Which value measured in millimeters of mercury indicates normal pulse pressure

Noninvasive Measurement of Aortic Stiffness and Central Aortic Pressure by Pulse Tonometry.

Aortic stiffness is both the cause and the consequence of isolated systolic hypertension.56 The central aortic pressure waveform is the sum of the pressure wave generated by the left ventricle and reflected waves from the peripheral circulation. When the large conduit arteries are healthy and compliant, the reflected wave merges with the incident wave during diastole, which enhances coronary blood flow. When the conduit arteries become stiff (as in ISH), however, pulse wave velocity increases such that the reflected and incident waves merge in systole, thereby augmenting systolic rather than diastolic pressure, which increases left ventricular afterload and reduces diastolic coronary flow. Sphymocor (AtCor Medical, Houston, Texas) is a commercial device that uses brachial artery BP and a generalized transfer function (proprietary software) to convert the radial waveform, measured by applanation tonography, to a derived central aortic BP waveform (seeeFig. 46.1). This device has received FDA approval for clinical use (CPT code 93784). Pulse tonometry provides two principal measures of aortic stiffness that are typically increased in hypertension: pulse wave velocity and augmentation index.40 Recently, a 24-hour ambulatory central BP monitor has received approval for clinical use.

EFIGURE 46.6. Computed tomography showing a left adrenal mass (arrow) and nodularity to the right adrenal gland. Adrenal vein sampling confirmed the diagnosis of a left aldosterone-producing adenoma. IVC, Inferior vena cava.

Pulse Pressure

Pulse pressure is the difference between systolic and diastolic blood pressure. Pulse pressure can be easily assessed by the clinician and has significant predictive value in cardiovascular disease. Pulse pressure examines cardiovascular compliance—the ability of the arteries to vasoconstrict and vasodilate to circulate blood to properly meet activity demands. Pulse pressure is calculated by subtracting diastolic blood pressure from systolic pressure. With age there is a decrease in compliance of the aorta and small arteries, which leads to an elevation of systolic pressure and a decline in diastolic pressure, causing an increase in pulse pressure. Pulse pressure can also be elevated with exercise, aortic insufficiency, and atherosclerosis, and when a patient has an elevated intracranial pressure, whereas it will narrow in the presence of aortic stenosis, HF, and pericarditis. As pulse pressure widens, there is an increase in the incidence of cardiovascular disease. Generally, a normal pulse pressure at rest is approximately 40 mmHg. A study conducted by Weiss et al. found that an increased pulse pressure in very old hospitalized patients was a predictor of higher mortality,50 and therefore, when pulse pressure exceeds 60 mmHg, a medical referral should promptly be made.

Pulse-Pressure Variation

Fluid resuscitation is an integral piece of the management of patients with circulatory failure, though administration of the proper amount and rate of parenteral fluids can be challenging. Fluid responsiveness, or the ability of the left ventricle to increase stroke volume in response to fluid administration, is an emerging concept that helps to address this challenge.135 This concept is based on the physiology of the Frank–Starling curve and the knowledge that pulse pressure (systolic pressure minus diastolic pressure) is directly proportional to stroke volume. The variation in pulse pressure seen with the respiratory cycle, orpulse-pressure variation, reflects the magnitude of respiratory change on stroke volume. This is best demonstrated by the influence of mechanical ventilation on right ventricular preload. Studies have shown that a pulse-pressure variation of greater than 13% is highly predictive of fluid responsiveness in mechanically ventilated patients.136

Though many methods exist to assess fluid responsiveness, the standard method is done with passive leg raising (PLR). This “self-volume challenge” increases preload through translocation of venous blood from the lower extremities to the thorax. A patient who exhibits a rise of more than 10% in their aortic blood flow (measured with esophageal Doppler) or cardiac index (measured with thermodilution) is considered a “fluid responder,” which is indicative of the need for further fluid administration.135 This concept is becoming increasingly useful in optimizing the fluid management of critically ill patients.

