptor blockade. However, mechanisms aside, at the same brachial artery pressures, losartan had a greater effect on central pressures than atenolol, illustrating that central PP is a more important clinical value than brachial PP.9, 10, 11 This makes an accurate, noninvasive measurement of central SBP and PP a worthy clinical goal.

Without placing a catheter in the central aorta, there are 2 paths toward the noninvasive estimation of central aortic pressure. The first is to calculate aortic pressures from peripheral arterial pulses. Because peripheral and central MBPs are the same, the second possibility is to accurately measure MBP at the brachial artery.

Central pressures can be calculated from noninvasive recordings of the carotid or radial artery pulses by applanation tonometry—the familiar method used to flatten the cornea for measurement of intraocular pressure. By similar flattening of the arterial wall, tonometry provides accurate pulse curves of the carotid or, the more easily recorded, radial artery, but unfortunately both radial and carotid pulses must be calibrated using brachial artery values. These calibrations are problematic because of the previously described inaccuracy of the auscultatory method. Several techniques using variations of these methods have been described, but they remain as yet unsuitable for widespread clinical use. Nonetheless, even the uncalibrated applanated radial pulse permits the calculation of the PP as a percentage of the MBP and, if the MBP were known, the actual radial PP could be calculated.

Mean BP, as well as PP, is a valuable predictor of CV risk and has the virtue of being unchanged throughout the arterial tree. However, MBP is not used widely because it must be calculated from the error prone auscultatory SBP and DBP. A possible solution lies in the measurement of the forearm MBP by oscillometry, where it is measured directly as the cuff pressure at maximum oscillation. Although the American National Standard1 has approved the clinical use of oscillometric SBP and DBP, their validation compared BPs to the auscultatory method because comparisons with direct intra-arterial data were sparse. However, the American National Standard has made no comparisons of the oscillometric and auscultatory MBP. There is another problem in that the accuracy and reproducibility of some oscillometric devices have been found to be unsatisfactory.12, 13 Those devices that are and are not recommended can be found at the Web site www.dableducational.com. Although conceptually attractive, the oscillometric MBP is affected by other factors including brachial arterial stiffness, inflated cuff volumes, irregular rhythms, and heart rate.14 SBP and DBP, by oscillometry, have already been used in several large studies,15, 16 but more validations of the oscillometric MBP must be made, comparing it with direct brachial artery and aortic pressures, before it can be introduced into future guidelines for the diagnosis and management of hypertension.

In conclusion, recognition of the limitations of the ausculatory BP method is growing. Aortic pressures would be an improvement over brachial artery pressures, but noninvasive techniques have either practical or theoretical disadvantages, limiting their usefulness as clinical tools. Applanation of the radial artery offers the possibility of PP measurement as a percentage of the MBP and MBP by cuff oscillometry may be the easiest first step forward. Manufacturers of oscillometric BP units should be encouraged to include MBP in their digital outputs and to press for further research to improve accuracy. However, the current widespread use of the auscultatory method has limitations that are becoming increasingly apparent. Oscillometric MBP measurements are practical and could easily be added to the clinical examination, but radial artery applanation requires some technical training and equipment for use in epidemiologic studies. These considerations underscore the importance of continuing efforts to develop and validate clinically acceptable methods that improve, or even eventually replace, the way we currently measure the BP.

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Addendum 

Since acceptance of this editorial, the CAFE trial results have been published showing that at similar brachial BP reductions, an Amlopidine regimen lowered central SBP and PP more than an Atenolol regimen and was associated with improved clinical outcomes.17

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References 

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PII: S0002-8703(06)00259-6

doi:10.1016/j.ahj.2006.03.016

American Heart Journal
Volume 152, Issue 3 , Pages 417-419, September 2006

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