Pulse Pressure and Risks for Cardiovascular Disease

Pulse pressure is defined as SBP minus DBP. In recent years, interest in pulse pressure as a risk factor for CVD has been intense. However, various investigators have struggled with how best to “anchor” the pulse pressure. For example, a patient with a BP of 120/70 mm Hg has the same pulse pressure (50 mm Hg) as a patient with a BP of 180/130 mm Hg, although the latter patient is clearly at higher risk for adverse events. Different investigators have anchored the pulse pressure to the DBP, the mean arterial pressure, and the SBP. As discussed earlier, Franklin and colleagues demonstrated that increasing pulse pressure was associated with marked increases in hazard of CHD for subjects with the same SBP.35 Chae and associates also found that pulse pressure was an independent predictor of HF in an elderly cohort, even after adjustment for mean arterial pressure, prevalent CHD, and other HF risk factors.43 In another study, Haider and colleagues observed that SBP and pulse pressure conferred similar risk for HF.44 However, other studies have found that SBP confers greater risk than pulse pressure, when SBP and pulse pressure are considered separately or as covariates in the same multivariable model.32 The Prospective Studies Collaboration, which pooled data from 61 large epidemiologic studies and nearly 1,000,000 men and women, found that the most informative measure of BP for prediction of CVD events was the mean of SBP and DBP, which was a better predictor than SBP or DBP alone and was much better than the pulse pressure.28 At present, JNC 7 recommends that clinical focus should remain on the SBP in determining need for therapy and achieving goal BP.1

Aging and Pulse Pressure

Both systolic and diastolic blood pressure are important.2c In industrialized societies, systolic blood pressure rises progressively with age; if individuals live long enough, almost all (>90%) will develop hypertension (Fig. 70-1). This age-dependent rise in blood pressure, especially systolic blood pressure, is not, however, an essential part of human biology. In less developed countries where consumption of salt and calories is low, blood pressure is lower and does not rise as much with age. In more developed countries, diastolic blood pressure rises until the age of 50 years and decreases thereafter, thereby producing a progressive rise in pulse pressure (systolic pressure minus diastolic pressure) (E-Fig. 70-1).

E-FIGURE 70-1. Aging and pulse pressure.

Schematic diagram showing the relation between aortic compliance and pulse pressure.

Different hemodynamic problems underlie hypertension in middle-age and older persons. Patients who develop hypertension before age 50 typically havecombined systolic and diastolic hypertension: systolic blood pressure140 mm Hg or higherand diastolic blood pressure 90 mm Hg or higher. The main hemodynamic problem is vasoconstriction at the level of the resistance arterioles. In contrast, most patients who develop hypertension after the age of 50 years haveisolated systolic hypertension: systolic blood pressure 140 mm Hg or higher but diastolic pressure below 90 mm Hg. In isolated systolic hypertension, the primary hemodynamic problem is decreased distensibility of the large conduit arteries. Collagen replaces elastin in the elastic lamina of the aorta, a process that is accelerated by both aging and hypertension. When pulse wave velocity increases sufficiently, the rapid return of the arterial pulse wave from the periphery augments aortic systolic pressure. The augmented systolic load on the left ventricle increases myocardial oxygen demand.

Pulse Pressure and Risks for Cardiovascular Disease

Pulse pressure is defined as the systolic minus the diastolic BP. In recent years there has been intense interest in PP as a risk factor for CVD. However, various investigators have struggled with how best to “anchor” the PP. For example, a patient with a BP of 120/60 has the same PP (60 mm Hg) as a patient with a BP of 150/90, although the latter patient is clearly at higher risk for adverse events. Different investigators have anchored the PP to the DBP, the mean arterial pressure, and the SBP. As discussed earlier, Franklin et al demonstrated that increasing PP was associated with marked increases in hazard of CHD for subjects with the same SBP.48 Chae et al also found that PP was an independent predictor of HF in an elderly cohort, even after adjustment for mean arterial pressure, prevalent CHD, and other HF risk factors.57 In another study, Haider and colleagues observed that SBP and PP conferred similar risk for HF.58 However, other studies have found that SBP confers greater risk than PP, when SBP and PP are considered separately or as covariates in the same multivariable model.45 The aforementioned Prospective Studies Collaboration, which pooled data from 61 large epidemiologic studies and around 1,000,000 men and women, found that the best measure of BP for prediction of CVD events was the mean of SBP and DBP, which predicted better than SBP or DBP alone, and much better than the PP.39 The recommendation of JNC 7 was that clinical focus should remain on the SBP in determining need for therapy and achieving goal BP.1

Mosley and colleagues compared the predictive utility of PP and other BP measures for diverse CVD outcomes (including hospitalizations and mortality from stroke, MI and HF) using long-term follow-up data from the Chicago Heart Association Detection Project in Industry.59 Baseline BP measures were assessed for predictive utility for fatal and nonfatal events over 33 years. Among 36,314 participants, who were a mean age of 39 years, 43.4% were women. In univariate analyses, hazards ratios for stroke death per one standard deviation of PP, SBP, and DBP, respectively, were 1.49, 1.75, and 1.71. Multiple metrics all indicated better predictive utility for SBP and DBP compared with PP. Results for CHD or HF death, and stroke, MI, or HF hospitalization outcomes were similar. PP had weaker predictive utility at all ages, but particularly for those younger than 50 years of age. Overall then, in this large cohort study, PP had predictive utility for CV events that was inferior to SBP or DBP. These findings tend to support the approach of current guidelines in the use of SBP and DBP to assess risk and the need for treatment.59

9 What does the term pulse pressure refer to?

Pulse pressure refers to the difference between systolic and diastolic blood pressure. Pulse pressure is also an independent predictor of cardiovascular complications. A wide pulse pressure is usually indicative of a noncompliant stiff aorta with a reduced ability to distend and recoil. During systolic ejection of blood from the left ventricle into the aorta and systemic circulation, the aorta does not distend, and the force of ejection is transmitted more forcefully into the peripheral vessels, causing an exaggerated systolic blood pressure level recording. During diastole, the elastic recoil of the aorta is more limited, contributing to a lower diastolic blood pressure. Thus a noncompliant aorta would increase systolic blood pressure and reduce diastolic blood pressure, resulting in a widened pulse pressure.

Pulse pressure and risk

Pulse pressure increases greatly after the age of 50 years as a result of arterial wall stiffening with the associated increase in SBP and fall in DBP. In older age groups in the Framingham study,13 coronary heart disease was found to be inversely related to DBP at any given level of SBP =120 mm Hg, suggesting that higher pulse pressure is as important, if not more so, than any other component of BP in predicting CHD risk (Figure 43-1). Pulse pressure was a better predictor than SBP, independent of DBP levels, for estimating the development of congestive heart failure (CHF); for each 10 mm Hg increase in pulse pressure there was a 14% increased risk of CHF, compared with a 9% increase for the same change in SBP.

Although SBP and PP are the best predictors of coronary heart disease, the same is not necessarily true for stroke. Mean arterial pressure has been found, in some studies at least, to be a better predictor of stroke than either SBP or PP. In the Systolic Hypertension in the Elderly Programme,14 a 10 mm Hg increase in PP was associated with a relative risk of stroke of 1.11 (1.01 to 1.22) compared with 1.20 (1.02 to 1.42) for a similar MAP rise.

The finding that PP is as good a predictor of coronary heart disease as SBP has potential implications for treating hypertension because there seems little point in lowering SBP and DBP to the same extent, (keeping PP unchanged) because this may contribute to maintaining some degree of CV risk. It would thus appear that, in elderly people, CHD events are more closely related to pulsatile load than steady-state components of blood pressure. This may explain why, overall, 30% to 60% of all CV events in the elderly population are attributable to mild or moderate hypertension.

CAVEATS IN EQUATING PULSE PRESSURE WITH CARDIOVASCULAR RISK

If PP is a surrogate for central artery stiffness, it is the stiffness that is the cardiovascular risk factor; strictly speaking, PP is a risk marker of stiffness. There are certain caveats to consider when using PP as a predictor of cardiovascular risk.

First, in middle-aged, healthy populations or older individuals with both systolic and diastolic hypertension, SBP and MAP may be equal or superior to PP as predictors of cardiovascular risk50–52; in this population, there is such high colinearity between SBP and PP that it often becomes impossible to show an advantage of one index over another in predicting risk. Only when SBP increases and DBP decreases, as described in most observational studies, does the superiority of PP over SBP as a predictor of cardiovascular risk become apparent in uncomplicated hypertension.

Second, with advanced age and after adjustment for cardinal risk factors, PP becomes an independent predictor of CHD risk. Therefore, despite the high colinearity between SBP with PP, the latter predominates as the single best predictor of CHD risk because of the contribution of pulsatile stress in a minority of subjects with discordantly low DBP values. It should be noted that the MAP equation (⅓ SBP + ⅔ DBP) grossly underestimates vascular resistance after ages 50 to 60 as DBP levels off and even falls.12 Hence, beyond middle-age, PP becomes a better predictor and the MAP a poorer predictor of cardiovascular risk. Paradoxically, the value or MAP has been highlighted with the recent publication of meta-analyses by the Prospective Studies Collaboration (PSC)53 and the Asian Pacific Cohort Studies Collaboration (APCSC),54 using 61 and 37 cohort studies, respectively. These investigators concluded that MAP, in both the young and old, was a far superior predictor of CHD risk than was PP. Their conclusions are in total disregard of the proven importance of arterial stiffness and early wave reflection as important risk factors in middle-aged and elderly individuals with ISH. A meta-analysis of a smaller number of well-performed, observational studies, rather than the multiple diverse studies included in the PSC and APCSC, might have provided a different picture of the importance of PP in predicting cardiovascular risk.

PP becomes an even stronger predictor of cardiovascular risk (1) when combined with a cluster of risk factors55; (2) in the presence of target organ damage, such as LVH56 or albuminuria57; (3) in association with diabetes58; and (4) in the presence of prior cardiovascular complications that lead to ventricular dysfunction.29–31

The totality of evidence supports PP as a surrogate risk marker for arterial stiffness, although at times an imperfect one. Despite high colinearity of PP with SBP, PP can be a more useful predictor of cardiovascular risk above and beyond the predictive power of MAP, SBP, or DBP. Clearly, these findings call into question the prevailing belief that elevation of SBP and DBP contribute equally to cardiovascular risk. However, there is as yet scanty evidence supporting the reduction of PP instead of SBP as a therapeutic goal. In addition, we have little information on the utility of using PP and SBP together, rather than SBP alone, to classify hypertensive risk. Furthermore, a public health recommendation that focuses on PP may detract from the importance of SBP in the diagnosis and treatment of hypertension. At present, it would be premature to modify current guidelines on the basis of prevailing data.

1 Abnormally Small Pulse Pressure

Since the pulse pressure depends on stroke volume, clinicians have tried for decades to use it as a way to quantify cardiac output. This relationship has been validated in one setting: patients with known left ventricular dysfunction. In these patients, the finding of a proportional pulse pressure less than 0.25 (proportional pulse pressure = pulse pressure divided by systolic pressure) detects a cardiac index less than 2.2 L/min/m2 with a sensitivity of 70% to 91%, specificity of 83% to 93%, positive LR = 6.9, and negative LR = 0.2.83,84

In contrast to conventional teachings, many patients with significant aortic stenosis have a normal pulse pressure (see Chapter 44).85 Chapter 70 discusses using changes in pulse pressure after passive leg elevation as a sign of volume responsiveness in critically ill patients.